Abdominal Wall Hernias

Springer Science+Business Media, LLC

Robert Bendavid, MD Jack Abrahamson, MD Maurice E. Arregui, MD Jean Bernard Flament, MD Edward H. Phillips, MD Editors

Abdominal Wall Hernias Principles and ManagelIlent Foreword by Raymond c. Read, MD Preface by Rene Stoppa, MD With 738 Figures, 46 in Full Color

Springer

Robert Bendavid, MD Toronto, Canada Jaek Abrahamson, MD Haifa, Israel Mauriee E. Arregui, MD Indianapolis, IN, USA Jean Bernard Flament, MD Reims, Franee Edward H. Phillips, MD Los Angeles, CA, USA

Library of Congress Cataloging-in-Publication Data Abdominal wall hernias : principles and management / editors, Robert Bendavid... [et all. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4612-6440-8 ISBN 978-1-4419-8574-3 (eBook) DOI 10.1007/978-1-4419-8574-3 1. Hernias-Surgery. 2. Hernias-Pathophysiology. I. Bendavid, Robert. [DNLM: 1. Hernia, Ventral. 2. Abdomen-pathology. 3. Abdomen-surgery. 4. Surgical Procedures, Operative. WI 955 A135 2000] RD621 .A193 2000 617.5'59----dc21 00-020620 Printed on acid-free paper. © 2001 Springer Science+Business Media New York Originally published by Springer-Verlag New York, Inc. in 2001 Softcover reprint of the hardcover 1st edition 2001 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use of general descriptive names, trade names, trademarks, etc., in this publication, even if the former are not especially identified, is not to be taken as a sign that such names, as understood by the Trade Marks and Merchandise Marks Act, may accordingly be used freely by anyone. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein.

Production coordinated by Chernow Editorial Services, Inc., and managed by Steven Pisano; manufacturing supervised by Jacqui Ashri. Typeset by Matrix Publishing Services, Inc., York, PA. 9 8 765 432 1 ISBN 978-1-4612-6440-8

SPIN 10750916

This book is dedicated, with love, to the memory of my first and most important teacher, my father. He was always there. R.B.

A powerful idea communicates some of its power to the man who contradicts it. MARCEL PROUST, 1919-In Search of Lost Time Who shall decide, when doctors disagree? ALEXANDER POPE,

1732-Epistle III: Of the Use of Riches

We are usually convinced more easily by reasons we have found ourselves than by those which have occurred to others. BLAISE PASCAL, 1670-Pensees He that will not apply new remedies must expect new evils; for time is the great innovator. SIR FRANCIS BACON, 1625-Essays 1597-1625; "On Innovation" The certainties of one age are the problems of the next.

R.H.

TAWNEY,

1926

Don't limit a child to your own learning, for he was born in another time. Rabbinic saying

Foreword

Herniology, during the latter part of the twentieth century, had become transformed by the realization that most abdominal defects in the adult are not predetermined by anatomic anomalies. Rather, they relate to connective tissue damage brought about by abnormal collagen metabolism, secondary to extended longevity, cigarette smoking, or impaired genetic expression. Surgeons now recognize that sutured repairs under tension are liable to give way sooner or later. Fortunately, bridging with prosthetic mesh has repeatedly been shown to be well tolerated and successful when the interposition is firmly anchored. The introduction of laparoscopic placement has led to the competitive development of minimally invasive open techniques which, by reducing postoperative pain, hasten recovery. The herniologist has emerged as a specialist, supported by a dedicated staff and clinic facilities, with a professional society and journal. Two of the heroes who, with their gold standard, led the way were the Shouldices, father and son. Therefore, it is fitting that this, the first new text of the third millenium, is edited by one of their colleagues. Robert Bendavid took a sabbatical year to write this book, with the help of his peers from around the world. Although educated in Canada, he was born overseas, and is multilingual. This skill has helped him edit the many foreign contributions in the light of his own enormous clinical experience. Robert, despite his promotion of the "Modern Bassini," has already put together an internationally recognized text on prostheses and abdominal wall hernias. He is well known for other original contributions-fletching and umbrella prostheses for groin defects, parapubic herniation, dysejaculation after hernia surgery, nomenclature, and a new understanding of the transversalis fascia. He has been a mainstay at international conferences on herniae during the past 15 years and has contributed 25 chapters to the textbooks of other editors. The text itself, as is expected from such a leading scholar in the field, encompasses all the new information that has so recently become available. It begins with history, anatomy, epidemiology, and pathology. Extensive documentation of new biomaterials is followed by adjuncts to surgery, techniques of repair, plastic surgery, emergencies, and pediatrics. The female hernia patient is followed by the elderly, incidental pathology, sports injuries, and ventral defects. Finally, complications are dealt with, along with unusual herniae and medicolegal aspects. It is a wonderfully fresh product that will serve as a point of reference for years to come. Dr. Bendavid and his co-editors have taken much time and trouble to provide us with a statement of what is known around the world today regarding herniology. Hopefully, this gift will enable us to better serve humanity. RAYMOND C. READ Little Rock, Arkansas, USA

Preface

It gives me particular pleasure to present the compilation Abdominal Wall Hernias: Principles and Management. One would not expect anything of less substance and quality from a textbook edited by Robert Bendavid, at the fateful start of the third millennium. Since Ephraim Chambers's and Denis Diderot's encyclopedic works, compilations such as this call for the collaboration of many experts, whose participation is obtained by virtue of the editor's own noteworthiness, unremitting work, and expertise in the subject. Is not every editor compelled to do better than his rivals in a strongly competitive field? This has been done-in the opinion of the most exacting among them. The coauthors have reconsidered all the accepted classics in the light of more recent additions, in accordance with the editor's plan. The necessary chapters on fundamentals begin with the historical evolution of some of the main themes of surgery, as seen by surgeons themselves. Then, by way of update, comes the discussion of the many techniques commonly used in surgery of the abdominal wall, some already established, others-more recent-still in the process of being evaluated. Prostheses have a significant legitimate place, for they have experienced a remarkable upsurge and are used not only in recurrent hernias and burst abdomens, but also very considerably in primary treatment. Laparoscopic surgery of hernias-a seductive product of high technology-was another item to be tackled with particular attention among the methods being currently evaluated. Thus, should readers wish to review a standard technique or one of its details, they will find it, more often than not, described by its inventor in this book. Should they be confronted by particular cases of rare hernias or exceptional circumstances, surgeons will be able to find exhaustive and up-twate information on these less familiar problems. Certain matters rarely approached in detail have also been notably considered, such as abdominal wall surgery for patients with ascites, for athletes, the obese, women, the elderly, even for the futuristic surgeon-the intellectual disciple of Jules Verne-technologies yet to be invented, in which robots will perhaps make their appearance, technologies to be welcomed cautiously and on the condition that they bring true benefit to the patient and to society. This book is a successful achievement, a tribute to the vitality of the surgeon of the abdominal wall. Remarkably illustrated, and with unvarying precision throughout, the work serves well its double purpose: to help readers to acquire fundamental, indispensable principles for up-twate understanding of abdominal wall pathology and to enhance their ability to make good choices of tactics or techniques, whatever the situation. This is the best one can ask for. Everyone knows that a consensus is unlikely, at present or in the near future, on the problem of the treatment of hernias. This question cannot be resolved solely by the contribution of scientific proofs, because it has "sociological" elements derived from the diversity of the many people concerned (the surgeons and their patients) and from the polymorphism of the lesions. One can promise that Abdominal Wall Hernias: Principles and Management will fulfill the ethical obligation to further the teaching of abdominal wall surgery and the control of its quality. This remains essential to this day. The 1998 Inquiry of the National Union of the Medical Press and Health Professionals in France revealed that written documents are the primary source of information in continued medical education, ahead of conferences and meetings. xi

Preface

xii

A book like this one must therefore have the support of many readers, as indeed one must hope it shall. But then, a simple glance at the table of contents is enough to disclose the difference between this and other comparable books, a difference in favor of the present work, which must take its place within reach of every surgeon's hand. These few words are thus no more than a deliberately brief preface to the feasts prepared for the satisfaction of the reader. RENE STOPPA

Amiens, France

Introduction

As we begin a new millennium, it seems fitting that a publication on hernias should meld the acquired knowledge and wisdom on the subject to constitute a state-of-the-science address-a century-ending statement before starting a new surgical period. This much has been attempted. The versatility and speed of today's communications have brought more than 120 surgeons from 16 countries into a futuristic "surgical village" dotted with satellite dishes and antennas. The abundance of scientific information has been difficult to contain, but an effort has been made to include all current concepts, theories, practices, operations, prostheses, and even gadgets: so much so that inclusion should not be construed as a recommendation, which brings to mind a quote from Sir Maximillian Beerbohm, "It distresses me, this failure to keep pace with the leaders of thought, as they pass into oblivion!" Foremost in my thoughts was an attempt to remain above controversy, to avoid bias, and to allow a generous exposure to all participants. To that end, I have to apologize for the elimination of certain chapters when authors were too opinionated too early, but also unshakeable in their attitude and presentation. The existence of an European Hernia Society and now the American Hernia Society has made it imperative that both sides of the Atlantic be given an even role in the elucidation of the hernia diathesis. This I feel was fairly accomplished. This book was made possible thanks to the generosity of each contributor who shared his time and knowledge. I know also that for some it meant a sacrifice. For that, I am grateful, and many readers will express the same feeling. My hope is that the result will meet with their warm approval. ROBERT BENDAVID

Toronto, Ontario, Canada

xiii

Contents

Foreword by Raymond C. Read ................................... ix Preface by Rene Stoppa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi Introduction ................................................ xiii Contributors ................................................ xxv

Part I History 1 Evolution and Present State of Groin Hernia Repair . . . . . . . . . . . . . . . . 3 RENE STOPPA, GEORGE E. WANTZ, GABRIELE MUNEGATO, AND ALFONSO PLUCHINOTTA

2 Use of the Preperitoneal Space in Inguinofemoral Herniorrhaphy: Historical Considerations ................................... 11 RAYMOND C. READ

3 Prostheses in Hernia Surgery: A Century of Evolution .............. 16 JAMES

DEBoRD

4 Evolution of Laparoscopic Hernia Repair ....................... 33 KARL LEBLANC AND RALPH GER

Part II Anatomy 5 Anatomy of the Abdominal Wall . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 JEAN BERNARD FLAMENT, CLAUDE AVISSE, AND JEAN FRANQOIS DELATTRE

6 Aponeurotic Hernias: Epigastric, Umbilical, Paraumbilical, Hypogastric . . . 64 OMAR M. ASKAR

Tribute to Omar M. Askar by John E. Skandalakis

7 Surgical Anatomy of the Inguinal Region from a Laparoscopic Perspective . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 RICCARDO ANNIBALI, ROBERT

J. FITZGIBBONS, JR., AND THOMAS QUINN

8 Fascial Anatomy of the Inguinal Region ........................ 86 JONATHAN D. SPITZ AND MAURICE E. ARREGUI xv

xvi

Contents

9 The Ligaments of Cooper and Thomson ....................... 92 J.P. RICHER, J.P. FAURE, M. CARRETIER, AND JACQUES BARBIER 10 The Transversalis Fascia: New Observations ..................... 97 ROBERT BENDAVID

The Space of Bogros and the Interparietoperitoneal Spaces ........ 101 J. HUREAU

Part III Epidemiology 12 Epidemiology of Inguinal Hernia: A Useful Aid for Adequate Surgical Decisions ....................................... 109 ALEJANDRO WEBER, DENZIL GARTEIZ, AND SALVADOR VALENCIA

13 Occult Hernias in the Male Patient ........................... 116 SAM G.G. SMEDBERG AND LEIF SPANGEN

14 Quality Control and Scientific Rigor .......................... 122 ERIK NILSSON AND STAFFAN HAAPANIEMI

Classification of Inguinal Hernias ............................ 128 V. SCHUMPELICK AND K- H. TREUTNER Commentary: An IDF Classification? IYy Robert Bendavid 130

Part W

Pathology

16 Mechanisms of Hernia Formation ............................ 133 JACK ABRAHAMSON

17 Metabolic Aspects of Hernia Disease . . . . . . . . . . . . . . . . . . . . . . . . .. 139 RAYMOND

C. READ

18 Pathological Tissue Changes and Hernia Formation .............. 143 ALAIN PANS

19 The Role of Collagen in Hernia Genesis ....................... 150 LARS NANNESTAD JORGENSEN AND FINN GoTTRUP

20 Recurrent Herniation: Etiology and Mechanisms

156

JACK ABRAHAMSON

Respiratory Pathophysiology and Giant Incisional Hernias ......... 166 GIOVANNI TRIVELLINI AND PIERGIORGIO DANELLI

Commentary IYy Robert Bendavid

172

Undescended and Cryptorchid Testes ......................... 173 M. HUTSON AND SUZANNE HASTHORPE Commentary by Robert Bendavid 178

JOHN

23 Testicular Atrophy ............................. :......... 179 ROBERT M. ZOLLINGER, JR. Commentary IYy Robert Bendavid 182

xvii

Contents

24 Unexpected Findings in Inguinal Hernia Surgery

184

ENRICO NICOLO

Soft Tissue Infection and Loss of Abdominal Wall Substance

....... 192

RONALD T. LEWIS

Part V Biomaterials 26 Biochemistry, Immunology, and Tissue Response to Prosthetic Material ....................................... 201 SUSANNE K. WOLOSON AND HOWARD P. GREISLER 27 Biomaterials: Structural and Mechanical Aspects of Prosthetic Herniorrhaphy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208

RJ. MINNS AND M.I.A. SELMIA

Biomaterials Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221 NIR KOSSOVSKY, CHARLES J. FREIMAN, AND DAVID HOWARTH

Carcinogenicity of Implantable Biomaterials .................... 235 B. KLOSTERHALFEN,

U. KLINGE, AND V. SCHUMPELICK

30 Suture Selection for Hernia Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . 237 PHILIP B. DOBRIN

Use of Fibrin Glues in the Surgical Treatment of Incisional Hernias ..................................... 246 J.P. CHEVREL AND A.M. RATH

32 Collagen-Based Prostheses for Hernia Repair ................... 250 P.B. VAN WACHEM, T.M. VAN GULIK, MJ.A. VAN LUYN, AND ROBERT P. BLEICHRODT

Clinical Applications of Stainless Steel Mesh .................... 258 JEAN JACQUES DURON

Commentary by Rnbert Bendavid

260

34 Repair of Abdominal Wall Defects by Intraperitoneal Implantation of Polytetrafluoroethylene (Teflon®) Mesh ..................... 262 M.L. DRUART, R. CHAMLOU, A. Commentary by Rnbert Bendavid

MEHDI, AND J.M. LIMBOSCH

265

Polyester (Dacron®) Mesh ................................. 266 MARC SOLER, PIERRE J. VERHAEGHE, AND RENE STOPPA

36 Polypropylene Prostheses PARVIZ K. AMID 37

272

Expanded Polytetrafluoroethylene ........................... 279 NICHOLAS

LAw

38 Vypro®: A New Generation of Polypropylene Mesh ............... 286 U. KLINGE, B. KLOSTERHALFEN, AND V. SCHUMPELICK

xviii

Contents

Combined Absorbable and Nonabsorbable Prostheses in the Treatment of Major Defects of the Abdominal Wall .............. 292 GIOVANNI TRIVELLINI

Commentary by Robert Bendavid

293

40 Prosthetic Materials and Adhesion Formation ................... 294 RICCARDO ANNIBALI

Intraperitoneal Prostheses ................................. 299 R.KJ. SIMMERMACHER

Use of Absorbable Mesh in the Staged Repair of Contaminated Abdominal Wall Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306 MERRIL T. DAYTON

Part VI Adjuncts to Surgery 43

Local Anesthesia ........................................ 317 ORESTE TERRANOVA, LUIGI DE SANTIS, AND FRANCESCO BATTOCCHIO

44 Antibiotics in Hernia Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324 JOHN M.A. BOHNEN

Imaging Hernias of the Abdominal Wall . . . . . . . . . . . . . . . . . . . . . . . 335 ]. ANDREW HAMLIN

46 Techniques of Pneumoperitoneum . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 LE6N HERSZAGE

47 Relaxing Incisions ....................................... 343 ROBERT BENDAVID

48 Drains in Hernia Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 347 PAOLO BOCCHI

Part VII Techniques of Open Groin Hernia Repair 353

Introduction to Pure Tissue Repairs ROBERT BENDAVID

49 The Bassini Operation .................................... 354 ORESTE TERRANOVA, LUIGI DE SANTIS, AND LUIGI CIARDO

Commentary by Robert Bendavid

360

50 The Dam Repair ........................................ 361 JACK ABRAHAMSON

The McVay Operation .................................... 365 JOHN]' RYAN

Commentary by Robert Bendavid

367

52 The Shouldice Repair. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 370 ROBERT BENDAVID

xix

Contents

376

Introduction to Tension-Free Repairs ROBERT BENDAVID

53 Gilbert's Repair of Inguinal Hernias .......................... 377 ARTHUR I. GILBERT, MICHAEL F. GRAHAM, AND WALTER]. VOIGT 54 The Mesh Plug Repair .................................... 382 IRA M. RUTKOW AND ALAN ROBBINS

55 Moran's Preperitoneal Mesh Repair for Inguinal Hernias .......... 388 ROBERT M. MORAN

Commentary by Rnhert Bendavid

389

56 The Nyhus Preperitoneal Repair of Groin Hernias ............... 391 JOSE F. PATINO

Commentary by Rnhert Bendavid

395

57 Unilateral Giant Prosthetic Reinforcement of the Visceral Sac: Preperitoneal Hernioplasties with Dacron® ..................... 396 GEORGE E. WANTZ AND EVA FISCHER 58 The Rives Technique: Treatment of Groin Hernias with Mersilene Mesh by an Inguinal Approach .............................. 401 JEAN BERNARD FLAMENT, CLAUDE AVISSE,JEAN-PIERRE PALOT, AND]. RIVES

Commentary by Rnhert Bendavid

405

59 The Gridiron Hernioplasty

407

FRANZ UGAHARY

60 Dynamic Self-Regulating Prosthesis (Protesi Autoregolantesi Dinamica) (PAD) ........................................ 412 G. VALENTI, A. TESTA, AND N. BARLETTA 61

Ventral Hernias: Use of the Kugel Patch ....................... 416 ROBERT D. KUGEL

62 Use ofVicryl Pads in Inguinal Hernia Repairs ................... 419 H.R

WILLMEN

63 Lichtenstein Tension-Free Hernioplasty for the Repair of Primary and Recurrent Inguinal Hernias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 423 PARVIZ K. AMID 64 Reinforcement of the Visceral Sac by a Preperitoneal Bilateral Mesh Prosthesis in Groin Hernia Repair . . . . . . . . . . . . . . . . . . . . . . . 428 RENE STOPPA

65 A Combined Abdominoinguinal Approach to Stoppa's Giant Prosthetic Reinforcement of the Visceral Sac Procedure ........... 437 VINCENZO MANDALA

66 Open Techniques of Femoral Hernia Repair .................... 439 JEAN-PIERRE PALOT AND CLAUDE AVISSE

Contents

Part VIII Laparoscopic Techniques of Groin Hernia Repair 67 Laparoscopic Intraperitoneal Onlay Mesh Repair ................ 451 MORRIS E. FRANKLIN,JR., AND JOSE ANTONIO DfAZ-ELIZONDO 68

Laparoscopic Transabdominal Preperitoneal Hernia Repair (TAPP) . . . 454 MICHAEL S. KAvlc AND SERGIO ROLL

Laparoscopic Totally Extraperitoneal Hernioplasty (TEP): Part I . . . . . 464 EDWARD L. FELIX

70 Laparoscopic Totally Extraperitoneal Repair for Inguinal Hernias (TEP): Part II ........................................... 472 JONATHAN D. SPITZ AND MAURICE E. ARREGUI

Part IX Open Techniques of Incisional Hernia Repair 71

The Shoelace Repair ..................................... 483 JACK ABRAHAMSON

Closure of Chronic Abdominal Wall Defects: The Components Separation Technique .................................... 487 OSCAR M. RAMIREZ AND JOHN A. GIROTTO

The Components Separation Technique Modified for Use with Enterostomies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497 SYLVESTER M. MAAs, TAMMO S. DE VRIES REILINGH, AND ROBERT P. BLEICHRODT

74 Treatment of Incisional Hernias by an Overlapping Herniorrhaphy and Onlay Prosthetic Implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 500 J.P. CHEVREL

75 The Kugel Repair for Groin Hernias ......................... 504 ROBERT D. KUGEL

76 Treatment of Major Incisional Hernias ........................ 508 JEAN BERNARD FLAMENT,JEAN-PIERRE PALOT, A. BURDE, JEAN FRANc,;;OIS DELATTRE, AND CLAUDE AVISSE

Part X Laparoscopic Techniques of Incisional Hernia Repair 77 Repair ofIncisional Hernias and Midline Defects .. . . . . . . . . . . . . . . 519 GUY R. VOELLER

Part XI Loss of Abdominal Wall Substance 78

Loss of Abdominal Wall Substance ........................... 527 J.P. CHEVREL

79 Acute Loss of Abdominal Wall Substance and Abdominal Compartment Syndrome H. HARLAN STONE

538

Contents

xxi

Part XII 80

Plastic Surgery of Abdominal Wall Reconstruction . . . . . . . . . . . . . . . . 547 A. BERGER AND J. LIEBAU Commentary by Rnlph Ger 553

Part XIII 81

Plastic and Reconstructive Surgery

Emergency Surgery

Should Prostheses Be Used in Emergency Hernia Surgery? XAVIER HENRY AND

........ 557

BOURAS-KARA TERKI

Groin Hernias in the Adult Presenting as Emergencies ... . . . . . . . . . 560 DAVID WATKIN

83 Abdominal Wound Dehiscence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 569 DIRK VAN GELDERE

84 Treatment of Strangulated Inguinal Hernias with Nonabsorbable Prostheses .................................. 577 ALAIN PANS,

C. DESAIVE, AND N. JACQUET

Use of Prosthetic Materials in Incisional Hernias with a Septic Risk ... 580 VINCENZO MANDALA

86 Incisional Hernias as Emergencies ........................... 582 DAVID V. FELICIANO

Part XIV Pediatrics 87

Pediatric Hernias ........................................ 591 BRADLEY M. RODGERS, EUGENE D. MCGAHREN, III, AND ROBERT

BURNS

Part XV The Female Hernia Patient 88

Epidemology of Hernias in the Female ........................ 613 ALEJANDRO WEBER, SALVADOR VALENCIA, DENZIL GARTEIZ, AND ALFREDO BURGUESS

89 Anesthesia for Hernia Repair in Pregnancy and Lactation

......... 620

STEPHEN HALPERN AND MARGARET SREBRNJAK

Nonpalpable Inguinal Hernia in Women

625

LEIF SPANGEN AND SAM G.G. SMEDBERG

Hernia and Chronic Pelvic Pain in Women ..................... 630 IBRAHIM M. DAOUD

Chronic Pelvic Pain in Women .............................. 632 MICHAEL S. KAVIC

xxii

Contents

93 Femoral Hernias in Females: Facts, Figures, and Fallacies

......... 639

ROBERT BENDAVID

Part XVI Special Problems 94 Hernias in the Elderly .................................... 643 PIERRE

J. VERHAEGHE, TSIRY B. ANDRIAMIHAMISOA,

AND FIDY M. RALAIMIARAMANANA

Elective Herniorrhaphy in an Aging Population ................. 646 STANLEY D. BERLINER AND NATHANIEL SPIER

Commentary by Robert Bendavid

651

96 Management of Genitourinary Tract Pathology Encountered During Inguinal Herniorrhaphy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 653 W. SCOTT McDOUGAL 97 Sports Injuries and Groin Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 657 OJ.A. GILMORE 98

Hernias and Patients with Ascites ............................ 662

J. BELGHITI AND M. HAKIM

Paraostomy Hernias: Prevention and Prosthetic Mesh Repair ....... 666 PAUL H. SUGARBAKER

100 Hernia and Obesity ...................................... 672 HARVEYj.SUGERMAN

101

Pneumoperitoneum in the Treatment of Giant Hernias, with Special Reference to Obesity ............................... 675 EDWARD E. MASON

Commentary by Robert Bendavid

679

102 Umbilical Hernias ....................................... 680 MAXIMO DEYSINE

Commentary by Robert Bendavid

684

103 Epigastric Hernias

685

MAXIMO DEYSINE

104 Acquired Lumbar Hernias ................................. 688 PARVIZ

Part XVII 105

AMID AND ROBERT BENDAVID

Complications of Hernia Repairs

Complications of Groin Hernia Surgery ....................... 693 ROBERT BENDAVID

106 Complications of Laparoscopic Inguinal Hernioplasty . . . . . . . . . . . . . 700 STEVEN M. FASS AND EDWARD H. PHILLIPS

107 Complications of the Use of Prostheses: Part I .................. 707 PARVIZ

AMID

xxiii

Contents

108

Complications of the Use of Prostheses: Part II .................. 714 GIANFRANCO FRANCIONI, PRO SPERO MAGISTRELLI, AND MARIO PRANDI

109

Infected Abdominal Wall Prosthesis .......................... 721 DONALD E. FRY

110

Chronic Pain Following Repair of a Groin Hernia ................ 726 PJ. O'DWYER AND M.G. SERPELL

111

Neuralgia Following Hernia Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . 730 C. TONS, J. HOER, AND V. SCHUMPELICK

112 Mesh Inguinodynia Mter Inguinal Herniorrhaphy . . . . . . . . . . . . . . . . 734 JAMES R. STARLING 113 Ilioinguinal/Iliohypogastric Neuropathy ....................... 737 R. GRAHAM VANDERLINDEN, RAJIV MIDHA, AND LOREN VANDERLINDEN 114 Sexual Dysfunction Following Inguinal Hernia Repair ............. 740 JERALD BAIN 115 Vascular Injuries from Hernia Surgery ........................ 743 JAMES R. DEBORD 116 Seromas............................................... 753 ROBERT BENDAVID AND MATTHIAS Kux 117 Dysejaculation .......................................... 757 ROBERT BENDAVID

Part XVIII

Other Considerations

118 Medicolegal Issues Relating to Herniorrhaphy ................... 761 ERLE E. PEACOCK 119 Ambulatory Hernia Surgery ................................ 767 MARTIN KURZER, PHILIP A. BELSHAM, AND ALLAN E. KARK 120 Telemedicine and Robotics in Surgery PETER M.N.Y.H. Go

772

Epilogue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 776 GEORGE E. WANTZ Index ..................................................... 777

Contributors

JACK ABRAHAMSON, MD

31 Kadimah Street, Haifa 34383, Israel PARVIZ

AMID, MD

Lichtenstein Hernia Institute, Los Angeles, CA 90069, USA B. ANDRIAMIHAMISOA Service de Chirurgie Viscerale et Digestive, Hopital Nord, Amiens 80054, France

TSIRY

RICCARDO ANNIBALI, MD

Department of Surgery, Section of Coloproctology, San Pio 10th Hospital, Milan 20159, Italy MAURICE E. ARREGUI, MD Department of General Surgery, St. Vincent Hospital and Healthcare Center, Indianapolis, IN 46260, USA

OMAR M. AsKAR, MDt Department of General Surgery and Anatomy, University of Cairo, Cairo, Egypt CLAUDE AVISSE, MD

Department of Surgery, Hopital Robert Debre, Reims 51100, France JERALD BAIN, MD

Department of Endocrinology, University of Toronto/Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada JACQUES BARBIER, MD

Service de Chirurgie Viscerale, Jean Bernard University Hospital, Poitiers 86021, France N. BARLETIA, MD Department of General Surgery, Ospedale G.B. Grassi, Rome 00189, Italy FRANCESCO BATIOCCHIO, MD

Division of Surgery, Hospital of Este, Este 35056, Italy

BELGHITI, MD

Hopital Beaujon, Clichy 92210, France xxv

xxvi

Contributors

PHILIP A. BELSHAM, MD The British Hernia Center, Hendon, London NW4 4RS, UK ROBERT BENDAVID, MD

18 Cedarcroft Boulevard, Toronto, Ontario M2R 2Z2, Canada

A. BERGER, MD Department of Plastic, Hand, and Reconstructive Surgery, Medical School of Hannover, D-30659 Hannover, Germany STANLEY D. BERLINER, MD

75-967 Hiona Street, Holualoa, HI 96725-9601, USA ROBERT P. BLEICHRODT, MD

Department of Surgery, Nijmegen University Medical Center, Nijmegen 6500HB, The Netherlands PAOLO BOCCHI, MD

Divisione Chirurgica, Ospedale Magiore di Parma, Parma 43100, Italy JOHN

M.A.

BOHNEN, MD

160 Wellesley Street East, Toronto, Ontario M4Y IJ3, Canada

A. BURDE, MD Department of Surgery, Hopital Robert Debre, Reims 51100, France ALFREDO BURGUESS, MD

Department of General Surgery, Hospital Angeles de las Lomas, Huixquilucan 52763, Mexico ROBERT C. BURNS, MD

Department of Surgery, University of Virginia Health Sciences, Charlottesville, VA 22906, USA

M. CARRETIER, MD Jean Bernard University Hospital, Poitiers 86021, France R. CHAMLOU, MD Centre Hospitalier Etterbeck-Ixelles, Brussels 1050, Belgium J.P. CHEVREL, MD

Service de Chirurgie Generale et Digestive Hopital Avicenne, Bobigny 93009, France LUIGI CIARDO, MD

Department of Surgical and Gastroenterological Sciences, University of Padua, Padua 35128, Italy PIERGIORGIO DANELLI, MD

Department of General Surgery, State University of Milan-"L. Sacco"University Hospital, Milan 20157, Italy

M. DAOUD, MD Department of Surgery, University of Connecticut and St. Francis Hospital and Medical Center, Hartford, CT 06105, USA IBRAHIM

xxvii

Contributors

MERRIL T. DAYTON, MD Department of Surgery, University of Utah, Salt Lake City, UT 84131, USA JAMES R. DEBORD, MD

Department of Surgery, University of Illinois College of Medicine at Peoria, Peoria, IL 61603, USA JEAN FRANCOIS DELATTRE, MD

Department of Surgery, Hopital Robert Debre, Reims 51100, France C.DESAIVE,MD

Department of Abdominal Surgery, Clinique A. Renard, Herstal 4040, Belgium LUIGI DE SANTIS, MD

Department of Surgical and Gastroenterological Sciences, University of Padua, Padua 35128, Italy MAxIMO DEYSINE, MD

Department of Surgery, State University of New York at Stony Brook and Mercy Medical Center, Rockville Center, NY 11570, USA JOSE ANTONIO DiAl-ELIZONDO, MD

Department of Surgery, University of Texas Health Sciences Center, San Antonio, TX 78222, USA PHILIP B. DOBRIN, MD, PHD

Department of Surgery, University of Missouri-Columbia, Harry S Truman Memorial Veterans' Hospital, Columbia, MO 65211, USA M.L. DRUART, MD

Centre Hospitalier Etterbeek-Ixelles, Brussels 1050, Belgium JEAN JACQUES DURON, MD

Department of Digestive Surgery, Pitie-Salpetriare, Paris 75013, France STEVEN M. FASS, MD

Department of Surgery, Cedars-Sinai Medical Center, University of California at Los Angeles, School of Medicine, Los Angeles, CA 90048, USA J.P. FAURE, MD

Jean Bernard University Hospital, Poitiers 86021, France DAVID V. FELICIANO, MD Department of Surgery, Emory University School of Medicine, Grady Memorial Hospital, Atlanta, GA 30303, USA EDWARD L. FELIX, MD

Department of Surgery, University of California, San Francisco, Fresno, CA 93710, USA EVA FISCHER, MD

Department of Surgery, The New York Hospital Cornell Medical Center, New York, NY 10021, USA ROBERT J. FITZGIBBONS, JR., MD

Department of Surgery, Creighton University School of Medicine, Omaha, NE 68131, USA JEAN BERNARD FLAMENT, MD

Department of Surgery, Hopital Robert Debre, Reims 51100, France

xxviii

GIANFRANCO FRANCIONI, MD Department of General Surgery, S. Andrea Hospital, La Spezia 19100, Italy MORRIS E. FRANKLIN,JR., MD Department of Surgery, University of Texas Health Sciences Center, San An~?nio, TX 78222, USA CHARLES J. FREIMAN, MD Department of Surgery, University of California at Los Angeles, School of Medicine, Los Angeles, CA 90095, USA DONALD E. FRy, MD Department of Surgery, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA DENZIL GARTEIZ, MD Department of General Surgery, Hospital Angeles de las Lomas, Huixquilucan 52763, Mexico RALPH GER, MD Department of Anatomy, Albert Einstein College of Medicine, Bronx, NY 10461-1975, USA ARTHUR I. GILBERT, MD Hernia Institute of Florida, Miami, FL 33143, USA OJA. GILMORE, MS, FRCS, FRCS (ED) The Groin and Hernia Clinic, London WIN 2ET, UK JOHN A. GIROTTO, MD Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA PETER M.N.YH. Go, MD St. Antonius Ziekenhuis, Nieuwegein 3430, The Netherlands FINN GoTTRUP, MD

Bispebjerg Hospital, University of Copenhagen, Copenhagen Wound Healing Center, Copenhagen NY, DK-2400 Denmark MICHAEL F. GRAHAM, MD Hernia Institute of Florida, Miami, FL 33143, USA HOWARD P. GREISLER, MD Department of Surgery, Loyola University Medical Center, Maywood, IL 60153, USA STAFFAN liAAPANIEMI, MD Department of Surgery, Vrinnevi Hospital, Norroping 60182, Sweden M. HAKIM, MD Department of Surgery, University of Paris, Paris 75343, France

STEPHEN HALPERN, MD Department Anesthesia, Sunnybrook and Women's College Health Sciences Centre, University of Toronto, Ontario M5S 1B2, Canada

Contributors

xxix

Contributors

J. ANDREW HAMLIN, MD Department of Radiology, St. John's Hospital, Santa Monica, CA 90404, and Department of Radiology, Century City Hospital, Los Angeles, CA 90065, USA STAFFAN HAPPANIEMI, MD

Department of Surgery, Vrinnevi Hospital, Norroping 60182, Sweden SUZANNE HAsTHORPE, PH.D.

Surgical Research, Royal Children's Hospital Research Institute, University of Melbourne, Parkville, Victoria 3052, Australia XAVIER HENRY, MD

Service de Chirurgie Viscerale et Disgestive, Hopital Nord, Amiens 80054, France LEON HERSZAGE, MD

Department of General Surgery, I. Pirovano Hospital, Buenos Aires, Argentina 1055

J. HOER, MD Department of Surgery, University of Aachen, Aachen 52076, Germany DAVID HOWARTH, MD

Department of Pathology, Mount Sinai Hospital, Toronto, Ontario M5G 1X4, Canada

J. HUREAU, MD

85 Avenue Emile Thibault, Paris 10362, France

JOHN M. HUTSON, MD, FRACS

Department of General Pediatric Surgery, Royal Children's Hospital Research Institute, University of Melbourne, Parkville, Victoria 3052, Australia N. JACQUET, MD

Department of Abdominal Surgery, CHU Saet Tilman, Liege 4000, Belgium LARs NANNESTAD JORGENSEN, MD

Department of Surgical Gastroenterology, Bispebjerg Hospital, University of Copenhagen, Copenhagen NY, DK-2400 Denmark E. KARK, MD The British Hernia Center, Hendon, London NW4 4RS, UK

ALLAN

MICHAEL S. KAVIC, MD

Department of Education and General Surgery, St. Elizabeth Health Center, Youngstown, OH 44501-1790, USA U. KLINGE, MD Department of Surgery, University of Aachen, Aachen 52076, Germany B. KLOSTERHALFEN, MD

Institute for Pathology, University of Aachen, Aachen 52076, Germany KossovsKY, MD Department of Surgery, University of California at Los Angeles, School of Medicine, Los Angeles, CA 90095, USA

NIR

xxx ROBERT D. KUGEL, MD

Hernia Treatment Center, Olympia, WA 98506, USA MARTIN KURZER, MD

The British Hernia Center, Hendon, London NW4 4RS, UK MATTHIAS Kux, MD

Department of Surgery, St. Joseph Hospital, Vienna 11130, Austria LAw, MD Case Far Hospital, The Ridgeway, Enfield, Middlesex EN2 8JL, UK

NICHOLAS

KARL LEBLANc, MD Department of Surgery, Louisiana State University, New Orleans, LA, and Surgical Specialty Group, Inc., Baton Rouge, LA 70808, USA RONALD T. LEWIS, MD Department of Surgery, McGill University, Montreal, Quebec H3A 1A1, Canada

LIEBAu, MD Department of Plastic, Hand, and Reconstructive Surgery, Medical School of Hannover, Hannover 30659, Germany

J.M. UMBOSCH, MD

Department of Surgery, Centre Hospitalier Etterbeck-Ixelles, Brussels 1050, Belgium M. MAAs, MD Department of Plastic and Reconstructive Surgery, Academic Hospital Maastricht, Maastricht 6202 AZ, The Netherlands

SYLVESTER

PROSPERO MAGISTRELLI, MD

Department of General Surgery, S. Andrea Hospital, La Spezia 19100, Italy VINCENZO MANDAIA, MD

Department of General and Emergency Surgery, Villa Sofia-CTO Hospital, Palermo 90015, Italy E. MAsON, MD University of Iowa College of Medicine, Iowa City, IA 52242, USA

EDWARD

W. SCOTT McDOUGAL, MD Department of Urology, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA EUGENE D. MCGAHREN, III, MD Department of Surgery, University of Virginia Health Sciences, Charlottesville, VA 22906, USA

A. MEHDI, MD Department of Surgery, Centre Hospitalier Etterbeck-Ixelles, Brussels 1050, Belgium

RAJIV MIDHA, MD Department of Neurosurgery, Sunnybrook and Womens College Health Sciences Centre, University of Toronto, Toronto, Ontario M4N 3M5, Canada RJ. MINNS, PH.D., DSCTECH

Department of Medical Physics, Dryburn Hospital, Durham DH1 5TW, UK

Contributors

xxxi

Contributors ROBERT M. MORAN, MD

National Ambulatory Hernia Institute, La Puente, CA 91744, USA GABRIELE MUNEGATO, MD

Department of Surgery, Clinique Chirurgicale de l'Universite, Centre Hospitalier Universitaire, Amiens 80054, France ENRICO NICOLO, MD, FACS

Department of Surgery, University of Pittsburgh Medical Center, McKeesport, PA 15132, USA ERIK NILSSON, MD, PH.D., FRCS

Department of Surgery, Motala Hospital, Linkoping University, Motala 5-591 85, Sweden PJ. O'DWYER, MH, FRCS

Department of Surgery, Western Infirmary, Glasgow G11 6NT, UK JEAN-PIERRE PALOT, MD

Service de Chirurgie Generale et Digestive, Universitaire de Reims, Reims 51687, France ALAIN PANS, PH.D.

Department of Abdominal Surgery, Clinique

Renard, Herstal 4040, Belgium

F. PATINO, MD Department of Surgery, Fundacion Santa Fe de Bogota, Bogota, Distrito Especial, Columbia

JosE

ERLE E. PEACOCK, MD Department of Surgery, University of North Carolina School of Medicine, Chapel Hill, NC 27514, USA

H. PHILLIPS, MD Department of Surgery, Cedars-Sinai Medical Center, University of California at Los Angeles, Los Angeles, CA 90048, USA EDWARD

ALFONSO PLUCHINOTTA, MD

Department of Surgery, Clinique Chirurgicale de l'Universite Centre Hospitalier Universitaire, Amiens 85004, France MARIo PRANDI, MD

Department of General Surgery, S. Andrea Hospital, La Spezia 19110, Italy THOMAS QUINN, MD

Department of Biomedical Sciences, Creighton University, Omaha, NE 68178, USA FIDY M. RALAIMIARAMANANA, MD

Service de Chirurgie Visceral et Digestive, Hopital Nord, Amiens 80054, France M. RAMIREZ, MD Department of Plastic Surgery, The Johns Hopkins University, Lutherville, MD 21093, USA

OSCAR

A.M. RATH, MD

Serivce de Chirurgie Generale et Digestive, Hopital de Bobigny, Bobigny 93009, France C. READ, MD Department of Thoracic Surgery, Central Arkansas Veterans Healthcare Center, Department of Surgery, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA

RAYMOND

xxxii

Contributors

TAMMO S. DE VRIES REIUNGH, MD

Department of Surgery, University Hospital "Vrije Universeiteit," 1081 HV Amsterdam, The Netherlands

JP. RICHER, MD jean Bernard University Hospital, Poitiers 86021, France

RIvEs, MD Universitaire de Reims, Reims 51687, France

ALAN ROBBINS, MD The Hernia Center, Freehold, Nj 07728, USA BRADLEY

M. RODGERS, MD

Department of Surgery, University of Virginia Health Sciences, Charlottesville, VA 22906, USA SERGIO ROLL, MD

Department of Surgery, University of Sao Paulo, Sao Paulo 04012-002, Brazil

IRA M. RUTKOW, MD Department of Surgery, University of Medicine and Dentistry of New jersey, New jersey Medical School, Newark, Nj 08903, USA JOHN

RYAN, MA, MB, BCH, FRCSI

Department of Surgery, University of South Dakota School of Medicine, Sioux Falls, SD 57105, USA V. SCHUMPEUCK, MD

Medizinische Fakultat RWTH, Chirurgischen Klinik, Aachen 52074, Germany

M.I.A. SELMIA, MD Department of General Surgery, South Cleveland Hospital-Middlesborough, Wickham, Newcastle-upon-Tyne NEll 9PW, UK M.G. SERPELL, MD Department of Surgery, Western Infirmary, Glasgow GIl 6NT, UK

R.KJ. SIMMERMACHER, MD

Department of Surgery, University Hospital, Utrecht 3508 GA, The Netherlands E. SKANDALAKIS, MD, PH.D. Center for Surgical Anatomy, Emory University School of Medicine, Atlanta, GA 30322, USA

JOHN

SAM G.G. SMEDBERG, MD, PH.D. Department of Surgery, Helsingborg Hospital, Helsingborg S-251 87, Sweden

MARc SOLER, MD

Chirurgie Generale, Clinique Saint jean, Cagnes sur Mer 06800, France LEIF SPANGEN, MD

Surgical Clinic, Central Hospital, S-651 85 Karlstad, Sweden NATHANIEL SPIER, MD

Department of Surgery, North Shore University Hospital, Manhasset, NY 11030, USA

xxxiii

Contributors

D. SPITZ, MD Department of General Surgery, St. Vincent Hospital and Healthcare Center, Indianapolis, IN 46260, USA

JONATHAN

MARGARET SREBIU-{JAK, MD, FRCPC

Department of Anaestesia, Sunnybrook and Women's College Health Sciences Centre, University of Toronto, Toronto, Ontario M5S IB2, Canada R. STARLING, MD Department of Surgery, University of Wisconsin, Madison, WI 53792, USA

JAMES

H. HARLAN

STONE, MD

Department of Surgery, University of Arizona College of Medicine, Phoenix, AZ 85032, USA RENE STOPPA, MD

Clinique Chirurgicale de l'Universite, Centre Hospitalier Universitaire, Amiens 80054, France PAUL H. SUGARBAKER, MD Department of Surgery, Washington Hospital Center, Washington, DC 20010, USA HARVEYJ. SUGERMAN,MD

Department of Surgery, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA 23298, USA

N. BOURAS-KARA TERKI, MD Service de Chirurgie Viscerale et Digestive, Hopital Nord, Amiens 80054, France ORESTE TERRANOVA, MD

Department of Surgical and Gastroenterological Sciences, Geriatric Surgical Clinic, University of Padua, Padua 35128, Italy A. TESTA, MD Department of General Surgery, Ospedale S. Pietro, Rome 00189, Italy

C. TONS, MD Department of Surgery, University of Aachen, Aachen 52076, Germany K-H. TREUTNER, MD Department of Surgery, University of Aachen, Aachen 52076, Germany GIOVANNI TRIVELLINI, MD

University of Milan, Milan 20142, Italy U GAHARY, MD Department of Surgery, Rivierenland Ziekenhuis Tiel, Tiel 4002, The Netherlands

FRANZ

SALVADOR VALENCIA, MD

Department of General Surgery, Hospital Angeles de las Lomas, Huixquilucan 52763, Mexico G. VALENTI, MD

Lungotevere Sanzeio 1, Rome 00153, Italy

xxxiv

Contributors

LOREN VANDERLINDEN, MD

Department of Neurosurgery, Trillium Health Centre, Mississauga, Ontario L5B 2V2, Canada R. GRAHAM VANDERLINDEN, MD Department of Neurosurgery, Trillium Health Centre, Mississauga, Ontario L5B 2V2, Canada DIRK VAN GELDERE, MD

Department of Surgery, Ziekenhuis Amstelveen 1180 AH, The Netherlands T.M. VAN GUUK, MD, PH.D. Department of Surgery, Academic Medical Center, 1100 DD, Amsterdam, The Netherlands MJ.A. VAN LUYN, PH.D. Department of Pathology, Laboratory Medicine, Medical Biology, University of Groningen, Groningen 9713 GZ, The Netherlands P.B. VAN WACHEM, PH.D. Department of Pathology, Laboratory Medicine, Medical Biology, University of Groningen, Groningen 9713 GZ, The Netherlands

PIERRE]' VERHAEGHE, MD Service de Chirurgie Viscerale et Digestive, Hopital Nord, Amiens 80054, France GUY R. VOELLER, MD

Department of Surgery, University of Tennessee-Memphis, Memphis, TN 38163, USA WALTER]. VOIGT, MD

Hernia Institute of Florida, Miami, FL 33143, USA E. WANTZ, MD Department of Surgery, The New York Hospital Cornell Medical Center, New York, NY 10021, USA GEORGE

DAVID WATKIN, MD, FRCS

Department of General Surgery, Leicester Royal Infirmary, Leicester LEI 5WW, UK ALEJANDRO WEBER, MD

Department of General Surgery, Hospital Angeles de las Lomas, Huixquilucan 52763, Mexico H.R. WILLMEN, MD Arzt fUr Chirurgie und Unfallchirurgie, Chirurgische Klinik, Kreiskrankenhaus Grevenbroich, 41515 Grevenbroich, Germany SUSANNE

WOLOSON, MD

Department of Surgery, Loyola University Medical Center, Maywood IL 60153, USA ROBERT M. ZOLUNGER, JR., MD

Department of Surgery, Case Western Reserve University School of Medicine, University Hospitals of Cleveland, Cleveland, OH 44106. USA

Part I History

1 Evolution and Present State of Groin Hernia Repair Rene Stoppa, George E. Wantz, Gabriele Munegato, and Alfonso Pluchinotta

Known since the beginning of the history of medicine, 1hernias have of patients and the community at large. On behalf of patients, there required help from the surgeon, mostly on the dramatic occurrence is a sort of ethical obligation, including patient information, safety, of strangulation (Figs 1.1-1.7). But when evaluating elective hernia and the benign nature of the operation, postoperative comfort, surgery a little more than a century ago, Paul Segond and William high degree of patient satisfaction, and long-term efficacy. On the Bull expressed the same sad opinion about the ill-named "hernia part of the community, there is an expectation of low postoperacure" of their time. In 1883, Segond said, "There is no operation tive disability, low direct and indirect costs, and permanent cure. in the past or present time which deserves the name of radical cure: Thus, surgical tactics have reached currently accepted policies this remains a chimera. Would radical cure be the unique aim of inspired by "minimum" as well as "maximum" rules of quality conthe surgeon, his duty should be never to operate."2 Later, in 1890, trol. These rules of quality are minimum anesthesia, surgical Bull remarked, "The use of the word cure for speaking of the op- trauma, postoperative disability, complications, and cost; maxierative treatment should be abandoned, and the results measured mum rapid learning, easy training, quick performance of the proby the period of relief before recurrence took place."3 cedure, and reproducibility of satisfactory results. The modem surgical era, facilitated by the advent of anestheThere are pertinent issues raised from past discussions and more sia and asepsis, began with Bassini4 who, in 1887, developed the recent assessments in classic hernia surgery. Attention given to the first modem, anatomically based hernia treatment. This procedure repair of the posterior inguinal wall, including the transversalis spread worldwide, but was often executed poorly, and hernia re- fascia, is vital for an effective cure. This is credited to Cooper (Fig. 1.8),9 Thomson,10 Bassini (Fig. 1.9 and 1.10),4 Shouldice,6 pair fell into a state of second class surgery. Forty years ago, in 1958, the meticulous work of American sur- Fruchaud,7 McVay,ll and Condon.l 2 Toward this goal, surgeons use geon Chester McVay and anatomist Barry Anson5 clarified the diverse techniques adapted to the various types of defects (Fig. 1.11). anatomy of the groin and popularized the Cooper's ligament inThe posterior approach has gained great popularity. First deguinal hernioplasty. In the late 1940s, Canadian surgeon E. scribed by Annandale,13 supported by Cheatle 14 and Henry,15 it Shouldice6 developed a hernioplasty similar to the Bassini opera- was promoted by Nyhus 16 and enthusiastically followed by Rives 17 tion. This procedure became extremely popular as well as the stan- and Stoppa. 18 The retroparietal cleavable spaces are excellent dard of the classic pure tissue hernioplasties. In France in 1956, approaches to the wall defect, and also perfect sites for the placeHenri Fruchaud7,8 published his wonderful anatomic study of the ment of synthetic meshes held in place by the positive intragroin, which became the bible for the European Hernia Society abdominal pressure, according to Pascal's hydrostatic principle. (GREPA) members. At the same time, convenient modem pros- We agree with Griffith, who said, "Equal familiarity with these two thetic materials appeared after World War II, and the innovations approaches allows one to suit the operation to the patient rather progressively became part of the surgical arsenal. Despite advances than the patient to the operation.... "19 Recently, laparoscopic in understanding about hernias, and with more than 200 tech- video-assisted hernia surgery, taking up the posterior approach, is niques described, a 5 to 10% recurrence rate continued to plague rediscovering the regional anatomy of the groin from inside the patients. This is where hernia surgery was when, in the early 1990s, abdomen. laparoscopic video-assisted surgery (a seductive product of high Compared to "pure tissue repairs" limited by tissue resistance technology) entered the field of hernia surgery. Today, hernia re- and suture tension, the prosthetic repair is logically more able to pair is still changing, discussions continue about important aspects reinforce or replace the weak layer of the groin as extensively as of open operations, while laparoscopic surgery, currently being necessary, and can provide tensionless repair for the largest deevaluated, struggles to gain popularity. fects and the most difficult procedures. The replacement or reinKey data on the evolution of the principles of hernia surgery forcement of the deep inguinal floor by using synthetic mesh are founded partly on the anthropologic nature of hernia, partly answers one of the questions of the day: mending the biologic ason a humanistic concern, and partly on its social appropriation. pect of the multifactorial mechanism of herniation, Peacock's Because hernias are a well-known common pathology, hernia re- "metabolic defect,"20 and Read's "metastatic emphysema."21 There pair is also a community problem. Demands have been recently is no scientific evidence of any late adverse effects after using prosexpressed by the media and accepted by the surgeons on behalf thetic materials in young patients. R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

FIGURE 1.1. Phoenician terracotta figurine showing an umbilical hernia (5th-4th century BC). (From Museo Arqueologico, Barcelona, Spain.)

FIGURE 1.3. Ancient "upside-down" treatment of a strangulated hernia. (From the Book ofCyrugia, Hieronymus Brunschwig, 1497.)

FIGURE 1.2. Surgical treatment of a scrotal hernia. From Rolandus Chirurgia, by Roger of Salerno (1l40-?). Twelfth century manuscript. (From Casanatense Library, Rome, Italy.)

FIGURE 1.4. Trusses for inguinal hernia. From Ambroise Pare, Of Tumours Against Nature in Genera~ 1649. This English translation and the multiple editions in French were the standard textbooks of surgery for a hundred years.

1. Evolution of Groin Hernia Repair

FIGURE 1.5. Woman with a femoral hernia. In Die Handschrift des Schnitt und Augenarteztes. Caspar Stromayr (l6th century). By Walter Brunn, 1925, Idra-Verlagsanstalt, Berlin.

FIGURE 1.6. Prolapsed fecal fistula after a strangulated hernia. In Wund Artzney by Fabricius Hildanus, 1652.

After World War II, synthetic meshes were introduced in France by Aquaviva who used nylon,22 and in the United States, Usher23 and Koontz24 using polypropylene. Experience with polyester mesh was reported in France by Rives 25 and Stoppa. 26 In clean hernia procedures, all modem fabrics have a similar good tolerance. Macroporosity is the most essential physical property to ensure rapid integration and resistance to infection. Microporous material is encysted, rather than integrated, and is not recommended. Synthetic meshes are used in various ways (plugs, patches, or large wrapping of the peritoneal sac), and can be placed in diverse anatomic sites. The underlay position between peritoneum and endoabdominal fascia seems to be the best one to fulfill Fruchaud's exhortation to "close the window, not the curtain," and give favorable working conditions to the hydrostatic principle of Pascal. Finally, prosthetic material must not be used in patients at risk for sepsis. This includes emergent operations for strangulated hernias. The diagnosis of hernia can be missed in some patients, as in the example of groin pain in obese or athletic patients. The ultrasonographic examination in supine and upright positions with a Valsalva maneuver has a diagnosis sensitivity and specificity of 90%. Computed tomography is rarely indicated. Herniography appears no longer justified in adults. Indications for hernia repair are diverse also, and the procedures are aimed at relieving symptoms and preventing the still deadly menace of strangulation. Only an asymptomatic direct hernia in the elderly can be observed under regular control, following the 1994 guidelines of the Royal College of Surgeons of England. 27 A femoral hernia, statistically more likely to strangulate, must be operated on as soon as diagnosed. In geriatric pa-

tients, delay can increase the risk of incarceration and emergency operation: elective herniorraphy can be safely performed after careful management of significant other ailments, and, whenever possible, under local anesthesia. There are still two tendencies in current hernia surgery. One is the routine use of a single operative technique for all types of hernias. This has contributed to perfection of the details of the procedures, but it also leads to a number of recurrences. We agree with many surgeons who prefer an individual approach, personalizing the operation to suit the patient as taught by Nyhus 28 and Devlin. 29 This takes into account the type and size of the defect, the status of groin anatomic structures, and the condition of the patient. Just as there is no panacea to cure all sicknesses, there is no gold standard operation to cure all hernias. Selective indications of diverse techniques rely on a nonuniversally adopted classification of groin hernias, based on the evaluation of the risk for recurrence. Several classifications have been published by, among others, McVay,I1 Harkins,30 Casten,31 Gilbert,32 Nyhus,28 and Bendavid.33 Many surgeons trust the Nyhus scheme 28 based on the state of the posterior wall, allowing recurrences to be related specifically to the type. In 1993, Stoppa34 adopted Nyhus's four hernia types, with some modifications to allow for aggravating factors. These include the characteristics of the hernia (size, multiplicity, sliding), patient condition (age, activity, associated diseases), and special surgical circumstances (infection risk, foreseen technical difficulties). Short hospital stay and ambulatory surgery, as well as early return to activity, have been demonstrated by comparative studies to provide long-term results for outpatient procedures that are the

Stoppa et al.

same as those for inpatient procedures, and with fewer complications. Initiated in Scotland by Nicoll,35 this is a currently accepted practice in North America. In spite of its economic advantages and the absence of disadvantages for the patient, ambulatory surgery has not gained popularity in Europe. The reasons for this include the lack of political and individual motivation and the fact that appropriate ambulatory surgical units are not readily available. The legal and professional responsibility of the surgeon is the same for an outpatient as it is for an inpatient setting. About anesthesia: a well-informed patient may participate in the choice between local, spinal, or general anesthesia. Local anesthesia can be widely used for primary, uncomplicated hernia repair if it is performed by experienced teams, in psychologically well-prepared, nonobese, nonallergic adults. Laparoscopic hernia repair has complicated anesthetic techniques because the pneumoperitoneum reduces cardiac output and produces hypercapnia. Epidural anesthesia, often used in open procedures, is of limited use in laparoscopic repair, mostly for rapid procedures in young patients because its hemodynamic effects add to those of the pneumoperitoneum. The current panorama of groin hernia classic repairs is as follows: current classic suture repairs are the popular Marcy (Figs. 1.11 and 1.12),36 Bassini,4 Shouldice,6 and McVayll operations. Current open prosthetic repairs include anterior onlays: Lichtenstein's tension free repair,37 Gilbert's sutureless hernioplasty,38 and their variations. Among preperitoneal underlays are Rives's operation (by inguinal approach),25 Stoppa's operation (by midline subumbilical approach),26 and Wantz's GPRVS39-42 (by the suprainguinal route). The success of their introduction on a large scale has been supported by their feasibility and efficiency. The controversy between open and laparoscopic hernia surgery supporters continues. Laparoscopic hernia surgery is not only

FIGURE 1.7. Technique of division of the deep inguinal ring for a strangulated hernia. Manual of Operative Surgery and Surgical Anatomy, Belliere: New York, 1855.

A FIGURE 1.8. (A) Posterior view of the groin showing the neck of a femoral hernia sac. From Astley Paston Cooper's famous book The Anatomy and Surgical Treatment of Inguinal and Congenital Hernia. Parts I and II. T Cox: London, England, 1804. (B) Posterior of a dissected groin showing the

neck of a femoral hernia sac. This anatomic dissection, made by Cooper, may have served as the model for the artist's rendition of the same. Courtesy of the UMDS Gordon Museum, London.

1. Evolution of Groin Hernia Repair

FIGURE 1.10. The Bassini inguinal hernioplasty as illustrated by his pupil A. Catterina. Catterina, upset because so many surgeons were doing the Bassini hernioplasty incorrectly, set out to educate surgeons in the correct technique. He stressed the fact that Bassini divided the cremaster muscle and also the floor of the inguinal canal, steps that most surgeons omitted. (From G.E. Wantz, The operation of Bassini as described by Attilio Catterina, Surg Gynecol Obstet 1989;168:67-80.)

FIGURE 1.9. Bassini's illustration of the surgical dissection for his inguinal hernioplasty. Note that the floor of the inguinal canal has been divided, exposing preperitoneal fat. This essential step of the hernioplasty was not mentioned in his written description and may explain why so many surgeons doing the Bassini hernioplasty never opened the posterior wall of the inguinal canal. From E. Bassini, Uber die Behandlung des Leistenlmtches, 1890. merely a different approach but a new method, using different tools, bringing a different type of physical contact with the patient, having different potential risks, and even a different philosophy. Its feasibility has been assessed by expert laparoscopic surgeons, but laparoscopic hernia surgery is more difficult than other laparoscopic procedures. It is more difficult than open hernia surgery to teach, to learn, and to perform. 4o The safety of laparoscopic repair, even when satisfactory in expert hands, is not universally acceptable. Rare but unacceptably severe complications are reported,41 mostly during the learning period. Some of these complications may be unrecognized intraoperatively (for example, a bowel injury), leading to catastrophic consequences related to delayed diagnosis. 42 Because every method has its limits, criteria for laparoscopic repair should be established. Laparoscopy's real benefit in terms of patient satisfaction has been investigated in several recent controlled studies. The principal criterion for the evaluation of a hernia cure is consensually the recurrence rate, after a follow-up of at least five years, preferably by a surgeon, on at least 90% of the total number of patients. Because this long-term follow-up is difficult to realize in active patient series, a logical exacting "maximum bias method" has been recently proposed. It consists of treating as recurrences all patients who have not changed addresses and who refuse to answer the surveys. Other criteria used in comparative evaluations are the postoperative com-

fort level, the complication rate and severity, the length of hospital stay, lost work time, and the cost of the procedure. Randomized clinical trials propose a quasi-metaphysical problem to the surgeon, who as a craftsman is naturally inclined to do the best possible work and is reluctant to proceed at random. Randomized studies are inconsistent with the principle of personalization of hernia cure. Comparison in hernia surgery is more difficult than in evaluations of medical treatments. Even the metaanalysis method, which is considered a statistical technique that limits personal and/ or institutional bias, should require organization to compare equivalent techniques applied to the same hernia types and to the same patient groups.

FIGURE 1.11. Halsted's illustration showing his first hernioplasty. All layers of the abdominal wall are cut through down to the peritoneum. The cord

is withdrawn to the subcutaneous tissues. The repair is done with mattress sutures that encompass all aponeurotic-muscular layers of the abdomen.

FIGURE 1.12. Illustration from Marcy's famous book showing simple ring closure. There is no doubt as to the nature of the repair. The transverse aponeurotic arch is sutured to the iIiopubic tract. From The Anatomy and Surgical Treatment of Hernia. New York: D. Appleton & Co, 1892.

However that may be, some controlled studies have compared laparoscopic techniques to nonlaparoscopic repairs (Brooks,43 Payne,44 Stoker,45 Barkun,46 Lawrence,47 Wilson,48 Filipi,49 Horeyseck, 50 Zieren,51 Champault,52 Heikkinen,53 Liem 54 ). Most of them are open to criticism on a statistical level, and most provide controversial conclusions, but they have merit and take some steps in the search for evidence. Compared to some current open repairs, laparoscopic hernia surgery does not reduce hospital stay. Postoperative pain is not less than it is after the Lichtenstein or Gilbert procedures. The return to normal activity occurs after nearly the same amount of time after each procedure in comparable groups of patients (same age, type of work). In long-term recurrence rate,

FIGURE 1.13. From an 1899 Ferguson paper showing the undissected spermatic cord and the repair that consisted of the approximation of the internal oblique abdominal muscle to the inguinal ligament.

R. Stoppa et a\.

FIGURE 1.14. Fruchaud's myopectineal orifice (10) delineated by the rectus muscle medially (11), the iliopsoas muscle laterally (6), the internal oblique muscle superiorly (1), and the pecten of the pubis inferiorly (12). The spermatic cord (9) and iliac vessels (7,14) cross the myopectineal orifice. Drawing by A. Moreaux in H.M. Fruchaud, Anatomie Chirurgicale des Hernie de [,Aine, Doin: Paris, 1956.

laparoscopic techniques do not provide better results than those of classic surgery. Studies comparing the two main laparoscopic procedures (TAPP vs TEP) are few: Khoury,55 Schrenk,56 Tschuydi.57 They have a low follow-up, but these reports indicate that the TAPP procedure is the easiest to learn and to perform. But the intra-abdominal manipulation, with incision of the peritoneum and extraperitoneal insertion of mesh (TAPP; transabdominal preperitoneal), much like the IPOM; intraperitoneal onlay patch repair which leaves mesh in the peritoneal cavity, exposes the patient to the risk of postoperative obstruction and may have a higher recurrence rate than the TEP technique. As far as individualization of the repair is concerned, laparoscopic procedures, which systematically use prosthetic material, are overtreatrnent for types I and II hernias. Because of the paucity of convincing studies favoring laparoscopic procedures and the need for a minimum of five years of follow-up, we must wait several years for reports of rigorous comparative results before we will know the most efficient procedures in terms of postoperative comfort, recurrence rate, and cost. Laparoscopic repair has not replaced open hernia operations, currently the most commonly performed. It is necessary and wise to continue to teach the classic procedures. Taking into account laparoscopic surgery's technical difficulty, highly technologic dependence, and its uncertain safety, it seems advisable not to introduce this hernia surgery on a large scale. Surgeons with experience and skill in laparoscopic repair can continue to operate this way, but they must think twice about pressuring the surgical community and influencing public opinion in exclusive favor of laparoscopic hernia repair (Wantz58 ). There remains the unresolved question of whether hernia surgery should be a surgical specialty. Indeed, it has an undeni-

1. Evolution of Groin Hernia Repair

able identity, composed of its anatomic and physiologic bases, its requirement for benignity and success, and its humanistic and social implications. There is a community of specially interested surgeons and great demands for these services. There are large differences in the results between experts and nonexperts. But hernia surgery, a very good example of a well-regulated surgery with rather simple basic procedures, is really a part of general surgery. Performing good hernia surgery has proved beneficial to the practices of young surgeons. Progress has not been made only by those surgeons devoted exclusively to inguinal hernioplasty. We believe that unnecessary specialization could impoverish hernia surgery, when maintaining it within general surgery would result in more creative exchanges. On condition that residents in general surgery be excellently taught the details of anatomy of the groin and thoroughly trained in hernia repair, hernia surgery is "a quintessential operation, which epitomizes surgery" (Wantz59 ). It falls to surgeons to continue to push hernia repair toward excellence, a duty assumed with close application by Chevrel and the GREPA members for more than 20 years,60 and by the American Hernia Society members, among others. This is an ethical service and, at the same time, a source of professional pride.

References 1. Stoppa R, Wantz G, Munegato G, et al. Hernia Healers. An IUustrated Histury. Paris: Arnette; 1998:175. 2. Segond P. Cure radicale des hernies. In: These du Concours d'Agregation, Paris: Masson; 1883. 3. Bull Wf. Notes on cases of hernia which have relapsed after various operations or radical cure. NY MedJ 1891;53:615. 4. Bassini E. Sulla cura radicale dell'ernia inguinale. Arch Soc ltal Chir. 1887;4-30. 5. Anson BJ, McVay CB. The anatomy of the inguinal region. Surg GynecolObstet. 1938;66:186-194. 6. Shouldice EE. Surgical treatment of hernia. Ontario Med Rev. 1945; 12:43. 7. Fruchaud H. Anatomie chirurgicale des hernies de l'aine. Paris: Doin; 1956. 8. Fruchaud H. Le traitement chirurgical des hernies de l'aine chez l'adulte. Paris: Doin; 1956. 9. Cooper AP. The Anatomy and Surgical Treatment ofAbdominal Hernia. London: Longman; 1804, 1807. 10. Thomson A. Cause anatomique de la hernie inguinale externe. Journal des connaissances medicales pratiques et de pharmacologie. 1836;4:137. 11. McVay CB, Chapp JD. Inguinal and femoral hernioplasty. Evaluation of a basic concept. Ann Surg. 1958;148:499. 12. Condon RE. Surgical anatomy of the transversus abdominis and transversalis fascia. Ann Surg. 1971; 173: 1. 13. Annandale T. Case in which a reducible oblique and direct inguinal and femoral hernia existed on the same side and were successfully treated by operation. Edinb MedJ 1876;21:1087. 14. Cheatle GL. An operation for the radical cure of inguinal and femoral hernia. Br Med J 1920;2:68. 15. Henry'AK. Operation for femoral hernia by a midline extraperitoneal approach: with a preliminary note on the use of this route for reducible inguinal hernia. Lancet. 1936;1:531. 16. Nyhus LM, Stevenson JK, Listerud MB, et al. Preperitoneal herniorrhaphy: a preliminary report on fifty patients. West J Surg. 1959;67:48. 17. Rives J, Stoppa R, Fortesa L, et al. Les pieces en Dacron et leur place dans la chirurgie des hernies de l'aine. Ann Chir. 1968;22:159. 18. Stoppa R, Petit J, Abourachid H. Procede original de plastie des hernies de l'aine. L'interposition sans fixation d'une prothese en tulle de Dacron par voie mediane sous-peritoneale. Chirurgie. 1973;99:119.

19. Griffith CA. Indirect inguinal hernia. With special reference to the Marcy operation. In: Nyhus LM, Harkins HN, eds. Hernia. 1st ed. Philadelphia: Lippincott; 1964. 20. Peacock EE, Jr, Madden JW. Studies on the biology and treatment of recurrent inguinal hernia: II. Morphological changes. Ann Surg. 1974; 179:567. 21. Read RC. Attenuation of rectus sheath in inguinal herniation. Am J Surg. 1970;120:610. 22. Aquaviva DE, Bourret P, Corti F. Considerations sur l'emploi des plaques de nylon dites crinoplaques comme materiel de plastie pamtale. Cong Fr de Chirugie, Paris: Masson; 1949:453. 23. Usher FC, Ochsner JL, Tuttle LL,Jr. Use of Marlex mesh in the repair of incisional hernias. Ann Surg. 1958;24:969. 24. Koontz AR, Kimberley RC. Tantalum and Marlex mesh (with a note on Marlex thread). An experimental and clinical comparison-preliminary report. Ann Surg. 1960;151:796. 25. RivesJ, Lardennois B, FlamentjV, et al. La piece en tulle de Dacron, traitement de choix des hernies de l'aine de l'adulte. A propos de 183 cas. Chirurgie. 1973;99:564. 26. Stoppa RE, Rives JL, Warlaumont CR, et al. The use of Dacron in the repair of hernias of the groin. Surg Clin North Am. 1984;64:269. 27. Royal College of Surgeons of England. Guidelines on the Management of Groin Hernia in Adults. Report of a Working Party Convened by the Royal College of Surgeons of England. London, 22 April 1993. 28. Nyhus LM, Klein MS, Rogers FB. Inguinal hernia in current surgical problems. Surgery XXXVIIII, St. Louis: Mosby Year Book, Inc., 1991; 6:403. 29. Devlin HB. Management of Abdominal Hernias. London: Butterworth, 1988. 30. Harkins HN. In: Nyhus LM, Stevenson JK, Listerud MB, et al., eds. Commentary on preperitoneal herniorraphy. Preliminary report on fifty patients. West J Surg. 1959;6:48. 31. Casten DF. Functional anatomy of the groin as related to the classification and treatment of groin hernias. Am J Surg. 1967;114:894. 32. Gilbert AI. An anatomic and functional classification for the diagnosis and treatment of inguinal hernia. Ann Surg. 1989;157:331. 33. Bendavid R The TSD classification. Diagrammatic representation of the various types and stages. A nomenclature for groin hernias. Monographie GREPA. 1993;15:12-14. 34. Stoppa RE, Warlaumont CR The midline preperitoneal approach and the prosthetic repair of groin hernia. In: Nyhus LM, Baker RJ, eds. Mastery of Surgery, 2nd ed. Boston: Little, Brown; 1992. 35. NicollJH. The surgery of infancy. Br MedJ 1909;ii:753-756. 36. Marcy HP. The cure of hernia by the antiseptic use of animal ligature. Trans lnt Med Congo 1891;2:446. 37. Lichtenstein IL. Hernia Repair Without Disability. St. Louis: C.Y. Mosby, 1970. 38. Gilbert AI. Inguinal hernia repair: biomaterials and sutureless repair. Perspec Gen Surg. 1991;2/1:113. 39. Wantz GE. Giant prosthetic reinforcement of the visceral sac. Surg Gynecol Obstet. 1989; 169:408. 40. Wantz GE. Atlas of Hernia Surgery. New York: Raven Press; 1991. 41. Wantz GE. The technique of giant prosthetic reinforcement of the visceral sac performed through an anterior groin incision. Surg Gynecol Obstet. 1993; 176:497. 42. Wantz GE. Properitoneal hernioplastywith Mersilene,® giant prosthetic reinforcement of the visceral sac (GPRVS). In: Bendavid R, ed. Prostheses and Abdominal Wall Hernias. Austin: RG. Landes Company; 1994. 43. Brooks DC. A prospective comparison oflaparoscopic and tension-free open herniorrhaphy. Arch Surg. 1994;129:361-366. 44. Payne JH, Grininger LM, Izawa MT, et al. Laparoscopic or open herniorrhaphy? A randomized prospective trial. Arch Surg. 1994;129: 973-981. 45. Stoker DL, Spiegelhalter DJ, Singh R, et al. Laparoscopic versus open inguinal hernia repair: randomised prospective trial. Lancet. 1994;343: 1243-1245.

10 46. BarkunJ, Wexler~, Hinchey EJ, et al. Laparoscopic versus open inguinal herniorrhaphy: preliminary results of a randomized controlled trial. Surgery. 1995;118:703-710. 47. Lawrence K, McWhinnie D, Goodwin A Randomised controlled trial of laparoscopic versus open repair of inguinal hernia; early results. Br MedJ 1995;311:981-985. 48. Wilson MS, Dean GT, Brough A Prospective trial comparing Lichtenstein with laparoscopic tension-free mesh repair of inguinal hernia. BrJ Surg. 1995;82:274-277. 49. Filipi Cj, Gaston:Johansson F, McBride PJ. An assessment of pain and return to normal activity. Laparoscopic herniorrhaphy vs open tensionfree Lichtenstein repair. Surg Endosc. 1996;10:983-986. 50. Horeyseck G, Roland F, Rolfes N. "Tension-free" repair of inguinal hernia: laparoscopy (TAPP) versus open (Lichtenstein) repair. Chirurgia. 1996;67:1036-1040. 51. Zieren J, Zieren HU, Wenger FA, et al. Laparoskopische oder Konventionelle Leistenhernienreparation mit oder ohne Implantat. Eine prospektiv-randomisierte Studie. Langebecks Arch ChiT. 1996;38:289-294. 52. Champault GG, Rizk N, CathelineJM, et al. Inguinal hernia repair: totally preperitoneal laparoscopic approach versus Stoppa operation. Randomized trial of 100 cases. Surg Laparosc Endosc. 1997;7:445-450.

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53. Heikkinen T, Haukipuro K, LeppalaJ, et al. Total costs oflaparoscopic and Lichtenstein inguinal repairs: a randomized prospective study. Surg Laparosc Endosc. 1997;7:1-5. 54. Liem MSL, van der GraafY, van Steensel Cj, et al. Comparison of conventional anterior surgery and laparoscopic surgery for inguinal hernia repair. N EnglJ Med. 1997;336:1541-1547. 55. Khoury N. A comparative study of laparoscopic extraperitoneal and transabdominal preperitoneal herniorrhaphy. ] Laparoendosc Surg. 1995;5:349-355. 56. Schrenk P, WoisetschHiger R, Rieger R, et al. Prospective randomized trial comparing postoperative pain and return to physical activity after transabdominal preperitoneal, total preperitoneal or Shouldice technique for inguinal hernia repair. BrJ Surg. 1996;83:1563-1566. 57. Tschuydi J, Wagner M, Klaiber C. Controlled multicenter trial of laparoscopic transabdominal preperitoneal hernioplasty vs Shouldice herniorrhaphy, early results. Surg Endosc. 1996;10:845-847. 58. Wantz GE: Editorial: The American Hernia Society. Hernia. 1997;1:3. 59. Wantz GE. Abdominal wall hernias. In: Schwartz S, Shires GT, Spencer FT, ed. Principles of Surgery. 6th ed. New York: McGraw-Hill; 1994. 60. Chevrel JP. Hernias and Surgery of the Abdominal Wan. 2nd ed. Paris Berlin Heidelburg: Springer-Verlag; 1998.

2 Use of the Preperitoneal Space in Inguinofemoral Herniorrhaphy: Historical Considerations Raymond C. Read

In ancient Egypt, groin hernias were treated only by external manipulation and bandaging, but celiotomy was used in India by the Hindus in the Brahmanic era (800-500 BC) and Praxagoras in Greece (350 BC) for the relief of obstructed and strangulated bowel resistant to taxis. Reduction of intestine, with or without incision of the hernial ring (kelotomy) or resection was accomplished through a small incision in the linea alba near the protrusion. During the Dark Ages, this procedure continued to be performed in the East. Most of the Greeks and all the Romans cut from below. I This dichotomy between the transabdominal (posterior) and the inguinal (anterior) routes continued. In the Middle Ages, the incisor Stromayr, in his manuscript of 1559,2 illustrated transfixion of the spermatic cord at the external inguinal ring. Cantemir reported on transperitoneal taxis and repair in his history of the Ottoman Empire. This was translated into French by Joncquieres3 in 1743, and Marcy published it in English in 1892.4 According to Chavasse,5 Crompton of Birmingham, England, used the transperitoneal posterior approach to the groin in a patient with strangulated umbilical herniation in 1860. Finding the gut gangrenous, he desisted and laid the sac open. Niven,6 the following year, suggested that femoral hernias could be similarly managed. The great Scottish surgeon, Annandale, repeated Crompton's procedure in 1873. Bowel obstruction relented, but the patient died two days later. He commented, "The ease with which a strangulated portion of the gut is relieved when gentle traction is made upon it, is remarkable."7 In the United States, Hutchinson (1878) reported on a case of inguinal herniation which, after multiple unsuccessful attempts at taxis under anesthesia, was operated upon in this manner. Bowel displaced through a tear in the peritoneum was found, and the reductio en masse was relieved, but gangrene supervened, resulting in the death of the patient. s A similar case treated successfully was described by Ward eight years later. 9 In the 1880s and 90s, a number of case reports appeared in British medical journals attesting to the value of this approach in the management of strangulated hernias. Maunsell, from New Zealand, published in support of this operation in 1887, and participated in a spirited discussion at the 1891 annual meeting of the British Medical Association. He propounded the importance of complementary closure of the femoral ring, which he achieved with transperitoneal placement of a silver wire mattress suture join-

R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

ing Poupart's, Gimbernat's and Cooper's ligaments. The suture was then passed down the femoral canal through the saphenous foramen and affixed to the skin of the thigh.lO One of the enthusiasts of "abdominal section for displaced hernia," Lawson Tait,n was a gynecologist who noticed the ease of incidental herniorrhaphy while operating in the pelvis in 1883. His patient had an ovarian cyst in association with an undiagnosed incarcerated femoral hernia. Mter resecting the tumor from the pelvis, he was able to reduce the herniated omentum and adherent intestine. He closed the femoral ring with a silk purse-string suture. This experience led him to recommend that the treatment of herniation by median abdominal section should be extended to nonstrangulated, reducible chronic hernias. He spelled out the advantages of the intraperitoneal approach to the elective "radical" cure of reducible hernias through a suprapubic linea alba incision in an extensive presentation to the section of surgery at the 1891 meeting of the British Medical Association. The benefits included: (a) ease of pulling out rather than pushing back herniated intestine or omentum; (b) rare need to dilate the hernial ring; (c) less hemorrhage; (d) laparotomy easily extended for intestinal resection; (e) no risk of reductio en masse; (f) quick repair; (g) no risk of injury to the intestine; (h) incision bloodless and easy to close; and (i) no damage to the inguinal canal, inferior epigastric vessels or the parietes. 12 A number of British surgeons enthusiastically supported him. Keetley (1886) summarized their case reports. Celiotomy was recommended for adults with large umbilical, inguinal or femoral protrusions and any others which presented difficulties. 13 In the United States, Kelly (1898), the first gynecologist-in-chief at Johns Hopkins Hospital, followed Tait's lead. He sometimes plugged the femoral canal from within, using a marble. 14 Later, Gillion (1891) published an article in Belgium,15 and Robins (1909) of Richmond, Virginia, another gynecologist, described a patient with recent strangulation of an inguinal protrusion. Finding the hernia irreducible from a groin incision, he extended it superiorly, split the rectus muscle, entered the abdominal cavity and reduced the bowel. Mter ligating the sac, he returned below and performed a repair. His patient made an uneventful recovery.l6 In 1919, LaRoque, also from Richmond, Virginia, published his intraperitoneal approach to all inguinal hernias. He used a muscle-splitting transverse incision in the internal oblique and transversus layers immediately above the internal inguinal ring to 11

perform celiotomy, closing the neck of the sac from within. A conventional herniorrhaphy followed. 17 In 1922, his technique was applied to femoral herniation. I8 In 1907, Moschcowitz recommended transperitoneal repair of femoral defects through a suprainguinal incision.l 9 In 1913, Bates applied Moschcowitz's operation to the elective intraperitoneal repair of indirect herniation. 20 LaRoque's operation was later recommended, particularly for sliding hernias, incarcerated or strangulated intestine, and cryptorchidism by Williams 2I until the end of World War II. It was revived by Dennis and Varco in 1947 for strangulated femoral herniation. 22 McEvedy (1966)23 and Wilkinson (1967) were the last to publish on the intraperitoneal technique. 24 The introduction of laparoscopic techniques (pioneered again by gynecologists) to groin herniorrhaphy in 1982 by Ger,25 resurrected the intraperitoneal posterior approach. Pari passu with the interest detailed above in the transabdominal (intraperitoneal) route to the groin, the anterior approach from below continued. In the early 19th century, repair was little different from that provided by the Romans, except that efforts were made not to include the spermatic cord in the ligature of the processus vaginalis. Later on, attempts were made to also obliterate the inguinal canal by external compression (trusses), sometimes supplemented by injected escharotics. The culmination of these efforts by, among others, Gerdy (1797-1856), a French surgeon who plugged the external inguinal ring with inverted scrotal skin held by sutures, and Wutzer (1789-1858), who secured it with a wooden plug, was Wood's operation (1863)26 and that of MacEwen (1886).27 They dissected up the hernial sac blindly from the external ring, and used it to plug the internal abdominal ring, being fixed, transcutaneously, by suture to the postero-Iateral abdominal wall using a Reverdin needle. Bassini employed this procedure which, he showed at autopsy, failed from eventual absorption of the sac. It was this experience which prompted him to develop his own operation (anterior approach), thus laying the foundation for modern herniology.28

The Use of the Preperitoneal Space

The Anterior Preperitoneal Approach to the Groin Remarkably, the first surgical use of the preperitoneal space was not for herniorrhaphy, but proximal ligation (Hunterian) of the epigastric or external iliac artery for aneurysm. An extraperitoneal approach was designed to avoid the risk of peritonitis (before antisepsis) from dividing the closely applied peritoneal layer with higher abdominal incisions. This procedure was undertaken from below, using the anterior approach to the groin, the roof and floor of the inguinal canal being divided. The operation, performed before the development of anesthesia, was described in an MD thesis to the University of Paris in 1823 by Bogros.29 This Professor of Surgical Anatomy at that institution had observed, "The external iliac artery terminates without a serosal cover ... The peritoneum extending from the anterior abdominal wall to the iliac fossa leaves in front a space 13.5 to 15.5 mm wide." Rouviere (1912), the great French anatomist, added, "... the outer layer of the peritoneum, in the shape of a gutter, concave above and behind, is in contact with the soft tissues of the iliac fossa from 1 to 1.5 cm above the inguinal ligaments. The peritoneum thus de-

R.e. Read

marcates with a dihedral angle formed by the fascia transversalis and the fascia iliaca inferiorly, a triangular prismatic interval filled with preperitoneal adipose tissue called the space of Bogros. "30 Further, Bogros described the inferior epigastric vessels as "first passing inferiorly, overlying the parent external iliac vessels, then turning anteriorly to enter the abdominal wall." Thus, their plexes run between Cooper's two laminae of transversalis fascia, not within the extraperitoneal space, as suggested by Condon and Bendavid. 31 That Bogros's space is avascular was demonstrated in 1972 by Tyson and Reichle, who used it for extraperitoneal femorofemoral arterial bypass. Nevertheless, illey reported that in a patient with iliac thrombophlebitis undergoing saphenofemoral venous bypass, vesical venous collaterals can be torn. 32 It would be 53 years before Annandale, and 62 years before Bassini, documented division of the external oblique aponeurosis and the transversalis fascial floor of the inguinal canal, for the repair of herniation. The topography of the midline pubovesical preperitoneal space of Retzius33 (1852) is well known. Amazingly, this Swedish anatomist was unaware of the space of Bogros since its description was documented only in a thesis, Bogros dying of pulmonary tuberculosis in 182~three years after his monumental contribution. However, as indicated above, Rouviere and other French anatomists at the beginning of the twentieth century pointed out that the lateral spaces of Bogros and the midline space of Retzius communicate. The first surgeon to use the preperitoneal space in the repair of groin herniation was Annandale, in 1876. He reported an operation he had performed on a 46-year-old man with unilateral, triple herniation, indirect, direct inguinal and femoral defects. The protrusions were so large that no truss could be fitted. The patient suffered from a dragging pain, and since the protrusions came down when he stood, walked, or coughed, he was unable to work. Annandale made an incision an inch above the inguinalligament and cut through the roof and floor of the inguinal canal, severing the epigastric vessels. The necks of the inguinal sacs were isolated close to the general peritoneum. Mter opening, they were ligated, all content being reduced. The femoral sac reduced spontaneously, and he plugged the femoral canal with the inguinal sac stitched below to the skin of the thigh, overlying the saphenous opening. The patient was seen three months later when he was doing well except for a femoral bulge, which was treated with a truss. 34 Annandale was thus the first to use the anterior preperitoneal approach for femoral and inguinal herniorrhaphy. He preceded Bassini (1884) in dividing the roof of the inguinal canal in the management of groin herniation. His operation was further developed by Ruggi (1892),35 in Italy, and Lotheissen (1898), a pupil of Billroth. 36 Bassini's operation (1887), which revolutionized the surgery of groin herniation, also made use of the preperitoneal space as reached from below through the anterior approach. Like Annandale, he not only divided the external oblique aponeurosis-the roof of the canal-but also transected the transversalis fascial floor as well, while preserving the epigastric vessels. He was followed closely by Halsted (1889).37 Unfortunately, numerous modifications soon replaced these preperitoneal procedures with suturing of the internal oblique muscle to the inguinal ligament. It took more than 60 years before the Shouldice Clinic reinstituted the modern Bassini and returned the operation to the preperitoneal position. Concern about tension and suture failure, especially with direct and recurrent herniation, led to the introduction of pros-

2. History of the Preperitoneal Space

muscle. The repair was performed internal to them in the avascular lateral preperitoneal space of Bogros. He commented upon finding "unsuspected and potential sacs" on the contralateral side, "dimples" of peritoneum and obliterated cords of processi vaginales. Occasionally, the urachus or a partially obliterated hypogastric artery (lateral umbilical fold) were seen. Ifhe encountered an incarcerated hernia, he opened the peritoneum and converted his operation to the intraperitoneal posterior procedure. Thus, Cheatle's particular contribution was entering the lateral suprainguinal parietoperitoneal space of Bogros via the space of Retzius, thereby providing access to bilateral groin herniation. Incidentally, he described concomitant appendectomy. He lived for 30 more years without publishing further on this procedure. It is The Posterior Preperitoneal remarkable that his landmark publication made so little impact that it was not even mentioned in his obituary ("No surgical inApproach to the Groin novations are associated with his name.") .48 His operation was reThe first procedure from above the pubis using the posterior discovered by Henry in 1936, who described bilateral closure of preperitoneal space in the repair of inguinofemoral herniation indirect inguinal sacs at their true neck next to the general periwas that of Cheatle in 1920. 44 George Lenthal Cheatle received his toneal envelope. 49 Nevertheless, little interest was shown in this medical education at King's College in London, graduating in procedure until after World War II. It was not even mentioned in 1887. He obtained his surgical training at the hospital under Edwards's authoritative review of herniology in 1943,50 or that of Joseph Lister, Chairman of Surgery (1877-1893), assisting the lat- Harkins in 1949. 51 The procedure was revived in the United States by Jennings and ter in the last operation he performed. Cheatle, who was blessed with an original mind and a passion for research, particularly in Anson (1942), who touted its advantages, exposure of the defect, regard to inflammation and cancer of the breast, loved the un- access to the deep transverse layer, importance of preperitoneal orthodox. He became a devoted disciple of Lister, from whom he fatty protrusion, high ligation of peritoneal sacs, less infection, and learned the virtues of enthusiasm, hard work, and attention to de- absence of injury to the spermatic cord and the accompanying tail. He spent his whole surgical career at King's College Hospital, nerves. 52 In 1949, Musgrove and McCready, at the Mayo Clinic, becoming senior surgeon in 1923, retiring in 1930. He is best recommended the Cheatle-Henry operation for femoral and known for his discovery of the association between Paget's disease obturator hernias. 53 Riba and Mehn (1952) described its associaof the nipple and underlying breast cancer, as well as his widely tion with retropubic prostatectomy.54 Hull and Ganey (1953),55 Mikkelsen and Berne (1954),56 Shandling and Thomson (1960),57 used dressing forceps. Herniology flourished at this institution. In 1863, Professor and Lipton (1961)58 then reported extensively on the procedure. Wood had published his book on hernia, which described subcu- The latter three contributors worked with children, emphasizing taneous fascial invagination and obliteration of the inguinal sac its use in cryptorchidism and incarcerated or recurrent herniawithin the canal, a procedure which was derived from the earlier tion. McVeigh and Barker (1954) pointed out disadvantagesGerdy (1820)45 and Wutzer (1838)46 inverted skin procedures. It local anesthesia could not be used, there was no easy way to perbecame widely used. Lister and his pupils from Britain and around form a relaxing incision, scrotal sacs could not be removed, good the world, including Annandale, Marcy, Bassini and Lucas-Cham- fascia was not always available in direct herniation, the external pionniere, searched for the radical cure. They had an advantage oblique layer could not be used in the repair, and its ring remained over many of their colleagues because they had not resisted, for a open. 59 The Cheatle-Henry approach was enthusiastically endecade or two, the application of antisepsis. They were thus able dorsed by Stoppa, who over the last quarter of a century has used to open up tissue planes, dissect, and use buried sutures. his giant prosthesis reinforcement of the visceral sac (GPRVS) to Cheatle's first description of his operation was brief, little more repair bilateral groin herniation. He has concentrated on difficult than haifa page. His first use ofa paramedian incision was adopted cases, many with recurrent disease. It is remarkable that he has because it was less liable to break down than the midline. It also been able to obtain a recurrence rate similar to most surgeons opdid not require as much retraction to work within the lateral erating on primary herniation. 60 Wantz has popularized this impreperitoneal suprainguinal space of Bogros. Like Henry later, he portant advance in the United States and developed his own pointed out that there is an intra-abdominal preperitoneal sper- unilateral variant. 61 Most laparoscopic repairs today use the posmatic cord which may contain an indirect sac between the inter- terior preperitoneal approach and attempt to reproduce Stoppa's prosthetic repair, avoiding any slit for the spermatic cord. nal ring and the general peritoneal cavity. The following year, in his second publication,47 Cheatle pointed Perhaps the most important post-World War II contribution to out that he was "led to devise a new method," the transabdominal posterior preperitoneal herniorrhaphy was made by P.G. McEvedy preperitoneal abdominal approach, because he had encountered in 1950. 62 He introduced the unilateral approach from above for a succession of cases which, from below, "presented difficulties in femoral herniation. His incision through the rectus sheath was the efficient excision of the sac." He had now reverted to median originally vertical, extending into the thigh where necessary to resection, conducted with a Pfannenstiel incision recommended by lieve incarceration. At the suggestion of Ogilvie and McNaught the gynecologist Victor Bonney, emphasizing again the influence (1956),63 the incision was made oblique with medial, rather than of this specialty and (later with Henry) urology on the develop- lateral, retraction of the rectus muscle. The same year, Reay'ment of herniology. Cheatle described retraction, within the space Young64 changed the approach to half a Pfannenstiel incision. of Retzius, of the inferior epigastric vasculature with the rectus The prime mover in posterior preperitoneal herniorrhaphy of theses by Acquaviva and Bourret (1948).38 Usher (1958) put anterior prosthetic repair on the map, using the preperitoneal approach. 39 Mahorner and Goss (1962), in two patients with recurrent herniation who had lost both inguinal and Cooper's ligaments, inserted a preperitoneal dermal graft from below. 4o Rives (1965), in France, used Mersilene® in the same way and stimulated his students, Stoppa and Flament, to further develop properitoneal prosthetic placement from both above and below. 41 More recently, Schumpelick42 and 143 have reported our experiences with anterior preperitoneal prosthetic repair.

the groin has been Nyhus (1960).65 He and his associates (1959)66 were stimulated by Mikkelsen and Berne to use the Cheatle-Henry approach. Visiting Professor John Bruce of Edinburgh, in discussion of their paper, recommended using the unilateral McEvedy approach. Taking his advice, Nyhus's group reported the following year on a large series using a modified McEvedy procedure, extended across the midline in bilateral defects. Nyhus's contribution sparked an explosion of interest in the approach from above and led to a better understanding of the anatomy of the preperitoneal suprainguinal space. Fowler (1975) ,67 an Australian pediatric surgeon, made an important contribution when he brought together previous observations of Bassini regarding peritoneal ligation in the iliac fossa (1890); Henry, true and false necks of the processes vaginalis (1936); and Lytle, the internal inguinal ring (1945).68 These were extended by Lampe for the preperitoneal fascia (1989)69 and Read, Cooper's posterior lamina of transversalis fascia (1992).70 The result was an understanding that the internal spermatic fascia was not derived from the internal inguinal ring and the anterior lamina of the transversalis fascia, but more internally from preperitoneal fascia and the posterior lamina of the transversalis fascia at the secondary internal ring close to the general peritoneal cavity. A preperitoneal spermatic cord, with or without a processus vaginalis, runs through the fatty avascular space of Bogros. High ligation of the sac demands dissection internal to the internal inguinal ring. Preperitoneal fat in the space of Bogros may therefore be a source of sliding herniation, with or without a processus vaginalis, and must be distinguished from cord lipomata. The inferior epigastric vasculature courses between the two laminae of transversalis fascia. Dissatisfaction with the results of sutured repairs through this approach prompted the application of prosthetics. This had been successfully performed in a large series from the anterior preperitoneal approach by Usher, et al. in 1958. Nyhus used a polyvinyl alcohol sponge in a patient (1959). Estrin and associates,71 in a series employing Usher's Marlex® (polypropylene) mesh (1963), pioneered their application from the posterior preperitoneal approach. I followed in 196772 and 1976. 73 Calne (1967)74 combined the anterior and posterior preperitoneal approaches, laying a large piece of Mersilene® mesh behind both rectus muscles after opening both groins for bilateral groin herniation. These many contributions have allowed the profusion of preperitoneal techniques available to the surgeon today for the management of patients presenting with herniation through the groin.

References 1. Read RC. The development of inguinal herniorrhaphy. Surg Clin Narth Am. 1984;64:185-196. 2. Read RC. Properitoneal herniorrhaphy: a historical review. WorldJ Surg. 1989; 13:532-540. 3. de Cantemir D. Histoire de l'agrandissement de l'empire Ottoman. Translated by M. De Joncquieres. 1743;2:397-401. 4. Marcy HO. The Anatomy and Surgical Treatment of Hernia. New York: D. Appleton Co.; 1892. 5. Chavasse TF. On a method of operating in strangulated umbilical hernia. Lancet. 1882;1:865. 6. Niven J. A new operation for the relief of hernia. Lancet 1861;1:276. 7. Annandale T. On a method of operating in certain cases of strangulated hernia. Edinb MedJ 1873-4;19:209-211.

RC. Read 8. Hutchinson E. Case of strangulated hernia operated on by abdominal section. Laparotomy. Ohio Med SurgJ 1878;3:499-502. 9. Ward E. Abdominal section for displaced hernia. Lancet. 1886;2:201203. 10. Maunsell HW. Radical cure of strangulated femoral hernia by suprapubic laparotomy. N Z MedJ 1887;1:23-25. 11. Tait L. On the radical cure of exomphalos. Br Med J 1883;2:1118. 12. Tait L. A discussion on treatment of hernia by median abdominal section. Br MedJ 1891(2):685-691. 13. Keetley CB. Thirteen cases of herniotomy for strangulated hernia. Br MedJ 1883;2:1093-1095. 14. Kelly HA. Femoral hernia. operative Gynecology. New York: D. Appleton Co.; 1898;Vol. 2:490-491. 15. Gillion L. Un nouveau procede de herniotomie, laparotomie pour hernie ombilicale. Clinique (Brux). 1891;5:758-760. 16. Robins CR Rectus incision for reduction of strangulated hernia with a report of a case of strangulated hernia in the sac of an undescended testicle. Old Dom J Med Surg. 1909;8:324-326. 17. LaRoque GP. The permanent cure of inguinal and femoral hernia: a modification of standard operative procedures. Surg Gynec Obstet. 1919; 29(5):507-511. 18. LaRoque GP. The intra-abdominal operation for femoral hernia. Ann Surg. 1922;75:110-112. 19. Moschcowitz AV. Femoral hernia: a new operation for the radical cure. JAMA. 1907;48:896-900. 20. Bates UC. New operation for the cure of indirect inguinal hernia. JAMA.1913;60:2032-2033. 21. Williams C. Repair of sliding inguinal hernia through the abdominal (LaRoque) approach. Ann Surg. 1947;126(4):612-623. 22. Dennis C, Varco RL. Femoral hernia with gangrenous bowel. Surgery. 1947;22:312-323. 23. McEvedy BV. The internal approach for inguinal herniae. Postgrad Med J 1966;42:548-550. 24. Wilkinson BW. LaRoque intra-abdominal approach for removal of hernia sac of inguinal and femoral hernia. W Va Med J 1967;63: 142-146. 25. Ger R The management of certain intra-abdominal hernias by intraabdominal closure of the sac. Ann R Coll Surg Engl. 1982;64:342-344. 26. Wood J. On Rupture, Inguinal, Crural and Umbilical; the Anatomy, Pathology, Diagnosis, Cause and Prevention with New Methods of Effecting a Radical and Permanent Cure, Embodying the Jacksonian Prize Essay of the Royal College of Surgeons of London. London: Davies; 1863. 27. MacEwen W. On the radical cure of oblique inguinal hernia by internal abdominal peritoneal pad and the restoration of the valved form of the inguinal canal. Ann Surg. 1886;4:89-119. 28. Bassini E. Nuovo metodo per la cura radicale dell'ernia inguinale. Atti Congre Assoc Med leal. 1887;2:179-182. 29. Bogros AJ. Essai sur l'anatomie chirurgicale de la region iliaque et description d'un nouveau procede pour faire la ligature des arteres epigastrique et iliaque externe. Th. Paris 1823, no. 153. A Paris, de l'imprimerie de Didot leJeune, imprimeur de la Faculte de medecine, rue des Ma-;ons, Sorbonne no. 13. 30. Rouviere H. Anatomie humaine descriptive, topographique et fonctionelle. Masson Edit, Paris, 1912. 31. Bendavid R The space of Bogros and the deep inguinal venous circulation. Surg Gynecol Obstet. 1992;174:355-358. 32. Tyson RR, Reichle FA. Retropubic femorofemoral bypass: a new route through the space of Retzius. Surgery. 1972;72(3):401-403. 33. Retzius AA. Some remarks on the proper design of the semilunar lines of Douglas. Edinb Med J 1858;3:865-867. 34. Annandale T. Case in which a reducible oblique and direct inguinal and femoral hernia existed on the same side and were successfully treated by operation. Edinb MedJ 1876;21:1087-1091. 35. Ruggi G. Metodo operativo nuovo per la cura radicale dell'ernia crurale. Bull Sci Med Bologna 1892;7(3):223.

2. History of the Preperitoneal Space 36. Lotheissen G. Zur Radikaloperation des Schenkelhernien. Centralbl ChiT. 1898;25:548-550. 37. Halsted WS. The radical cure ofhernia.]ohns Hopkins HospBull. 1889; 1:12-13. 38. Acquaviva DE, Bourret P. Cure des eventrations par plaques de nylon. Presse Med. 1948;56:892. 39. Read RC. Francis C. Usher: the herniologist of the twentieth century. Hernia. 1999;3:57-61. 40. Mahorner H, Goss CM. Herniation following destruction of Poupart's and Cooper's ligaments: a method of repair. Ann Surg. 1962;155(5): 741-748. 41. Rives J. Surgical treatment of the inguinal hernia with Dacron® patch. Principles, indications, technique and results. Int Surg. 1967;47(4):360-361. 42. Schumpelick V. Atlas of Hernia Surgery. Philadelphia: B.C. Decker Inc; 1990. 43. Read RC, Barone GW, Hauer:Jensen M, Yoder G. Properitoneal prosthetic placement through the groin: the anterior (Mahorner-Goss, Rives-Stoppa) approach. Surg Clin Narth Amer. 1993;73(3):545-555. 44. Cheade GL. An operation for the radical cure of inguinal and femoral hernia. Br MedJ 1920;2:68-69. 45. Gerdy PN. Nouvelles operations pour guerir radicalement les hernies du ventre. Gaz Hop. 1836;1:10. 46. Wutzer CWo Ueber radicale Heilung beweglicher Leistein-Bruche. In Naumann MEA, Wutzer CW, Kilian HF (eds): Organ fur die gesammte Heilkunde. Bonn: Henry and Cohen; 1841:1-55. 47. Cheade GL. An operation for inguinal hernia. Br Med J 1921; 2:1025-1026. 48. Obituary. GL Cheade. Lancet. 1951;1:115-116. 49. Henry AK. Operation for femoral hernia by a midline extraperitoneal approach. With a preliminary note on the use of this route for reducible inguinal hernia. Lancet. 1936;1:531-533. 50. Edwards H. Critical review: inguinal hernia. Br] Surg. 1943;31(122): 172-185. 51. Harkins HN. The repair of groin hernias: progress in the past decade. Surg Clin North Am. 1949;29:1457-1482. 52. Jennings WK, Anson BJ, Wright RR. A new method of repair for indirect inguinal hernia considered in reference to parietal anatomy. Surg Cynec Obst. 1942;74:697-707. 53. Musgrove JE, McCready FJ. The Henry approach to femoral hernia: report of two cases. Surgery. 1949;26(4):608-611. 54. Riba LW, Mehn WH. Retropubic prostatectomy and inguinal hernia repair. ] Urnl. 1952;67 (1): 106--116. 55. Hull HC, Ganey JB. The Henry approach to femoral hernia. Ann Surg. 1953;137:57-60.

15 56. Mikkelsen WP, Berne CJ. Femoral hernioplasty: suprapubic extraperitoneal (Cheade-Henry) approach. Surgery. 1954;35:743-748. 57. Shandling B, Thompson S. The Cheade-Henry approach for inguinal herniotomy in infants and children: The Hospital for Sick Children, Toronto. Can] Surg. 1963;6:484-488. 58. Lipton S. Use of the Cheade-Henry approach in the treatment of cryptorchidism. Surgery. 1961;50(5):846--848. 59. McVeigh HJ, Barker WF. The midline extraperitoneal approach for the repair of inguinal and femoral hernias. West] Surg Obstet Cynec. 1954;62:534-538. 60. Stoppa RE, RivesJL, Warlaumont CR, PalotjP, Verhaeghe PJ, Delattre JF. The use of Dacron in the repair of hernias of the groin. Surg Clin N. Amer. 1984;64(2):269-285. 61. Wantz GE. Giant prosthetic reinforcement of the visceral sac. Surg GynecoIObstet.1989;169:408-417. 62. McEvedy PG. Femoral hernia. Ann R Coll Surg Engl. 1950;7:484-496. 63. McNaught GHD. Femoral hernia: the rectus sheath operation of McEvedy. ] R Coll Surg Edinb. 1956; 1:309-311. 64. Reay-Young PS. Repair offemoral hernia. Lancet. 1956;2:1217-1218. 65. Nyhus LM, Condon RE, Harkins HN. Clinical experiences with preperitoneal hernial repair for all types of hernia of the groin. Am] Surg. 1960;100:234-243. 66. Nyhus LM, Stevenson JK, Listerud MB, Harkins HN. Preperitoneal herniorrhaphy: a preliminary report in fifty patients: with particular reference to the importance of transversalis fascia analogues. West] Surg Obstet Cynec. 1959;67:48-54. 67. Fowler R. The applied surgical anatomy of the peritoneal fascia of the groin and the "secondary" internal inguinal ring. Aust N Z] Surg. 1975;45(1):8-14. 68. Lytle "J. The internal inguinal ring. Br] Surg. 1945;32(128):441446. 69. Lampe EW. Experiences with preperitoneal hernioplasty. In: Nyhus LM, Condon RE, eds. Hernia. 3rd ed. Philadelphia: J.B. Lippincott; 1989: 178-184. 70. Read RC. Cooper's posterior lamina of transversalis fascia. Surg Cynecol Obstet. 1992; 174( 5) :426--434. 71. EstrinJ, Lipton S, Block IR. The posterior approach to inguinal and femoral hernias. Surg Cynecol Obstet. 1963;116:547-550. 72. McVay CB, Read RC, Ravitch MM. Inguinal hernia. Curr Prohl Surg. 1967;Oct:I-50. 73. Read RC. Preperitoneal prosthetic inguinal herniorrhaphy without a relaxing incision. Am] Surg. 1976;132:749-752. 74. Calne RY. Repair of bilateral hernia: a technique using Mersilene® mesh behind the rectus abdominis. Br] Surg. 1967;54:917-920.

3 Prostheses in Hernia Surgery: A Century of Evolution James R. DeBord

Introduction "A serious consideration of prophylactic and remedial measures in large hernia, of whatever nature, is surely justified by the knowledge that the individual thus afflicted can be nothing but a miserable invalid. Not even the best fitting supporter can render life more than bearable, nor is it possible for such a person to make any severe exertion, whether it be in the pursuance of an occupation or in the enjoyment of an athletic sport." (Willard Bartlett, M.D., Washington University, St. Louis, Mo., 19031)

From the beginning of modern anatomical hernia surgery, ushered in by Bassini in 1887,2 recurrences have plagued and frustrated surgeons of all ages, experience, skill, and nationality. Over the past century, it has become clear even to the most recalcitrant devotee of autologous tissue repairs that prosthetic biomaterials will sometimes be required to bridge or reinforce natural and unnatural defects in the integrity of the abdominal wall, inguinal canal, and chest wall.

Autologous Repair Techniques for the use of free pedicle-based autografts of external oblique aponeurosis and fascia lata were developed and utilized for the repair of hernias from 1901 to the present-day use of the tensor fasciae latae myocutaneous flap, which provides both vascularized fascia and viable soft tissue and skin coverage.3-11 While the advantages of autogenous fascia are apparent, and each patient can provide his own perfectly biocompatible tissue with good tensile strength and long-term viability, the disadvantages of these techniques have prevented the use of autologous fascial transplants from becoming more popular. The disadvantages center primarily on the negative aspects of a second operation to harvest the autologous graft, which involves the added operating room time and expense, the discomfort and scar associated with the donor wound, and the potential for surgical complications at the donor site. These same objections apply to the use of autologous skin and dermal grafts, which have been used with some success, but also have been associated with added local complications such as sinus tracts, cyst formation, and epidermoid carcinoma related to retained epidermal elements which cannot be completely removed from these grafts.I 2- 17 R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

Preserved fascial homografts and xenografts were the next logical step in the development of tissue patches for hernia repair. Over the years these have included "freeze-dried" human fascia lata,18.19 lyophilized homologous aorta,20 preserved human dura mater,21.22 heterologous bovine (ox) fascia,23 and porcine dermal collagen. 24.25 While these biomaterials have had anecdotal success in hernia repair and appear to provide an adequate matrix for autologous fibroblastic ingrowth, there remain problems related to the host local inflammatory reaction to these nonautologous tissues as well as the modern concerns about occult viral disease (HIV) transmission, however remote, that might possibly occur whenever "preserved" tissues are transplanted. There remains, however, a role for careful autologous closure of large abdominal wall defects using local tissue transfer techniques such as the bilateral advancement flap technique of Lucas and Ledgerwood, which mobilizes the external oblique and recti muscles medially via a lateral relaxing incision. 26

Metal Prostheses

Silver Filigrees The earliest use of man-made prosthetic reinforcements for hernia repair was the placement of silver wire coils on the floor of the inguinal canal by Phelps in 1894.27 This concept was expanded by the German surgeons Witzel 28 and Goepel,29 who utilized for hernia repair hand-made silver wire filigrees. Filigree is a term originally referring to fine, lace-like ornamental work of intertwined wire of gold or silver; in surgery, it describes an open arrangement of fine silver wire into a prosthesis for hernia repair. The filigree became the first prosthetic "mesh" to be routinely incorporated into the surgical armamentarium for repair of difficult or recurrent hernias, and many variations of the silver wire filigree were developed (Fig. 3.1). Seemingly crude by today's standards, the use of filigrees in the repair of hernias nevertheless persisted, with refinements, over a longer period than any other prosthetic material, including the most popular meshes in use today. Meyer in 1902,30 and Bartlett1 in 1903, utilizing different styles of filigrees (wire netting versus a wire loop filigree), reported small series of successful repairs of difficult hernias, the first reports in the North American literature on this technique. Lawrie McGavin ofthe Sea-

3. Prostheses in H ernia Surgery

spite these results, the use of silver filigrees gradually faded from the surgical scene primarily because of the discomfort reported by some patients due to silver wire's lack of pliability and its tendency to become work-hardened, as well as its lack of inertness in human tissues which, while stimulating a fibrous reaction, also led to fluid accumulation, sinus tract formation with occasional persistent drainage, and an increased potential for infection. The emerging development of newer prosthetic biomaterials at the time of Ball's report ended the long experience of surgeons with silver wire filigrees for hernia repair.

Tantalum Gauze

FIGURE 3.1. Examples of early silver wire filigrees for hernia repair. 30.32

Tantalum approaches glass in resistance to acid and alkalis, making it inert in the physiochemical environment ofliving tissue. This element possesses high tensile strength, ductility, and malleability, allowing it to be drawn into fine wire and woven into a gauze (Fig. 3.2). In 1940, Burke introduced tantalum for general use in surgery and described its reaction and tolerance to human tissues. 34 Tantalum gauze became popular in hernia surgery after the reports of Throckmorton,35 Koontz,36 Douglas,37 and Lam and colleagues. 38 All were published in 1948. The clinical success reported in these four initial papers prompted an increase in the popularity of this procedure, as did the favorable report of Dunlop in 1950. 39 In 1951, Koontz reported on 77 patients with large direct inguinal hernias and poor tissues using tantalum gauze to buttress a McVay-Cooper's ligament repair, with one recurrence over a 25-month follow-up.4o Also in 1951 , Flynn et al. reported on 45 ventral incisional hernia repairs with tantalum mesh, with only one recurrence in a follow-up of four and one-half years. 41 A few years later, Burton42 and Adler43 reported several disadvantages to the use of tantalum gauze. These problems with the tantalum gauze became apparent only after a period of adequate follow-up and evaluation, and related primarily to fatigue fractures of the gauze mesh with resultant patient discomfort,

man's Hospital in England, reported on his technique of the double filigree method of hernia repair in 1907. 31 In this technique one filigree was placed deep to the transversalis aponeurotic arch, which was sutured over the filigree to the shelving edge of Poupart's ligament, and the superficial filigree was placed above the cord and beneath the external oblique apopneurosis. Percival Cole reviewed the extensive experience of the Seaman's Hospital with the double filigree technique of McGavin in 1941 and noted that from 1920-1940, 23% of the inguinal hernia operations performed at that institution were done with silver wire filigree implants. 32 Ball, in 1958, reported from Melbourne on his use of a larger silver wire filigree placed in the preperitoneal space and covering the entire posterior floor of the groin.33 Ball stated, "Silver wire filigrees appear to be the best method of repair if properly used, and I believe that the method has fallen into some disrepute because of technical faults in the placing of the filigree. It must be placed in a properly prepared bed and kept perfectly flat. The silver wire does slowly disintegrate and therefore is a mild tissue irritant and stimulates the production of fibrous tissue." In this series of 500 patients, Ball reported only two known recurrences, and this probably reflects the known benefits of the preperitoneal placement of any prosthesis in hernia surgery. De-

FIGURE 3.2. Tantalum gauze fabric in two mesh sizes (below) compared with older silver wire prosthesis (above).34

J.R. DeBord

irregularities in the abdominal wall contour, and even to recurrent herniation through the area of mesh fracture despite the associated fibrous ingrowth surrounding the tantalum gauze. Seroma formation was also frequently noted postoperatively, as was the problem of the dense adhesions to any underlying bowel or the difficulty in removing the prosthesis if it should ever be necessary.

Stainless Steel Annealed stainless steel wire surgical sutures have been used since the 1920s, and screens or mesh made from fine stainless steel wire were readily available for many industrial uses when Babcock began to apply this material to the surgical problems of hernia, thoracic wall defects, orthopedic problems, and cosmetic surgery problems in 1952.44 Earlier studies in dogs found no evidence of foreign body reaction to the stainless steel mesh, and tissue incorporation with reperitonealization had occurred without adhesion formation within two weeks. 45 To improve on the flexibility and conformability of steel mesh, Haas and Ritter developed a stainless steel ring chain net made up of larger lO to 11 mm flat rings connected by smaller round rings of 3 to 4 mm diameter. 46 This net was based on the original design of Goepel, who described a ring chain net made of silver wire in 1928 (Fig. 3.3).47 Preston and Richards in 1973 reviewed more than 2,000 cases over a 24-year period using annealed stainless steel mesh in the treatment of hernia. 48 They found this prosthesis to demonstrate excellent strength and durability, resistance to and tolerance of infection, freedom from the problem of "work hardening" and metal fatigue, and good acceptance by their patients. While they reported an infection rate of only 0.1 %, they did not report a recurrence rate or provide any clinical barometer of the effectiveness of their techniques. Mathieson and James, Bapat and Patel reported on the successful use of stainless steel mesh in inguinal hernia repair in 1975. 49.50 As recently as 1986, Validire 51 et al. reported on 150 large abdominal incisional hernias repaired by fascial approximation and stainless steel mesh reinforcement. They achieved a primary success rate of 90% and a secondary success rate of more than 95% in these difficult cases over an average follow-up of four years.

FIGURE 3.3. Goepel's original silver wire ring chain net, later fabricated in stainless steel. 47

Annealed fine stainless steel mesh appears to have features that make it a useful surgical prosthesis, especially in the presence of infection. It should be noted, however, that metallic implants contraindicate the use of magnetic resonance imaging.

Nonmetallic Synthetic Prostheses In 1959, Koontz and Kimberly stated, "We believe that one of the great needs in surgery is some nonmetallic, nonabsorbable material which can be used both for sutures and for prostheses and which will not cause trouble in the presence of infection."52 In their experiments, they tested in dogs numerous fabrics both in aseptic and septic conditions. They examined Dacron® fabric, Dacron and nylon cloth, fiberglass, mylar, nylon mesh, Orlon® cloth, polyethylene, polyvinyl sponge, Teflon® mesh, Teflon and nylon cloth, and vinyon-N cloth. In the absence of infection, OrIon cloth showed the most promise with better infiltration by fibroblasts and a stronger end result than any of the other materials. There was also good fibroblast infiltration into the Dacron fabric, fiberglass, and nylon mesh, but this did not produce the strength of the Orlon cloth. None of these materials withstood infection, however, and as a rule the infected implanted material was found floating in an abscess cavity in the weeks following implantation. They did point out, however, that occasionally good healing without infection occurred when most of these materials were used, even in the presence of contamination.

Fortisan Fabric Narat and Khedroo described their efforts in 1952 to overcome the shortcomings of tantalum and stainless steel meshes with the biologically inert, regenerated cellulose fabric fortisan. 53 However, in the presence of infection the fortisan fabric became a rolledup foreign body in an abscess cavity or caused persistent sinus tract formation. Fortisan fabric never became clinically useful for hernia repair. 54

Polyvinyl Sponge Polyvinyl sponge (Ivalon®) is a polymer of polyvinyl alcohol with formaldehyde in which air is blown through the liquid plastic to form a solid, white, odorless, tasteless "sponge" which, when allowed to dry, becomes firm and rigid and can then be cut into sheets for surgical use that have an appearance on cross-section of a "slice of bread" (Fig. 3.4). Ivalon was first introduced in 1949 as a plombage following pneumonectomy in dogs. 55 In the decade or so following its initial use, Ivalon was used for nearly every feasible surgical application. 56 Shilling et al. described very little foreign body reaction in tissues to Ivalon sponge and showed complete fibroblastic invasion into the mesh, forming a framework of fibrous tissue providing strength to the repaired wound. 57 Schofield and colleagues reported that polyvinyl sponge met all of the requirements of a foreign material for use in hernia repair and recommended its clinical use. 58 In 1957, Abrahams and Jonassen published their clinical experience with Ivalon sponge in the repair of 16 recurrent hernias. 59 They used 2 mm-thick slices of polyvinyl sponge and sutured the prosthesis well beyond the

3. Prostheses in Hernia Surgery

FIGURE

3.5. Thin, medium, and thick nylon netting (left to right).68

3.4. Polyvinyl sponge (Ivalon®).55

margins of the defect under moderate tension. There were two cases of wound infection which healed completely, and in followup to 30 months there were no recurrences. Schofield as well as Koontz and Kimberly, however, reported experimental data clearly indicating that, in the presence of infection, polyvinyl sponge would not be a satisfactory prosthesis in hernia repair.52,60 Adler and Darby thoroughly studied the tissue responses to Ivalon sponge and also the tensile strength of this prosthesis after implantation. 56 ,61 They concluded that most of the desirable features of Ivalon sponge were altered in vivo, that the material was poorly tolerated by the body in the presence of infection, and that the sponge may fragment and dissolve with time.

Nylon Nylon as a suture material is well accepted by surgeons as a strong and reliable material that initiates minimal tissue reaction and remains in common use in modern surgery. A technique utilizing nylon sutures to weave or darn the groin floor to repair hernias with a tension-free lattice was reported by Maloney in 1948, and 10 years later he reviewed his experience with this technique. 62 ,63 He reported a recurrence rate of less than 1 % in 253 hernia repairs followed for more than five years. 64 Callum et al. reported their results with the nylon darn technique in 1974 with a recurrence rate of 7.5% in 186 repairs with a follow-up of five to 12 years. 65 Abrahamson and Eldar performed this repair on 780 patients over a 10-year period and reported in 1988 a recurrence rate of 1.8% with a minimum follow-up of three years.66 Cumberland, in 1952, issued a preliminary report on the use of a prefabricated nylon mesh for the repair of ventral hernia. 67 He used the nylon weave to repair ventral hernias in seven patients in which there were no recurrences during the brief follow-up that averaged less than eight months. The large experience of Doran, Gibbins, and Whitehead with various forms of nylon net in hernia repair was published in 1961 (Fig. 3.5).68 They found that a thin net in 86 patients had a sepsis rate of 1.2%, but a two-year recurrence rate of over 20%. A thick net was used in only 15 cases and abandoned due to a sepsis rate of 53%. A medium thickness net was employed in 212 repairs with an acceptable sepsis incidence of 2.8% and a failure rate

in those patients followed for two years of 4.7%. All six patients with medium net repairs who developed infection had to have the nylon net removed. Kron, in 1984, reported on the use of the French nylon mesh crinoplaque in the preperitoneal repair of bilateral inguinal hernias. 69 He reported no recurrences and no serious septic complications in 200 cases. Koontz's experiments with nylon mesh demonstrated that in the absence of infection the mesh may undergo excellent infiltration by fibrous tissue, but be entirely unreliable in the presence of infection .52 Adler and Firme pointed out that nylon tended to lose its tensile strength and deteriorate when implanted into tissues, and Ludington and Woodward demonstrated that nylon loses 80% of its strength due to hydrolysis and chemical denaturing in vivo. 70, 71

Silastic Silicones are polymers of alternate silicon and oxygen atoms with branching alkyl groups. The longer chain polymers form a rubbery solid called silastic. Prostheses for abdominal wall repair are made by combining the silastic with Dacron or nylon mesh, with the mesh sandwiched between two layers of the silicone. This reinforced silicone elastomer is a relatively thick material that initiates only a minimal inflammatory reaction. This material was introduced and utilized primarily by pediatric surgeons for the correction of large omphalocele and gastroschisis defects in neonates. 72- 76 While apparently successful in a small number of hernia patients, silastic sheeting continues to be used clinically with regularity only in pediatric surgery in the temporary silo closure of neonatal congenital abdominal wall defects.

Teflon Teflon (polytetrafluoroethylene or PTFE) was developed by E.I. DuPont & Co. of Wilmington, Delaware. Teflon became most famous for its use as a nonstick surface in cookware and its unique physical property that it cannot be wet with water. Nothing will adhere to it, and this singular physical property of this chemically inert plastic prompted its study as a biomaterial for surgical use. LeVeen and Barberia, in 1949, studied the tissue reaction to Teflon in dogs. They noted, after varying intervals, that Teflon

J.R. DeBord

FIGURE

3.6. Close-up view of Teflon®mesh.

chips implanted in the peritoneal cavity were lying free with no acute inflammatory changes and no gross evidence of tissue reaction. 77 Ten years later, Ludington and Woodward used PTFE mesh in the repair of abdominal wall defects in 26 patients. 71 Based on a six- to 12-month follow-up of their patients with no recurrences, they felt their results warranted further clinical trials of Teflon mesh in hernia repair (Fig. 3.6). In 1964, Gibson and Stafford reported on 25 patients with large or recurrent ventral incisional hernias with Teflon mesh repair.78 They reported a 50% wound complication rate, and five of the 25 patients had to have the mesh removed to achieve healing. They suggested that the enthusiasm for the use of prosthetic materials be reappraised and tempered because of the excessive morbidity in their experience. In 1968, Copello reported from Argentina on the use of Teflon mesh in the repair of complicated recurrent groin hernia. 79 In 35 cases followed for two years or more, there was no infection or sinus tract formation and no rejection or removal of the mesh. There were no recurrences. Snijders's 1969 paper on the use of Teflon gauze in the treatment of medial and recurrent inguinal hernias reviewed 150 hernia repairs with two to six years' fOllowup, and found a 2.7% recurrence rate. 80 No wound infections or fistulas occurred. In 1974, Kalsbeek reported his series of 34 patients with ventral incisional hernias with an intraperitoneal implant of Teflon mesh. 81 There were 12 failures in 34 patients in this group, with an average follow-up of 4.6 years. Ten of the cases developed fistulas. Blondiau et aI., in 1979, described 56 cases of recurrent or bilateral inguinal hernia treated by a preperitoneal approach with a Teflon mesh implantation. 82 Forty-eight of these patients were available for follow-up six to 42 months postoperatively, and there were no recurrences or infectious sequelae. Similar results using the same preperitoneal approach with Teflon mesh was reported by Azagra et al. in 1987.83 Repair of ventral incisional hernias with an intraperitoneal implant of PTFE prosthesis was performed in 23 cases by Druart and Limbosch in 1988.84 With a mean follow-up of 18 months, only one recurrence (4.3%) was noted. They noted also that Teflon mesh was remarkably well tolerated by the body when implanted intraperitoneally. The effectiveness of Teflon mesh was evaluated in 54 patients

with 58 recurrent inguinal hernias by Van Ooijen and Kalsbeek in 1989.85 With a mean follow-up of 5.2 years, there were five recurrences (9%) and one deep wound infection that led to removal of the Teflon patch. At the time of final follow-up, there were no signs of infection or sinus tracts. They attributed the low rerecurrence rates as much to the tension-free technique they employed as to the Teflon mesh prosthesis. They felt the disadvantages of Teflon mesh for hernia repair were minimal. In 1992, Mozingo et al. reported on 100 recurrent inguinal hernias in 84 men repaired by a preperitoneal approach using a Teflon prosthesis. 86 In follow-up of six months to five years, there were three recurrences, all in cases where the mesh slipped. No postoperative infections or testicular complications occurred. Despite some success, especially with the intraperitoneal or preperitoneal implantation, original Teflon mesh is not incorporated into body tissues, is not tolerant of infection, and has too high a rate of wound complications to be recommended for routine use in hernia repair.

Carbon Fiber Flexible filamentous carbon fiber, which can be produced in various shapes for surgical implantation, is well tolerated in living tissue and attracts a significant fibroblastic ingrowth producing a dense fibrous tissue response that can mimic tendon and fascia. This material's usefulness in orthopedic surgery has been documen ted. 87 ,88 In 1980, Johnson-Nurse and Jenkins produced large experimental abdominal hernias in sheep and repaired them, comparing Dacron mesh with a reefing suture repair using continuous braided carbon fiber.89 They noted that the braided carbon fiber material was well tolerated in the tissues, with a strong stimulus to collagen formation and fibrosis even within the matrix of the braided carbon. Concern about the possibility of carbon being a carcinogenic agent was raised because of the association of coal dust to lung cancer. To date there are no data to support this contention. Tayton et al. in 1982 studied the long-term effects of carbon fiber on soft tissues in a rat model and found no signs of malignant change after an average period of over 17 months. 9o In 1982, Minns et al. fabricated a carbon fiber mesh and implanted it in the dorsal lumbar fascia in rabbits and compared this to Dacron mesh. 91 The carbon fiber mesh tensile strength was initially very weak, but the force to rupture increased as the postimplantation time increased. Greenstein et aI., in 1984, presented an experimental study in rats using an absorbable polylactic acid polymer-coated filamentous carbon mesh for ventral herniorrhaphy.92 Polylactic acid is a biodegradable polyester of lactic acid. They concluded that the carbon-polylactic acid mesh was a more appropriate synthetic biomaterial for a large ventral herniorrhaphy. In 1985, Cameron and Taylor confirmed Greenstein's findings, again using rats to compare a carbon fiber darn repair with polypropylene mesh repair of ventral hernias. 93 Tensiometry of the excised abdominal wall showed no difference in the strength of the two repairs. Morris et aI., in 1990, studied tissue ingrowth occurring in carbon fibers implanted in rats for up to 12 months in induced abdominal wall defects. 94 Compared to polypropylene mesh, carbon fibers induced significantly more tissue ingrowth at six to 12 months postoperatively.

3. Prostheses in Hernia Surgery

In an October 20, 1990 editorial, Lancet reviewed in general terms the literature established regarding carbon fibers and hernia repair. 95 It was concluded that carbon fiber implants may be useful for reinforcing abdominal wall defects in man. They noted carbon fibers are very biocompatible and induce the formation of new connective tissue that is similar in appearance and strength to normal ligaments. Morris et aI., in 1998, studied a carbon fiber mesh in the repair of facial defects created in dogs. 96 The authors felt a randomized clinical trial in patients undergoing hernia repair was justified. Nevertheless, despite the appealing characteristics of composite carbon fiber mesh and its apparent advantages over polypropylene mesh in experimental studies, there has not yet been a significant clinical experience reported in humans to assess the long-term results of carbon fiber prostheses in the repair of hernias.

Polyester Dacron Mesh A polyester polymer from ethylene glycol and terephthalic acid was developed in 1939 and introduced to the United States in 1946.97 By the late 1950s, this material, known as Dacron, was machine-knitted into a fabric mesh and marketed by Ethicon Inc. of Somerville, NJ, under the trade name Mersilene.® All products described as polyester mesh or Dacron mesh or Mersilene mesh are referring essentially to the same product. Wolstenholme, in 1956, became reluctant to implant the stiff metal prostheses available then and utilized a commercial Dacron fabric in the repair of 15 inguinal and four ventral hernias. 98 He was encouraged by his initial results, as all patients healed from their wounds without complications, but no long-term follow-up was reported. A large series of over 3,000 patients was reported by Bellis in 1969 using Mersilene mesh in a tension-free technique under local anesthesia. 99 He reported only 19 failures, 14 of which were due to "rejection" of the mesh. Durden and Pemberton, in 1974, emphasized that successful hernia repair with Dacron mesh requires careful and meticulous surgical technique. IOO They repaired 96 large direct inguinal hernias with Mersilene mesh with one seroma, one recurrence, and no infections. In a group of 13 patients undergoing ventral herniorrhaphy with Dacron mesh as a bridge across the defect, complications included five seromas, no recurrences, and one patient with infection. The follow-up period for all patients was two to five years. No patient with Dacron mesh had difficulty with fragmentation of the implant, extrusion of the mesh, or pain from the presence of the prosthesis. They felt that Dacron mesh met many of the criteria for an ideal prosthesis for hernia repair. Polyester mesh was used by Abul-Husn in 1974 to repair 23 hernias. 101 He noted that the mesh is fine and light, yet strong and pliable, durable, moderately elastic, can be autoclaved, and, because of its interlocking polyester fibers (Fig. 3.7), can be cut with scissors to any shape desired by the surgeon without its edges fraying. He reported the recurrence in 16 inguinal hernia repairs, but no recurrences in the two umbilical hernias and five ventral incisional hernias repaired with polyester mesh. Also in 1974, Caine reported on the use of Mersilene mesh to repair bilateral inguinal hernias from the preperitoneal approach through a single suprapubic incision and passing the mesh behind the rectus abdominus.102 Twenty-six patients were followed for more than one year, and there were six unilateral recurrences, one

FIGURE 3.7. High-power view of the interlocking polyester fibers of Mersilene® mesh.

bilateral recurrence, and one infection requiring removal of the mesh. Caine felt that this technique utilizing Mersilene mesh was especially useful for difficult large or recurrent bilateral groin hernias, but did not recommend it in patients with small bilateral hernias who have good tissues. Casebolt, in 1975, reported on the use of fabric mesh repair in 35 cases of abdominal wall defects. 103 He used polyester and polypropylene meshes in equal amounts in a variety of hernia problems with two recurrences after a mean follow-up of 36 months. There was a 14% incidence of minor wound complications and an 8% incidence of deep infections involving the mesh. In 1975, Haskey and Bigler repaired 20 ventral incisional hernias with Mersilene mesh without major complications. 97 They used an inlay technique successfully with no recurrences reported. Stoppa et al. described their use of a very large, unsutured Dacron prosthesis for repair of difficult groin hernia using a preperitoneal approach through a low midline incision in 1975.104 The easy bloodless dissection in the subperitoneal spaces of Retzius and Bogros, the excellent exposure of the myopectineal orifice to be repaired, and the opportunity to repair several inguinal floor defects by a single approach appealed to the authors. Stoppa and Warlaumont reviewed a more recent assessment of this unsutured pre peritoneal Dacron prosthetic repair of groin hernia in 1989 and reported a long-term recurrence rate of 1.4% in 604 repairs. 105 Cerise et aI., in both an experimental and clinical study, evaluated Mersilene mesh in 100 consecutive hernia repairs in humans (87 groin, 13 ventral), noting only one recurrence with follow-up of one to 4.5 years, and only one significant complication consisting of recurrent abscesses and sinus formation at 20 months postsurgery.106 Using a scanning electron microscope, Minns and Tinckler, in 1976, studied transversalis fascia and Mersilene mesh to analyze their structural features. 107 These studies, not surprisingly, showed hernia fascia to be weaker than normal fascia and mesh to be stronger than either fascia. In 1985, van Damme reported a series of 100 consecutive patients who underwent prosthetic repair of inguinal hernia through a preperitoneal approach.l 08 In 49%, the hernia was recurrent. Using a technique similar to Stoppa's, which has now become known as "giant prosthetic reinforcement of the visceral sac" or GPRVS,109 he used mostly Dacron mesh to achieve a lOO% success

J.R. DeBord

22 rate with one chronic draining sinus tract, one hematoma, and two hydroceles as complications. Van Damme emphasized that if there were no technical errors with this technique, there was no recurrence. In classical herniorrhaphy, however, even after a perfect operation recurrence is always possible, even many years later, because the result does not only depend upon the surgeon but also to a large extent on the tissues and the strain to which they are subjected. In 1987, Adloff and Arnaud described their technique for the surgical repair of large incisional hernias utilizing an intraperitoneal Mersilene mesh in conjunction with a plasty of the anterior rectus sheath. 110 In 130 repairs with a follow-up of one to eight years, there were six recurrences (4.5%), which were all a result of lateral detachment of the mesh. Overall, more than 90% of the patients who underwent surgical treatment of their large incisional hernia fully recovered. In 1989, Wantz reviewed his results using the procedure of GPRVS with 237 hernias of the groin in patients at high risk for recurrence. 11l- 114 He used primarily Mersilene prostheses, and his data emphasized that Dacron is the mesh of choice for GPRVS because it does not become rolled up or folded upon itself in the preperitoneal space. There were nine recurrences, most of which were noted within six months of surgery, and all successfully rerepaired. Five of the recurrences were due to nonfixation of the mesh (four Marlex,® one Gore-Tex®) and four recurrences with Mersilene mesh were due to inadequate positioning of the mesh by the surgeon. Complications were very few, and the overall recurrence rate for these problem hernias of 3.7% was extremely good. Wantz stated, "Herniation after GPRVS is inconceivable, providing the mesh suitably adheres, does not disintegrate, and is correctly sized, shaped, and placed." Thill and Hopkins confirmed the utility of Mersilene mesh in the repair of adult groin hernias compared with a standard Bassini repair in their 1994 report involving 303 patients with 364 groin hernias.1l5 The complication rates were similar between the two repairs, but the recurrence rate at an average follow-up of five years was 11.5% for the Bassini repair and 3.3% for the polyester mesh repair. A unique polyester mesh was introduced for laparoscopic repair of abdominal wall hernias by Helfrich and Gianturco in 1995.1 16 The mesh incorporated a removable internal wire to maintain its circular shape of either 7 em or 10 cm diameter. Dacron mesh was the first popular nonmetallic mesh to stand the test of time, and it remains in active clinical use today, although its use has decreased as polypropylene mesh has become popular.

Polypropylene Mesh Usher introduced a new polyethylene plastic mesh called Marlex50 in a series of experimental and early clinical papers in 1958 to 1959. 117- 1l9 Usher and Wallace placed various plastics into the peritoneal cavities of dogs and found Teflon and Marlex caused less foreign-body reaction than did nylon, Orlon, or Dacron. They described this new material as possessing high tensile strength (50,000-150,000 lb/sq-in) and pliability; being impervious to water and resistant to most chemicals; with a softening temperature of 260 F, so sterilization by boiling was no problem; and as an implant it became infiltrated by connective tissue. Ponka, in 1959, tested this new polyethylene mesh in dogs and 0

found it uniformly successful in replacing segments of abdominal wall without infection and with little microscopic evidence of foreign-body reaction. 120 In 1960 and 1962, Usher reported a collected review of 541 cases of hernia repair with Marlex mesh. 121 ,122 The mesh was used only for large and more difficult hernias with a high risk for recurrence, and 240 cases had minimum follow-up of one year. There was a recurrence rate of 10.2% for incisional hernias and 5.9% for inguinal hernias, with complication rates of 15% and 4.3% respectively. In six of 358 incisional hernias, the mesh had to be removed because of infection. This was not necessary in any of the 183 inguinal hernia repairs. Adler found, in a survey of general surgeons throughout the United States in 1962, that 20% were using it for complicated hernia repair. 43 In 1963, an improved version of Marlex was introduced by Usher, based on a new knitted mesh of polypropylene monofilament fiber, used initially as a suture material. This prosthesis remains in use today, marketed by C.R. Bard, Inc. of BielIe rica, MA, as Marlex, though the name was later changed to Bard® Mesh (Fig. 3.8) .123,124 Jacobs and colleagues, in 1965, found knitted Marlex mesh to be useful in the repair of difficult incisional hernias as have many published authors since. 125-139 In 1987, Bendavid devised a clever umbrella-shaped Marlex prosthesis for insertion from below into the preperitoneal space through the femoral defect for treatment of femoral hernia.1 40 This "umbrella" consisted of an 8 cm disk of Marlex with a stem to facilitate handling and ease of insertion. The stem is eventually resected when the disk portion has been properly inserted and sutured. In 30 patients operated on for femoral hernia, there have been no recurrences after insertion of the Marlex umbrella, although two patients developed postoperative seroma. The number of umbrella repairs without recurrence reached 81 in a later report. 141 Nyhus and colleagues reported in 1988 on the evolution of their preperitoneal approach to the problem of recurrent groin hernia.1 42 Over a 100year period they came to believe that the procedure of choice for recurrent groin hernia was a preperitoneal primary tissue repair of the defect with application of a Marlex mesh buttress also placed posteriorly. They reported a 1. 7% rerecurrence rate with this technique with follow-up from six months to 10 years. Bendavid described, in 1989, a complete mesh reconstruction of the groin floor and inguinal ligament using polypropylene mesh prepared as a three-leafed "fletching."141 This complicated prosthetic repair is well illustrated in the text and is indicated in the repair of the multirecurrent groin hernia, where total destruction of the inguinal ligament may have occurred and the defect extends to the anterior superior iliac spine. He reported 26 such cases with no infection, no testicular atrophy, and two seromas. There was one recurrence 10 months after surgery due to detachment of the fletching from the remnant of the inguinalligament near the iliac spine. This was successfully rerepaired by resuturing the mesh. In an editorial in the February 1989 American Journal of Surgery, Peacock concluded that the continued effort to repair direct inguinal hernias by tissue approximation with sutures should be abandoned. 143 "The modem biologically based concept for repair of groin hernia acquired during adult life is application of a patch, avoidance of tension, and use of local anesthesia so that the result can be tested intraoperatively."

3. Prostheses in Hernia Surgery

~IH

'V4.

\l!

r..~

~~1

..., B

FIGURE 3.8. Marlex® mesh: (A) gross appearance, (B) close-up view, (C) scanning electron microscope view of monofilament knitted interstices.

t-:

'),

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In this same journal issue, Lichtenstein and associates reported on 1,000 consecutive patients with primary repair of inguinal hernia using a "tension-free" repair employing a Marlex mesh prosthesis to bridge the direct floor of the groin without approximation of the tissue defect. 144 Jones and Jurkovich, in 1989, reviewed their own experience and that of others with polypropylene mesh in closure of infected abdominal wounds. 145 They described five patients of their own in whom polypropylene mesh was used to close the abdomen following celiotomy for intra-abdominal sepsis. Complications directly related to the mesh placement occurred in four patients (80%) : a small bowel fistula developed in all four patients, and a wound dehiscence also occurred in one. All eventually had the mesh removed. Using a preperitoneal approach, Bendavid, described in 1990 the use of Marlex mesh to repair a series of seven incisional parapubic hernias. 146 This unusual hernia is the result of previous surgery that has disrupted the insertion of the musculotendinous elements of the abdominal wall on the pubis. The defect, usually round and 5 to 8 cm in diameter, emerges just above the pubis and requires a prosthetic repair. The Marlex is sutured to both Cooper's ligaments and the arcu ate pubic ligament below and to the full thickness abdominal wall structures above. Ben-

david reported successful repairs in all of the patients with this technique. Many additional reports confirm the good results of polypropylene as a prosthesis or prosthetic device. 147- 164 However, not being complacent or easily satisfied, surgeons will continue to spearhead, along with bioengineers, the development of improved biomaterials for surgical reconstruction of the human body.

Expanded Polytetrafluoroethylene PTFE is a fully fluorinated polymer with the chemical formula (CF2-CF2)n. It was discovered accidentally in 1938 by RJ. Plunkett of E.I. DuPont & Co., Inc.I 65 Its unique chemical and physical properties are well documented. 166 Its use as a biomaterial for hernia repair has been reviewed earlier in this chapter. In 1963, Shinsaburo Oshige of Sumitoma Electric Industries, Osaka, Japan, discovered a process for expanding PTFE to produce a highly uniform, continuous fibrous, porous structure which, after sintering, retained its microstructure with vastly improved mechanical strength. 167 The technique for expanding PTFE was ultimately refined by Robert W. Gore l68 and initially applied clinically to the development of a functional vascular pros-

J.R. DeBord

FIGURE

thesis that was introduced to the market in 1975 by both Impra, Inc. of Tempe, Arizona, and W.L. Gore and Associates, Inc. of Flagstaff, Arizona. Subsequent to the development of the expanded PTFE (ePTFE) vascular graft, ePTFE was radially expanded to provide a sheet material that would meet the demands of a prosthesis used in the repair of hernias and other soft tissue deficiencies. This new biomaterial was first used clinically in 1983. The ePTFE patch is composed of pillar-shaped nodes of PTFE that are connected by fine fibrils of PTFE with a multidirectional arrangement of the fibrils in the surface view which imparts balanced strength properties to the patch in all directions (Fig. 3.9). The average internodal fibril length (that is, pore size) is 20 to

25 J-L, and this unique porous microstructure provides a flexible, soft, nonfraying, conformable biomaterial that allows cellular infiltration and tissue incorporation into the patch (Fig. 3.10). Expanded PTFE has been documented to have adequate material tensile strength for safe clinical use, and, using industrial testing methods, the Gore-Tex® soft tissue patch (STP) has been shown to be stronger than Marlex, Prolene,® or Mersilene mesh and equivalent to these materials in terms of suture retention strength (Table 3.1).169-170 From the late 1970s to the mid 1990s, numerous experimental and clinical papers described the utilization of e-PTFE in many different arenas from orthopedic to dental to plastic surgery to

3.10. Tissue incorporation into Gore-Tex® soft tissue patch 27 months after hernia repair: (A) Milligan's Trichrome stain, 25X magnification of fibrous tissue adherent to both patch surfaces with collagen pen-

FIGURE

3.9. Gore-Tex® soft tissue patch.

etration of the patch interstices; (B) Hand E stain, 50X magnification of fibroblasts and a few macrophages with collagen fibers within the patch spaces.

3. Prostheses in Hernia Surgery TABLE 3.1. High rate strength comparison l Prosthetic material Gore-Tex® soft tissue patch (2 mm) Gore-Tx soft tissue patch (1 mm) Marlex® mesh Prolene® mesh Mersilene® mesh

Material strength 2

Suture retention 3

30.0 kg/cm

3.4 kg/pin

14.8 kg/cm

1.92 kg/pin

3.5 kg/cm 6.4 kg/cm 1.0 kg/cm

1.46 kg/pin 2.06 kg/pin 0.46 kg/pin

lFifteen samples were tested in each case. Data reported are mean values. 2All materials were tested by rupturing a notched rectangular sample at a strain rate of 9000%/sec and measuring the maximum force sustained by the sample. 3All materials were tested by pulling five small diameter pins (spaced 4 mm in from an edge and 2 mm apart) out of a sample at a rate of approximately lOO cm/sec. The pins were of approximately the same diameter as suture materials used in prosthetic hernia repairs. Data from W.L. Gore and Associates, Inc., Patch Project Work Plan #215. (170) .

chest wall reconstruction and, of course, to inguinal and ventral incisional hernia repair. These reports are reviewed in more detail in the earlier edition of this book and in a recent review by this author.171-217 The repair oflarge primary and recurrent ventral incisional hernias is the most demanding of all hernia repairs and is accompanied by high recurrence rates if a prosthetic biomaterial is not used. Techniques for the laparoscopic repair of these difficult hernias have been described, and early results appear promising and offer relief from many of the wound complications associated with open repair.218-221 Standard to all of these reports is the use of ePTFE prostheses and transabdominal fixation sutures augmented by staples. Low rates of hernia recurrence and complications, along with short hospital stays and earlier return to normal activities, continue to be the outcome advantage promoted by surgical laparoscopists. Despite its appeal to many, the technical challenge and learning curve of laparoscopic ventral hernia repair leave a majority of surgeons currently utilizing open prosthetic repair as their preferred approach and the technique with which they are most comfortable and confident. Gillion et al. published a 1997 review of 158 patients with incisional hernias repaired with an open technique using ePTFE patches. 222 Their infection rate (4%) and recurrence rate (4%) were low, with a mean follow-up of 37 months. Similar results were reported by Balen et al. in 1998, with one recurrence in 45 operations with a mean follow-up of 39 months. 223 In 1999, Gonzalez et al. of Spain and Bauer et al. of New York published their results on 84 and 98 complex repairs with ePTFE respectively.224,225 Gonzalez's data with 1-3 years' follow-up showed an infection rate of only 1.7% and a recurrence rate of 2.4%. Twenty-five percent of his cases were recurrent hernia operations. Bauer, with one-half of his patients presenting with recurrent hernias, had an overall 19% recurrence rate, but nine of these were due to removal of infected patches. Recurrence occurred with an intact patch in 10 patients (10.2%), with a mean implant duration of 6.2 years. There were no bowel complications

related to the intraperitoneal placement of the ePTFE prosthesis in either series. Since its first clinical use in 1983, the e-PTFE patch has been found to be an effective biomaterial for a wide array of clinical problems. The ultimate role of this biomaterial in modern surgery is still being evolved, and it is now just under two decades since its first clinical applications, so long-term follow-up data will now become available.

Absorbable Mesh Polyglycolic acid (Dexon®-Davis and Geck, Inc. Manati, PRJ and polyglactin 910 (Vicryl®-Ethicon, Inc. Somerville, NJ) meshes have been developed as outgrowths of the successful utilization of these slowly absorbable synthetic fibers as suture material. Dexon mesh is a wide weave of polyglycolic acid braided fibers which produces a soft, pliable, and stretchable prosthetic netting which is biodegradable and is gradually absorbed over a period of about 90 days.226 Vicryl mesh, on the other hand, is a tightly woven broadcloth, which is flexible although not elastic, and shares similar physical and biodegradable properties as Dexon mesh. 227 Both of these biomaterials are absorbed and should not be used as the sole prosthesis for repair of abdominal hernia. In experimental studies, Delany et aI., in 1982, showed that Dexon mesh could be used to wrap the injured spleen of dogs and successfully tamponade the parenchymal hemorrhage. 226 Lamb and colleagues, in 1983, repaired clean rabbit abdominal wall defects using Vicryl mesh and found, at three weeks, there was no weakness when compared with nonabsorbable meshes. 228 However, at 12 weeks, the bursting strength of the polyglactin 910 repair was significantly less than that of nonabsorbable meshes. In addition, 40% of the animals repaired with Vicryl mesh developed a hernia due to inadequate fibrous tissue incorporation into the mesh before hydrolysis of the prosthesis occurred. They concluded that Vicryl mesh was not a suitable biomaterial for permanent repair of abdominal wall defects. Jenkins et ai., in 1983, compared prosthetic materials in rats for abdominal wall repair and found no difference in bursting strength, up to eight weeks, when Vicryl mesh was compared with Marlex and Gore-Tex prosthesesP4 In this study, the best longterm protection against adhesions was provided by the absorbable mesh. Their eight-week follow-up may not have been long enough to detect hernia recurrence following absorption of the Vicryl mesh. In 1985, the first clinical application of absorbable mesh for repair of the spleen was reported in six patients by Delany et ai. 229 The repairs were performed using the Dexon mesh in several ways with good results and with no complications directly related to the presence of the mesh. Similar results with the successful Dexon mesh repair of the injured spleen and kidney have been reported by others. 230 ,231 Reconstruction of the pelvic peritoneum is an additional application for absorbable mesh material as described by Delany et al. in 1985. 232 This sling-type peritoneal substitution procedure suspended the small intestine out of the pelvis and out of the field used for postoperative radiation following resection for rectal cancer.

J.R. DeBord

The use of Dexon mesh to repair contaminated abdominal wall defects in patients was reported by Dayton and colleagues in 1986. 233 As an alternative to placing polypropylene mesh in a contaminated field, they used polyglycolic acid mesh to repair infected abdominal wall defects in eight patients. In follow-up studies up to 18 months, six of the eight patients (75%) developed hernias at the site of the absorbable mesh repair. They concluded that postoperative hernia development was probable in patients whose defects were repaired with absorbable mesh. However, this complication has to be balanced against the serious complications of sepsis, fistula, bleeding, skin erosion, and drainage, which require removal of nonabsorbable prostheses in a large percen tage of cases when the latter are used in contaminated areas. The authors felt placement of absorbable mesh for temporary abdominal wall support until wound contamination resolved might enhance the likelihood of subsequent successful placement of a permanent prosthesis. When compared with Marlex mesh in a dog model over a 16week period, Dexon mesh was shown by Delany et al., in 1992,234 to produce fewer intraperitoneal adhesions and, unlike Marlex, these adhesions and acute tissue reaction diminished over time as the prosthesis was absorbed. While absorbable mesh, as common sense would predict, does not provide adequate support for hernia repair, Pans et al. studied its role in hernia prevention in morbidity obese patients undergoing bariatric surgery.235 A total of 288 patients were randomized to primary closure with polyglactin sutures alone or with the same sutures plus a polyglactin mesh placed above the omentum but not fixed with any sutures. Not surprisingly, there was no significant benefit of the mesh in reducing the incidence of incisional hernia during the follow-up period. The two main predictive factors in the overall 26% incidence of incisional hernia in these patients were patient age and preoperative weight.

The Ideal Prosthesis Zimmerman said in 1968, "The use of artificial materials in the repair of hernia has created an interest and evoked a literature which probably exceeds the importance of this innovation. From this chaotic volume, numerous materials and various techniques have been, and continue to be, promulgated, but few factual conclusions can be drawn. "236 In the 32 years since that statement was made, some would say that its sentiments are still applicable. It seems, however, that some conclusions can be drawn from the current accumulation of data, but it is doubtful that we have yet seen, in any currently available form the "ideal" prosthetic biomaterial. Cumberland67 and Scales,237 in the 1950s, developed eight still pertinent criteria for the ideal implantable biomaterial. These have been more recently enumerated by Hamer-Hodges and Scott. I78 The material: 1. 2. 3. 4. 5. 6.

Should Should Should Should Should Should

not be physically modified by tissue fluids; be chemically inert; not excite an inflammatory or foreign-body reaction; be noncarcinogenic; not produce a state of allergy or hypersensitivity; be capable of resisting mechanical strains;

7. Should be capable of being fabricated in the form required; 8. Should be capable of being sterilized. It has become apparent that there is no single ideal operation that exists for the permanent cure of hernia, and it is unlikely that a single ideal prosthesis to augment hernia repair will be developed that is universally adaptable. Three biomaterials in hernia repair currently in widespread use throughout the world are well tolerated by the body: polyester mesh, polypropylene mesh, and expanded polytetrafluoroethylene patch. None of these materials has been shown to be carcinogenic or to elicit an allergic reaction in tissues. While ePTFE material strength and suture retention strength exceed those of polyester and polypropylene mesh, no clinical failures of any of these biomaterials has ever been reported due to mechanical prosthesis failure. These three biomaterials have all been shown, both macroscopically and microscopically, to allow tissue ingrowth into the prosthesis. The more coarse macro porous meshes clearly differ from the smooth microporous ePTFE patch in this regard. The polyester and polypropylene meshes incite a more proliferative, although disorganized, fibrous collagenous response that many feel creates a more secure bond with the surrounding fascia. The only prosthetic material that seems to elicit a strong, orderly, and organized collagen response, aligned in the direction of the stress applied, is carbon fiber-based material that has had little clinical use reported. The micro porous ePTFE patch does support tissue ingrowth into its internodal spaces, and this has been histologically well confirmed. When implanted as a replacement for the abdominal wall, without peritoneal coverage, the ePTFE patch supports the rapid development of a mesothelial-like cellular monolayer, which acts to "reperitonealize" the visceral surface of the patch. The resulting decrease in adhesion formation and bowel complications in this setting has been reported in numerous experimental and clinical papers reviewed earlier. The rationale for the selection of a prosthetic biomaterial in hernia repair must be based on a sound knowledge of the properties of the various available prostheses as reviewed by DeBord238 and Goldstein. 239 Future biomaterials must meet three additional criteria to more nearly match the Cumberland and Scales requirements for the ideal prosthetic material: 1. They must be resistant to infection; 2. They must provide a barrier to adhesions on the visceral side; 3. They must respond in vivo more like autologous tissue-allowing tissue incorporation for good fixation and a strong, lasting repair, without encouraging the scarring and encapsulation problems seen with many of today's prostheses. Amid and associates combined biomaterials in an effort to find a combination that might promote the desirable incorporation of the mesh with the abdominal wall while preventing the undesirable adherence of the biomaterial to the intestine. 240 Of all the combinations of prosthetic material used in this rabbit model, only the polypropylene mesh/polypropylene sheeting combination met these dual criteria. No clinical experience has been reported. In 1996, Velitchkav et al. described an extensive experience with a new biomaterial developed in Bulgaria. 241 Ampoxen, a multifil-

3. Prostheses in Hernia Surgery amen ted polycaproamide impregnated with 5-nitro-8-hydroxyquinolinum (Medica, SA, Sandanski, Bulgaria) was developed in 1975 and is widely available and inexpensive in Bulgaria. This mesh is nonabsorbable and impregnated with the broad-spectrum antiseptic nitroxoline to which bacterial resistance has not been seen. This mesh has a rapid fibrinous fixation in the tissues and avoids seroma formation. Within seven days of implantation, it is difficult to separate Arnpoxen mesh from host tissues. The mesh is elastic, which facilitates its handling characteristics. These authors reported 846 inguinal hernia repairs using Arnpoxen mesh and a Lichtenstein technique, with no recurrences and very low general complications. Unfortunately, outside Bulgaria there has been little reported experience with this biomaterial. A new prototype mesh consisting of a knitted polyester structure treated with a fluoropolymer and impregnated with gelatin was described in 1996 by Soares et al. 242 The FluoropassiV® mesh (Vascutek Ltd., Inchinnan, Scotland) has a polyester wrap-knitted structure made by knitting texturized multifilament polyester yams into a two-bar reverse lockknit fabric. It is then coated with a fluoropolymer solution using proprietary technology and impregnated with gelatin that has been cross-linked with formaldehyde and softened with glycerol. In this study, Fluoropassiv mesh was compared with polypropylene and ePTFE in experimentally induced abdominal hernias in piglets. In this study, the new mesh provided adequate mechanical strength and compared favorably with the standard products with respect to systemic or in situ reactions, tissue incorporation, handling characteristics, and flexibility. No clinical data are available. Klinge and associates, in 1988, using a rat model, constructed and tested a new mesh (soft hernia mesh (SHM» based on a combination of nonabsorbable polypropylene and absorbable polyglactin 9lO. 243 The amount of nonabsorbable material was reduced to less than 30% of that in the Marlex controls, while still maintaining adequate tensile strength but vastly superior flexibility. Histologic examination showed a pronounced reduction in the inflammatory reaction in the tissues, and the collagen bundles were oriented more favorably. There is little doubt that infection remains the "bete noir" of implantation of any prosthetic material in human surgery, and clearly it is the leading cause of failure in hernia repair no matter what biomaterial is used. Dent et aI., in 1992, presented experimental data using Gore-Tex STPs impregnated with silver and chlorhexidine in a contaminated rat model. 244 Adherence ofbacteria to the prosthetic material is the initial step in the pathogenesis of prosthesis colonization. 245 Impregnation of broad-spectrum antimicrobial agents, such as silver and chlorhexidine, into implantable devices has been shown to reduce bacterial colonization. 246,247 In this study, 100% of the control patches were colonized compared with only 30% of the antimicrobial impregnated patches. In the control group, patches had more than 105 colony forming units (CFU) of bacteria, whereas only 10 to 200 CFU were detected in the silver-chlorhexidine group. Preliminary evaluation in rats showed prolonged retention of drugs by the patches (more than three weeks). Systemic antibiotics often fail to prevent patch infections clinically because the drugs cannot penetrate the bacterial biofilm that forms on the surface of the prosthesis. 248 This may lead to bacterial adherence to the prosthesis, resulting in infection and potentially fatal septic complications. Impregnation of silver and chlorhexidene into the ePTFE patch ap-

pears to prevent bacterial colonization and subsequent infection. DeBord et al. have recently studied both laboratory and clinical findings after implantation of this antimicrobial agent-impregnated ePTFE patch in patients and found no untoward effects from this biomaterial (Dual Mesh Plus,® W.L. Gore and Associates, Inc., Flagstaff, Arizona).249 Clinical data should develop now that this modified ePTFE patch is commercially available to determine whether or not this silver-chlorhexidine impregnation reduces the risk of clinical infection when implanting this patch for hernia repair. Thus, it appears that an antimicrobial-impregnated prosthesis that allows well-organized fibrous ingrowth on one side and has anti-adhesion properties on the other side would approach the brass ring of an ideal prosthetic biomaterial for abdominal wall reconstruction. "Prostheses, whatever their value, cannot replace a full knowledge of the underlying anatomy and pathology of hernia, or substitute for the exercise of time-honored principles of surgical technique."236

References 1. Bartlett W. An improved filigree for the repair oflarge defects in the abdominal wall. Ann Surg. 1903;38:47. 2. Bassini E. Sulla cura radicale dell'ernia inguinale. Arch Soc Ital Chir. 1887;4:380. 3. McArthur LL. Autoplastic suture in hernia and other diastases: preliminary report. JAMA. 1901;37:1162. 4. McArthur lL. Autoplastic suture in hernia and other diastases: final report. JAMA. 1904;43:1039. 5. Kirschner M. Die praktischen ergenbisse der freien fascien-transplantation. Arch Klin ChiT. 1910;92:888. 6. Gallie WE, LeMesurier AB. The use of living sutures in operative surgery. Can Med Assoc J 1921;2:504. 7. Gallie WE, LeMesurier AB. The use of free transplants offascia as living sutures in the treatment of hernia. Arch Surg. 1924;9:516. 8. Feldt-Rasmussen K, Jensen OA. Large ventral herniae treated with free fascial grafts. Acta Chir Scand. 1956; III :403. 9. Burton CC. Classification and techniques of fascial grafts in repair of inguinal hernia. Int Abs Surg. 1957;105:521. 10. HamiitonJE. The repair oflarge or difficult hernias with mattressed onlay grafts offascia lata: a 21-year experience. Ann Surg. 1968;167:85. 11. Cederna JP, Davies BW. Total abdominal wall reconstruction. Ann Plast Surg. 1990;25:65.

12. Uihlein A Jr. Use of the cutis graft in plastic operations. Arch Surg. 1939;38:118. 13. Cannaday JE. Some of the uses of the cutis graft in surgery. AmJ Surg. 1943;59:409. 14. Chodoff RJ. The use of full thickness skin grafts in the repair oflarge hernia. Ann Surg. 1949;129:119. 15. Strahan AWB. Hernial repair by whole-skin graft with report on 413 cases. Br J Surg. 1951;38:276. 16. Clarke SHC. The formation of inclusion dermoid cysts following whole thickness skin graft repair of hernia. BrJ Surg. 1952;39:346. 17. GomezJ, WylieJH, PonkaJL. Epidermoid carcinoma in a cutis graft after repair of an incisional hernia. Rev Surg. 1972;29:381. 18. Koontz AR. Preserved fascia in hernia repair. Arch Surg. 1933;26:500. 19. Usher FC. Use of freeze dried human fascia lata in the repair of incisional hernias. Am Surgeon. 1955;21:364. 20. Fogelson SJ,Jackson CR. The repair of tissue deficient hernias byaortic implants. Surg Gynecol Obstet. 1959;109:245.

28 21. Mason MS, Raaf J. Use of homologous dura mater in the repair of hernias. Arch Surg. 1961;82:856. 22. Rodgers BM, MaherJW, TalbertJL. The use of preserved human dura for closure of abdominal wall and diaphragmatic defects. Ann Surg. 1981;193:606. 23. El-Domeiri AA. Repair of abdominal and thoracic wall defects by bovine fascia (ox fascia). Anh Surg. 1976;111:172. 24. Hall-Allen RTJ. Porcine dermal collagen repair of inguinal hernias. ] R Col Surg Edinb. 1984;29:154. 25. Sarmak BD, Hall-Allen R1J. Porcine dermal collagen repair of incisional herniae. Br] Surg. 1984;71:524. 26. Lucas CE, Ledgerwood AM. Autologous closure of giant abdominal wall defects. Am Surg. 1998;64:607. 27. Phelps AM. A new operation for hernia. NY MedJ 1894;60:291. 28. Witzel O. Ueber den Verschluss von Bauchwunden und Bruchpforten durch versenkte Silberdrahtnetze (Einheifung von Filigranpelotten). Centralhl Chir Lepiz. 1900;27:257. 29. Goepel R. Ueber die Verschliessung von Bruchpforten durch Einheilung geflochtener fertiger Silberdrahtnetze (Silberdrahtpelotten). Verh Dtsch Ges Chir. 1900; 19: 174. 30. Meyer W. The implantation of silver filigree for the closure of large hernial apertures. Ann Surg. 1902;36:767. 31. McGavin L. The use of filigrees of silver wire in the cure of hernia usually considered inoperable. Br MedJ 1907;2:1395. 32. Cole PP. The filigree operation for inguinal hernia. Br] Surg. 1941; 29:168. 33. Ball L. The repair of inguinal hernia and the use of filigrees. Br] Surg. 1958;45:562. 34. Burke GL. Corrosion of metals in tissues and an introduction to tantalum. Can Med AssocJ 1940;43:125. 35. Throckmorton TD. Tantalum gauze in the repair of hernias complicated by tissue deficiency. Surgery. 1948;23:32. 36. Koontz AR. Preliminary report on the use of tantalum mesh in the repair of ventral hernias. Ann Surg. 1948;127:1079. 37. Douglas DM. Repair of large hernia with tantalum gauze. Lancet. 1948;1:936. 38. Lam CR, Szilagyi DE, Puppendahl M. Tantalum gauze in the repair oflarge postoperative ventral hernias. Anh Surg. 1948;57:234. 39. Dunlop GR. The use of tantalum gauze in the repair of hernias with tissue deficiencies. New Eng!] Med. 1950;242:542. 40. Koontz AR. The use of tantalum mesh in inguinal hernia repair. Surg CynecolObstet. 1951;92:101. 41. Flynn "'J, Brant AE, Nelson GG. A four and one-half year analysis of tantalum gauze used in the repair of ventral hernia. Ann Surg. 1951;134:1027. 42. Burton CC. Fascia lata cutis and tantalum grafts in repair of massive abdominal incisional hernias. Surg Cynec Obstet. 1959;109:621. 43. Adler RH. An evaluation of surgical mesh in the repair of hernias and tissue defects. Anh Surg. 1962;85:156. 44. Babcock WW. The range of usefulness of commercial stainless steel cloths in general and special forms of surgical practice. Ann West Med Surg. 1952;6:15. 45. Jonas KC. Stainless steel cloth as internal prosthesis. Anh Surg. 1950;60:1205. 46. Haas A, Ritter SA. Use of stainless steel ring chain net for reinforcement in the repair of large and recurrent hernias of the anterior abdominal wall. Am] Surg. 1958;95:87. 47. Goepel R. Der Verschluss von Nabel und Bauchwand hernien unter Verwendung gegliederter Silberdrahtnetze. Munch Med Wochebnschr. 1928;75:127. 48. Preston DJ, Richards CF. Use of wire mesh prostheses in the treatment of hernia. Surg Clin North Am. 1973;53:549. 49. Mathieson AJM, James JH. A review of inguinal hernia repair using stainless steel mesh.] R Col Surg Edinb. 1975;20:58. 50. Bapat RD, Patel RA. Stainless steel mesh: a neglected implant for inguinal hernia repair.] Postgrad Med. 1975;20:94.

J.R. DeBord 51. ValidireJ, Imbaud P, Dutet D, et al. Large abdominal incisional hernias: repair by fascial approximation reinforced with a stainless steel mesh. Br] Surg.' 1986;73:8. 52. Koontz AR, Kimberly RC. Further experimental work on prostheses for hernia repair. Surg Gynecol Obstet. 1959;109:321. 53. NaratJK, Khedroo LG. Repair of abdominal wall defects with Fortisan fabric. Ann Surg. 1952;136:272. 54. Koontz AR, Kimberly RC. An evaluation of the usefulness of Fortisan fabric in hernia repair. Ann Surg. 1954;139:644. 55. Grindlay JH, Clogett ~T. Plastic sponge prosthesis for use after pneumonectomy. Proc Staff Meet Mayo Clinic. 1949;24:538. 56. Adler RH, Darby C. Use of a porous synthetic sponge (Ivalon) in surgery. I. Tissue responses after implantation. US Armed Fones Med J 1960;11:1349. 57. Schilling JA, Joel W, Shurley HM. A comparative study of the histochemical changes in granulation tissue contained in stainless steel wire mesh and polyvinyl sponge cylinders. Surgery. 1959;46:702. 58. Schofield TL, Hallenbeck GA, Grindlay JH, et al. Use of polyvinyl sponge in repair of experimentally produced defects in the abdominal wall. Anh Surg. 1954;68:191. 59. AbrahamsJI,Jonassen ~T. The use of polyvinyl sponge in the repair of abdominal wall hernias. Surgery. 1957;42:336. 60. Schofield TL. Polyvinyl alcohol sponge; an inert plastic for use as a prosthesis in the repair oflarge hernias. Br] Surg. 1955;42:618. 61. Adler RH, Darby C. Use of a porous synthetic sponge (Ivalon) in surgery II. Studies of tensile strength. US Armed Forces Med J 1960; 11:1466. 62. Maloney GE, Gill WG, Barclay RC. Operations for hernia: technique of nylon dam. Lancet. 1948;2:45. 63. Maloney GE. Results of nylon-darn repair of herniae. Lancet. 1958;1:273. 64. Maloney GE. Daming inguinal hernias. Anh Surg. 1972;104:129. 65. Callum KG, Doig RL, KimmonthJB. The results of nylon darn repair for inguinal hernia. Anh Surg. 1974;108:25. 66. Abrahamson J, Eldar S. The nylon dam repair for primary and recurrent inguinal hernias. Contemp Surg. 1988;32:33. 67. Cumberland VH. A preliminary report on the use of prefabricated nylon weave in the repair of ventral hernia. Med] Aust. 1952;1: 143. 68. Doran FSA, Gibbins RE, Whitehead R. A report on 313 inguinal herniae repaired with nylon nets. Br] Surg. 1961;48:430. 69. Kron B. Un nouveau materiel et une technique simplifiee pour la cure des hernies bilaterales recidivees ou non par voie pre-peritoneale ou sous-peritoneale.] Chir (Paris). 1984; 121 :491. 70. Adler RH, Firme C. The use of nylon prostheses for diaphragmatic defects. Surg Gynecol Obstet. 1957;104:669. 71. Ludington LG, Woodward ER. Use of Teflon® mesh in repair of musculofascial defects. Surgery. 1959;46:364. 72. Schuster RF. A new method for the staged repair of large omphaloceles. Surg Cynecol Obstet. 1967;125:837. 73. Gilbert MG, Mencia LF, Brown WT, et al. Staged surgical repair of large omphaloceles and gastroschisis.] Pediatr Surg. 1968;6:702. 74. Ein SH, Fallis JC, Simpson JS. Silon sheeting in the staged repair of massive ventral hernias in children. Can] Surg. 1970;13:127. 75. Cudmore RE, Zachary RB, Lister J. Silastic sheeting for abdominalwall defects. Letter to the editor. Lancet. September 1970;II:666:26. 76. Linn BS, Vargas A. Use of temporary prostheses to repair difficult hernias. South MedJ 1973;66:925. 77. LeVeen HH, BarberiaJR. Tissue reaction to plastics used in surgery with special reference to Teflon®. Ann Surg. 1949;129:74. 78. Gibson LD, Stafford CE. Synthetic mesh repair of abdominal wall defects. Am Surg. 1964;30:481. 79. Copello AJ. Technique and results of Teflon® mesh repair of complicated re-recurrent groin hernias. Rev Surg. 1968;25:95. 80. Snijders H. The use of Teflon® gauze in the treatment of medial and recurrent inguinal hernias. Arch Chir Neerl. 1969;21:199.

3. Prostheses in Hernia Surgery 8l. Kalsbeek HL. Experience with the use of Teflon® mesh in the repair ofincisional hernias. Arch Chir Neerl. 1974;26:7l. 82. Blondiau]V, Verheyen V, Coland M. Cure des hernies inguinocrurales par voie mediane preperitoneale et prothese en Teflon.® Acta Chir Belg. 1979;78:317. 83. Azagra JS, Alle JL, Esselen M, et al. Nonante-quatre hernies de l'aine traitees par prothese interposee par voie mediane en preperitoneal. Acta Chir Belg. 1987;87:15. 84. Druart ML, Limbosch JM. Traitement des eventrations par implantation intraperitoneale de voile en Teflon.® Ann Chir. 1988;42:39. 85. Van Ooijen B, Kalsbeek HL. Recurrent inguinal hernia repaired with mesh (Teflon®). Neth] Surg. 1989;41:6l. 86. Mozingo DW, Walters MJ, Otchy DP, et al. Properitoneal synthetic mesh repair of recurrent inguinal hernias. Surg Gynecol Obstet. 1992;174:33; 87. Forster lW, Ralis ZA, McKibbin B, et al. Biological reaction to carbon fiber implants. Clin Orthop. 1978;131:299. 88. Jenkins DHR, McKibbin B. The role of flexible carbon-fibre implants as tendon and ligament substitutes in clinical practice. ] Bone Joint Surg. 1980;62-B:497. 89. Johnson-Nurse C, Jenkins DHR The use of flexible carbon fibre in the repair of experimental large abdominal incisional hernias. Br] Surg. 1980;67:135. 90. Tayton K, Phillips G, Ralis Z. Long-term effects of carbon fibre on soft tissues.] Bone Joint Surg. 1982;64-B:112. 9l. Minns~, Denton MJ, Dunstone GH, et al. An experimental study of the use of a carbon fibre patch as a· hernia prosthesis material. Biomaterials. 1982;3:199. 92. Greenstein SM, Murphy TF, Rush BF, et al. The experimental evaluation of a carbon-polylactic acid mesh for a ventral herniorrhaphy. Curr Surg. 1984;41 :358. 93. Cameron AEP, Taylor DEM. Carbon-fibre versus Marlex mesh in the repair of experimental abdominal wall defects in rats. Br ] Surg. 1985;72:648. 94. Morris DM, Haskins R, Marino AA, et al. Use of carbon fibers for repair of abdominal-wall defects in rats. Surgery. 1990;107:627. 95. Editorial. Lancet. October 1990;976. 96. Morris DM, HindmanJ, Marino AA. Repair offascial defects in dogs using carbon fibers.] Surg Res. 1998;80:300. 97. Haskey RS, Bigler FC. Difficult hernias.] Kans Med Soc. 1975;76:239. 98. Wolstenhohne]T. Use of commercial Dacron fabric in the repair ofinguinal hernias and abdominal wall defects. Arch Surg. 1956;73:1004. 99. Bellis CJ. Immediate unrestricted activity after inguinal herniorrhaphy. International Surg. 1969;52:107. 100. Durden JG, Pemberton LB. Dacron® mesh in ventral and inguinal hernias. Am Surgeon. 1974;40:662. 101. Abul-Husn S. The use of polyester mesh in hernia repair. Lebanese MedJ 1974;27:437. 102. CaIne RY. Repair of bilateral hernia with Mersilene® mesh behind rectus abdominis. Arch Surg. 1974;109:532. 103. Casebolt BT. Use offabric mesh in abdominal wall defects.] Missouri St Med Assoc. 1975;72:7l. 104. Stoppa R, PetitJ, Henry X. Unsutured Dacron® prosthesis in groin hernias. Int Surg. 1975;60:41l. 105. Stoppa RE, Warlaumont CR The preperitoneal approach and prosthetic repair of groin hernia. In: Nyhus LM, Condon RE, eds. Hernia. 3rd ed. Phiiadelphia:JB Lippincott, 1989:199-225. 106. Cerise EJ, Busuttil RW, Craighead, et al. The use of Mersilene® mesh in repair of abdominal wall hernias: a clinical and experimental study. Ann Surg. 1975;181:728. 107. Minns ~, Tinckler LF. Structural and mechanical aspects of prosthetic herniorrhaphy.] Biomech. 1976;9:435. 108. Van Damme J-PJ. A preperitoneal approach in the prosthetic repair of inguinal hernia. Int Surg. 1985;70:223. 109. Nyhus LM, Klein MS, Rogers FB. Inguinal hernia. Curr Prabl Surg. 1991;28-6:427.

29 1l0. Adloff M, Arnaud J-P. Surgical management of large incisional hernias by an intraperitoneal Mersilene® mesh and an aponeurotic graft. Surg Gynecol Obstet. 1987;165:204. lll. Wantz GE. Giant prosthetic reinforcement of the visceral sac. Surg GynecolObstet. 1989;169:408. 112. Stoppa RE. The treatment of complicated groin and incisional hernias. World] Surg. 1989;13:545. 113. Wantz GE. Incisional hernioplasty with Mersilene.® Surg Gynecol Obstet. 1991;172:129. 114. Solorzano CC, Minter RM, Childers TC, et al. Prospective evaluation of the giant prosthetic reinforcement of the visceral sac for recurrent and complex bilateral inguinal hernias. Am] Surg. 1999; 177:19. 115. Thill RH, Hopkins WM. The use ofMersilene® mesh in adult inguinal and femoral hernia repairs: a comparison with classic techniques. Am Surg. 1994;60:553. 116. Helfrich RB, Gianturco C. Abdominal wall hernia repair: use of the Gianturco-Helfrich-Eberbach hernia mesh.] Laparoendosc Surg. 1995; 5:9l. 117. Usher FC, Ochsner J, Tuttle LLD Jr. Use of Marlex® mesh in the repair of incisional hernias. Am Surg. 1958;24:969. 118. Usher FC, Wallace SA. Tissue reaction to plastics; comparisoJ;l of nylon, Orlon,® Dacron,® and Teflon.® Arch Surg. 1958;76:997. 119. Usher FC, GannonJP. Marlex® mesh; a new plastic mesh for replacing tissue defects; I. Experimental studies. Arch Surg. 1959;78:13l. 120. PonkaJL, Wylie JH, Chaikof L, et al. Marlex® mesh-a new plastic mesh for the repair of hernia. Henry Ford Hosp Med J 1959;7:278. 121. Usher FC, CoganJE, Lowry TI. A new technique for the repair of inguinal and incisional hernias. Arch Surg. 1960;81:847. 122. Usher FC. Hernia repair with Marlex® mesh. Arch Surg. 1962;84:73. 123. Usher FC, Allen JE Jr, Crosthwait RW, et al. Polypropylene monofilament; a new biologically inert suture for closing contaminated wounds. ]AMA. 11962;79:780. 124. Usher FC. Hernia repair with knitted polypropylene mesh. Surg Gynecol Obstet. 1963;117:239. 125. Jacobs E, Blaisdell FW, Hall AD. Use of knitted Marlex® mesh in the repair of ventral hernias. Am] Surg. 1965;1l0:897. 126. Collier HS, Griswold RA. Repair of direct inguinal hernia without tension. Am Surg. 1967;33:715. 127. Schmitt HJ Jr, Grinna GLB. Use of Marlex® mesh in infected abdominal war wounds. Am Surg. 1967;113:825. 128. Drainer IK, Reid DK Recurrence-free ventral herniorrhaphy using a polypropylene mesh prosthesis.] R Coll Surg Edinb. 1972;17:253. 129. Gilsdorf RB, Shea MM. Repair of massive septic abdominal wall defects with Marlex® mesh. Am] Surg. 1975;130:634. 130. Walker PM, Langer B. Marlex® mesh for repair of abdominal wall defects. Can] Surg. 1976;19:21l. 13l. Boyd WC. Use of Marlex® mesh in acute loss of the abdominal wall due to infection. Surg Gynecol Obstet. 1977;144:251. 132. Abdu RA. Repair of paracolostomy hernias with Marlex® mesh. Dis Colon Rectum. 1982;25:529. 133. Gamjobst W, Sullivan ES. Repair of paraileostomy hernia with polypropylene mesh reinforcement. Dis Colon Rectum. 1984;27:268. 134. Sugarbaker PH. Peritoneal approach to prosthetic mesh repair of paraostomy hernias. Ann Surg. 1985;201:344. 135. Morris-Stiff G, Hughes LE. The continuing challenge of parastomal hernia: failure of a novel polypropylene mesh repair. Ann R Coll Surg EngL 1998;80:184. 136. Martin RE, Sureik S, Clossen IN. Polypropylene mesh in 450 hernia repairs: evaluation of wound infections. Contemp Surg. 1982; 20:46. 137. Chan STF, Esufali ST. Extended indications for polypropylene mesh closure of the abdominal wall. Br] Surg. 1986;73:3. 138. Down NK, Falk RE, Makowka L. Excision of abdominal wall tumours and reconstruction with Marlex® mesh. Can] Surg. 1986;29:19l. 139. Bayer I, Kyzer S, Chaimoff C. A new approach to primary strength-

30 ening of colostomy with Marlex® mesh to prevent paracolostomy hernia. Surg Gynecol Obstet. 1986;163:579. 140. Bendavid R. A femoral "umbrella" for femoral hernia repair. Surg GynecolObstet. 1987;165:153. 141. Bendavid R. New techniques in hernia repair. World] Surg. 1989; 13:522. 142. Nyhus LM, Pollak R, Bombeck CT, et al. The preperitoneal approach and prosthetic buttress repair for recurrent hernia. Ann Surg. 1988; 208:733. 143. Peacock EEJr. Here we are: behind again! Editorial. Am] Surg. 1989; 157:187. 144. Lichtenstein IL, Schulman AG, Amid PK, et al. The tension-free hernioplasty. Am] Surg. 1989;157:188. 145. Jones jW, Jurkovich GJ. Polypropylene mesh closure of infected abdominal wounds. Am Surg. 1989;55:73. 146. Bendavid R. Incisional parapubic hernias. Surgery. 1990;108:898. 147. Molloy RG, Moran KT, Waldron RP, et al. Massive incisional hernia: abdominal wall replacement with Marlex® mesh. Br] Surg. 1991;78: 242. 148. Nyhus LM. The recurrent groin hernia: therapeutic solutions. World ] Surg. 1989;13:541. 149. Matapurkar BG, Gupta AK, Agarwal AK. A new technique of "Marlex®-Peritoneal Sandwich" in the repair of large incisional hernias. World] Surg. 1991;15:768. 150. Caldron A, Vorwald P, Merono E, et al. A single technique for polypropylene mesh hernioplasty of inguinal and femoral hernias. Surg Gynecol Obstet. 1992;175:359. 151. Gilbert AI. Sutureless repair of inguinal hernia. Am] Surg. 1992; 163:331. 152. Lichtenstein IL. Hernia Repair Without Disability. 2nd ed. St. Louis: Ishiyaku EuroAmerica: 1986. 153. Robbins AW, Rutkow 1M. The mesh plug hernioplasty. Surg Clin North Am. 1993;73:501. 154. Rutkow 1M, Robbins AW. Mesh plug hernia repair: a follow-up report. Surgery. 1995;117:597. 155. Robbins AW, Rutkow 1M. Mesh plug repair and groin hernia surgery. Surg Clin North Am. 1998;78:1007. 156. McGreevy JM. Groin hernia and surgical truth. Am] Surg. 1998; 176:301. 157. Janu PG, Sellers KD, Mangiante EC. Mesh inguinal herniorrhaphy: a ten-year review. Am Surg. 1997;63:1065. 158. Temudom T, Siadati M, Sarr MG. Repair of complex giant or recurrent ventral hernias by using tension-free intraparietal prosthetic mesh (Stoppa technique): lessons learned from our initial experience (fifty patients). Surgery. 1996;120:738. 159. Corbitt JD Jr. Laparoscopic herniorrhaphy. Surg Laparosc Endosc. 1991;1:23. 160. Felix EL, Michas CA, McKnight RL. Laparoscopic repair of recurrent hernias. Surg Endosc. 1995;9:135. 161. Fitzgibbons RJ Jr, Camps J, Comet DA, et al. Laparoscopic inguinal herniorrhaphy; results of a multicenter trial. Ann Surg. 1995;221:3. 162. Crawford DL, Phillips EH. Laparoscopic repair and groin hernia surgery. Surg Clin North Am. 1998;78:1047. 163. Horton MD, Florence MG. Simplified preperitoneal Marlex® hernia repair. Am] Surg. 1993;165:595. 164. Moran RM, BraunsJ, Petrie CR, et al. Moran repair for inguinal hernias. Am Surg. 1997;63:430. 165. Plunkett RJ. US Patent 2230654 (to Kinetic Chemicals, Inc). 1941; Feb 4. 166. Gangal sv. Polytetrafluoroethylene. In: Kirk-Othmer Encyclopedia of Chemical Technology. Vol II. 3rd ed. New York: John Wiley & Sons Inc., 1980. 167. Oshige S. Japanese Patent No 42-13560 (67/13560). 1967;Aug. 168. Gore RW. US Patent 3953566 (to WL Gore and Assoc, Inc). 1976; April 27. 169. McClurken ME, McHaney JM, Colone WM. Physical properties and

J.R. DeBord

170. 171. 172.

173. 174. 175.

176.

177.

178.

179. 180. 181. 182. 183.

184.

185. 186. 187. 188.

189.

190. 191.

192.

193. . 194.

test methods for expanded polytetrafluoroethylene (PTFE) grafts. In: Kambic HE, Kantrowitz A, Sung P, eds. Vascular Graft Update: Safety and Performance ASTM STP 898. Philadelphia: American Society for Testing and Materials; 1986. WL Gore and Assoc, Inc. Patch Project Work Plan #215. DeBord JR. The historical development of prosthetics in hernia surgery. Surg Clin North Am. 1998;78:973. Elliott MP, Juler GL. Comparison of Marlex® mesh, microporous Teflon® sheets when used for hernia repair in the experimental animal. Am] Surg. 1979;137:342. Sher W, Pollack D, Paulides CA, et al. Repair of abdominal wall defects: Gore-Tex® vs Marlex® graft. Am Surg. 1980;46:618. Jenkins SD, Klamer TW, PartekalJ, et al. A comparison of prosthetic materials used to repair abdominal wall defects. Surgery. 1983;94:392. Neel HB III. Implants of Gore-Tex;® Comparisons with Teflon®coated polytetrafluoroethylene carbon and porous polyethylene implants. Arch Otolaryngol. 1983;109:427. Brown GL, Richardson JD, Malangoni MA, et al. Comparison of prosthetic materials for abdominal wall reconstruction in the presence of contamination and infection. Ann Surg. 1985;201:705. Wool NL, Strauss AK, Roseman DL. Clinical experience with the Gore-Tex® Soft Tissue Patch in hernia repair: a preliminary report. Proc lnst Med Chic. 1985;38:33. Hamer-Hodges DW, Scott NB. Replacement of an abdominal wall defect using expanded PTFE sheet (Gore-Tex®).] R Coll Surg Edinb. 1985;30:65. Pairolero PC, Arnold PG. Thoracic wall defects: surgical management of 205 consecutive patients. Mayo Clin Proc. 1986;61:557. Arnold PG, Pairolero PC. Chest-wall reconstruction: an account of 500 consecutive patients. Plastic Reconstr Surg. 1996;98:804. McMahon JD, Ripstein CB. Rectal prolapse-an update on the rectal sling procedure. Am Surg. 1987;53:37. Pailler JL, ManaaJ, Vicq PH, et al. Cure des hernies de l'aine avec interposition d'une prothese de PTFE. La Lettre Chirurg. 1987;55:13. Pasqualitti P, Miracco C. Esperienza clinica sull'impiego di un materiale protesico (PTFE espanso) nelle riparazioni di ernie e laparocelio Osp ltal ChiT. 1987;XL:375. Bauer lJ, Salky BA, Gelernt 1M, et al. Repair of large abdominal wall defects with expanded polytetrafluoroethylene (PTFE). Ann Surg. 1987;206:765. Law NW, Ellis H. Adhesion formation and peritoneal healing on prosthetic materials. Clin Mater. 1988;3:95. Druart ML, Limbosch JM. Traitement des eventrations par implantation intraperitoneale de voile en Teflon.® Ann ChiT. 1988;42:39. Lampl IH, Loeprecht H. Chest wall resection-alloplastic replacement. Thorac Cardiovasc Surg. 1988;36:157. Horbach NS, Blanco JS, Ostergard DR, et al. A suburethral sling procedure with polytetrafluoroethylene for the treatment of genuine stress incontinence in patients with low urethral closure pressure. Obstet Gynecol. 1988;71 :648. Antonini R, Biandrate F, Piccolini M, et al. Nostra esperienza suiI' utilizzo di un materiale protesico (PTFE) nel trattamento di laparoceli voluminosi ed iterativi. Acta Chir Mediterr. 1988;4:537. Berman M. The use of Gore-Tex® materials in the practice of cosmetic surgery. Am] Cosmet Surg. 1989;6:13. Van der Lei B, Bleichrodt RP, Simmermacher RKJ, et al. Expanded polytetrafluoroethylene patch for the repair of large abdominal wall defects. Br] Surg. 1989;76:803. Smith S, Gantt N, Rowe MI, et al. Dura versus Gore-Tex® as an abdominal wall prosthesis in an open and closed infected model.] Pediatr Surg. 1989;24:519. Murphy JL, Freeman]B, Dionne PG. Comparison of Marlex® and Gore-Tex® to repair abdominal wall defects in the rat. Can] Surg. 1989;32:244. Bleichrodt RP, Wijnen R. The use of polypropylene polytetrafluoroethylene and porcine corium implant to repair contaminated ab-

3. Prostheses in Hernia Surgery dominal wall defects in rats (abstract). Surgical Infection SocietyEurope, Amsterdam, The Netherlands. 1988; June. Published in Surgical Research Communications 1989;3(Suppll):28. 195. Law NW. A comparison of polypropylene mesh, expanded polytetrafluoroethylene patch and polyglycolic acid mesh for the repair of experimental abdominal wall defects. Acta Chir Scand. 1990;156:759. 196. Campanini A, Poddie D, Argnani M, L'accesso pre-peritoneale nel trattamento dell'ernia inguinale recidiva con protesi di PTFE. Chirurgia. 1990;3:315. 197. Law NW, Ellis H. Preliminary results for the repair of difficult recurrent inguinal hernias using expanded PTFE patch. Acta Chir Scand. 1990;156:609. 198. Debeugny P, Canarelli JP, Bonnevalle M, et al. Laparoschisis indication du patch en Teflon dans la reparation parietale. Cir Pidiatr. 1990;31:18. 199. Pailler JL, Essoussi H, de Calan L. Eventrations post operatoires: les protheses. Moniteur Hospitalier. 1990;27. 200. Harrison MR, Adzick NS, Longaker MT, et al. Successful repair in utero of a fetal diaphragmatic hernia after removal of herniated viscera from the left thorax. N Engl] Med. 1990;322:1582. 201. Monaghan RA, Meban S. Expanded polytetrafluoroethylene patch in hernia repair: a review of clinical experience. Can] Surg. 1991;34:502. 202. Spaw AT, Ennis BW, Spaw LP. Laparoscopic hernia repair: the anatomic basis.] Laparoendosc Surg. 1991;1:269. 203. Toy FK, Smoot RT Jr. Toy-Smoot laparoscopic hernioplasty. Surg Laparosc Endosc. 1991;1:151. 204. Campos LI, Sipes EK. Laparoscopic repair of diaphragmatic hernia. ] Laparoendosc Surg. 1991;1:369. 205. Colombo PL, Roveda S, Belisomo M, et al. Considerazioni sui grandi laparoceli abdominali l'utilizzo di protesi. Minerva Chir. 1992;47:161. 206. Konior RJ. Facial paralysis reconstruction with Gore-Tex® soft tissue patch. Arch Otolaryngol Head Neck Surg. 1992;118:1188. 207. Pans A, Pierard GE. A comparison of intraperitoneal prostheses for the repair of abdominal muscular wall defects in rats. Eur Surg Res. 1992;24:54. 208. Deysine M. Hernia repair with expanded polytetrafluoroethylene. Am ] Surg. 1992;163:422. 209. LeBlanc KA, Booth WV. Repair of primary and secondary inguinal hernias using an expanded polytetrafluoroethylene patch. Contemp Surg. 1992;41:29. 210. DeBord JR, Wyffels PL, Marshall JS, et al. Repair of large ventral incisional hernias with expanded polytetrafluoroethylene prosthetic patches. Postgrad Gen Surg. 1992;4:156. 211. LeBlanc KA, Booth WV. Laparoscopic repair of incisional abdominal hernias using expanded polytetrafluoroethylene: preliminary findings. Surg Laparosc Endosc. 1993;3:39. 212. Berliner SD. Clinical experience with an inlay expanded polytetrafluoroethylene soft tissue patch as an adjunct in inguinal hernia repair. Surg Gynecol Obstet. 1993;176:323. 213. Georgiades AH, Bauer WF. Repeat abdominal access. Surg Gynecol Obstet. 1993; 176:393. 214. Kennedy GM, Matyas JA. Use of expanded polytetrafluoroethylene in the repair of the difficult hernia. Am] Surg. 1994; 168:304. 215. Felix EL, Michas C. Laparoscopic repair of Spigelian hernias. Surg Laparosc Endosc. 1994;4:308. 216. Paul MG, DeRosa RP, Petrucci PE, et al. Laparoscopic tension-free repair oflarge paraesophogeal hernias. Surg Endosc. 1997;11:303. 217. Willekes CL, Edoga JK, Frezza EE. Laparoscopic repair of paraesophogeal hernia. Ann Surg. 1997;225:31. 218. Park A, Gagner M, Pomp A. Laparoscopic repair of large incisional hernias. Surg Laparosc Endosc. 1996;6:123. 219. Toy FK, Bailey RW, Carey S, et al. Prospective multicenter study oflaparoscopic ventral hernioplasty. Surg Endosc. 11998;2:955. 220. Tsimoyiannis EC, Tassi A, Glantzounis G, et al. Laparoscopic intraperitoneal onlay mesh repair of incisional hernia. Surg Laparosc

Endosc. 1998;8:360.

221. Costanza MJ, Heniford BT, Arca MJ, et al. Laparoscopic repair of recurrent ventral hernias. Am Surgeon. 1998;64:1121. 222. Gillion JF, Begin GF, Marecos C, et al. Expanded polytetrafluoroethylene patches used in the intraperitoneal or extraperitoneal position for repair of incisional hernias of the anterolateral abdominal wall. Am] Surg. 1997;174:16. 223. Balen EM, Diez-Caballero A, Hernandez-Lizoain JL, et al. Repair of ventral hernias with expanded polytetrafluoroethylene patch. Br] Surg. 1998;85:1415. 224. Gonzalez AU, de la Portlier de Juan F, Albarran GC. Large incisional hernia repair using intraperitoneal placement of expanded polytetrafluoroethylene. Am] Surg. 1999;177:291. 225. Bauer Harris MT, Kreel I, et al. Twelve-year experience with expanded polytetrafluoroethylene in the repair of abdominal wall defects. Mt Sinai] Med. 1999;66:20. 226. Delany HM, Porreca F, Mitsudo S, et al. Splenic capping: an experimental study of a new technique for splenorrhaphy using woven polyglycolic acid mesh. Ann Surg. 11982;96:187. 227. Condon RE. Prosthetic repair of abdominal hernia. In: Nyhus LM, Condon RE, eds. Hernia. 3rd ed. Philadelphia: JB Lippincott; 1989. 228. Lamb JP, Vitale T, Kaminskin DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery. 1983;93:643. 229. Delany HM, Rudavsky A, Lan S. Preliminary clinical experience with the use of absorbable mesh splenorrhaphy.] Trauma. 1985;25:909. 230. Lange DA, Zaret P, Merlotti GJ, et al. The use of absorbable mesh in splenic trauma.] Trauma. 1988;28:269. 231. White R, Ramos S, Delany H. Renorrhaphy using polyglycolic acid mesh.] Trauma. 1987;27:689. 232. Delany HM, Solanki B, Driscoll WB. Use of absorbable mesh for splenorrhaphy and pelvic peritoneum reconstruction. Contemp Surg. 1985; 27:11. 233. Dayton MT, Buchele BA, Shirazi SS, et al. Use of an absorbable mesh to repair contaminated abdominal wall defects. Arch Surg. 1986;121: 954. 234. Delany HM, Li J, Kim ES. Extent of peritoneal adhesions and local tissue reaction in response to absorbable vs nonabsorbable mesh. Contemp Surg. 1992;40:29. 235. Pans A, Elen P, Dewe W, et al. Long-term results of polyglactin mesh for the prevention of incisional hernias in obese patients. World] Surg. 1998;22:479. 236. Zimmerman LM. The use of prosthetic materials in the repair of hernias. Surg Clin North Am. 1968;48:143. 237. Scales JT. Discussion on metals and synthetic materials in relation to soft tissues; tissue reaction to synthetic materials. Proc R Soc Med. 1953;46:647. 238. DeBord JR. The rationale for the selection of a prosthetic biomaterial in hernia repair. Prohl Gen Surg. 1995;12:75. 239. Goldstein HS. Selecting the right mesh. Hernia. 1999;3:23. 240. Amid PK, Shulman AG, Lichtenstein IL, et al. Experimental evaluation of a new composite mesh with the selective property of incorporation to the abdominal wall without adhering to the intestines . .J Biomed Mater Res. 1994;28:373. 241. Velitchkov NG, LosanoffJE, Iqossev KT, et al. The Lichtenstein open tension-free inguinal hernia repair using a new prosthetic meshBulgarian Irresorbable Ampoxen. Int Surg. 1996;81:205. 242. Soares BM, Guidoin RG, Marois Y, et al. In vivo characterization of a fluoropassivated gelatin-impregnated polyester mesh for hernia repair.] Biomed Mater Res. 1996;32:293. 243. Klinge U, Klosterhalfen B, Conze J, et al. Modified mesh for hernia repair that is adapted to the physiology of the abdominal wall. Eur .J Surg. 1998;164:951. 244. Dent L, Modak S, Sam path L, et al. Evaluation of an infectionresistant silver-chlorhexidine-impregnated PTFE soft tissue patch. Surg Forum. 1992;XLIII:70. 245. Brewer AR, Stromberg BV. In vitro adherence of bacteria to prosthetic grafting materials. Ann Plast Surg. 1990;24:134.

32 246. Modak S, Sampath L. Development and evaluation of a new polyurethene central venous antiseptic catheter: reducing central venous catheter infections. Complications Surg. 1992; 11 :23. 247. Veenstra DL, Saint S, Sullivan SD. Cost-effectiveness of antisepticimpregnated central venous catheters for the prevention of catheterrelated bloodstream infection. JAMA. 1999;282:554.

J.R. DeBord 248. Costerton jW, Irwin RT, Chen KJ. The bacterial glycocalyx in nature and disease. Annu Rev Microbiol. 1981;35:299. 249. DeBord JR, Bauer jJ, Grischkan DM, et aI. Short-term study on the safety of antimicrobial-agent-impregnated ePTFE patches for hernia repair. Hernia 2000. In press.

Evolution of Laparoscopic Hernia Repair Karl LeBlanc and Ralph Ger

The concept of a posterior approach to the repair of abdominal wall hernias had its earliest beginnings in North America in 1878 in Utica, New York, when E. Hutchinson reported a case of inguinal hernia that was strangulated at the internal ring. Hutchinson made a midline incision between the umbilicus and the pubis. Entering the peritoneal cavity, he released the gangrenous bowel, but the patient died the following day.1 Annandale was the first (1876) to enter the preperitoneal space through an incision parallel to Poupart's ligament for the purpose of treating an indirect and femoral hernia. 2 But it was 50 years earlier still, in 1823, that the first surgeon entered the preperitoneal space: searching for a safer approach to the ligation of the external iliac artery, A. J. Bogros investigated and described the space now known by his name. s Tait (1891), Cheatle (1920), Henry (1936) and McEvedy (1966) described this "newer" approach to hernia repair through the preperitoneal space. 4 This approach was rediscovered and established by Nyhus (1959) as an effective method of herniorraphy.5 The benefits of using a prosthetic mesh placed in the preperitoneal space were shown by Rignault,6 NyhUS,' Stoppa,8 and Wantz. 9 These surgeons did not have access to laparoscopic methodology at that time to investigate this method of access to the abdominal or preperitoneal spaces.

First Use The first report of the use of the laparoscope in the repair of an abdominal hernia was made by Ger in 1982. 10 He reported a series of 13 patients treated in the 1970s in which he closed the peritoneal opening of the sac using Michel clips. All but the last patient in this series was repaired through an open incision. The thirteenth patient was repaired in 1979 under laparoscopic guidance with a special stapling device. The first report of the use of the laparoscope in the repair of abdominal hernias was made by Ger in 1982. 10 He reported a series of 12 patients treated in the 1970s in which he closed the peritoneal opening of the sac through an open abdominal incision using Michel clips. In a thirteenth patient the repair was carried out in 1979 under laparoscopic guidance with a special stapling device. The patient was lost to follow up after a short period. Ger continued his efforts to repair these hernias laparoscopically. He reported the closure of the neck of

R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

the hernia sac using a prototype instrument called the "herniostat" in beagle dogs.!1 The results in these models seemed promising. In that same article, he reported the potential benefits of the laparoscopic approach to groin hernia repair as: (1) creation of puncture wounds rather than formal incisions; (2) minimal dissection; (3) less risk of spermatic cord injury and ischemic orchitis; (4) minimal risk of bladder injury; (5) decreased incidence of neuralgias; (6) possibility of an outpatient procedure; (7) ability to achieve the highest possible ligation of the hernial sac; (8) minimal postoperative discomfort; (9) a faster recovery time; and (10) ability to perform simultaneous diagnostic laparoscopy and to diagnose and treat bilateral inguinal hernias. These potential advantages and advances in the laparoscopic repair of hernias continue to be the recognized goals of each method. Since the publication of Ger's article, most inguinal hernia repairs have been carried out on an outpatient basis.

Techniques Developed Bogojavalensky initially presented the use of a prosthetic biomaterial with laparoscopy in 1989. 12 He placed a roll of polypropylene mesh into indirect hernias offemale patients. POpplS repaired a coincidental direct hernia that was found at the time of a uterine myomectomy. He recognized the need to provide coverage of a wider area than that of the defect itself. To accomplish this, he placed a 4 cm by 5 cm patch of dehydrated dura mater over the defect. This was secured to the peritoneum with catgut sutures that were tied extracorporeally. Popp expressed concerns that the intra-abdominal repair of inguinal hernia could lead to adhesive complications and suggested that a preperitoneal approach might be preferable. Schultz reported the first patient series of laparoscopic herniorraphy14 in 1990. He used a combination of rolls of polypropylene that were packed into the hernial orifice and the placement of two or three flat sheets of polypropylene mesh (2.5 cm by 5 cm) over the defect. The rolls of mesh were not secured to either the fascia or the peritoneum, which was closed using clips. This was probably the earliest attempt at a type of transabdominal preperitoneal (TAPP) repair that is commonly used today. Corbitt15 modified this technique by inverting the hernia sac and performing a high ligation with sutures or with an endoscopic stapling device. The 33

initial reports were promising, but longer follow-up revealed recurrence rates of 15 to 20%.1 6 Because of this, both of these methods were abandoned. Nevertheless, the avoidance of extensive dissection by these methods was appealing. A similar concept was applied in the intraperitoneal onlay patch (IPOM) technique. This repair was investigated by Salerno, Fitzgibbons, and Filipi,17 using a polypropylene patch in a porcine model. They placed rectangular prostheses against the abdominal wall, covering the internal inguinal ring and secured it with a stapling device. The success of these repairs led them to apply the method in clinical trials. At about the same time, Toy and Smoot18 reported upon their first 10 patients repaired with the IPOM technique. They secured an expanded polytetrafluoroethylene (PTFE) patch to the inguinal floor with staples, using a prototype stapling device of their own design. A subsequent report of their first 75 patients was published in 1992. 19 In this later series, the same prosthetic biomaterial (7.5 cm by 10 cm) was attached with the Endopath EMS® stapler. Mter a follow-up of up to 20 months, the recurrence rate was 2.4%. They noted a significant decrease in postoperative pain and earlier return to normal activity, as compared to the open repair of inguinal hernia. Others reported similar results. 20-22 Fitzgibbons 23 later abandoned the IPOM repair except for simple indirect inguinal hernias. He found that the patch material could be displaced into the hernial defect because it was anchored to the peritoneum alone rather than the fascia. He used the TAPP approach, which had also been reported by Arregui24 for the other types of groin hernias. In this repair, the peritoneum is incised and dissected away from the transversalis fascia to expose the posterior inguinal wall. The mesh material is then secured to that fascia, which was believed to ensure superior fixation and tissue ingrowth. Popp25 described a method of dissecting the peritoneum away from the abdominal wall prior to the incision of the peritoneum in the TAPP repair. This technique used saline injected by a transcutaneous syringe. This "aquadissection" probably led to the idea that the entire dissection could be accomplished from within the preperitoneal space, eliminating the need to enter the abdominal cavity. Other operations that were attempted at that time included the "ring-plasty" and a preperitoneal iliopubic tract repair. Ring-plasty is a sutured repair that approximates the deep structures of the lateral iliopubic tract to the proximal arching musculotendinous fibers of the transversus abdominis muscle. 20 ,26 The preperitoneal iliopubic tract repair sutures the iliopubic tract to the transversus abdominis muscle. 27,28 While this repair incorporated the use of a prosthetic material, it had the disadvantage of tension. As techniques of laparoscopic inguinal herniorrhaphy matured, the predominant method was the TAPP repair using either a polypropylene mesh 16,29 or an expanded polytetrafluoroethylene material (ePTFE).30 Arregui31 and Phillips32 introduced a technique that did not involve a peritoneal incision in the repair of the posterior inguinal wall. The dissection of the preperitoneal space was accomplished instead under direct visualization of the area through a laparoscope placed in the peritoneal cavity. The laparoscope was then moved into the newly dissected preperitoneal space to complete the repair. Dulucq33,34 was the first surgeon to perform the laparoscopic repair of an inguinal hernia without entering the peritoneal cavity. Ferzli35 and McKernan36 later popularized this technique. Using the "open" entry into the preperitoneal space, the dissection of the space was carried out

K. LeBlanc and R. Ger

under direct visualization in that space. The completed totally extraperitoneal (TEP) repair was identical to that of the TAPP but decreased the risk of injury to intra-abdominal organs.

Results These publications proved that the repair of inguinal hernias could be accomplished with the laparoscopic technique. Controversy persisted,37 then as well as now, as to whether or not these operations should be done. Part of the controversy concerns the variety of new complications, such as bowel and bladder injury,19 inferior epigastric and iliac artery laceration,38 trocar herniation,36 genitofemoral neuralgia,38,39 and lateral femoral cutaneous neuralgia. 16,38 Additionally, the laparoscopic repair was more difficult to master, operating times were longer, and the instrumentation was more costly.35 A multicenter analysis40 of the procedure, using most of the methods noted above, verified that the repair had a recurrence rate of 0.4-3% and a low incidence of complications in experienced hands. Currently, the majority of laparoscopic inguinal hernia repairs are approached by either the TAPP or TEP method and utilize a polypropylene prosthesis. Most of the surgeons who perform the TEP repair use the commercially available dissection balloons to prepare the preperitoneal space. In a recent report,41 the recurrence rate of these repairs was 0.4% in 10,053 repairs with a median follow-up of 36 months. The surgeons that continue to perform laparoscopic herniorrhaphy believe that the goals anticipated by Cerll have been realized. The improvement in recovery in the laparoscopic cholecystectomy and herniorrhaphy patients led us to attempt the repair of ventral and incisional hernias in 1992.42 This initial report involved only five patients, but the quick recovery and the safety of the procedure were encouraging. These patients are free of recurrence after more than seven years. The fixation was that of the "box type" of hernia stapler without the use of sutures. With more patients and follow-up, no recurrences were noted. 43 ,44 The use of ePTFE prostheses is preferred by us given its in-growth characteristics and relative freedom from the development of intra-abdominal adhesions. 45 In 1995, Barie46 proposed the use of a polyester material covered on the visceral side with a mesh of absorbable polyglactin. However, Stoppa and Soler demonstrated that transmigration through the bowel was still a threat when the polyglactin was absorbed. They abandoned the idea as early as 1991. 47 Park48 modified our technique for the repair of large ventral hernias by utilizing the transfixion of the ePTFE patch or Prolene® mesh with transabdominally placed Prolene sutures passed through a Keith needle. In their series of 30 cases, one recurrence was noted. This repair used a fascial overlap of 2 cm. Holzman49 placed Marlex® prostheses with a 4 cm overlap onto normal fascial edges and secured them with an endoscopic stapler. He found this technique to be safe and effective. In separate investigations, Holzman49 and Park50 found that the laparoscopic repair took longer to accomplish but was associated with fewer postoperative complications and a shorter hospital stay. Currently, it is felt that a minimum of a 3 cm overlap is required for an adequate repair. The prosthesis is preferably fixed to the abdominal wall with both transabdominal sutures and the use of the helical tacking device. The size of the mesh and the method of fixation determine the success of a hernia repair. The recur-

4. Evolution of Laparoscopic Hernia Repair

rence rate declines with better fixation methods, as shown by comparing the results of using staples alone (15%), helical tacks alone (8%), or tacks with transabdominal sutures (0%).51 The history of open inguinal hernia repair spans many centuries. The use of the laparoscope in the repair of inguinal and ventral hernias is still in its infancy by comparison. In experienced hands, the recurrence rate is comparable to the open tension-free repair, the complication rate is low, and recovery is rapid. Operating times have diminished, but many believe that laparoscopic herniorrhaphy does not achieve an appropriate cost-benefit profile. Improved technology, continued innovation and refinement of techniques, and long-term results will ultimately determine whether it will become a generally accepted, standard procedure.

References 1. Hutchinson E. Case of strangulated hernia operated by abdominal section laparotomy. Ohio M & SJ 1878;3:499. 2. Annandale T. A case in which a reducible oblique and direct inguinal and femoral existed on the same side and were successfully treated by operation. Edinb MedJ 1876;21:1087-1091. 3. Bendavid R. The space of Bogros. Postgrad Gen Surg. 1995;6(1):1. 4. Read RC. Preperitoneal herniorrhaphy: a historical review. World] Surg. 1989; 13:532-540. 5. Nyhus LM. Preperitoneal herniorrhaphy. West] Surg, Obstet Gynecol. 1959;7:48-54. 6. Rignault DP. Preperitoneal prosthetic inguinal herniorrhaphy through a Pfannenstiel approach. Surg Gynecol Obstet. 1986;162:465. 7. Nyhus LM, Pollak R, Bombeck TC, et al. The preperitoneal approach and prosthetic buttress repair of recurrent hernia. Ann Surg. 1988; 208:722-727. 8. Stoppa RE, Warlaumont CR. The preperitoneal approach and prosthetic repair of groin hernia. In: Nyhus LM, Condon RE, eds. Hernia. Philadelphia: Lippincott; 1989: 199-225. 9. Wantz GE. Prosthetic repair groin hernioplasties. In: Atlas of Hernia Surgery. New York: Raven Press; 1991;101-151. 10. Ger R. The management of certain abdominal herniae by intraabdominal closure of the neck of the sac. Ann R Coll Surg Engl. 1982; 64:342-344. 11. Ger R, Monro K, Duvivier R, et al. Management of inguinal hernias by laparoscopic closure of the neck of the sac. Am] Surg. 1990;159: 370-373. 12. Bogojavalensky S. Laparoscopic treatment of inguinal and femoral hernia (video presentation). 18th Annual Meeting of the American Association of Gynecological Laparoscopists. Washington, DC; 1989. 13. Popp LW. Endoscopic patch repair of inguinal hernia in a female paltient. Surg Endosc. 1990;5:10-12. 14.' Schultz L, Graber j, Pietrafittaj, et al. Laser laparoscopic herniorrhaphy: a clinical trial, preliminary results.]Laparoendosc Surg. 1990;1:41-45. 15. Corbitt J. Laparoscopic heniorrhaphy. Surg Laparosc Endosc. 1991;1: 23-25. 16. Corbitt J. Laparoscopic herniorrhaphy: a preperitoneal tension-free approach. Surg Endosc. 1993;7:550-555. 17. Salerno GM, Fitzgibbons Rj, Filipi C. Laparoscopic inguinal hernia repair. In: Zucker KA, ed. Surgicallaparoscopy. St. Louis: Quality Medical Publishing; 1991:281-293. 18. Toy FK, Smoot RT. Toy-Smoot laparoscopic hernioplasty. Surg Laparosc Endosc. 1991;1:151-155. 19. Toy FK, Smoot RT. Laparoscopic hernioplasty update. 1992;2(5): 197-205. 20. Spaw AT, Ennis BW, Spaw LP. Laparoscopic hernia repair: the anatomical basis.] Laparoendosc Surg. 1991;1:269-277.

35 21. LeBlanc KA, Booth WV. Avoiding complications with laparoscopic herniorrhaphy. Surg Laparosc Endosc. 1993;3 (5) :420-424. 22. LeBlanc KA, Spaw AT, Booth WV. Inguinal herniorrhaphy using intraperitoneal placement of an expanded polytetrafluoroethylene patch. In: Arregui ME, Nagan RF, eds. Inguinal hernia: advances or controversies? Oxford: Radcliffe Medical Press; 1994:437-439. 23. Fitzgibbons RP. Laparoscopic inguinal hernia repair. In: Zucker KA, ed. Surgical laparoscopy update, St. Louis: Quality Medical Publishing; 1993:373-934. 24. Arregui ME. Preperitoneal repair of direct inguinal hernia with mesh. Advanced Laparoscopic Surgery: The International Experience. Indianapolis, Ind.: May 20--22; 1991. 25. Popp LW. Improvement in endoscopic hernioplasty: transcutaneous aquadissection of the musculofascial defect and preperitoneal endoscopic patch repair.] Laparoendosc Surg. 1991; 1 (2) :83-90. 26. Dion YM, Morin J. Laparoscopic inguinal herniorrhaphy. Can] Surg. 1992;35:209-212. 27. Gazayerli MM. Anatomic laparoscopic repair of direct or indirect hernias using the transversalis fascia and iliopubic tract. Surg Laparosc Endosc. 1992;2:49-52. 28. Gazayerli MM, Arregui ME, Helmy HS. Alternative technique: laparoscopic iliopubic tract (IPTR) inguinal hernia repair with inlay buttress of polypropylene mesh. In: Ballantyne GH, Leahy PF, Modlin IR, eds. Laparoscopic surgery. Philadelphia: WB Saunders; 1993. 29. Kavic MS. Laparoscopic hernia repair. Surg Endosc. 1993;7:163-167. 30. Campos L, Sipes E. Laparoscopic hernia repair: use of a fenestrated PTFE graft with endo-clips. Surg Laparosc Endosc. 1993;3(1);35-38. 31. Arregui ME, Navarrette j, Davis Cj, et al. Laparoscopic inguinal herniorrhaphy: techniques and controversies. Surg Clin North Am. 1993;73(3): 513-527. 32. Phillips EH, Carroll Bj, Fallas MJ. Laparoscopic preperitoneal inguinal hernia repair without peritoneal incision: technique and early clinical results. Surg Endosc. 1993;7:159-162. 33. Dulucq jL. Treatment of inguinal hernia by insertion of a subperitoneal patch under preperitoneoscopy. Chirurgie. 1992;118(1-2): 83-85. 34. Dulucq JL. Treatment of inguinal hernias by insertion of mesh through retroperitoneoscopy. Post Grad Surg. 1992;4(2):173-174. 35. Ferzli GS, Massad A, Albert P. Extraperitoneal endoscopic inguinal hernia repair.] Laparoendosc Surg. 1992;2(6):281-286. 36. McKernan jB, Laws HL. Laparoscopic repair of inguinal hernias using a totally extraperitoneal prosthetic approach. Surg Endosc. 1993; 7:26-28. 37. Rutkow IJ. Laparoscopic hernia repair. The socioeconomic tyranny of surgical technology. Arch Surg. 1992;127(11):1271. 38. Felix EL, Michas C. Double-buttress laparoscopic herniorrhaphy.] Laparoendosc Surg. 1993;3(1):1-8. 39. Geis WP, Crafton WB, Novak Mj, et al. Laparoscopic herniorrhaphy: results and technical aspects in 450 consecutive procedures. Surgery. 1993;114:765-774. 40. Tetik C, Arregui ME, DulucqjL, et al. Complications and recurrences associated with laparoscopic repair of groin hernias: a multi-institutional retrospective analysis. Surg Endosc. 1994;8:1316-1323. 41. Felix E, Scott S, Crafton B, et al. Causes of recurrence after laparoscopic hernioplasty. Surg Endosc. 1998;12:226-231. 42. LeBlanc KA, Booth wv. Laparoscopic repair of incisional abdominal hernias using expanded polytetrafluoroethylene: preliminary findings. Surg Laparosc Endosc. 1993;3(1):39-41. 43. LeBlanc KA, Booth WV, Spaw AT. Laparoscopic ventral herniorrhaphy using an intraperitoneal onlay patch of expanded polytetrafluoroethylene. In: Arregui ME, Nagan RF, eds. Inguinal hernia: advances or controversies? Oxford: Radcliffe Medical Press; 1994:501-510. 44. LeBlanc KA, Booth WV, Whitaker jM. Laparoscopic repair of ventral hernias using an intraperitoneal onlay patch: report of current results. Contemp Surg. 1994;45(4):211-214. 45. LeBlanc KA. Two-phase in vivo comparison studies of the tissue re-

sponse to polypropylene, polyester, and expanded polytetrafluonr ethylene grafts used in the repair of abdominal wall defects. In: Treuter KH, SchumpeJick, eds. Peritoneal adhesions. Berlin: Springer-Verlag; 1997:352-362. 46. Barie PS, Mack CA, Thompson WA. A technique for laparoscopic repair of herniation of the anterior abdominal wall using a composite mesh prosthesis. Am] Surg. 1995; 170:62-63. 47. Soler M. Eventrations post operatoires, etude de deux nouveaux procedes. Doctoral thesis. University of Picardie: 1991.

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48. Park A, Gagner M, Pomp A. Laparoscopic repair of large incisional hernias. Surg Laparosc Endosc. 1996;6(2):123-128. 49. Holzman MD, Parut CM, Reintgen K, et al. Laparoscopic ventral and incisional hernioplasty. 1997;11:32-35. 50. Park A, Birch DW, Lovrics P, et al. Laparoscopic and open incisional hernia repair: a comparison study. Surgery. 1998;124:816-822. 51. LeBlanc KA. Current considerations in laparoscopic incisional and ventral herniorrhaphy. Submitted.

Part II Anatomy

5 Anatomy of the Abdominal Wall Jean Bernard Flament, Claude Avisse, and Jean

Fran~ois

The Anterolateral Abdominal Wall The anterolateral abdominal wall occupies a hexagonal area limited cranially by the angle of the xiphoid process and the costochondral margins; laterally, the limit is the midaxillary line and caudally the anterior part of the pelvic skeleton and pubic symphysis. We will describe successively the different aspects of the anterolateral abdominal wall which the surgeon must know when performing a laparotomy, closing a laparotomy, or managing de novo or incisional hernias of the abdominal wall.

Muscles of the Anterolateral Abdominal Wall Rectus Abdominis The rectus muscles of the abdomen run vertically, like two pillars, from the anteroinferior thoracic skeleton to the pubic region. Each rectus is attached on the thorax by three digitations to the anterior part of the fIfth rib, the sixth rib and its cartilage, and the seventh costal cartilage and xiphoid process. The body of the rectus is wide in its upper half (10-12 cm at the level of the costal ridge and 5-8 cm near the umbilicus). The muscle ends in a fibrous tendon measuring 2-3 cm in width at the level of the pubis (Fig.5.1A). Three to five tendinous intersections cross the rectus muscle. This polygastric arrangement is a reminder of the primitive metameric segmentation of the abdominal musculature, and the fibrous intersections may be considered the equivalent of abdominal ribs. These interesting fibrous bands are usually incomplete in both the anteroposterior and the transverse direction (Fig. 5.1B).

Flat Muscles The triple layer of the flat abdominal muscles lies on each side of the two central paramedian pillars formed by the rectus muscles. The fibers of these three large muscles run obliquely in different directions: the external oblique has its fibers oriented downward and forward, the internal oblique fibers run upward and forward, while the transversus abdominis fibers run horizontally.

Delattre

These muscles are myoaponeurotic systems comprising a muscle body extended by a wide aponeurosis. The transversus abdominis displays two systems of aponeuroses, one anterior and the other posterior. These different aponeuroses form the sheath of the rectus muscle and are arranged differently in the upper twothirds and lower one-third of the abdominal wall. External Oblique The muscular fIbers of this flat muscle arise from

the lateral part of the thoracic wall (the lateral surface of the lowest seven or eight ribs) by slips that interdigitate with those of the anterior serratus. The fibers of the muscle take an oblique course downward and toward the midline. The posterior and superior part of the external oblique is composed of fleshy muscular fIbers inserting on the anterior end of the iliac crest and the anterior superior iliac spine. Its anterior aponeurosis spreads out in front of the rectus. Along the line extending from the xiphoid process to the pubic symphysis, the fibers of the external oblique on one side interdigitate with those of the other side to form a chevron pattern. This pattern shows progressive accentuation in the lower part of the abdominal wall. The lower fIbers of the aponeurosis of the external oblique split from each other inferiorly and medially to form the opening of the superfIcial inguinal ring. The aponeurotic fIbers form the superior (medial) and inferior (lateral) crura of the superficial inguinal ring. Arcuate fibers arch over the superior rim of this slit-like opening in the aponeurosis of the external oblique. They are known as intercrural fibers (Fig. 5.2). The inferior crus (lateral crus) inserts into the pubic tubercle and pecten; the superior or medial crus inserts anterior to the pubic bone and symphysis. The insertion of the inferior crus is, in part, by way of the lacunar ligament. Fibers from the superior crus cross the midline to insert on the opposite pubic tubercle. The innominate fascia of Gallaudet, or fascia of the external oblique muscle, is a tissue-thin membrane that covers the external oblique muscle and aponeurosis. It forms the intercrural fibers in the superfIcial ring and follows the spermatic cord to form the external spermatic fascia. The external oblique lowers the ribs (expiratory muscle), bringing the thorax closer to the pelvis. InternalOblique The internal oblique muscle lies deep to the ex-

ternal oblique with its fibers running in an opposite direction to those of the external oblique. The muscle is inserted on the pelvic 39

R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

J.B.

Flament et al.

FIGURE 5.1. Rectus muscle and its sheath. (A) Anterior view; (B) sagittal section.

skeleton and stretches upward, forward, and medially to the thoracic border and linea alba. The aponeurotic fibers of the internal oblique are classically considered to be the major constituent of the sheath of the rectus. The insertions of the internal oblique are the following: the anterior two-thirds of the intermediate line of the iliac crest; the aponeurosis of the lumbosacral muscles; the anterior superior iliac spine; the lateral third of the inguinal ligament; and the iliopsoas fascia. The fibers of the muscle are oriented in an upward direction. The posterior fascicles are composed only of fleshy

FIGURE 5.2. Aponeurosis of the external oblique: 3 = lateral crus; 4 = medial crus; 5 = intercrural fibers. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 43, p. 77, with permission.)

fibers over the entire length, and they insert on the cartilage of the lowest three ribs. The main part of the muscle continues into its aponeurosis, which blends into its homologues from the other side in the region of the linea alba, splits into two laminae (upper two-thirds of the aponeurosis) which pass around the anterior and posterior surfaces of the rectus. At the level of the lower third of the rectus, the anterior passage of all the aponeurotic fibers causes a rupture in the posterior wall of the fibrous rectus sheath referred to as the semicircular line of Douglas (arcuate line). The fibers of the internal oblique, originating from the anterior superior iliac spine and lateral third of the inguinal ligament, run medially and slightly downward to fan out over the anterior surface of the rectus. These muscle fibers form the anterior part of the conjoined tendon (falx inguinalis). The lower part of the internal oblique continues on to the spermatic cord as the cremaster muscle (Fig. 5.3). The action of this muscle is comparable to that of the external oblique, although its unilateral contraction leads to rotation and lowering of the thorax on the side of the contraction. Transversus Abdominis Muscle The transversus, from its cranial to caudal parts, is inserted posteriorly on the six lower ribs, lumbodorsal fascia, iliac crest, and iliopsoas fascia. The thoracic insertions of this muscle are on the medial surface of the cartilage of the lowest seven or eight ribs and interdigitate with the insertions of the diaphragm. The transversus may be considered as a veritable antagonist of the diaphragm and the main expiratory muscle. In the lumbar region, the muscle is inserted on the tips of the costal processes of the lumbar vertebrae and, by its aponeurotic sheet, on the thoracolumbar fascia. In the pelvic region, the transversus abdominis inserts on the anterior half of the medial edge (labium internum) of the iliac crest, the anterior superior iliac spine, and classically, the lateral third of the inguinal ligament medial to the insertions of the internal oblique. In reality, these fibers of the transversus abdominis are attached to the iliac fascia behind the inguinal ligament and then run forward and inward and come to lie almost parallel to

5. Anatomy of the Abdominal Wall

FIGURE 5.3. Disposition of the internal oblique muscle: 1 = internal oblique fibers; 2 = internal oblique fibers; 3 = cremasteric muscle; 4 = rectus muscle. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. C. Doin; 1956, Fig. 51, p. 87, with permission.)

the deep surface of the internal oblique. These fibers form the "conjoined tendon," and contribute to the formation of the cremaster (Fig. 5.4). The fleshy body of the transversus abdominis, except for its lowermost part, blends into the anterior aponeurosis of the muscle. The boundary between its muscular and fibrous parts is rather sinuous and will be described later as the semilunar line of Spiegel. The aponeurotic fibers of the transversus abdominis above the arcuate line (semicircular line, or fold of Douglas) pass posterior to the rectus abdominis muscle, while those below this level generally pass anteriorly and thus contribute to the anterior portion of the rectus sheath. The transversus is the main muscle in the retention of the abdominal viscera. This muscle is very important in respiration, since it displaces or blocks the visceral mass under the diaphragm at the end of the initial stage of diaphragmatic inspiration. The powerful traction of this muscle on the linea alba tends to separate the margins of a laparotomy incision. This accounts for the high frequency of wound dehiscence subsequent to vertical midline incision of the abdominal wall. Furthermore, the rapid retraction of the transversus explains the persistence of the dehiscence and the difficulties encountered in its treatment, even in the absence of loss of abdominal wall tissue .

FIGURE 5.4. Transversus abdominis muscle in a classical textbook of anatomy. (From Bourgery, Atlas of Anatomy, 1832.)

Cooper, in the 1827 edition of his work, described the transversalis fascia as follows: "When the lower portions of the internal oblique and transversalis muscles [sic] are raised from the subjacent attachments, a layer of fascia is found to be interposed between them and the peritoneum, through which the spermatic vessels emerge from the abdomen. This fascia, which I have ventured to name fascia transversalis, varies in density, being strong and unyielding towards the ilium, but weak and more cellular towards the pubis." [Editor's Note: "Transversalis muscle" was a term used for the transversus abdominis muscle.]

The fascia propria, an areolar adipose layer of variable thickness in different individuals, is often referred to as the subperitoneal fat. It separates the transversalis fascia from the peritoneum, except at the level of the umbilicus, where it is practically absent. It penetrates between the bladder and the pubis into the space of Retzius (retropubic space) and laterally (in contact with the iliac fascia) into the space of Bogros (retroinguinal space). The fascia propria is a loosely organized and largely intercommunicating layer.

The Rectus Sheath

Transversalis Fascia This fibrous layer lines the deep surface of the transversus abdominis and can be easily separated from the muscle over most of its surface. Its mechanical resistance is very weak above the umbilicus. However, below the umbilicus, it gains a certain structural consistency, which is more pronounced in the inguinal region. At this level, the transversalis fascia displays the properties of a true aponeurosis, as pointed out by Cooper in 1827, tightly adhering to the posterior surface of the transversus abdominis, even seeming to extend the muscle downward (Fig. 5.5) .

The rectus muscle is enclosed in a stout sheath formed by the bilaminar aponeuroses of the three flat muscles, which split and pass anteriorly and posteriorly around the muscle, starting at the lateral border of the rectus abdominis, forming the linea alba medially, and continuing in a complicated way to the opposite side. The crossing of these fibers, at the midline, is the real insertion of the fleshy bodies of the flat muscles of the anterior abdominal wall.

J.B. Flament et al.

FIGURE 5.6. Structure of rectus sheath: 1 and 8 = internal oblique; 2 = external oblique; 3 = transversus abdominis; 4 and 11 = transversalis fascia; 5 = inguinal ligament; 6 = rectus sheath; 7 = aponeurotic fiber of the external oblique ending on the rectus sheath; 10 = rectus muscle; 9 = public tubercle. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 146, p. 244, with permission.)

FIGURE 5.5. Transversus abdominis muscle and transversalis fascia: 1 = external oblique; 2 = internal oblique; 3 = transversus abdominis muscle; 4 = inguinal ligament (schematic); 5 = iliopubic tract; 6 = epigastric artery; 7 = Gimbernat's ligament; 8 = Cooper's ligament. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 65, p. 103, with permission.)

Below a limit formed by the semicircular line, the posterior lamina of the rectus sheath is no longer present and is replaced by the transversalis fascia. The Anterior Lamina of the Rectus Sheath (Fig. 5.6) This is formed by the fibers of the oblique muscles, forming an overlapping chevron pattern facing upward or downward at an angle of 90-110°. This arrangement of the fibers of the sheath flattens out in the umbilical region, which probably accounts for the relative weakness of transverse sutures in this zone. The Posterior Lamina of the Sheath This is derived mainly from the aponeurosis of the transversus abdominis. Neurovascular trunks penetrate the rectus sheath through small openings in the posterior lamina. Midway between the xiphoid and the umbilicus, the arrangement of the aponeurotic layers is such that the external oblique aponeurosis passes in front of the rectus abdominis muscle. The internal oblique aponeurosis divides into two laminae at the lateral margin of the rectus abdominis muscle. One layer passes in front of the rectus to form a portion of its anterior sheath, while the other layer contributes to the formation of the posterior rectus sheath (Figs. 5.7 and 5.8). Below the arcuate line, (linea semicircularis of Douglas), layers forming the rectus sheath have another arrangement: the aponeurosis of the external oblique, the internal oblique, and the transversus abdominis muscles all pass anterior to the rectus abdominis

muscle. The transversalis fascia forms the only fascial layer posterior to the rectus abdominis muscles below the level of the arcuate line, midway between the umbilicus and the symphysis pubis. As previously noted, the posterior rectus sheath in this area is composed of peritoneum, areolar tissue, and transversalis fascia as clearly shown in Figure 5.9. The Arcuate Line (Semicircular Line ofDouglas) The arcuate line lies roughly along the line joining the right and left anterior superior iliac spines. It is usually a clearly defined, rather sharp structure. Sometimes, it is marked by a progressive zone of transition where the resistant posterior lamina of the rectus sheath continues into the much weaker transversalis fascia. This zone of transition is a weak area, lined posteriorly by the umbilico-prevesical aponeurosis, which narrows upward. So the zone of weakness lies usually at

FIGURE 5.7. Posterior view of the rectus sheath. On the left side, the muscle has been resected to show the anterior lamina of the rectus sheath. (From Bougery, Atlas oj Anatomy, 1832.)

5. Anatomy of the Abdominal Wall

is very weak. Thus, the muscle can be freed very easily. This dissection is totally bloodless. It provides a retromuscular, prefascial plane that we have widely used for the placement of a prosthesis in the treatment of incisional hernias.

Linea Alba

FIGURE 5.8. Posterior view of the abdominal wall after section of urachus and the umbilical arteries: 1 = arcuate ligament; 2 = probe placed between transversalis fascia and transversus abdominis muscle; 3 = transversalis fascia; 4 = inferior epigastric artery with an anastomosis to obturator artery; 5 = suprapubic artery; 6 = external iliac vein; 7 = umbilicoprevesical aponeurosis; 8 = umbilical artery; 9 = ductus deferens; 10 = 51 and 52 roots; 11 = superior gluteal artery; 12 = urachus. (Reprinted from A. Hovelacque etJ. Turchini, Anatomie et histologie de l'appareil urinaire et de l'appareil genital de l'homme. G. Doin; 1938, with permission.)

the most lateral part of the arcuate line. In this region, herniation (so-called Spigelian hernia) may occur. Adherence of the Rectus Abdominis to the Laminae of Its Sheath The rectus can be easily mobilized within its sheath, except at the level of the fibrous intersections, which adhere to the anterior lamina. The adherence of the rectus to the posterior lamina of the sheath

The linea alba is formed by decussating aponeurotic fibers of the rectus sheath. It is a solid median raphe running vertically down the abdominal wall. The linea alba represents the site of insertion of the flat muscles of the abdominal wall, and the most frequently used approach to the abdominal cavity. It is therefore the most common site for incisional hernias. Midline incisions at this level can and should allow the surgeon to dissect between the rectus muscles without opening their sheath. Below the umbilicus, and especially below the arcuate line, the fibrous separation of the rectus muscles is less obvious. Indeed, the medial borders of the two rectus muscles are often in contact with each other and may even overlap slightly. Identification of the interstitium between the two muscles is further complicated inferiorly by the presence of the small pyramidal muscles (in 90% of subjects), extending from the pubis to the center of the subumbilical midline. In a recent anatomico-radiological study, A.M. Rath and J.P. Chevrel 2 have shown that the average length of the linea alba (in 40 cadaveric dissections) was 29.11 cm (20-40 em). It is wider at the level of the umbilicus (2.24 cm) than above it (1.72 cm) or below (0.66 cm). They compared the cadaveric data with the results obtained from 40 tomodensitometric slices. The values they found in vivo were somewhat different: the average width of the linea alba being 8.3 ± 5.63 cm above, 21.2 ± 8.07 cm at, and 9.3 ± 6.74 em below, umbilical level. There is thus a considerable difference between the two studies at the supraumbilical level.

Semilunar (Spigelian) Line

FIGURE 5.9. Posterior view of the transversalis fascia: 1and 7 = transversalis fascia; 2 = fascia iliaca; 3 = inferior epigastric trunk; 4 = spermatic artery; 5 = vas deferens; 6 = obturator artery. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956; Fig. 185, p. 328, with permission. )

A. van der Spiegel (1578-1625) described the semilunar line as the boundary between the muscle body and the anterior aponeurosis of the transversus abdominis. Indeed, in most subjects, the semilunar line describes a medially concave line, since the upper and lower parts of the body of the transverse approach the abdominal midline, whereas the middle part of the muscle lies in a more lateral position, especially in the region of the anterior superior iliac spine. Owing to the fact that the myoaponeurotic boundary between the internal and external oblique does not correspond to the boundary of the transversus abdominis, the use of the term "laterallinea alba" to designate the semilunar line is not appropriate. This zone resembles a lateroreetus band rather than a true line. It is traversed by vessels arranged stepwise and thus offers a limited route of approach if one is to avoid destructive incisions. The intersection between the semilunar line and the arcuate line is a point of weakness. The passage in this area of the inferior epigastric vessels running along the posterior surface of the rectus abdominis contributes also to the weakness of this region where the rare Spigelian hernia may arise. This type of hernia is found in the triangle

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bounded laterally by the semilunar line, superiorly by the lateral part of the arcuate line, and inferiorly and medially by the oblique course of the inferior epigastric vessels.

Vascularization of the Anterolateral Abdominal Wall Arterial Vascularization The general pattern of the arterial vascularization of the anterolateral abdominal wall is formed by a vertical axis, reinforced by metameric arrangement of the lateral vessels. The vertical arterial axis, lying along the posterior surface of the rectus muscle, is formed by the inferior and superior epigastric arteries. This vertical axis is reinforced by the metameric arrangement of the lateral vessels originating from the intercostal and lumbar arteries. The inferior epigastric artery, which is the predominant artery, arises from the external iliac artery just behind the inguinal ligament. It runs cranially and medially, pierces the transversalis fascia and then lies anterior to it. It is accompanied by Hesselbach's (interfoveolar) ligament, which is a thickening of this fascia. The artery then has a variable course toward the lateral border of the rectus, crossed at a point situated 4 to 8 cm above the pubis. Posterior to the rectus, the artery divides into a descending branch running toward the pubis, and an ascending branch, the larger of the two. The ascending branch may persist as a single, dominant axis, which splits into parallel ascending branches, or divide into two main branches running about 1 cm from the lateral and medial margins of the rectus. Direct anastomosis between the inferior and superior epigastric arteries is relatively rare. The superior epigastric artery is an abdominal branch of the internal thoracic artery, descending through Larey's cleft (the sternocostal triangle). Regardless of the anastomotic pattern, communication between the two arteries is well developed, since the opacification of one of them immediately leads to massive reflux of contrast material into the other. The lateral arterial system is a reminder of the initial metameric arrangement of the trunk arteries. These transverse arteries are supplied by the diaphragmatic branch of the internal thoracic artery, which is anastomosed to the termination of the intercostal arteries and the lumbar arteries. The latter show many communications with the deep circumflex iliac artery, a branch of the external iliac artery. There are significant vertical anastomoses joining these metameric arteries to form a ladder-like system. Accordingly, in the flanks, there is a parietal arterial plexus supplying the perforating branches, which, along with nerve filaments, enter the rectus sheath and anastomose to the vertical arterial axis. The superficial perforating arteries arise from the horizontal arterial system. Nevertheless, these perforating arteries are also supplied by the vertical epigastric arterial axis. As previously pointed out, the subcutaneous abdominal (superficial epigastric) and superficial circumflex iliac arteries form a remarkable inferior cutaneous arterial system. At the level of the flat abdominal muscles, the arterial branches are found mainly in two layers, one on each side of the internal oblique.

Venous Drainage The system of venous drainage has a pattern similar to that of the arteries. The inferior epigastric veins (two per artery), join together to form a short common terminal trunk drained by the external iliac vein. The inferior epigastric veins run along the medial border of the artery for about 1 cm and then leave it to join the external iliac vein. The terminal trunk of these veins measures usually 3 cm in length. This venous trunk can be reached by the classic inguinal approach or by a vertical pararectus route exposing the origin of the venous trunk. The latter route allows catheterization of the vein if required at a safe distance from structures which might be injured.

Lymphatic Drainage The upper part of the muscular abdominal wall is drained by the internal thoracic lymph nodes, while in the lower part drainage is provided by the external iliac nodes. Finally, lateral lymphatic drainage is provided by the lumbar nodes.

Innervation of the Anterolateral Abdominal Wall A precise knowledge of the nerve distribution to the abdominal wall is very important to the surgeon who performs abdominal operations. Section of a single nerve results in little harm, even for the sensory functions, since adjacent nerves overlap the area. Division of two nerve trunks is not advisable, but the harm is not yet serious. If a third nerve trunk is divided, a particular type of pseudohernia, or diffuse weakness, will result. Hence, the distribution of the intercostal nerves should be known to all who may incise the abdominal wall.

Skin Innervation The segmental distribution of the intercostal nerves is well known. The anterior rami are found between the internal oblique and the transversus abdominis muscles. These nerves run medially and penetrate the internal oblique muscle as they approach the rectus sheath. At the lateral margin of the rectus abdominis muscle, the nerves supply the muscle and its sheath. The 6th or 7th thoracic nerve applies the epigastric area; the 10th innervates the area to the level of the umbilicus, while the 12th thoracic nerve reaches the area just above the groin. The anterior rami of the first lumbar nerve complete the nerve supply to the inguinal area through the iliohypogastric and ilioinguinal nerves. The iliohypogastric and ilioinguinal nerves supply sensory innervation to an oblique band of the abdominal wall comprising the lower part of the iliac fossa, the inguinal region, and part of the external genital organs. The genitofemoral nerve arises from the first and second lumbar nerves and contributes to the sensory innervation of the root of the external genital organs. It is also the motor nerve of the cremaster (Fig. 5.10). The lateral cutaneous nerve of the thigh, originating from the second lumbar nerve, is not involved in the superficial innervation of the abdominal wall.

5. Anatomy of the Abdominal Wall

The Skin and Its vessels Cutaneous and Subcutaneous Layer

FIGURE 5.10. Innervation of the anterolateral abdominal wall: 1 = seventh intercostal nerve; 2 = external oblique; 3 = eighth intercostal nerve; 4 = internal oblique muscle; 5 = anterior lamina of the rectus sheath; 6 = external oblique aponeurosis; 7 = internal oblique aponeurosis; 8 = ninth intercostal nerve; 9 = 10th intercostal nerve with nerves to internal oblique; 10 = 11th intercostal nerve; 11 = 12th intercostal nerve; 12 = nerve to the internal oblique; 13 = cutaneous branch; 14 = iliohypogastric nerve. (Reprinted from A. Hovelacque, Anatomie des nerfs craniens et rachidiens. G. Doin; 1927, with permission.)

The structure and organization of the cutaneous and subcutaneous layers have considerable influence on the planning of abdominal wall incisions. Vascularization is a determining factor in the mobilization of surgical flaps. Finally, knowledge of the innervation of this layer is of importance from the point of view of symptomatology, since referred visceral pain often projects to the cutaneous layer of the abdominal wall. The skin is relatively mobile over the myofasciallayers of the anterolateral abdominal wall, although its medial area is stabilized by the umbilicus which acts like a central "thumbtack." The loosely organized subcutaneous tissue forms a pad, which may be very thick, containing within it the superficial fascia. The major feature of this layer is the elastic traction lines or Langer's lines. These lines run transversely across the anterolateral abdominal area. Their direction is practically horizontal in the supraumbilical region, but below they slant downward to outline an arc of increasing superior concavity as they progress toward the pubic region. The surgeon should be aware of the direction of Langer's lines if, after abdominal section, the incision is to heal with minimal scarring (Fig. 5.11). In 1941 Cox4 studied the cleavage lines of the skin with precision and presented his findings clearly. Vertical incisions across these lines produce widely gaping wounds, and although they do heal, with the passage of time the scar tends to widen. Generally speaking, there is far less spreading of the wound edges when transverse or oblique incisions are made.

Parietal Muscle Innervation The 7th through 12th intercostal nerves, along with the iliohypogastric and ilioinguinal nerves, supply the motor innervation of the anterolateral abdominal wall. The classic pattern of this motor innervation has been described by Hovelacque in 1927.3 The 7th, 8th, and 9th intercostal nerves distribute to the supraumbilical part of the rectus. The 10th intercostal nerve runs toward the umbilicus along an imaginary line extending across the midline to the anterior superior iliac spine on the opposite side. The 11 th intercostal nerve passes below the umbilicus in the direction of the contralateral inguinal ligament. Finally, the 12th intercostal nerve runs in a very inferior position in the direction of the pubic tubercle on the opposite side. The motor branch of the iliohypogastric nerve reaches the inferior part of the rectus and the pyramidalis muscle, while that of the ilioinguinal nerve terminates in the flat abdominal muscles. The nerve trunks run first between the internal oblique and the transversus abdominis to reach the rectus at a point slightly medial to its lateral margin (Fig. 5.10).

FIGURE 5.11. Langer's lines, usual disposition. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 156, p. 265, with permission.)

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Flament et al.

Arterial Vascularization of Cutaneous Layers of the Abdomen The arterial vascularization of the cutaneous layers of the abdominal wall is rich. Many vessels emerge from the anterior surface of the rectus sheath and then ramify extensively under the skin. Some of these vessels perforate the aponeurosis of the external oblique in the mid-axillary line, while others emerge from the anterior lamina of the sheath of the rectus abdominis. There are usually four supraumbilical and three subumbilical vessels on each side. The umbilicus is surrounded by four highly anastomosed perforating arteries (periumbilical arterial circle). The perforating arteries, arising deep in the cutaneous layers, are supplied by the lateral vessels of the abdominal wall, that is, by the lower intercostal and the lumbar arteries. These lateral vessels show many anastomoses with the deep circumflex iliac network. There are also specific cutaneous arterial systems running upward from the inguinal region. The superficial epigastric and superficial circumflex iliac arteries arise from the femoral artery. These two superficial arteries are highly anastomosed to one another and to the deep arterial network. The territory supplied by them extends a few centimeters lateral to the midline and ends about halfway between the umbilicus and the xiphoid process.

Venous Drainage The system of venous drainage runs parallel to the arterial system. In the region of the umbilicus, the venous system of the abdominal wall may communicate above with a patent ligamentum teres hepatis (Cruveilhier-Baumgarten syndrome) and below with the pelvic veins running along the allantoic sheath.

FIGURE 5.12. The myopectineal orifice: 1 = iliacus muscle; 2 = fascia iliaca; 3 = external oblique muscle; 4 = internal oblique muscle; 5 = superior iliac spine; 6 = femoral nerve; 7 = iliopsoas muscle; 8 = pectineus muscle; 9 = rectus muscle; 10 = internal oblique muscle; 11 = iliopectineal tract; 12 = fascia iliaca; 13 = Cooper's ligament; 14 = pubic tubercle (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 193, p. 338, with permission.)

dominis muscles which form the falx inguinalis or conjoined tendon. Laterally, the myopectineal orifice is bounded by the iliopsoas muscle, with its thick aponeurosis, the fascia iliaca, covering the femoral nerve, while the medial border is formed by the rectus muscle with the ligament of Henle (Fig. 5.13).

Lymphatic Drainage The system oflymphatic drainage is extremely diffuse, fanning out from the umbilicus. This system communicates with the deep hepatic and pelvic lymphatic networks. The lymphatic ducts of the abdominal wall run downward to the inguinal region, join the deep lymphatic trunks of the lumbar region laterally, and connect above with the intercostal and internal mammary systems. These different lymph vessels form a channel on each side and along the mammillary line. Primary cancer of the breast or of a supernumerary nipple may seed neoplastic nodes along this line. 6 _____ _

Groin Anatomy

General Concept of the Inguinofemoral Area Henri Rene Fruchaud5 emphasized the fact that all hernias of the groin originate within a single weak area which he named the myopectineal orifice (Fig. 5.12). According to Fruchaud, the myopectineal orifice forms a single orifice bounded below by the bony margin of the pelvis, which here forms part of the anterior border of the ilium, covered by the pectineal ligament, and the pectineus muscle, and above by the flat (broad) muscles of the anterolateral abdominal wall. These are arranged in two layers, a superficial layer constituted by the external oblique muscle, and a deep layer constituted by the internal oblique and transversus ab-

FIGURE 5.13. Myopectineal orifice with femoral vessels: 1 = internal oblique; 2 = iliopsoas muscle; 3 = fascia iliaca; 4 = iliopectineal tract; 5 = Cooper's ligament; 6 = pubic tubercle; 7 = rectus muscle; 8 = inguinalligament; 9 = femoral vein; 10 = femoral canal. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 195, p. 341, with permission.)

5. Anatomy of the Abdominal Wall

--r1~m~~----------e

If!!f'->L-- f ~--~t---- g

H-~H"--- h

FIGURE 5.14. Sagittal section of the myopectineal orifice. (A) Inguinal and femoral canals according to Testut: 1 = spermatic cord; 2 = femoral vein; 13 = Cooper's ligament; 14 = iliopubic ramus of the pelvic bone. (From L. Testut, Traiti d 'anatomie humaine. G. Doin; 1923.) (B) Inguinal and femoral canals according to Fruchaud; a = inguinal canal; b = transversus abdominis muscle; c = external oblique muscle; d = external oblique aponeurosis; e = transversalis fascia; f = iliac artery; g = transversalis fascia; h = spermatic cord; i = inguinal ligament; j = Cooper's ligament; k = femoral artery. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 30, p. 54, with permission.). (C) Frozen cadaveric sagittal section. (From the collection of the Department of Anatomy, Reims University.)

The Myopectineal Orifice Superficially, the myopectineal orifice is divided into two levels by an aponeurotic structure, the inguinal ligament (or crural arch), which represents the termination of the aponeurosis of the external oblique muscle. Figure 5.12 represents the original conception of Fruchaud's myopectineal orifice, as it was reproduced by Wantz in his Atlas of Hernia Surgery.6 The superior, inguinal level provides a passage for the spermatic cord (or round ligament), while the inferior, femoral (or crural) level provides a passage for the femoral vessels (Fig. 5.14A,B) as schematically described in the sagittal theoretical cross section. Roughly quadrangular, the myopectineal orifice has four margins, inferior, superior, medial, and lateral, as they were described by Fruchaud.

Inferior Margin of the Myopectineal Orifice The inguinofemoral region is constructed at the anterior border of the iliac bone (Fig. 5.15), which presents from above downward and from without inward the anterior superior iliac spine, an unnamed notch, the anterior inferior iliac spine, the iliopubic eminence (a bony prominence over the acetabulum), and last the pectineal surface of the superior ramus of the pubic bone, bounded behind by the pecten of the pubis and medially by the pubic tubercle. The pubic bone is lined in its upper part by the pectineal ligament of Cooper, l to which the sutures can be firmly anchored.

c The pectineal ligament (Cooper's ligament) is a very resistant, composite structure reinforcing the periosteum of the pubic pectin between the pubic tubercle and the iliopectineal eminence. This ligament joins the inguinal ligament medially where it forms the lacunar ligament of Gimbernat but diverges laterally from it when it runs in a much deeper position. The pectineal ligament is a heterogeneous structure comprising three layers. The deep layer is in continuity with the periosteum of the superior pubic ramus. The middle, muscular layer is formed by fibers of the pectineus muscle. This muscle, which belongs mainly to the muscular floor of the femoral triangle, arises from the pectineal surface and pecten of the pubis. The muscle belly, oblique downward, terminates at the pectineal line on the posterior aspect of the superior epiphysis of the femur. The superficial (aponeurotic) layer is very resistant, being formed by the overlapping of the vertical fibers of the aponeurosis of the pectineal muscle and transverse fibers running along the innominate line of the pelvis (arcuate line). Some of these fibers seem to emanate from the psoas minor. The pectineal ligament displays an extreme degree of mechanical resistance. Although it is only a few millimeters thick, wires passed under the ligament in contact with the bone can be used to virtually lift up the whole body (Fig. 5.16).

Medial Margin of the Myopectineal Orifice The terminal part of the rectus and the overlying pyramidalis form the medial boundary of the fibromuscular frame. The rectus ter-

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izontally. It is formed by the fusion of the lower fibers of the internal oblique and transversus abdominis muscles. The muscle fibers of the conjoined tendon arise laterally, not from the inguinal but rather from the iliac fascia of the psoas major and iliac muscles and from the anterior superior iliac spine. These fibers initially run parallel to the inguinal ligament and are connected to it by fibrous bands. The fibers of the conjoint tendon then run upward and horizontally above the inguinal ligament, to terminate as a reinforcement of the prerectus aponeurotic layer.

Lateral Margin

minates inferiorly on the surface extending from the pubic symphysis to the pubic tubercle. The anterior surface of the muscle is covered by a thick aponeurosis, while its posterior surface is lined by the transversalis fascia only. The margin of the rectus sometimes presents a lateral expansion which goes to the pubic tubercle and is referred to as Henle's ligament (this ligament is present in 30 to 50% of patients and is fused with the transversalis fascia).

The lateral margin of the myopectineal orifice is formed by the iliopsoas muscle and the iliopectineal arch (Figs. 5.17, 5.18). The iliopsoas muscle, arising from its origins at the lumbar vertebrae and internal iliac fossa, goes from the abdomen to the thigh in front of the iliopubic eminence to terminate at the posterior aspect of the lesser trochanter of the femur. It is surrounded by its sheath, the iliac fascia, beneath which the femoral nerve is situated in the space separating the two muscle heads. The iliopectineal arch is the medial thickening of the iliac fascia covering the iliacus muscle where the muscle leaves the pelvis. This arch attaches laterally to the anterosuperior iliac spine and medially to the iliopectineal eminence. It is never used directly by the surgeon, but it is important as a common junction site of the following structures of the lateral groin: the insertion of fibers of the external oblique aponeurosis (fibers of the inguinal ligament) , the origin of some fibers of the internal oblique muscle; the transversus abdominis muscle; and the lateral attachment of the iliopubic tract. The iliopectineal arch also contributes to the lateral wall of the femoral sheath.

Superior Margin of the Myopectineal Orifice

Closure of the Myopectineal Orifice

The superior boundary is formed by the so-called conjoined tendon (falx inguinalis), a twin muscular layer running roughly hor-

Superficially, the myopectineal orifice is divided into two levels by an aponeurotic structure, the inguinal ligament, which represents

FIGURE 5.15. Anterior border of the iliac bone: 1 = iliopectineal tract; 2 = Cooper's ligament; 3 = iliopubic tract; 4 = Gimbernat's ligament; 5 = pubic tubercle. (Reprinted from H. Fruchaud, Anatomie chirurgicale cles hernies de l'aine. G. Doin; 1956, Fig. 131, p. 213, with permission.)

____ 9 _ ___10

FIGURE 5.16. Pectineal (Cooper's) ligament. (A) Sagittal cross section of the inguinal canal showing precisely the structure of the Cooper ligament: 1 = inferior epigastric trunk; 2 = iliopubic tract; 3 = inguinal ligament; 4 = Gimbernat ligament; 5 = pectineus muscle; 6 = pubic bone; 7 = transversus abdominis muscle; 8 = internal oblique muscle; 9 = peritoneum;

10 = external oblique aponeurosis; 11 = spermatic cord; 12 = Cooper's ligament; 13 = urinary bladder; 14 = endopelvic fascia. (Reprinted from H. Fruchaud, Anatomie chirurgicale cles hernies cle l'aine. G. Doin; 1956, Fig. 53, p. 89, with permission.) (B) Dissection (left side). (From the collection of the Department of Anatomy, Reims University.)

5. Anatomy of the Abdominal Wall

FIGURE 5.17. Inguinal and femoral canals: 1 = inguinal ligament; 2 = iliopsoas muscle; 3 = femoral artery; 4 = iliopectineal tract; 5 = Cooper's ligament; 6 = Gimbernat's ligament; 7 = pubic tubercle. (Reprinted from H. Fruchaud, Anatomie chirurgicale dRs hernies de l'aine. G. Doin; 1956, Fig. 38, p. 68, with permission.) the termination of the aponeurosis of the external oblique muscle. The superior, inguinal, level provides a passage for the spermatic cord (or round ligament), while the inferior, femoral (or crural), level provides a passage for the femoral vessels. Deeply, the myopectineal orifice is closed by the transversalis fascia, which becomes evaginated around the spermatic or femoral structures passing through the region.

The Inguinal Ligament The inguinal ligament forms the reinforced inferior edge of the external oblique aponeurosis. Opening this aponeurosis to approach an inguinal hernia exposes this ligament as a whitish, ribbon-like structure which spreads out when the aponeurosis is pulled downward and laterally. The inferior margin of the inguinal ligament is not completely free, since it is in continuity with the fibrous structures blending above with the transversalis fascia and below with the femoral sheath (Fig. 5.19A and B). The question may be asked whether there is truly a discrete fibrous structure (Poupart's ligament) stretched between the anterior superior iliac spine and pubic tubercle. The existence of the inguinal ligament was questioned by many authors, especially by Winckler, who demonstrated that the so-called inguinal ligament was only the inferior edge of the external oblique aponeurosis (Fig. 5.20A and B).

Transversalis Fascia (Fig. 5.21A) The frame of the myopectineal orifice is closed by the lower part of the transversalis fascia. This fascia, which is rather weak elsewhere, constitutes a veritable aponeurosis in this region, where it extends under the inferior margin of the transversus abdominis.

FIGURE 5.18. Inguinal ligament, inguinal canal, and femoral canal: 1 = inguinal ligament, extended by iliopubic tract; 2 = iliopsoas muscle; 3 = iliopectineal tract; 4 = femoral canal; 5 = Cooper's ligament; 6 = Gimbernat's ligament; 7 = pubic tubercle; 8= external oblique aponeurosis; 9 = spermatic cord. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 36, p. 62, with permission. [Editor's note: In his comment on this drawing, Fruchaud states that, though it is conventional, it is wrong.]) In this area, the transversalis fascia presents arcuate reinforcements. Henle's ligament has already been described. Hesselbach's ligament (ligamentum interfoveolare) is a fibrous reinforcement of the sheath of the inferior epigastric vessels at the medial side of the inguinal ring. Laterally, the transversalis fascia adheres rather tightly to the iliac fascia, and inferiorly, to the inguinalligament and the pectineal ligament in the medial part of this region. According to McVay and Anson 7 (1940), the pectineal ligament is the true inferior insertion of the medial part of the transversalis fascia, whereas the areolar layer lying anterior to the fascia and adhering to the inguinal ligament should not be considered mechanically significant. At a more lateral site, the transversalis fascia separates from the pectineal ligament to blend with the femoral sheath anterior to the femoral vessels, thus delimiting a prevascular funnel about 3 cm long (the funnel of Anson and McVay).

Reinforcement of the Transversalis Fascia (Fig. 5.21B) The interfoveolar ligament (of Hesselbach) is an apparent thickening of the transversalis fascia at the medial side of the internal inguinal ring. Like a spider web, it lies in front of the inferior epigastric vessels. When well developed, it gives the impression that it is only a lateral condensation of the ligament of Henle. However, it is not a true ligament. The iliopubic tract, posterior to the lower margin of the external oblique aponeurosis, is a fibrous structure sometimes called the bandelette of Thomson. Attached medially near the pubic tu-

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FIGURE 5.19. The inguinal ligament. (A) True position of the inguinalligament, of the ligament of Gimbernat, and of the myopectineal orifice: 1 = external oblique resected; 2 = internal oblique muscle; 3 = inguinal ligament; 4 = iliopsoas muscle; 5 = iliopsoas muscle; 6 = internal oblique muscle; 7 = external oblique resected; 8 = rectus sheath; 9 = fascia iliaca; 10 = Cooper's ligament; 11 = Gimbernat's ligament; 12 = pubic tubercle.

(Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. Doin; 1956, Fig. 90, p. 137, with permission.) (8) Personal dissection showing the termination of flat muscles and the rectus sheath. Dissection can create an artificial "inguinal ligament." Compare with (A). (From the collection of the Department of Anatomy, Reims University.)

berc1e and running laterally to the iliac fascia, the tract continues more laterally to the anterior superior spine of the ilium. Medially, it forms the lower border of the internal ring, crossing the femoral vessels to form the anterior margin of the femoral sheath. The tract curves around the medial surface of the femoral sheath to attach to the pectineal ligament. The iliopubic tract was pres-

ent in 98% of Condon's dissections. This author notes that it is often confused with the inguinal ligament. 7 Although nearby, this ligament belongs to the anterior lamina (superficial myoaponeurotic layer), while the iliopubic tract is part of the deeper layer (postlaminar structures). Every surgeon who repairs groin hernias must understand the

A FIGURE 5.20. (A) Anterior view of external oblique muscle and its aponeurosis, forming the inguinal ligament, according to Winckler (in Fruchaud); 1 = muscular fibers of the external oblique; 2 = external oblique fibers going to anterior superior iliac spine; 3 = external oblique fibers going to fascia iliaca; 4 = lateral cutaneous femoral nerve; 5 = fascia iliaca; 6 = superficial inguinal ring; 7 = lateral crus; 8 = medial crus; 9 = pectineus

B muscle aponeurosis. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 41, p . 75, with permission.) (8) Inguinal ligament and myopectineal orifice: 1 = external oblique; 2 = internal oblique; 3 = inferior edge of the external oblique aponeurosis forming the inguinal ligament. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 128, p. 205, with permission.)

5. Anatomy of the Abdominal Wall

FIGURE 5.21. Transversalis fascia and its reinforcement. (A) Hesselbach's ligament. (From H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 85, p. 131. With permission.) (8) Fascia transversalis and internal ring; 1 = semicircular line; 2 = inferior epigastric artery; 3 = vas

deferens; 4 = Hesselbach's triangle; 5 = anastomosis between inferior epigastric and obturator trunks. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 86, p. 132, with permission.)

boundaries of Hesselbach's triangle. This knowledge is basic to understanding and successful repair of direct and indirect inguinal hernias. The medial margin is made up of the lateral border of the rectus abdominis muscle and its sheath; at the inferior margin lies the inguinal ligament. [Editor's Note: When originally described by Hesselbach, the lower margin was the ligament of Cooper.] The lateral border of the triangle is marked by the inferior epigastric artery (Fig. 5.22). This artery arises from the external iliac artery

just before it passes under the inguinal ligament. The spermatic cord lies anterior to the floor of this triangle after it emerges from the abdomen just lateral to the inferior epigastric artery. Indirect inguinal hernias arise lateral to the inferior epigastric artery, then continue on an oblique path along the cord from the internal abdominal ring, through the inguinal canal and the external ring, into the scrotum. Direct hernias take an anterior path directly through the abdominal wall medial to the inferior epigastric artery.

Peritoneum

FIGURE 5.22. Fascia transversalis and Hesselbach's triangle. 1 = external oblique aponeurosis; 2 = conjoined tendon; 3 = spermatic cord; 4 = inferior epigastric trunk; 5 = Hesselbach's triangle; 6 = inguinal ligament; 7 = iliopubic tract. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 70, p. 109, with permission.)

The peritoneum is the innermost layer of the abdominal wall and, therefore, of the inguinal area. It is loosely connected with the transversalis fascia in most areas, with the exception of the internal ring, where the connection is stronger. The processes vaginalis, a peritoneal diverticulum, is embryologically related to the deep inguinal ring (Fig. 5.23). The ascending fibrous and vascular structures interposed between the transversalis fascia and peritoneum push up against the latter to form three inguinal depressions. From medial to lateral, these depressions are: the internal inguinal fossa, lying between the obliterated urachus (median umbilical ligament) and umbilical artery (medial umbilical ligament) ; the middle inguinal fossa, lying between the umbilical artery and the inferior epigastric vessels; and the external inguinal fossa, located lateral to the umbilical vessels and corresponding to the deep inguinal ring. The external inguinal fossa is a peritoneal infundibulum corresponding to the mouth of the embryonic vaginoperitoneal canal. This fossa is the natural course of sliding indirect hernia, whereas direct hernia results from the progressive distension of the middle inguinal fossa. Sliding direct hernia via the supravesical fossa is an exceptional finding.

J.B. Flament et al. space is considered to be the lower prolongation of the great posterior paravesical space. The space of Bogros, according to Bendavid,9 is a lateral extension of the retropubic space of Retzius and may be explored by incising the transversalis fascia, or better, the floor of the canal from the internal ring to the pubic crest. He also reported that a venous network is located at the lower and anterior part of the space of Bogros. The Bendavid "venous circle," located at the subinguinal space of Bogros, is composed of the inferior epigastric vein, the iliopubic vein, the rectusial vein, the retropubic vein, and the communicating rectusio-epigastric vein. Attached to the anterior wall, this venous circular network is variable (Fig. 5.24A and B). Familiarity with this venous circle is advised, particularly for those surgeons using prosthetic material, and for laparoscopic surgeons.

Inguinal Canal

FIGURE 5.23. Posterior view of the peritoneal fossae: 1 = urachus; 2 = bladder; 3 = umbilical artery; 4 = spermatic trunk; 5 = vas deferens; a = external inguinal fossa; b = middle inguinal fossa; c= internal inguinal fossa. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 201, p. 351, with permission.)

The inguinal canal is an oblique rift measuring approximately 4 cm in length. It is located 2 to 4 cm above the inguinal ligament between the internal (deep inguinal) ring and the external (superficial inguinal) ring opening. The inguinal canal contains either the spermatic cord or the round ligament of the uterus.

Preperitoneal Space The Limits of the Inguinal Canal (Fig. 5.25)

Fat and other connective tissue lie within a space between the peritoneum and the transversalis fascia. Fibrous bands, and occasionally lipomas similar to those in the spermatic cord, also are present. The preperitoneal space is exposed by the reflection of the parietal peritoneum toward the iliac fossa before it reaches the pubic bone. The surgical anatomy of the iliac region was discussed by French anatomist and surgeon Bogros in 1823. 8 He described a triangular space with the following boundaries: laterally, it is limited by the iliac fascia, anteriorly by the transversalis fascia, and medially by the parietal peritoneum. This cleavable interparieto-peritoneal

The anterior wall is formed by the aponeurosis of the external oblique muscle, together with the internal oblique muscle laterally. The posterior wall, or floor, is the most important wall of the inguinal canal. It is formed primarily by fusion of the aponeurosis of the transversus abdominis muscle and the transversalis fascia in 75% of subjects, and in the remaining 25% by the transversalis fascia only. The deep inguinal ring is an opening in the upper lateral part of the transversalis fascia, an evagination like the lining of a jacket,

rT,T7J~.Ktelllal ring

..., ............ _..........

•......-......... .......••••

.1'.-

.••...

••••••

.....................

FIGURE 5.24. (A) The deep inguinal venous vasculature within the space of Bogros. (B) Variations in the pattern of the deep inguinal venous sys-

B tern. (Reprinted from Surg Gynecol Obstet; 1992;174:335-338, with permission.)

5. Anatomy of the Abdominal Wall

1 2 3_~

4------7, 5.25. The limits of the inguinal canal. Fruchaud's conception: 3 = external oblique aponeurosis; 6 = transversalis fascia; 11 = inguinal ligament; 12 = iliopubic tract. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 67, p. 105, with permission.)

FIGURE

5.26. Anterior wall of the inguinal canal and superficial inguinal ring. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 32, p. 56, with permission.)

FIGURE

where the transversalis fascia joins the fibrous coat of the spermatic cord. This fibrous spermatic cord envelope is embryologically equivalent to the fascia, although it does not display similar mechanical properties. The deep inguinal ring is strengthened from below and medially by the passage of the inferior epigastric vessels and the reinforcement of Hesselbach's ligament (ligamentum interfoveolare), an apparent thickening of the transversalis fascia at the medial side of the internal inguinal ring. Hesselbach's ligament has been considered a mechanically important structure. Tension on this ligament elevates and closes the deep inguinal ring, thus acting in opposition to the forces acting on the external inguinal fossa. The superficial inguinal ring (annulus inguinal is superficialis) is located above the pubic tubercle in the medial part of this fascial layer. In this region the spermatic cord lies in the highly vascular areolar subcutaneous tissue. Accordingly, care must be taken when dissection is done in this area. Subsequent to incision made parallel to the fibers of the aponeurosis of the external oblique, the first step in the approach to this region is the debridement of the superficial inguinal ring (Fig. 5.26). In children, the inguinal canal is short (1 to l.5 cm), and the internal and external rings are nearly superimposed upon one another.

The Spermatic Cord The spermatic cord is a matrix of connective tissue continuous proximally with the preperitoneal collective tissue. It holds the ductus deferens, three arteries, three veins plus the pampiniform plexus, and two nerves concentrically invested by three layers of tissue. One other nerve, the ilioinguinal, lies just lateral to the components of the cord. The most anterior of the elements of the spermatic cord is the pampiniform plexus; posterior are the ductus and the remnant of the processus vaginalis, or hernial sac. These entities, as well as others, are covered by the spermatic fascia. Medial to the superficial inguinal ring, the spermatic cord lies deep to the fascia of Scarpa and Colles. Scarpa's fascia is so well developed that the surgeon may mis-

take it for the aponeurosis of the external oblique muscle, which may lead to treating a superficial ectopic testicle as an inguinal cryptorchidism. There may be a layer of fat between the fascia and the aponeurosis.

Arteries of the Spermatic Cord The arteries of the testis and epididymis are shown in Fig. 5.27. The internal spermatic, or testicular, artery is a branch of the aorta. The artery of the ductus deferens originates from the inferior vesical artery. The external spermatic, or cremasteric, artery arises from the inferior epigastric artery. Anastomoses are present between the gonadal and deferential arteries in all patients. There are also some anastomoses between these and the cremasteric arteries in approximately two-thirds of patients. Upon division of the cord, collateral circulation is sufficient to prevent gangrene of the testis in 98% of patients. Testicular atrophy will nevertheless occur in 80%. If the surgeon accidentally divides the cord, it is advisable to leave the testicle in the scrotum and not bring it into the surgical field, to preserve the collateral circulation from the scrotal artery, the prostatic artery, and the inferior vesical artery, which may save the testicle. Between the upper and middle third of the testicle, the testicular artery bifurcates into the main testicular and epididymal branches. During epididymectomy, dissection of the epididymis should start at the lower pole of the testicle and proceed upward (approximately 2.5 cm) . From there, the surgeon should find the bifurcation and ligate only the epididymal branch.

Veins of the Spermatic Cord In the spermatic cord, the pampiniform venous plexus is composed of 10 to 12 veins (Fig. 5.28). These are separated into anterior and posterior groups which are drained by three or four

J.B. Flament et al.

Nerves of the Spermatic Cord The genital branch of the genitofemoral nerve (Ll, L2) enters the inguinal canal through the internal inguinal ring. The cremaster muscle is innervated by the genital branch. The ilioinguinal nerve (Ll) emerges between the external and internal oblique muscle near the anterior superior iliac spine. It then enters the canal and emerges from the external inguinal ring. There, the ilioinguinal nerve supplies the skin of the penile root and the upper part of the scrotum. The arteries of the cord and the ductus deferens are innervated by sympathetic fibers which come from the prostatic portion of the pelvic plexus.

Fasciae of the Spermatic Cord

FIGURE 5.27. Arteries, veins and nerves of the testicles. External view. 1 = artery of the ductus deferens; 7 = testicular artery; 8 = spermatic veins. (Reprinted from A. Hovelacque, Anatomie des ncrfs craniens et rachidiens. G. Doin; 1927, Fig. 113, p. 753, with permission.)

veins which join to become two veins proximal to the deep inguinal ring. These veins run in the extraperitoneal space on either side of the testicular artery. The vein on the right opens directly into the inferior vena cava, that on the left enters the left renal vein. The cremasteric vein flows into the inferior epigastric veins, while the deferential vein drains into the pelvic plexus.

The ductus deferens and the accompanying blood vessels of the spermatic cord are surrounded by three layers of fascia: the external spermatic fascia, a continuation of the fascia of the external oblique muscle (Gallaudet's); the cremasteric fascia, which is continuous with the musculature and fascia of the internal oblique and possibly the transversus abdominis muscles; and the internal spermatic fascia, an extension of the transversalis fascia. The subcutaneous superficial fascia in the scrotum contains little adipose tissue. This is replaced by smooth muscle, which forms the tunica dartos scroti. The rugal folds of the scrotal skin are formed by the attachment of these muscle fibers to the skin.

The Round Ligament In the female, the round ligament of the uterus lies in the inguinal canal. It is the homologue of the gubernaculum testis, not of the spermatic cord of the descended testis. The gubernaculum in the female also becomes the ligament of the ovary. Both round and ovarian ligaments are attached laterally to the side of the uterine wall just under the fallopian tubes. If necessary, the round liga-

ment may be resected without adverse effects.

Scrotum and Labia Majora

FIGURE 5.28. Fascia of the spermatic cord: 1 and 2 = external spermatic fascia; 10 = testicular artery. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hcrnies de l'aine. G. Doin; 1956, Fig. 163, p . 285, with permission.)

The skin of the scrotum is elastic and corrugated. It is thinner and more pigmented than the inguinal skin. Mter puberty, the scrotum has less hair than inguinal skin but possibly has more sebaceous and sweat glands. The raphe between the right and left halves of the scrotum is a median ridge continuous with the raphe of the penis and perineum. The dartos is the superficial fascia of the scrotum. The superficial portion is contributed by Camper's fascia, which covers the abdominal wall, penis, perineum, thigh, and buttocks. The deep portion derives from Scarpa's fascia and is continuous over the abdominal wall to the penis (Buck's fascia) and to the perineum (Colles' fascia). The dartos is composed of connective tissue and smooth muscle fibers and is attached to the skin. Colles' fascia is attached laterally to the periosteum of the pubic arch of the lower abdominal wall. The space deep to the dartos may allow extravasated urine to collect. The skin of the labia majora is composed of elongated bilateral folds with lateral and medial surfaces. The lateral surface starts at

5. Anatomy of the Abdominal Wall

the mons pubis, a rounded eminence formed by an accumulation of fat in front of and above the symphysis pubis and ends with the skin of the thigh. The lateral surface is more pigmented but somewhat less hairy than the inguinal skin. The medial surface is smooth and hairless, studded with large sebaceous follicles. Starting from the anterior commissure, which is the union of the inner surfaces of the right and left labia majora anteriorly, it ends at the posterior commissure, which is an ill-defined union of both inner surfaces posteriorly. (In the majority of individuals, such a union does not occur.) Sebaceous and sweat glands are present on the lateral surface. Smooth muscle fibers, arranged irregularly, form a counterpart for the tunica dartos of the male. The round ligament ends in the subcutaneous tissue of the labium majus.

Skin and Subcutaneous Layer The hairy skin of the inguinal region is marked by the flexion fold of the thigh, which runs parallel to the inguinal ligament 2 or 3 cm below it. The bony landmarks of the inguinal ligament, that is, the anterior superior iliac spine and pubic tubercle, are easy to find, even in obese patients. The areolar subcutaneous tissue of the inguinal region is richly vascularized, sometimes referred to as Thomson's "vascular layer." In addition to the veins and arteries, this tissue contains lymph vessels which are invisible to the naked eye. The genital branch of the genitofemoral nerve lies within the inguinal canal. It arises from the first and second lumbar nerves and gives branches to the cremaster muscle. The ilioinguinal nerve arises from the first lumbar spinal nerve, passes down the canal, and emerges from the external inguinal ring. It supplies the skin of the penile root and the upper part of the scrotum (Fig. 5.29). Sympathetic fibers from the prostatic portion of the pelvic plexus serve the ductus deferens. Similar fibers from the pelvic plexus supply the arteries of the cord. Sympathetic and sensory

fibers from cutaneous nerves of the region supply the scrotum. These include the ilioinguinal nerve, genital branch of the genitofemoral nerve, which supplies the labia majora, perineal branches of the pudendal nerve, and the perineal branch of the posterior femoral cutaneous nerve. Any incision in this area should be located parallel to, and at least one or two fingers above, the inguinal ligament.

Superficial Fascia This fascia consists of two portions: a superficial layer (Camper's fascia) and a deep layer (Scarpa's fascia). The superficial fascia consists of subcutaneous fat. The deep layer is thin and membranous. These two layers are well developed in the inguinal area and are clearly defined in most cases.

The Femoral Canal and the Femoral Sheath Between the inguinal ligament anteriorly and the linea terminalis (iliopectineal line) posteriorly, the femoral level of the myopectineal orifice is a space organized into three compartments (Fig. 5.30). The most lateral of these compartments is the neuromuscular compartment, which contains the iliopsoas muscle, the femoral nerve, and the lateral femoral cutaneous nerve. Medially, the vascular compartment contains the femoral artery and vein. Still more medial is the compartment of the femoral canal. The femoral sheath , an extension of the transversalis fascia of the abdomen, envelops the femoral artery, vein, and femoral canal (Fig. 5.31) .

3 45 ______ _

FIGURE 5.29. Nerves of the spermatic cord: 1 = iliohypogastric nerve; 2 = internal oblique; 3 = ilioinguinal nerve; 4 = cremasteric; 5 = spermatic cord; 6 = external oblique aponeurosis. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 31, p. 55, with permission.)

FIGURE 5.30. Iliofemoral trunks in the femoral canal: 2 = transversus abdominis and transversalis fascia; 6 = inferior epigastric artery; 7 = femoral artery and vein; 8 = iliopsoas muscle; 9 = pectineus muscle. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 150, p. 255, with permission.)

J.B. Flament et al.

FIGURE 5.31. The femoral sheath. Jean Rives's personal interpretation of Fruchaud's conception. (Reprinted from H. Fruchaud, Anatomie chirurgicale rks hernies rk l'aine. G. Doin; 1956, Fig. 127, p. 204, with permission.)

The femoral canal is conical, approximately 1.25 to 2 cm in length. The fossa ovalis, the opening for the great saphenous vein, is at its apex inferiorly. Thus, a femoral hernia may present as a bulge of the skin over the fossa ovalis. The femoral ring is inflexible. Its transverse diameter ranges from 8 to 27 mm, and the anteroposterior diameter ranges from 9 to 19 mm. However, in 70% of patients these diameters are 10 to 14 mm and 12 to 16 mm respectively.I o The lateral boundary is the femoral vein and connective tissue. The posterior boundary is Cooper's ligament. The iliopubic tract or the inguinal ligament, or both, form the anterior boundary. The transversalis fascia, aponeurotic insertion of the transversus abdominis muscle, and the lacunar ligament form the medial boundary (Fig. 5.32).

are associated with the superficial epigastric and the external pudendal vessels as far as 1 cm above the inguinal ligament. In zone 3, inferomedial nodes were absent in 29% of specimens examined by Daseler and colleagues, and only a single node was present in 37% . In zone 4, the inferolateral quarter, a chain of nodes lies lateral to the great saphenous vein; a node is always present at the junction of the great and accessory saphenous veins. In zone 5, the central zone, 84% of specimens had no nodes and 15% had only a single node.

Lymphatics of the Inguinal Area Inguinal lymph nodes may be categorized into the following: superficial nodes (between the superficial fascia and the fascia lata), deep inguinal nodes (beneath the fascia lata), and aberrant inguinal nodes (within the inguinal canal).

Superficial Inguinal Nodes These nodes have been divided into five arbitrary groups called "zones" for nearly 100 years. These groups, centered on the termination of the great saphenous vein, are shown in Fig. 5.33. The number of nodes, varying from 4 to 25, is inversely proportional to the size of the individual nodes. Despite the small number of superficial nodes (Daseler et al. II found an average of only 8.25 nodes per limb dissected), they form possibly the largest single group of lymph nodes in the body. The nodes lie along the blood vessels of the region within the zones. In zone 1, the superolateral nodes extend along the superficial circumflex iliac vein below the inguinal ligament. Haagensen et al. found a few above the ligament on the aponeurosis of the external oblique muscle. In zone 2, the superomedial nodes

FIGURE 5.32. The medial angle of the inguinal area: 5 = iIiopubic tract; 6 = transversalis fascia; 7 = Cooper's ligament; 8 = inguinal ligament. (Reprinted from H. Fruchaud, Anatomie chirurgicale rks hernies de l'aine. G. Doin; 1956, Fig. 64, p. 101, with permission.)

5. Anatomy of the Abdominal Wall

FIGURE 5.33. Superficial inguinal nodes and vessels: 4 = superficial circumflex iliac vessels; 7 = superior external pudendal vessels. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies d el'aine. G. Doin, 1956, Fig. 159, p. 269, with permission.)

Deep Inguinal Nodes Two or three small nodes lie below the fascia lata along the femoral vein. The largest, the node of Cloquet, is located at the femoral ring between the vein and the lacunar ligament and is almost always present.

Aberrant Nodes Aberrant nodes include some small nodes in the inguinal canal, over the symphysis pubis, and at the base of the penis. Drainage from the glans penis or glans clitoris is believed to be to the deep inguinal nodes. Efferent lymphatics from the superficial nodes, especially lower ones, pass to the deep nodes. Those from the inferior groups (zones 3, 4, and 5) pass to superior nodes (zones 1 and 2) and then upward to the lowest iliac nodes along the external iliac vessels. Lymph from the testes passes to aortic and renal nodes, along the arterial supply of the gonads.

anterior layers. The posterior and middle layers are around the sacrospinalis muscle. The middle layer envelops the quadratus lumborum and continues laterally to the transversus abdominis aponeurosis by fusion of all three layers. A middle muscular layer is formed of sacrospinalis, internal oblique, and serratus posterior inferior muscles. A deep muscular layer, composed of the quadratus lumborum and psoas muscles, is covered by the transversalis fascia, the preperitoneal fat, and the peritoneum. This posterior abdominal wall, less a "surgical" structure than the anterior abdominal wall, shows significant direct relations to the three main retroperitoneal sheaths. The posterior abdominal wall is in contact with the lumbar neural ganglia, and contains within its muscles the lumbar plexus and an entire vascular network. The classical zones of posterior weakness are Grynfeltt's lumbar quadrangle (tetragonum lumbale) and Petit's lumbar triangle (trigonum lumbale). Lumbar hernia rarely occurs at these sites; parietal weakness of the posterior abdominal wall is most often of postoperative or traumatic origin. The deep layer of the posterior abdominal wall comprises, in the midline, the lumbosacral spine flanked laterally by the iliopsoas and quadratus lumborum which mask the lumbar intertransverse muscles.

Median Spinal Axis The lumbar spine, markedly convex anteriorly, is entirely covered by a fibrous coat consisting of the anterior longitudinal ligament, which terminates at the level of the second sacral vertebra, and the diaphragmatic crura. The right crus, the larger, lies over the bodies of L-2 and L-3 and the neighboring intervertebral disks. The left crus is usually smaller, lying over the body of L-2 and the neighboring intervertebral disks. From their insertions on the spine, the diaphragmatic crura run forward to form the aortic hiatus. Fleshy fibers arise from the upper margin of the fibrous arch of the hiatus. In this way, the diaphragmatic crura constitute the classic "afibrous bed" of the aorta in front of the lumbar spine. The flared part of the right crus penetrates between the aorta and the inferior vena cava. The first two intercostal arteries on the right and left sides pierce the fleshy part of the diaphragmatic crura as they run tangential to the bodies of the vertebrae (Fig. 5.34) .

Surgical Anatomy of the Posterior (Lumbar) Body Wall This lumbar area of the posterior body wall is limited superiorly by the 12th rib, inferiorly by the crest of the ilium, posteriorly by the erector spinae (sacrospinalis) muscles, and anteriorly by the posterior border of the external oblique muscle. This posterior wall is composed superficially of a thick, tough skin and two layers of fibrous tissue with fat between them (superficial fascia) . A superficial muscle layer is formed posterolaterally by the latissimus dorsi muscle and anterolaterally by the external oblique muscle. The thoracolumbar fascia contains posterior, middle, and

FIGURE 5.34. Median spinal axis, lumbar spine and crus of the diaphragm. (From M.:J. Bourgery, Atlas of Anatomy, 1832.)

The promontory of the sacrum protrudes into the space between the common iliac vessels like a bracket above the pelvis. The pelvic viscera are suspended from the promontory, through the thick fibrous coat covering it and the L5-S1 intervertebral space. The middle sacral vessels run anteriorly over the promontory. The danger point formed by the left common iliac vein, running obliquely across this region, should be kept in mind. The sacrum, forming the posterior wall of the pelvis, contains the cavum durale down to the level of S-2. The vegetative nerves distributing to the sphincters and genital organs emerge through the third and fourth anterior sacral foramina. The position of these nerves should be borne in mind when using the transsacral approach to the rectum. Resection through the fourth sacral foramina can be done, whereas in the course of a more superior route it is imperative to preserve at least one of the third sacral foramina. The boundary between the sigmoid colon and rectum classically lies at the level of the anterior part of S2-S3. The. median osteofibrous spinal axis extends laterally in cruciform fashion by the posterior part of the iliac crests. This crest seems to divide the muscles into two step-like layers. The upper layer is formed by the greater psoas lying medially and the quadratus lumborum laterally. The lower layer consists of the greater psoas flanked by the iliacus. The iliac crest thus resembles a very thick intersection reinforced by the iliolumbar ligament, which runs behind the greater psoas and spreads out on the anteromedial lip of the bony crest.

Lateral Spinal Muscles Iliopsoas Muscles (Fig. 5.35) The psoas major is a voluminous muscle extending from the 12th thoracic vertebra to the lesser trochanter. It runs from the lumbar spine along the innominate line of the iliac bone, to leave the ab-

5.35. Iliopsoas muscle, schematic view: 1 = promontory; 2 = recti; 3 and 6 = psoas major; 4 = iliacus; 5 = psoas minor; 7 = Cooper's ligament; 8 = pectineus muscle; 9 = pubic tubercle. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 142, p. 235, with permission.)

FIGURE

J.B. Flament et al.

dominal region via the muscular lacuna beneath the inguinal ligament, in the inferior part of the myopectineal orifice. The psoas major is a muscle comprising two layers. The anterior layer (corporeal) and the posterior layer (costiform) are joined together laterally. The space between them contains the lumbar plexus, the ramifications of the lumbar arteries, the lumbar veins and their longitudinal anastomosis, and the ascending lumbar vein. The anterior corporeal layer of the muscle is attached to the spine from the 12th thoracic to the fourth lumbar vertebrae. The insertions are mainly on the intervertebral disks rather than on the vertebral bodies themselves and are joined to one another by fibrous arches. These fibrous arches, arranged in opposition to the concavity of the lateral surfaces of the bodies of the vertebrae, form small openings for the passage of the lumbar vascular trunks and sympathetic communicating branches. On the right, these arcuate fibers are most often covered anteriorly by the right margin of the inferior vena cava. Because of this arrangement, surgical identification of the sympathetic ganglia may be dangerous. The posterior (costiform) layer of the greater psoas inserts on the anterior surface of the transverse processes of all five lumbar vertebrae. The greater psoas is thus well formed in the upper lumbar region. It leaves the diaphragm by passing under the medial arcuate ligament, sometimes referred to as the arch of the psoas. The iliac fascia is attached to the inferior margin of this ligament and lines the psoas major. An abscess originating from the 12th thoracic vertebra can thus travel downward along the fascia. The psoas minor arises from vertical fascicles inserted on the 12th thoracic and first lumbar vertebrae. This muscle runs along the medial boundary of the psoas major to attach to the innominate line and iliopectineal eminence. The psoas minor is not a constant muscle (present in less than 50% of subjects) . Its lowermost fibers may be seen to extend down to the pectineal ligament. Finally, it is also attached to the deep surface of the iliac fascia and thus acts to stretch this fascia. The iliacus muscle originates from the greater part of the internal iliac fossa and stretches downward to the level of the anterior inferior iliac spine. The muscle fibers, grouped together along the lateral margin of the psoas major, form, along with the latter, a groove for the femoral nerve. The iliacus fibers then wind around the terminal tendon of the psoas major and finally pass anterior to the latter to insert on the lesser trochanter and below; that is, these fibers extend below the femoral insertion of the psoas major. The iliacus fascia is a fibrous sheath common to the psoas major and iliac muscles. It is relatively thin in its upper part, but becomes very thick at the level of the iliac crest. Deep to the inguinal ligament, the iliacus fascia is reinforced, forming the iliopectineal arch, which separates the vascular and muscular lacunae. The iliac fascia can be stretched only slightly. This finding accounts for the rapidly compressive complications of hematomas originating from the rich vascular network within the psoas major. This type of hematoma occurs frequently in patients taking anticoagulants, and it may lead to severe damage of the lumbar plexus, especially to the femoral nerve.

Quadratus Lumborum Muscle This muscle extends behind and lateral to the psoas major in the space bounded by the 12th rib, the tips of the transverse processes

5. Anatomy of the Abdominal Wall

matic lymphatic channels form a direct communication between the retroperitoneal region and the subpleural space. This accounts for the rapid thoracic and mediastinal extension of certain pathological processes involving the retroperitoneal region, such as pancreatitis.

Innervation

5.36. Posterior abdominal wall and its innervation: 1 = twelfth intercostal nerve; 2 = iliohypogastric nerve; 4 = ilioinguinal nerve; 12 = genitofemoral nerve; obturator nerve. (Reprinted from A. Hovelacque, Anatomie des nerfs craniens et rachidiens. G. Doin; 1927, with permission.)

FIGURE

of the lumbar vertebrae, and the posterior part of the iliac crest. The muscle body, resembling a rectangle rather than a square, is composed of interlacing multidirectional fibers originating from the different bony margins listed above (Fig. 5.36). The anterior part of the quadratus lumborum muscle is essentially composed of fibers extending from the iliolumbar ligament and the deep part of the iliac crest to the inferior margin of the 12th rib and the tip of the transverse processes of the lumbar vertebrae. The thinner posterior layer of the muscle extends down the 12th rib to the lumbar transverse processes.

Arterial Vascularization and Venous Drainage The arterial supply to the posterior abdominal wall comes from the lumbar arteries, which form a complex anastomotic network between the 12th intercostal (subcostal) artery above and the deep circumflex iliac artery below. The venous drainage of the posterior abdominal wall is particularly well developed, especially within the psoas major, where the veins communicate with the intraspinal venous plexuses by way of conjugate vessels and the arches of the psoas with the inferior vena cava. The ascending lumbar vein is one of the roots of the azygos system. The venous network of the posterior abdominal wall (iliolumbar, lumbar, and ascending lumbar veins) is able to shunt most of the caval blood after a subrenal ligation of the inferior vena cava.

Lymphatic Network The upper part of the posterior abdominal wall is drained by the lateral caval and lateral aortic lymph nodes. The transdiaphrag-

The posterior abdominal wall is innervated by the lumbar plexus. The psoas m,yor receives branches at different levels from the first through fourth lumbar nerves, and the psoas minor receives branches from the first and second lumbar nerves. Filaments arising from the femoral nerve supply the iliacus. The motor innervation of the quadratus lumborum is from the 12th intercostal nerve and branches from the first three lumbar spinal roots (Fig. 5.36). The iliohypogastric and ilioinguinal nerves emerge from the lateral margin of the greater psoas at the level of the L-I-L-2 intervertebral disk and then run along the anterior surface of the quadratus lumborum posterior to the kidney. These nerves follow the iliac crest to finally enter the inguinal region. The lateral femoral cutaneous nerve exits from the anterior surface of the psoas m,yor at the level of the lower end of the third lumbar vertebra or the L-3-L-4 intervertebral disk. It runs obliquely outward and downward to cross over the lateral margin of the psoas major at the level of the L-4-L-5 intervertebral disk and then runs along the surface of the iliac bone to finally enter the muscular lacuna medial to the anterior superior iliac spine. The genitofemoral nerve appears on the anterior surface of the psoas major at a point slightly medial and inferior to the lateral femoral cutaneous nerve (L-4-L-5 intervertebral disk). It then descends parallel to the fibers of the psoas major just behind the inguinal ligament where it divides into terminal branches. The femoral nerve leaves the lateral margin of the psoas major, becoming visible in the groove between the latter and the iliacus at the level of the sacral promontory. This nerve divides just below the inguinal ligament. The obturator nerve emerges from the medial border of the psoas major at about the same level as the preceding nerve, that is, at the site where the medial margin of this muscle crosses over the ala of the sacrum (the fossette of Cuneo and Marcille). In this region, it is accompanied by the fifth lumbar nerve root, which receives the first sacral nerve root to form the lumbosacral trunk.

Action of the Deep Muscles of the Posterior Abdominal Wall The iliopsoas, inserted on the pelvis and spine, acts mainly to flex and laterally rotate the thigh, and thus is very important for walking. Acting on the axial skeleton, the psoas major resembles a polyarticular muscle, leading to lateral flexion and slight rotation of the spine on the side opposite the muscle. When both psoas major act simultaneously with the subject supine, they elevate the upper and lower parts of the trunk. The psoas minor, which flexes the lumbar spine with respect to the pelvis, is a tensor muscle of the iliac fascia. The quadratus lumborum acts as a lateral brace of the lumbar spine by pulling the iliac crest and the 11 th rib closer to one another. This muscle can also be considered to depress the 11 th rib, and thus acts as an accessory respiratory muscle.

J.B.

Superficial Layer of the Posterior Abdominal Wall Two layers of flat muscles and aponeuroses lie posterior to the deep muscle layer and extend laterally to continue into the anterolateral abdominal wall. From anterior to posterior, the first of these layers is that of the posterior aponeurosis of the transversus abdominis. This aponeurosis, lying posterior to the quadratus lumborum, is attached to the tips of the transverse processes of the lumbar vertebrae.

Deep Weak Area Framed by muscle bodies, this aponeurotic layer constitutes a zone of weakness, the classic Grynfeltt's lumbar quadrangle. The medial or posterior boundary of this area is formed by the erector muscles of the spine inserted on the posterior part of the iliac crest, the posterior iliac spines, and the posterior surface of the sacrum. These muscles spread out from their origin toward the ribs. This muscular mass is invested with a very resistant aponeurosis, which, along with the arches of the lumbar vertebrae and posterior surface of the transverse processes, forms a veritable osteofibrous canal (thoracolumbar fascia) through which the muscles pass. The inferior lateral boundary of the lumbar quadrangle is formed by the internal oblique, which runs upward and forward to make an acute angle with the mass of spinal muscles. Moreover, the internal oblique is inserted on the thoracolumbar fascia and the posterior part of the iliac crest, extending up to the inferior margin of the 12th rib. The superior medial boundary of the lumbar quadrangle is formed by the serratus posterior inferior. This muscle, extending over the mass of the spinal muscles, is attached by its inferior digitation to the inferior edge of the 12th rib. Finally, a short part of the inferior margin of the 12th rib forms the superior lateral boundary of Grynfeltt's lumbar quadrangle. The floor of the triangle is the aponeurosis of the transversus abdominis muscle arising by fusion of the layers of the thoracolumbar fascia. The roof is the external oblique and latissimus dorsi muscles.

Flament et al.

the superficial lamina of the latter. Its floor is the internal oblique muscle, with contributions from the transversus abdominis muscle and posterior lamina of the thoracolumbar fascia and the internal oblique muscle. Superficial fascia and skin cover the triangle. A lumbar hernia in the area of the lumbar quadrangle (usually the upper part), which may enter into Petit's lumbar triangle, is a rare finding. In such cases, the neck of the hernial sac is narrow, and treatment can thus be achieved with relative ease. Conversely, postoperative incisional hernia in this region is far more problematic. Hernias also sometimes occur following closed trauma, which causes destruction or detachment of the muscles in this region. Significant tissue loss, often accompanied by paralysis of the abdominal strap resulting from motor nerve injury, requires the use of foreign or autoplastic material to achieve repair, that is, large flaps of fascia lata cut in the external iliac fossa and reflected upward onto the iliac crest, as in Koontz's operation.

Surgical Anatomy of the Pelvic Wall The pelvis, like a box, lies open below the abdominal cavity, limited laterally by an anterior (obturator) area and a posterior (sciatic) area. It is closed, inferiorly, by the perineal diaphragm.

Obturator Area The obturator region is bound superiorly by the horizontal ramus of the pubic bone, laterally by the hip joint and the shaft of the femur, medially by the pubic arch, the perineum, and the gracilis muscle, and inferiorly by the insertion of the adductor magnus on the adductor tubercle of the femur (Fig. 5.37). The obturator foramen is formed by the rami of the ischium and pubis. It lies inferior to the acetabulum on the anterolateral

Superficial Weak Area This muscular layer is lined posteriorly by a layer containing the superficial weak area of the region, that is, Petit's lumbar triangle. The lumbar triangle is bounded by the following structures: below, the base of the triangle is formed by the posterior part of the iliac crest; laterally and anteriorly, the side of the triangle is formed by the posterior margin of the external oblique running downward and forward, the anterior part of this muscle being entirely composed of fleshy fibers from the 12th rib to the iliac crest; and medially, the posterior (lumbar) side is formed by the lateral margin of the latissimus dorsi, which runs upward and laterally. This muscle originates from a large aponeurotic sheet attached to the spinous processes of the thoracic and lumbar vertebrae, the sacral crest, and the posterior iliac spine. This fibrous sheet continues medially with the thoracolumbar fascia and is often described as

FIGURE 5.37. Pelvic bone and the limits of the pelvic wall. (Reprinted from H. Fruchaud, Anatomie chirurgicale des hernies de l'aine. G. Doin; 1956, Fig. 134, p . 215, with permission.)

5. Anatomy of the Abdominal Wall

FIGURE 5.38. The obturator region, coronal schematic cross section: 3 = rectum; 9 = levator and internal obturator muscle; 10 = obturator externus muscle; 11 = ischiopubic ramus of the pelvic bone. (Reprinted from A. Hovelacque etJ. Turchini, Anatomie et histologie de l'appareil urinaire et de l'appareil genital de l'homme. G. Doin; 1936, Fig. 55, p. 105, with permission.)

wall of the pelvis. Except for a small area, the obturator canal, the foramen is closed by the obturator membrane. Fibers of the membrane are continuous with the periosteum of the surrounding bones and with the tendons of the internal and obturator externus muscles. [Editor's Note: Embryologically, the foramen and its membrane represent an area of potential bone formation that never proceeds to completion. In this sense, the obturator foramen is a lacuna, and the obturator canal is the true foramen] (Fig. 5.38). The obturator canal is a tunnel 2 to 3 cm long beginning in the pelvis at the defect in the obturator membrane. It passes obliquely downward to end outside the pelvis in the obturator region of the thigh. The canal is bound cranially and laterally by the obturator groove of the pubis and caudally by the free edge of the obtura-

FIGURE 5.39. Obturator hernia. (A) Obturator vessels and nerve emerging from obturator canal. (B) hernia through the obturator externus muscle; hernia and nerve exit above the obturator external muscle; the nerve exits above and the hernia below the obturator externus muscle. (Reprinted from V. Schumpelick, Atlas ofHernia Surgery; 1990, B.C. Decker, Inc., with permission.)

tor membrane and the internal and obturator externus muscles. Through this canal pass the obturator artery, vein, and nerve. The obturator nerve is usually superior to the artery and vein. The nerve separates into anterior and posterior divisions as it leaves the canal. A hernial sac may follow either division of the nerve. The obturator artery divides to form an arterial ring around the foramen. An obturator hernia is an abnormal protrusion of preperitoneal fat or an intestinal loop through the obturator foramen. It characteristically affects the right side of middle-aged women. The herniated fat or ileal loop or, rarely, the urinary bladder, compresses the obturator nerve, affecting either or both divisions to produce the characteristic hip-knee pain (Howship-Romberg sign) present in about one-half of the patients with obturator hernia. The formation of an obturator hernia begins with a "pilot tag" ofretroperitoneal fat in the first stage, followed by the appearance of a peritoneal dimple in the second stage into which a knuckle of viscus may be partially incarcerated (Richter's hernia) in the third stage. Eventually, the incarceration of an ileal loop produces complete obstruction. The frequency of pilot tags in cadavers and the rarity of actual obturator hernias in patients suggest that most obturator hernias do not progress beyond the first and second stages of development (Fig. 5.39A and B) .

Surgical Anatomy of the Sciatic Region A sciatic hernia is a protrusion of a peritoneal sac and its contents through the greater or lesser sciatic foramen. It also has been called a "sacrosciatic," "gluteal," or "ischiatic" hernia. There are three potential apertures through which a sciatic hernia may occur. Two are through the greater sciatic foramen above (suprapiriformic) or below (infrapiriformic) the piriformis muscle, which also passes through the foramen. A third potential hernia (subspinous) may pass through the lesser sciatic foramen below the sacrospinous ligament. All three hernial sites are covered by the gluteus maximus muscle (Fig. 5.40) . The suprapiriformic foramen is formed by the anterior sacroil-

J.B. Flament et al.

Perineal Area The Pelvic Diaphragm

FIGURE 5.40. Sciatic hernias: I = suprapiriformis; 2 = infrapiriformis; 3 = spinotuberous. (Reprinted from V. Schumpelick, Atlas of Hernia Surgery; 1990, B.C. Decker, Inc., with permission.)

iac ligament anteriorly, the upper border of the piriformis muscle inferiorly, the ilium laterally, and the sacrotuberous ligament and the upper part of the sacrum medially. The infrapiriformic foramen is bound above by the lower border of the piriformis muscle, below by the sacrospinous ligament, posteriorly by the sacrotuberous ligament, and anteriorly by the ilium. A subspinous hernia, through the lesser foramen, has a ring composed of the ischial tuberosity anteriorly, the sacrospinous ligament and ischial spine superiorly, and the sacrotuberous ligament posteriorly. Through the lesser foramen pass the tendon and the nerve of the internal obturator muscle, the pudendal nerve, and the internal pudendal vessels.

FIGURE 5.41. (A) Anatomy of the pelvic floor: I = pubic symphysis; 2 = deep transverse perineal muscle; 3, 4 = obturator canal and muscle; 5 = anal canal; 6 = levator ani muscle; 7 = coccygeus muscle; 8 = piriformis muscle; 9 = sacrum; 10 = fIfth lumbar vertebra; II = paravesical hernia; 12 = retrovesical hernia; 13 = obturator hernia; 14 = ischiorectal hernia;

The pelvic diaphragm is composed of two paired muscles, the levator ani and coccygeus. They form the floor of the pelvis and the roof of the perineum (Fig. 5.41A). The levator ani is itself formed by the iliococcygeus and pubococcygeus muscles. A subdivision of the pubococcygeus, the puborectalis muscle, is important to rectal continence. The puborectalis muscle originates from the body of the pubic bone and the superior layer of the deep perineal pouch (urogenital diaphragm). Fibers from the two puborectalis muscles pass posteriorly and join posterior to the rectum, forming a welldefined sling. The puborectalis, with the superficial and deep parts of the external sphincter and the proximal part of the internal sphincter, form the so-called anorectal ring. This ring can be palpated, and, because cutting through it will produce incontinence, it must be identified and protected during surgical procedures. It is at the approximation of these divisions of levator ani that weak areas may permit a posterior perineal hernia to bulge. The peritoneum envelops the front and sides of the upper third of the rectum. As the rectum passes deeper into the pelvis, however, progressively more fat is interposed between the peritoneum and the rectal musculature. Finally, the peritoneum separates completely from the rectum and passes anteriorly and superiorly over the uterus or, in males, over the bladder. This creates a depression called either the rectouterine or rectovesical pouch. There are three areas of weakness in the wall of the ischiorectal fossa through which an abscess of the fossa may pass. Of these three areas, the weakest is medial, through the anal wall. Slightly stronger is the inferior boundary of skin, and strongest is a medial pathway through the levator ani muscle or between its components. This last pathway can be taken in the opposite direction by a perineal hernia of the ischiorectal type.

c IS = spinotuberous hernia; 16 = infrapiriformis hernia; 17 = suprapiriform is hernia. (8) Anterior and posterior pelvic floor hernias in the female (labial, pudendal, vaginolabia.) (C) Posterior perineal hernia in the male. (Reprinted from V. Schumpelick, Atlas of Hernia Surgery; 1990, B.C. Decker Inc., with permission.)

5. Anatomy of the Abdominal Wall

Sites of Perineal Hernia

References

A primary perineal hernia may occur anterior or posterior to the superficial transverse perineal muscle. An anterior perineal hernia passes through the pelvic and urogenital diaphragms, lateral to the urinary bladder and vagina, and anterior to the urethra. It has been variously called pudendal, labial, lateral, or vaginolabial. It is found only in women (Fig. 5.4IB). A posterior perineal hernia passes between components of the pelvic diaphragm or through the hiatus of Schwalbe, when present, lateral to the urethra, vagina, and rectum. The hiatus is formed by the nonunion of the obturator internus and levator ani muscles. There are two possible locations: (1) an upper posterior hernia between the pubococcygeus and iliococcygeus muscles; and (2) a lower posterior hernia between the iliococcygeus and coccygeus muscles, below the lower margin of the gluteus maximus muscle (Fig. 5.41C). In males, the perineal hernia enters the ischiorectal fossa. In females, it may enter the fossa or the labium majus, or it may lie close to the vaginal wall or below the lower margin of the gluteus maximus muscle.

1. Cooper A. The anatomy and surgical treatment of abdominal hernia. London: Longman and Co.; 1804. 2. Rath, AM, Chevrel]p. The abdominal linea alba. Surg Rt.u1iol Anat. 1996;18:281-288. 3. Hovelacque A. Anatomie des ncrfs craniens et rachidiens. Paris: G. Doin; 1956. 4. Cox, 1941. 5. Fruchaud H. Anatomie chirurgicale des hernies de l'aine. Paris: G. Doin; 1956. 6. Wantz GE. Atlas of hernia surgery. New York: Raven Press; 1991. 7. Nyhus LM, Condon RE, eds. Hernia. Philadelphia:JB Lippincott Company; 1995. 8. Bogros, AJ. Essais sur l'anatomie chirurgicale de la region iliaque et description d'un nouveau procede pour faire la ligature des arteres epigastriques et iliaque externe. These Mid, Paris. No. 153, 29 Aout 1823. Paris: Didot Ie Jeune Edit.; 1823. 9. Bendavid R. The space of Bogros and the deep inguinal venous circulation. Surg Gynecol Obstet. 1992;174:355-358. 10. Skandalakis LJ, Colborn GL. Surgical anatomy of the abdominal wall. In: Bendavid R, ed. Prostheses and abdominal waU hernias. Austin: R.G. Landes Company; 1994.

6 Aponeurotic Hernias: Epigastric, Umbilical, Paraumbilical, Hypogastric Omar M. Askar

Aponeurotic Hernias The term aponeurotic hernia distinguishes epigastric, paraumbilical, umbilical, and hypogastric hernias from other types of abdominal hernias because of the very special characteristics of the central abdominal wall aponeuroses through which these hernias make their appearance. Appreciation of the structural and functional significance of these aponeuroses is essential to the planning of surgically and physiologically sound repairs of hernial defects in the aponeurotic area of the anterior abdominal wall. A reasonable explanation for the high rate of recurrence following a certain type of repair or the use of a specific technique may be given.

Surgical Anatomy The Aponeurotic Sheets of the Anterior Abdominal Wall The abdominal wall aponeuroses were long looked upon as inert sheets of fascia into which the flat muscles of the anterior abdominal wall are inserted. Recent studies 1,2 have shown these aponeurotic sheets to be an intricately interwoven fabric, the threads of which are fine, glistening tendons invested with loose areolar tissues to ensure their free mobility over each other (Fig. 6.1). Each of these fine tendons belongs to a small fleshy muscular belly in one of the three strata of abdominal muscles. Six strata of fine, tendinous aponeurotic slips emerge from the three layers of abdominal muscles. They flow medially to form two aponeurotic sheets which invest the rectus abdominis muscle, forming the rectus sheath. Three strata of aponeurotic tendinous fibers can be seen in both anterior and posterior rectus sheaths disposed in a crisscross triple-ply pattern. At the medial borders of the two recti, the aponeurotic fibers from the anterior and the posterior rectus sheaths blend together to form one narrow sheet of aponeurosis: the midline aponeurotic zone, or linea alba (Fig. 6.2). The tendinous fibers of one side cross the median by passing through the midline aponeurotic linea alba. There they join their counterparts from the other side to form, in effect, one digastric muscle from the mirror-image muscle of the two sides of the abdominal wall 64

R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

(Fig. 6.3A,B, and C). The digastric pattern ensures the perfectly harmonized function of the anterior abdominal wall musculature. In fact, the function of any single muscle in the anterior abdominal wall cannot be worked out independently of the others.

The Midline Aponeurotic ZoneThe Linea Alba Between the two rectus sheaths lies an aponeurotic sheet (Fig. 6.4). The term linea alba does not serve to explain the real nature of this midline aponeurotic zone. It is a zone of an aponeurotic fabric, the threads of which are fine tendinous strands interwoven together. They are the tendinous fibers of the abdominal muscles crossing the midline on their way to join their counterpart from the opposite side. In their course across the midline aponeurotic zone, the fibers of one side decussate with their analogues coming from the opposite side. In some 30% of individuals, the decussation of the tendinous fibers coming from the two sides occurs only once at the midline "single decussation" (Fig.6.5). In the other 70%, two additional lines of decussation are seen, one on either side of the midline "triple decussation" (Fig. 6.6). In addition to reinforcing the aponeurotic texture, the two additional lines of decussation seem to protect the midline decussation. In a single decussation, a hernial defect will be seen at the midline (Fig. 6.7), while in a triple decussation the hernial defect lies on one side of the midline. The force that produced the hernia acted outside the triple decussation (Fig. 6.8). This may explain why some patients appear more prone to develop herniation through the abdominal aponeuroses than others. More hernia repair failures may be expected on the weaker lineae albae with single line decussations, which will be more susceptible to fraying and allowing sutures to slip off. Extra lines of decussation were also seen in some individuals, denoting a firmer aponeurotic fabric. 3,4 The firmness given to the abdominal wall aponeurosis by the additional lines of decussation may be appreciated when the midline aponeurotic zone of man is compared to that of quadrupeds. In quadrupeds, the linea alba is much wider and thinner, but because of the tightly interwoven texture produced by many more lines of decussation4-6 the aponeurotic fabric, though wide and thin, almost membranous,

6. Aponeurotic Hernias

6.1. Anterior rectus sheath (above the umbilicus) as seen under the dissecting microscope, showing the glistening fine tendinous fibers in the aponeurotic sheath bound together by loose areolar tissue and disposed in a crisscross pattern.

FIGURE

attains greater strength; it has to stand the weight of all the abdominal viscera in addition to a pregnant uterus that often contains twins. Aponeurotic hernias are not as common in quadrupeds as in man. Three distinct functional zones can be identified in the midline aponeurotic zone: an upper, mobile respiratory or "epigastric zone," a middle "umbilical zone," and a lower, fairly fixed hypogastric or "belly support zone" (Fig. 6.4) .1,7 Each of the three zones has its own aponeurotic pattern which bears direct relation to its function as well as to the mechanism by which a hernial defect may be produced. This fact should be taken into consideration when planning the type of repair needed for a hernial defect in each zone and when looking for a cause of recurrence following such a repair.

6.3. Diagrams showing the digastric pattern of the muscles of the abdominal wall: (A) between the (right) external oblique and (left) internaloblique (anterior lamina); (B) between the (left) internal oblique

FIGURE

6.2. Right paramedian incision. The rectus muscle is retracted to show anterior and posterior rectus sheath blending together to form the midaponeurotic zone or linea alba.

FIGURE

The Epigastric Zone In the epigastric zone, the aponeurotic fibers take an oblique upward medial and downward medial direction (Fig. 6.5, 6.6). This obliqueness allows the linea alba and the whole aponeurosis in the epigastric zone to shorten and lengthen to adapt to the movements of the trunk (Fig. 6.9 and 6.10) and to stretch in response to respiration.1.3 As a result of the oblique direction of the aponeu-

c (posterior lamina) and the (right) transversus; (C) between the two transversus abdominis muscles.

FIGURE 6.4. Transilluminated silhouette of anterior abdominal wall in normal adult (postmortem specimen) showing the midline aponeurotic zone (linea alba) between the two rectus abdominis muscles: (A) epigastric, expansile, respiratory zone; (8) tendinous intersection; (C) lower, strong subumbilical portion of rectus muscle.

rotic fibers, lengthening is accompanied by narrowing of the fabric (Fig. 6.11). Thus, in abdominal distension, the midline aponeurotic zone increases in length but not in breadth, resulting in downward displacement of the umbilicus, a physical sign noted in cases of chronic abdominal distension. Stretching of the aponeurosis in its transverse dimension would result in divarication of the two recti, and possibly contribute to widening of the subcostal angle.

FIGURE 6.5. Linea alba above the umbilicus (at operation), single line of decussation.

O .M. Askar

FIGURE 6.6. Diagram of single line of decussation between the aponeurotic fibers of the two external oblique aponeuroses.

The Relation of the Epigastric Zone to the Diaphragm On the posterior aspect, the linea alba in the epigastric zone receives aponeurotic fibers descending from the sternocostal portion of the diaphragm. These fibers terminate about midway between the xyphoid and the umbilicus by intermingling with the tendinous fibers coming from the posterior rectus sheaths, as well as those derived from the middle tendinous intersection (Fig. 6.12). These fibers appear to synchronize the movements of the epigastric zone with those of the diaphragm. Herniation through the epigastric zone often occurs as a complication of its main function, respiration. A sudden severe stretch of the aponeurosis, such as that produced by vigorous coughing

FIGURE

6.7. Midline hernias in patient with a single line of decussation.

6. Aponeurotic Hernias

FIGURE

6.10. The effects of stretching obliquely oriented woven fabrics.

A midline epigastric incision can cause herniation in the epigastric zone, especially when done in a weak midline aponeurosis with a single line of decussation. Lacking interwoven texture, the weak aponeurotic fabric allows the sutures to slip along the slippery aponeurotic fibers. Other types of epigastric hernial defects such as congenital defect (Fig. 6.14) are much less frequent. 6.8. Diagram showing triple decussation on the anterior surface of the midline aponeurosis

FIGURE

or straining, may create a force strong enough to tear open an epigastric aponeurosis with a weak single line of decussation. The point receiving the maximal load of this fo:ce wo~ld be w~ere. t~e aponeurotic fibers from the middle tendmous mtersectIon Jom those from the anterior and posterior rectus sheaths as well as those descending from the diaphragm. This point lies about midway between the xyphoid and umbilicus, where an epigastric hernia would develop. Such a hernia is often seen in robust, adult males (Fig. 6.13) . The old theory that epigastric hernias are caused by protuding extraperitoneal fat finding its way through the aponeurosis, entering and enlarging a fascial foramen created by the passage of a blood vessel that pierces the linea alba,1.6 was not supported by many investigators. 7- JO

The Umbilical Zone In the umbilical zone, the linea alba widens (Fig. 6.4). In addition to their obliqueness, the aponeurotic fibers take an S-shaped course (Fig. 6.9). This allows even more stretch in the midregion; pregnancy converts this curvature to a straight line. Abdominal distension exceeding the physiologically permissible limits would load this area around the umbilicus; paraumbilical hernias are often seen in women who have borne children. Abdominal distension pressing on the midaponeurotic "umbilical zone" tends to stretch the aponeurosis in both the longitudinal and the transverse axes. Unlike the epigastric zone, the umbilical zone stretches

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Y~A.~ ', ' y&"S: · fK.x.:< "

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6.9. Hernia to one side of the midline, in patient with triple decussation.

FIGURE

fabrics.

6.11. Diagram of effects of stretching obliquely oriented woven

O.M. Askar

6.12. Tendinous aponeurotic slips descending from the sternocostal portion of the diaphragm to join the midline aponeurosis about halfWay between xiphoid process and umbilicus. FIGURE

FIGURE

more transversely than longitudinally. This fact seems to have caught the attention of Mayo,n who suggested a transverse overlap for the repair of hernial defects in the midaponeurotic umbilical zone. The upper flap is provided by the elongated epigastric zone.

The Hypogastric "Belly Support" Zone In the lower hypogastric zone,I,12 the linea alba tapers at its lower end on the os pubis. Most of the aponeurotic fibers on the pos-

6.14. Congenital epigastric and paraumbilical hernias in a male

patient.

terior rectus sheath escape forward to join those of the anterior rectus sheath in forming a fairly strong cover to a well-developed lower part of the rectus muscle. The relatively few remaining posterior aponeurotic fibers pass behind the rectus muscle to end in the arcuate line. Very few fibers pass along the fascia transversalis in the region of the inguinal canal. Most of the aponeurotic fibers in the hypogastric region are directed downward and medially. The linea alba is thin and is formed by a single line of decussation only.I3 The strong lower subumbilical segment of the rectus muscles thus forms the main constituent of the belly support mechanism. The medial edges of the two recti often overlap or may even blend together to make one strong sheet of muscle. The surgeon must reconstitute the two recti in the closure of a midline subumbilical incision, for these muscles form the main barrier in the repair of a subumbiIical hernial defect.

The Tendinous Intersections

FIGURE

6.13. Epigastric hernia in a robust male.

The tendinous intersections are three to five pairs of horizontal tendinous septa along the course of the flat rectus muscle. They are formed by fine tendinous slips which emerge from the muscular bellies of the rectus muscle (Fig. 6.15). Some of them pass straight up from one segment of the intersected rectus muscle to the next, acting as intermediate tendons (Fig. 6.16A). The others curve forward to join the anterior rectus sheath, some of them acquiring an upward medial direction, then join the aponeurotic fibers of the anterior rectus sheath lying in the same orientation, namely, those of the anterior lamina of the internal oblique aponeurosis. Other tendinous slips run downward and medially (Fig. 6.16B). In this very short course between the rectus muscle and its sheath, the upward tendinous fibers decussate with their downward counterparts, forming a transverse line of decussation along which the rectus muscle gains attachment to its anterior

6. Aponeurotic Hernias

tt .-

...

itt 1

---t

6.17. Diagram of mechanism of transformation, through the tendinous intersections, of the vertical force of longitudinal contraction of the rectus abdominis muscle into a lateral pull of the midline aponeurosis (linea alba).

FIGURE

6.15. Right paramedian incision (intraoperative photograph) . Tendinous aponeurotic fibers of a tendinous intersection emerging from the rectus muscle (left) to join the anterior rectus sheath (right). FIGURE

sheath. A fairly strong band of aponeurotic tendinous slips emerges from the medial border of the rectus muscle and passes directly medially to join the midline aponeurotic zone, sharing in the formation of its aponeurotic fabric (Fig. 6.16C). These fibers may be of special importance as they transmit the longitudinal contracting force of the rectus muscle into a lateral pull on the

midline aponeurotic zone (Fig. 6.17) . A forcible lateral pull at a critical spot in the weak midline aponeurosis of a single decussation pattern may be strong enough to tear open the aponeurosis and produce a hernial defect. It can be seen (Fig. 6.4) that all the tendinous intersections are situated in relation to the mobile areas of the anterior abdominal wall, namely, the upper expansile respiratory and umbilical zones. The lower tendinous intersection joins the linea alba at a point just above the umbilicus. Its functional importance is that it demarcates the fairly fixed lower belly support zone from the upper respiratory and umbilical zones. The point at which this lower tendinous intersection joins the midline aponeurotic zone is a critical spot for the development of paraumbilical hernial defects (Fig. 6.18) . In a few instances, one or both lower tendinous intersections may gain attachment to the linea alba at a point just below the umbilicus. These can give rise to an infraumbilical paraumbilical hernial defect. The middle tendinous intersection joins the linea alba at a point about midway between the xyphoid process and the umbilicus, where the aponeurotic slips descending from the sternocostal portion of the diaphragm join the posterior aspect of the midline aponeurosis. This constitutes another critical spot for the development of an epigastric hernial defect, especially in a weak alba with a single line of decussation (Fig. 6.19).

The Relation of the Skin to the Midline Aponeurosis

6.16. Diagram of aponeurotic fibers of three types of tendinous intersections: (A) fibers acting as intermediate tendons between the rectus muscle bellies; (B) fibers passing forward to join the rectus sheath (as in Fig. 6.10); (C) fibers emerging from the medial edge of the rectus muscle to join the midline aponeurosis. FIGURE

Above the umbilicus, at the midline, the skin of the anterior abdominal wall has a form of attachment to the midline aponeurosis. This was found to be due to the presence of fine tendinous slips that emerge from the anterior surface of the midline aponeurosis: they pass forward through the subcutaneous tissues to gain attachment to the dermis at the midline. In their path from the aponeurosis to the skin they describe an x-shaped pattern. These tendinous bands must be cut to allow reflection of the skin of the anterior abdominal wall at the midline. Lateral to their attach-

O.M. Askar

-----i2

SK1N~

"NT~ :_-----::::---__=;-----

SHtATH .:_?±~~~;.~~ pOST. R£Q .::::------------- .~---------------::: SHEATHl

6.20. Diagram of x-shaped aponeurotic slips attaching the skin in the umbilical area to the midline aponeurosis.

FIGURE

6.18. Diagram of mechanism of paraumbilical hernia creation in pregnancy and labor: RM = rectus muscle; ARS = anterior rectus sheath; PRS = posterior rectus sheath; U = umbilicus. FIGURE

ment, the skin may be peeled offwith blunt dissection (Fig. 6.20). These x-shaped aponeurotic bands are responsible for the loculations seen in paraumbilical and epigastric hernias, but rarely in other hernias. The presence of these bands above the umbilicus but not below may have a significance in the formation of a pendulous belly below rather than above the umbilicus. In obesity, the deposition of fat above the umbilicus occurs away from the midline over the hypochondria. It is through these aponeurotic bands that the heavy weight of a pendulous belly can be transmitted to the aponeurosis above the umbilicus. Resection of an obese pendulous belly would help to relieve the harmful downward traction on the aponeurosis, quite apart from its cosmetic effect (Fig. 6.21).2,14 Also, the umbilical scar, being a fixed point on the anterior wall aponeurosis, provides another means whereby the pendulous obese belly can exert harmful downward traction on the linea alba; it should, for this reason, be disconnected from the skin. Attempts at refashioning an artificial umbilicus by joining the skin to the aponeurosis with a suture, are often followed by recurrence of the hernial defect at the site of the suture.

The Umbilical Orifice The umbilical orifice is a natural defect in the midline aponeurosis to allow the passage of the umbilical cord structures during fetal life. During development, the aponeurotic fibers of the

FIGURE 6.19. Diagram of the mechanism of epigastric hernia defect creation: arrows indicate directions of force in spasmodic effort. Diaphragmatic tendinous slips join the midline aponeurosis, intermingling with those of the middle tendinous intersection fibers.

FIGURE 6.21. Diagram of the harmful effects of downward traction on the aponeurosis by a heavy, pendulous belly below the umbilicus.

6. Aponeurotic Hernias

References 1. Askar o. Surgical anatomy of the anterior abdominal wall aponeurosis. Ann R Coll Surg. 1977;59:313. 2. Askar O. A new concept of the aetiology and surgical repair of the paraumbilical and epigastric hernias. Ann R Coll Surg of England. 1978;60:42. 3. Askar O. Aponeurotic hernias. Surg Clin North Am. 1984;64:315. 4. Askar 0, et al. The umbilical ring. 1993. 5. Burton C. Fingered fascia lata grafts for repair of incisional hernia. Surg Gynecol Obstet. 1959;109:621.

6. Cullen TS. Method of dealing with intestinal loops densely adherent to an umbilical hernia. JAMA. 1922;78:564. 7. Wilkinson WR Epigastric hernia. WV MedJ 1949;45:328. 8. Anson BJ, McVay CB. The anatomy of hernial regions. SurgGynecol Obstet. 1949;89:417.

FIGURE 6.22. Diagram of the arrangement of tendinous aponeurotic fibers around the umbilical ring.

developing anterior abdominal wall pass around the umbilical cord so that when the development of the anterior abdominal wall is completed, the umbilical cord passes through a rounded aperture in the anterior abdominal wall aponeurosis, the umbilical ring. The umbilical ring is formed by aponeurotic fibers of both lower tendinous intersections, supplemented from the two sides by aponeurotic fibers from the external oblique, internal oblique and transversus abdominis (Fig. 6.22). These tendinous aponeurotic fibers surround the umbilical ring in a way similar to the shutter mechanism used in optical instruments (Fig. 6.1).1 5 The free mobility of the aponeurotic tendinous fibers surrounding the umbilical ring allows the shutter mechanism to close the umbilical ring when the abdominal muscles contract. Immediately after birth, the infant takes its first breath by the first contraction of its diaphragm. This is followed by a forcible contraction of the abdominal muscles which creates a positive intrathoracic pressure which helps to compress air within the lungs to open up the collapsed alveoli and expel excess air up through the larynx, giving the first cry of life, by which the newborn announces the start of respiration. This forcible contraction of the abdominal wail muscles will put the midline aponeurosis on stretch. The tendinous aponeurotic fibers encircling the umbilical orifice, acted upon by the contracting abdominal muscles, constrict the umbilical ring so that the vessels passing in the umbilical cord through the constricted umbilicus become completely occluded: a very clever device provided by nature to help the newborn to sever relations with the placenta. Failure to produce efficient constriction of the umbilical ring during or shortly after birth, as would occur in mild grades of fetal distress in a difficult labor, would delay the healing and closure of the umbilical stump, and at the same time leave a patulous umbilical ring through which a hernial sac could find its way. An umbilical hernia is thus quite different from other conditions like exomphalos, where the problem resides with failure of development of a part of the anterior abdominal wall.

9. Moschowitz AY. The pathogenesis and treatment of herniae of the linea alba. Surg Gynecol Obstet. 1914;18:504. 10. Pollock LH. Epigastric hernia. Am J Surg. 1936;34:376. 11. Mayo WV. Radical cure of umbilical hernia.JAMA. 1907;48:1842. 12. Wolmsly WR. The sheath of the rectus abdominis.J Anat. 1937;71:404. 13. Rizk N. The aponeurotic expansions of the anterior abdominal wall. Anatomy thesis. Cairo University, Faculty of Medicine; 1975. 14. Lathrop G. Abdominallipectomy.JAMA. 1916;67:487. 15. McVay CB. In: Christopher textbook of surgery. 7th ed. MD Davis, ed. Philadelphia: WB Saunders; 1960, pp. 518-540.

Tribute to Omar M. Askar " ... I was watching a butcher in my fann deskinning [sic] a lamb which was killed for a party. The criss-cross decussating pattern of the lamb's wide linea alba struck me. I took its abdominal wall aponeurosis and looked at it with a magnifYing lens. I saw fine glistening tendons... ." (Omar M. Askar: personal communication, 27 January, 1991.) I am deeply grateful to Dr. Robert Bendavid for presenting the work of my friend and for asking me to write a few words about a good man, a great anatomist, and an excellent surgeon, Prof. Omar M. Askar. The late Omar M. Askar, of Cairo, Egypt, was a true student of the anterior abdominal wall. His work is classic, and will remain in the annals of surgical anatomy. I corresponded with Prof. Askar for many years before I finally had the opportunity to meet him. I was invited to visit Cairo for the Egyptian Society of Surgeons meeting in 1993. My dear friend Omar rolled out the red carpet for me and my wife. It was a great joy, honor, and privilege to discuss with Omar the anatomy and surgical dimensions of the anterior abdominal wail. His specimens were well preserved and clarified for me the bilaminar formation of the aponeuroses of the parietal muscles, as well as the formation of the linea alba by the decussating fibers of the rectus sheath. In 1995, Prof. Askar came to Atlanta, and I had the pleasure of having him as a guest in my home. His lecture on recurrent paraumbilical hernias at Grand Rounds for the Department of Surgery at Emory University School of Medicine was memorable. I was reminded ofa line in another letter, dated 15 March 1994: "I always say, 'A good father is a good teacher.''' His chapter is part of his teaching legacy. John E. Skandalakis Atlanta, Georgia

Surgical Anatomy of the Inguinal Region from a Laparoscopic Perspective Riccardo Annibali, Robert]. Fitzgibbons,Jr., and Thomas Quinn

Introduction "The operating surgeon knows little of the posterior wall of the inguinal canal, so well is it hidden from his view." (WJ. Lytle, 1945)1

In 1969, Ravitch stated that the "operations for the cure of hernia would seem to be established and well known beyond the possible need for further discussion and demonstration."2 Actually, before the introduction oflaparoscopic surgery, the "problem hernia" seemed to be well defined. The term indicated "the protrusion of a loop or knuckle of an organ or tissue through an abnormal opening,"3 that needed to be repositioned and kept in place with some type of repair. The only variable factor was the choice of herniorrhaphy. Today, laparoscopic hernia repair challenges the surgeon with a new perspective of hernia. Most anatomy and surgery textbooks describe the groin and its layers in the sequence of dissection, proceeding from the superficial to the deep, and giving little consideration to the interior view of the abdominal wall. To prepare for laparoscopic hernia repair, it is necessary to reverse this approach and begin our anatomical study with the deepest layers.

Terminology Concepts of superior and inferior, superficial and deep, anterior and posterior have been established by time-honored convention and are adhered to even though the surgeon does not operate on patients standing in the "anatomical position." Use of terms like "down" to mean under the surgeon's hand and "up" to mean toward the ceiling is inevitable in communication among members of an operating team, but in formal notes and descriptions of anatomy and surgical procedure, standard terminology is essential. Ambiguity is particularly worrisome in discussions of the laparoscopic view. When two structures cross, which one is "in front" of the other? It is helpful to remember that the patient's physical disposition in space does not depend on the surgeon's point of view; with this in mind, when the laparoscopic surgeon says "in front" he will always mean "anterior to" in the conventional sense.

72 R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

Methods of Dissection To identify the anatomical structures that compose the deep surface of the anterior abdominal wall and the inguinal region, we have performed 14 dissections in 10 male and 4 female cadavers whose age ranged from 63 to 100. For the study of the layers of the abdominal wall in the majority of the specimens, we initiated the dissection with a standard midline incision. In the last two dissections, however, we began with an enlarged bilateral subcostal incision in order to preserve the anterior abdominal wall intact. In all cases, the abdominal viscera were removed to allow unobstructed visualization of the anatomical details in the retroperitoneal space of the lower trunk. Peritoneum that covered the internal surface of the abdominal wall above the inguinal ligament was initially left intact to preserve the laparoscopic view.

Peritoneum The deep surface of the abdominal wall above the inguinal ligament is covered by peritoneum (Figs. 7.1, 7.2A and B, and 7.3; see color insert). Five peritoneal folds formed by peritoneal reflections over three underlying cord-like structures in the center, and two vascular bundles peripherally, are visible below the umbilicus. The median umbilical ligament, which represents the obliterated remnant of the embryonic urachus, lies in the midline and extends from the fundus of the bladder to the umbilicus. Two other peritoneal folds, the medial and lateral umbilical ligaments, are bilaterally symmetrical. The medial umbilical ligament consists of a fold of peritoneum covering the distal portion of the umbilical artery. This is usually atrophied and cord-like in the adult, but it is normally patent proximally, and gives off the superior vesical arteries to the urinary bladder (Figs. 7.1, 7.4, 7.SA, 7.9, 7.10, 7.14B; see color insert). Occasionally, the entire umbilical artery may remain patent. 4 In some patients, the medial umbilical fold is particularly prominent and may hinder proper dissection. 5 The lateral umbilicalligament consists of a fold of peritoneum around the inferior epigastric vessels, together with a variable amount of fatty tissue. It should be noted that some older texts define the fold outlined by the umbilical artery as the lateral umbilical ligament, while the fold associated with the inferior epigastric vessels has been

7. Surgical Anatomy of the Inguinal Region 7.1. Drawing illustrating the anatomy of the internal surface of the lower abdominal wall, inguinal region and lower trunk. (See color insert.)

Remnant of umbilical a.

FIGURE

Medial umbilical ligament

Linea semicircularis Rectus abdom . m. Inferior epigastric a. and v.

Urachus (median umbilical ligament)

Testicular artery and vein Falx inguinalis (Henle's lig.)

Anastomotic pubic Medial fossa

Aponeurotic arch

Lateral fossa

Superior and inferior crura (transversalis fascia sling)

Femoral canal --'---"7lIIF:~~F.:.t;~"

Femoral ring Pectineal (Cooper's) a. and v. Psoas minor tendon

lIiopubic tract Deep circumflex iliac a. and v. Iliopectineal arch AnI. pubic branch and iliopubic vein Vas deferens Obturator foramen, nerve, artery, vein Femoral nerve Lateral femoral cutaneous nerve Ilioinguinal ne rve Iliohypogastric nerve Genitofemoral nerve Genital branch + Femoral branch·

called plica epigastrica.3.4.6 In this chapter, we will use more contemporary terminology (Table 7.1).7-12 On either side of the midline, the medial and lateral umbilical ligaments delineate three shallow fossae (Figs. 7.1, 7.2A,B,C, 7.3) . The lateral fossa lies lateral to the inferior epigastric vessels. It is the site where indirect hernias pass through the internal inguinal ring. The medial fossa is defined as the space between the lateral and the medial umbilical ligament and corresponds to the site of development of direct inguinal hernias. The location and size of the medial umbilical ligament is variable; it is sometimes superimposed on the lateral umbilical ligament and should, therefore, not be considered a consistent landmark. Finally, the supravesical fossa lies between the medial and the median umbilical ligaments. It is more or less evident, depending on its depth. The rectus abdominis muscle and its sheath confer greater strength to this area, making supravesical hernias rare. 8 Condon observed that "the umbilical fossae are rarely noted during intra-abdominal operations and are of no surgical importance in regard to either the etiology or the repair of groin hernias." 7 Since the development of laparoscopic techniques for hernia repair, however, increased attention has been paid to the internal aspect of the abdominal wall: a consistent relationship between inguinal herniation and the umbilical fossae has been routinely observed.

Preperitoneal Space The preperitoneal space of Bogros contains a variable amount of connective tissue, which may be areolar, fatty, or semimembranous (Figs. 7.1, 7.4, 7.5A,B, 7.6, 7.9, 7.14B).7-9 It is in direct communi-

cation with the retropubic space of R.etzius. 13 A precise knowledge of the vascular and neurological structures included in the preperitoneal space of the lower trunk is essential for the laparoscopic surgeon intending to perform a hernia repair. After removal of the peritoneum, the preperitoneal space is entered. Tobin and, more recently, Arregui, have described a thin fascial layer superficial to the peritoneum known as the preperitoneal fascia. 14-J 7 The magnification obtained with the laparoscope allows a better identification of this fascia, while in the embalmed cadaver its identification is somewhat difficult. In the course of 187 laparoscopic hernia repairs in 145 patients, Arregui has demonstrated that the preperitoneal fascia divides the preperitoneal space into two different compartments, and its opening is required to enter the preperitoneal space of Bogros proper. As described by Arregui,17 the space between the peritoneum and the preperitoneal fascia contains a small amount of adipose and areolar tissue, the remnant of the umbilical artery, and the inferior epigastric vessels, which produce the two peritoneal folds on either side of the midline. Arregui also maintains that at the level of the internal inguinal ring, the preperitoneal fascia is intimately fused with the peritoneum and provides the conical sheath that is visible laparoscopically around the vas deferens and the internal spermatic (testicular) vessels (Fig. 7.6) . It then continues distally, following the spermatic cord, to form the inner component of the internal spermatic fascia.15 During laparoscopic repair of an indirect hernia, this conical fascial covering must be entered to clear the sac from the other structures of the cord in order to reduce, ligate, and transect the hernial sac. Arreguil7 has also pointed out that the plane between the peritoneum and the preperitoneal fascia may be mistakenly entered either during a laparoscopic transabdominal preperitoneal procedure or a totally extraperitoneal

FIGURE 7.2. (A) View of the deep surface of the anterior abdominal wall in a cadaver preparation, which demonstrates the peritoneal folds and fossae. (B) The peritoneal fossae are better demonstrated with transillumination of the lower anterior abdominal wall: UM = umbilicus; FB = fundus of the bladder; U = median umbilical ligament; ML = medial umbilical ligament; LL = lateral umbilical ligament (inferior epigastric vessels); SF = supravesical fossa; MF = medial fossa; LF = lateral fossa; IS = internal spermatic (testicular) vessels; VD = vas deferens; EI = external iliac vessels; A = abdominal aorta. The arrow indicates the deep inguinal ring. (C) Exterior view of the anterior abdominal wall and inguinal region transilluminated: UM = umbilicus; RM = sheath of rectus muscle; AA = aponeurotic arch of transversus abdominis muscle; SC = spermatic cord; IR = area corresponding to the internal inguinal ring; IE = inferior epigastric vessels; LF = lateral fossa; IL = inguinal ligament. Dotted outline indicates the weak areas included within the inguinal triangle through which direct hernias occur. (See color insert.)

FIGURE 7.3. Peritoneal folds and fossae, as seen at laparoscopy. A direct

hernia is visible bilaterally and appears as a circular defect included between the aponeurotic arch of the transversus abdominis muscle superiorly and the iliopubic tract inferiorly: U = median umbilical ligament; ML = medial umbilical ligament; LL = lateral umbilical ligament; AA = aponeurotic arch of the transversus abdominis muscle; IP = iliopubic tract; SF = supravesical fossa; MF = medial fossa; LF = lateral fossa; VD = vas deferens; IS = in ternal spermatic (testicular) vessels; EI = external iliac vessels; B= bladder with Foley catheter inserted. (See color insert.)

FIGURE 7.4. Panoramic view of the internal surface of the anterior lower abdominal wall, inguinal regions, lower trunk, and pelvis in a cadaver dissection: UM = umbilicus; LS = linea semicircularis; RM = rectus abdominis muscle; HT = inguinal (Hesselbach's) triangle; IE = inferior epigastric vessels; AP = anterior pubic branch and iliopubic vein; TS = transversalis fascia sling; U = urachus; CL = Cooper's ligament; UA = umbilical artery; AO = anomalous obturator artery; SV = superior vesical artery; PB = anastomotic pubic branches; IV = external iliac vein; IA = external iliac artery; VD = vas deferens; PA = iliopectineal arch; IP = ilio-

A FIGURE 7.5. (A) Photograph of a cadaver preparation (right side) showing the preperitoneal space at the level of the inguinal area, after removal of the peritoneum and preperitoneal adipose tissue (the urachus has been resected and the bladder retracted posteriorly). (B) Same view of (A), but in a different cadaver. Note the staples correctly positioned just above the iliopubic tract to tack the inferior border of the mesh. The internal spermatic (testicular) vessels have been moved slightly laterally to better show the external iliac vessels on the floor of the "Triangle of Doom." RM = rectus abdominis muscle; IE = inferior epigastric vessels; IP = iliopubic tract; CL = Cooper's pectineal ligament; IS = internal spermatic (testicular) vessels; ES = external spermatic vessels; VD = vas deferens; IA = external iliac artery; IV = external iliac vein; EI = external iliac vessels; IPA =

pubic tract; DC = deep circumflex iliac vessels; GN = genitofemoral nerve; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; LC = lateral femoral cutaneous nerve; IL = ilioinguinal nerve; 1M = iliacus muscle; PM = psoas major muscle; IS = internal spermatic (testicular) vessels; UR = ureter; A = abdominal aorta; LV = iliolumbar vessels. Thick black arrow indicates deep inguinal ring; white arrow, obturator foramen; short arrow, femoral ring. (See color insert.)

B iliopectineal arch; GN = genitofemoral nerve; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; LC = lateral femoral cutaneous nerve; IL = ilioinguinal nerve; DC = deep circumflex iliac vessels; V = seminal vesicles; UA = umbilical artery; PB = anastomotic pubic branch; AP = anterior pubic branch and accompanying iliopubic vein; RP = retropubic vein; LV = iliolumbar vessels; B= bladder; CI = common iliac artery; M = aponeurotic arch of the transversus abdominis muscle; UR = ureter; 1M = iliacus muscle; PM = psoas major muscle; TF = transversalis fascia; IF = iliac fascia (reflected in Part (B»; TM = transversus abdominis muscle. (See color insert.) 75

R. Annibali et al.

TABLE 7.1. Different terminologies used to indicate the peritoneal folds of the deep surface of the anterior abdominal wall Nomina anatomica

terminology Median umbilical ligament Medial umbilical ligament Lateral umbilical ligament

Structure determining the fold

AI ternative terminologyb

Urachus Obliterated umbilical artery Inferior epigastric vessels

Median umbilical ligament Lateral umbilical ligament Plica epigastrica

'Nomina Anatomica, 198012 ; Condon, 19787; Ponka, 19808 ; Gray's Anatomy, 198910; Skandalakis, 1991 21 bZimmermann, 19673; Thorek, 19624; Gullmo, 19846 ; Hollinshead, 1961 43 ; Schaffer, 1953.50

repair. This could result in injury to the bladder if the dissection is carried medial to the medial umbilical ligament.

Vessels of the Retroperitoneal and Preperitoneal Space The importance of a thorough understanding of the vasculature for surgeons who staple prosthetic mesh in the preperitoneal space is self-evident: the vascular structures can easily be damaged, with serious results. The external iliac vessels run on the medial aspect of the psoas muscle over its investing fascia, before passing behind the iliopubic tract and the inguinal ligament to become the femoral vessels, within the femoral sheath (Figs. 7.1, 7.2B, 7.3, 7.4, 7.SA,B, 7.7.A, 7.9, 7.10, 7.14B) . The inferior epigastric vessels normally originate from the external i1iacs (Figs. 7.1, 7.2A,B,C, 7.4, 7.SA,B, 7.6, 7.7A,B, 7.9, 7.10, 7.14B). They run superiorly and medially toward the umbilicus from a point midway between the anterior superior iliac spine and the symphysis pubis, ascend obliquely along the medial margin of the internal inguinal ring between the transversalis fascia and the peritoneum, and finally

7.6. Preperitoneal space seen laparoscopically during a hernia repair: PF = peritoneal flap reflected; IS = internal spermatic (testicular) vessels; VD = vas deferens; CL = Cooper's pectineal ligament; ML = medial umbilical ligament; PB = anastomotic pubic branch; PV = iliopubic vein; IE = inferior epigastric vessels; SC = superior crus of the transversalis fascia sling; IP = iliopubic tract; AA = aponeurotic arch of the transversus abdominis muscle. The arrow points to the deep inguinal ring. (See color insert.) FIGURE

pierce the transversalis fascia to enter the sheath of the rectus muscle. The inferior epigastric arteries usually give rise to two branches in the inguinal region: the cremasteric artery, known formerly as the external spermatic artery (Figs. 7.SA, 7.10, 7.14B), and the anastomoticpubicbranch (Figs. 7.1, 7.4, 7.SA, 7.6, 7.7A,B, 7.9, 7.14B). The cremasteric artery runs upward from its origin along the medial aspect of the internal inguinal ring, pierces the transversalis fascia, and crosses the preperitoneal space to join the spermatic cord. The pubic branch courses inferiorly toward the obturator foramen, where it anastomoses with the obturator artery. The anastomotic pubic artery sometimes gives rise to an inconstant small branch, called the anterior pubic branch, as it crosses the superior ramus of the pubis. The anterior pubic branch runs along the superior ramus of pubis, toward the body of this bone. This anastomotic ring of arteries, together with their corresponding veins, is sometimes known as the "corona mortis" ("crown of death") because of the bleeding which occurs if it is injured while suturing or applying staples to the pectinal (Cooper's) ligament, or in blind medial incision of the lacunar ligament when attempting to free an incarcerated femoral hernia. An obturator artery originating from the inferior epigastric or external iliac has been observed in approximately 30% of the specimens studied. I 6-19 When the obturator artery is anomalous in its origin, it usually appears as a sizable branch from the inferior epigastric vessels (Figs. 7.4, 7.9, 7.10). Laceration of these branches during surgery leads to hematomas in the preperitoneal space. The iliopubic vein courses deep to the iliopubic tract (Figs. 7.1, 7.4, 7.SA, 7.6, 7.9, 7.10, 7.14B) and accompanies the anterior pubic branch when this is present. It either empties directly into the inferior epigastric vein, or joins the venous anastomotic pubic branch to form a common trunk that drains into the inferior epigastric vein. 13 Another tributary of the inferior epigastric vein, the rectusial vein, runs along or is embedded within the lower lateral fibers of the rectus muscle (Figs. 7.9 and 7.10) . According to Bendavid, who first named this vessel, it consistently forms a venous anastomotic ring by joining the iliopubic vein above the pubic crest. 13 We were able to demonstrate this connection in cadaver dissections; however, these venous anastomoses are better identified at the operating table than in the anatomy laboratory, as the small veins are often collapsed and empty in the cadaver, but darkened in color and engorged in the patient undergoing surgery. Finally, a small collateral branch of the anastomotic pubic vein is commonly observed on the lower posterior aspect of the pubic ramus, beneath Cooper's pectineal ligament, and has been called the retropubic vein (Figs. 7.SA, 7.9, 7.10, 7.14B). For all surgeons interested in placing prosthetic materials in the preperitoneal space, the importance of familiarity with the deep inguinal venous cir-

7. Surgical Anatomy of the Inguinal Region

FIGURE 7.7. (A) Cadaver preparation of the inguinal region. Close-up of the area of the right deep inguinal ring. (B) Laparoscopic view of the left internal inguinal ring. TS = transversalis fascia sling; SC = superior crus of the transversalis fascia sling; IC = inferior crus of the transversalis fascia sling; IS = internal spermatic (testicular) vessels; VD = vas deferens; IV = external iliac vein; IA = external iliac artery; IP = iliopubic tract;

IE = inferior epigastric vessels; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; PA = iliopectineal arch; M = aponeurotic arch of the transversus abdominis muscle; DC = deep circumflex iliac vessels; 1M = iliacus muscle; PB = anastomotic pubic branch. (See color insert.)

culation is self-evident: damage to these structures is easy and usually leads to hematoma formation. The external iliac vessels are also the origin of the deep circumflex iliac artery and vein (Figs. 7.1, 7.4, 7.5A,B, 7.7A, 7.14B). These cross laterally over the femoral sheath, run between the iliopubic tract and the iliopectineal arch, pierce the transversalis fascia, and finally end in the space between the transversus abdominis and the internal oblique muscles. It is important to note that an anastomosis exists between the circumflex iliac vessels and the iliolumbar and suPerior gluteal vessels (Figs. 7.1, 7.4, 7.5A, 7.14B).7,20 In males, the testicular arteries (formerly called internal spermatic), originate from the aorta below the renal arteries (Figs. 7.1, 7.2A, 7.3,7.4, 7.5A,B, 7.6, 7.7A,B, 7.9, 7.10, 7.14B, 7.15, 7.16) . They then pass inferolaterally behind the peritoneum covering the psoas major muscle. Each passes in front of the genitofemoral nerve, the ureter, and the inferior part of the external iliac vessels. Each testicular artery joins the vas deferens as it enters the inguinal canal through the deep inguinal ring, accompanied by its corresponding testicular vein. The left testicular vein drains into the renal vein, while the right empties into the vena cava. The laparoscopic surgeon must appreciate the interrelations of these vessels to avoid their inadvertent damage during laparoscopic hernia repair.

names corresponding to the structure covered, such as transversalis, psoas, obturator, or iliac, but it is a single fascial envelope that invests the entire abdominal cavity.3 The term transversalis fascia was coined by Sir Astley Cooper to designate the portion of the endoabdominal fascia that covers the internal surface of the transversus abdominis muscle. 21 .22 In his original description, Cooper reported that the transversalis fascia is composed of an outer (or anterior), and an inner (or posterior) lamina. 23 This bilaminar arrangement has also been reported by Cleland and MacKay,24 but McVay, Anson, and Condon dispute this. 25 Those who propound the bilaminar transversalis fascia describe an anterior layer closely related to the aponeurosis of the transversus abdominis and attached inferiorly to the pectineal ligament of Cooper and medially to the rectus sheath. 26 In this scheme, the posterior layer blends superiorly with the linea semicircularis of Douglas and medially with the linea alba, and inserts inferiorly on the superior ramus of pubis. According to Read, the inferior epigastric vessels do not lie in the preperitoneal space proper, but are contained instead between the two layers of the transversalis fascia.22 While the anterior layer of the transversalis fascia is clearly identifiable during anatomical dissections on an embalmed cadaver, the same is not uniformly true for the posterior layer. Other authors have identified the structure that Cooper considered the posterior layer of the transversalis fascia with the preperitoneal fascia, discussed earlier. 1,27.28 Since the transversalis fascia is a layer through which inguinal hernias must pass, it has considerable importance for surgeons. 8 There is, however, significant confusion and uncertainty about the precise role that the transversalis fascia plays in both the origin and the repair of inguinal hernias. 23,29,30 Some authors feel that

Transversalis Fascia External to the preperitoneal space is the endoabdominal fascia. This fascia covers separate muscles, aponeuroses, or becomes attached to the periosteum of interposed bony structures. It acquires

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the transversalis fascia is a thin, weak layer with no intrinsic strength. 7,2l,29 Others argue that a resistant and strong transversalis fascia is essential to the avoidance ofherniation. 8 Indeed, Griffith stated that "the fact that transversalis fascia may be destroyed by large direct hernias in obese elderly men has led to the concept that the transversalis fascia is unimportant. Nothing could be further from the truth. "31 There is general agreement, however, that the deep elements of the abdominal wall, including the transversus abdominis muscle with its aponeurosis and the transversalis fascia, constitute the structure that supports the pressure of the intra-abdominal organs and prevents herniation. 8,32-34 The internal (or deep) inguinal ring is located in the lateral fossa about 1.25 cm above and slightly lateral to the middle of the inguinalligament (Figs. 7.1, 7.4, 7.5A,B, 7.6, 7.7.A,B, 7.9, 7.10, 7.13, 7.14B).29,33,34 It is the internal opening of the inguinal canal, allowing passage of the vas deferens, the testicular vessels and, normally, the genital branch of the genitofemoral nerve. It is usually reported as being 2 cm in circumference, but appears nearly closed when viewed laparoscopically. During fetal development, the testicle descends from its abdominallocation to the scrotum. It is accompanied by an oblique cone of transversalis fascia. 7,29,31 This cone of fascia is oriented inferomedially, but less obliquely than the direction of the cord. It is therefore redundant on the medial side of the cord and forms a sling-shaped, thickened condensation of the transversalis fascia that reinforces the medial aspect of the deep ring. 20 ,34 This is called the transversalis fascia sling; it has superior and inferior extensions known as the superior and inferior crura (Figs. 7.1, 7.7A,B).7,8 This anatomical structure is physiologically important, as it plays a key role in the sphincteric or valvular mechanism of the internal inguinal ring. When the muscular fibers of the transversus abdominis contract, the transversalis fascia moves along with them, displacing the internal ring laterally and cranially under the muscular edge of the internal abdominal oblique. 1,35 This action also causes

PsQlS

the crura to approximate with each other, further reinforcing the closure of the internal ring and preventing indirect herniation. 7,9,33 The iliopubic tract is a fascial condensation connected laterally with the inner lip of the iliac crest, the anterior superior iliac spine, and the iliopectineal arch. It runs parallel to the inguinal ligament, but in a plane posterior to it, crosses the femoral vessels anteriorly and forms an inferior border of the deep inguinal ring before and finally fanning out to attach to the medial portion of Cooper's ligament and the pubic tubercle 21 ,29,33,34,36 (Figs. 7.1, 7.3, 7.4, 7.5A,B, 7.6, 7.7A,B, 7.8, 7.9, 7.10, 7.13, 7.14B, 7.16). From time to time, this structure has been referred to as the "bandelette of Thomson," the "bandelette ilio-pubienne," and the "deep femoral arch." None of these terms is commonly used in North America, where the name "iliopubic tract" has been popularized by Nyhus, Condon, and others. 7,29,37 According to some authors, the iliopubic tract is a tough cord essential for hernia repair. 34,48 Lichtenstein, however, has found it to be of significant strength only in a small number of cases (25%), and does not regard it as a supportive structure. 39,40 In a series of 151 dissections of embalmed inguinal regions and in serial sagittal sections of four body halves, Gilroy and coworkers could identifY a substantial structure corresponding to the iliopubic tract and useful for hernia repair in 42% of the specimens. 41 The pectineal (or Cooper's) ligament is difficult to define since the original description of Sir Astley Cooper23 ,30 has been often modified (Figs. 7.1, 7.4, 7.5A,B, 7.6, 7.8, 7.9, 7.10, 7.14B). Some have described it as the fusion of the periosteum covering the superior ramus of the pubis lateral to the pubic tubercle with the transversalis fascia and the iliopubic tract. 7,21,33,38,42 Others believe it is simply a lateral extension of tendinous fibers from the lacunar ligament. 43 Still others have questioned whether it is appropriate to refer to it as a separate ligament. 21 Regardless of its origin or exact makeup, for practical purposes, the pectineal (Cooper's) ligament is the shiny, fibrous structure covering the superior pubic

minot mUlde - - - - - - - - -

Plo.. ""jOt muscle - - - - - - - - - : . . Ouadr,"'" "mbonJm mlSdl - - - - - ;

E.tetnal oblique musdo - - - InlOrNl oblique muscIo - - - - - - . . ,• •,.

T'",,.,.,susobdOtnlnlsmusclo - - _ IliohypogastJit neM!

----""1

lIloingui....."" -

- -- - -

lIi.lcusmuscio - - -- --

Genitolemotai .."" - - - - ... tetll ..motai"'_""' ..... ---~~ Ing«tinellmh - - --

----remOtllbronch ------~ GeniQlbrallch - - - - - - - - remOtaitino

----------:It

lIiOllUbic tract

-------'""/1

F,mcnl.he.th

lI_olS tendon

_------C-

------""""'11. FIGURE 7.8. Anatomy of the inguinal and femoral region. (See color insert.)

7. Surgical Anatomy of the Inguinal Region

7.9. The internal surface of the lower anterior abdominal wall prepared in a cadaver. The weak areas inside the inguinal triangles through which direct herniations occur, and included between the aponeurotic arch of the transversus abdominis muscle superiorly and Cooper's pectineal ligament inferiorly, are better demonstrated here by transillumination of the lower anterior abdominal wall. The urachus and the bladder have been reflected posteriorly. (See color insert.) FIGURE

"co~oined tendon."7,44 This combination, however, has been found in only 3 to 5% of cases. 7,33,43 In fact, McVay and others have argued that the conjoined tendon does not exist and that it is only an artifact of dissection. 38 ,44 A second physiological system, known as the shutter mechanism, functions in the prevention of direct and indirect herniation. It is activated when, during straining, the internal oblique and the transversus abdominis muscle contract simultaneously and approximate the transversus aponeurotic arch to the iliopubic tract and inguinal ligament, thus reinforcing the posterior wall of the inguinal cana1. 7,9,35 In approximately 25% of individuals, however, the arch cannot descend far enough to reach the inguinal ligament. It may be located too far superiorly or simply be poorly developed. 9,45 In these cases, a portion of the lower deep abdominal wall lacks the reinforcement of the aponeurotic arch and is supported only by the transversalis fascia (Fig. 7.10) .32 The inguinal (or Hesselbach's) triangle is the Achilles heel of the groin (Figs. 7.1, 7.4, 7.5A,B, 7.9, 7.10). According to the original description, its boundaries are the inferior epigastric vessels superolaterally, the rectus sheath medially, and Cooper's ligament inferiorly.8,20,21,34 These borders have been modified since then by the substitution of the inguinal ligament for Cooper's ligament, to allow easier identification of the area by surgeons who use the traditional anterior approach for herniorrhaphy. For the laparo-

ramus. 5 It is easily identified during laparoscopic surgery and in the anatomical dissecting room. The iliopectineal arch is a condensation of the transversalis fascia on the medial side of the iliac fascia. It is attached laterally to the anterior superior iliac spine, and medially with the iliopectineal eminence. It crosses the lateral aspect of the femoral sheath (Figs. 7.1, 7.4, 7.5A,B, 7.7A, 7.8, 7.9, 7.l4B, 7.16). Part of the fibers of the external oblique, the internal oblique, the transversus abdominis muscles, and the iliopubic tract originate from this fibrous structure. The iliopectineal arch is also an important landmark because it divides the medial vascular compartment (lacuna vasorum) and the femoral canal from the lateral muscular compartment (lacuna musculorum) (Figs. 7.8, 7.14B, 7.16) . In the former, the femoral vessels and the femoral canal are found; the latter is occupied primarily by the iliopsoas muscle, but contains also the femoral nerve and the lateral femoral cutaneous nerve (see below) .

Transversus Abdominis Muscle The transversus abdominis muscle takes its origin from the lower six ribs, the lumbodorsal fascia, the iliac crest, the iliopubic tract and the iliopsoas fascia. These fibers pass transversely around the lateral abdomen to the midline, to form part of the lateral abdominal wall. Lateral to the rectus muscle, the fibers of the transversus abdominis insert on a tendinous aponeurosis. The lower fibers cross downward and medially to form an aponeurotic arch that bridges over the superior margin of the internal inguinal ring before inserting at the pubic tubercle and the medial side of the pectineal (Cooper's) ligament (Figs. 7.1, 7.2C, 7.3, 7.5A,B, 7.6, 7.7A,B, 7.9, 7.10) .8 Occasionally, these fibers join with parallel lower fibers of the internal oblique as they insert on the pubic tubercle and the superior ramus of the pubis to form the so-called

7.10. Same preparation as Fig. 7.9. Close-up of the area of the left inguinal (Hesselbach's) triangle: RM = lateral border of the rectus abdominis muscle; LS = linea semicircularis (of Douglas); IE = inferior epigastric vessels; ES = external spermatic (cremasteric) vessels; RV = rectusial vein; CL = Cooper's pectineal ligament; IP = iliopubic tract; VA = umbilical arteries; SV = superior vesical artery; HL = falx inguinalis (or Henle's ligament); AA = aponeurotic arch of the transversus abdominis muscle; VD = vas deferens; IS = internal spermatic (testicular) vessels; PB = anastomotic pubic branch; AP = anterior pubic branch and iliopubic vein; PV = iliopubic vein; RP = retropubic vein; AO = anomalous obturator artery; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; LC = lateral femoral cutaneous nerve; TS = transversalis fascia sling; CI = common iliac artery; IA = external iliac artery; IV = external iliac vein; PA = iliopectineal arch; FN = femoral nerve; PM = psoas major muscle; 1M = iliacus muscle; A = abdominal aorta. The thick arrows point to the deep inguinal ring. The thin arrow indicates the femoral ring. (See color insert.) FIGURE

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scopic procedure, however, it seems more appropriate to return to Hesselbach's original description, since the inguinal ligament is not visible laparoscopically. The inferior portion of the triangle includes the weak area previously seen in the medial umbilical fossa,7,21 where direct hernias develop. Its boundaries are the aponeurotic arch superiorly and the iliopubic tract inferiorly (Figs. 7.1, 7.2C, 7.9, 7.10). Cranial to a line located approximately midway between the umbilicus and the symphysis pubis, called the linea semicircularis,4,8,10 the aponeurotic fibers of the transversus abdominis pass posterior to the rectus abdominis muscle, thus contributing to the formation of the posterior rectus sheath, while caudal to that level they usually cross anteriorly as part of the anterior rectus sheath, leaving the rectus sheath deficient below the linea semicircularis, and the rectus abdominis lined only by the transversalis fascia and the peritoneum (Figs. 7.1, 7.4, 7.9, 7.10). In many cases, the aponeurotic lower portion of the transversus abdominis muscle does not end at the rectus sheath but curves down to insert onto the superior ramus of the pubis.7 This slip is identified by some as the falx inguinalis. 20 ,33,34 According to others, however, the term "falx inguinalis" should be reserved for a vertical extension (sometimes referred to as the ligament of Henle) of the sheath of rectus muscle that occurs in 30-50% of patients. It attaches to the symphysis pubis and Cooper's ligament (Figs. 7.1, 7.9).21,38

Internal and External Oblique Muscles The internal and external oblique muscles form part of the anterior and the lateral abdominal wall. They play a minimal role in inguinal hernia formation, limited to an influence on the direction of a hernial bulge. 21 ,32 The most inferior portion of the aponeurosis of the external oblique forms the inguinal (or Poupart's) ligament, which extends from the anterior superior iliac spine laterally to the pubic tubercle medially. Medially, some of its fibers turn to insert in the pectineal (Cooper's) ligament, thus forming the lacunar (or Gimbernat's) ligament (Fig. 7.9).7,20

Inguinal Canal and Spermatic Cord The inguinal canal is an oblique passage approximately 4 cm long (Fig. 7.11). It begins at the deep inguinal ring and extends downward and medially through a gap in the transversus abdominis and the internal oblique muscles at a point approximately midway between the anterior superior iliac spine and the pubic tubercle to end at the external (or superficial) inguinal ring. This "ring" is actually a triangular opening in the aponeurosis of the external oblique muscle which is located superior to the inguinal ligament and immediately lateral to its insertion on the pubic tubercle. The inguinal canal is limited inferiorly by the inguinal ligament, inferomedially by the lacunar ligament, anteriorly by the aponeurosis of the external oblique muscle, laterally and superiorly by the fibers of the internal oblique muscle and the aponeurotic arch of the transversus abdominus. 20 The posterior wall, between the aponeurotic arch superiorly and the iliopubic tract inferiorly, is formed by the transversalis fascia alone. The inguinal canal is the passageway for the spermatic cord, which is formed at the internal inguinal ring where the vas deferens and the internal spermatic (testicular) vessels join together with a matrix of connective tissue that is continuous with the preperitoneal connective tissue. The processus vaginaliJB,29,33 is the portion of peritoneum that accompanies the testicle during its descent toward the scrotum in embryonic life. Its funicular portion is commonly obliterated in the adult, while the testicular portion constitutes the tunica vaginalis testis. However, 30% to 40% of children three to four months old have a patent processus vaginalis. 46 According to Russell, all indirect inguinal hernias have a congenital origin due to patency of all or part of the processus vaginalis.47 The cord also includes the cremasteric vessels and the artery of the ductus deferens, as well as the genital branch of the genitofemoral nerve and ilioinguinal nerve. The spermatic vein drains blood from the pampiniform plexus, a network of smaller veins within the cord, and empties into the renal vein on the left and into the inferior vena cava on the right. The cord is covered by three layers acquired when crossing the abdominal wall (Fig. 7.11). The internal spermatic fascia is provided

Peritoneum

Deep inguinal ring----HTransversus abdominis mU!;Cle·--.,r\1

Median umbilical ligament Rectus abdominis muscle Pyramidalis muscle

Internal oblique Aponeurosis of external oblique muscle ------'~

Iil,.-,;-o--Superficial inguinal ring

Inguinal _ _ _ _ _ _ _~~~~.p.~~~~~~ ligament Intennediate inguinal ring

External spermatic fascia

Internal spermatic fascia

FIGURE 7.11. The inguinal canal. (Modified from Yaeger W.L. Intermediate inguinal ring. Clin Anatomy, 5:289-295, 1992. Reproduced with permission.)

7. Surgical Anatomy of the Inguinal Region

by the transversalis fascia at the deep inguinal ring and is the innermost layer. The fibers of the cremaster muscle and its investing fascia are derived from the internal oblique muscle and its fascia on the lateral aspect of the inguinal canal: this forms the middle layer. Yeager has proposed the use of the term intermediate inguinal ring to indicate the oval area from which the lower fibers of the internal oblique emerge to form the cremaster layer. 48 Finally, at the external inguinal ring, the external oblique muscle fascia reflects onto the cord, forming the external spermatic fascia.9,2o,33

The Femoral Sheath and Femoral Canal The femoral sheath is a tubular, funnel-shaped expansion of the endoabdominal fascia that encompasses the femoral artery, femoral vein, and the femoral canal in the upper thigh (Figs. 7.8, 7.16). The lateral wall of the sheath is almost vertical, whereas the medial wall points obliquely inferolaterally.3,29 The anterior wall of the femoral sheath is formed by the transversalis fascia and is reinforced by the iliopubic tract. It is important to notice that the inguinal ligament is not in direct contact with the anterior surface of the femoral sheath, since the iliopubic tract is interposed between the two structures. 8,29 Posteriorly, reinforcement is provided by a slip of the pectineus and iliopsoas fascia.8.21.38 The lateral wall is in contact with the iliopectineal arch and is pierced distally by the femoral branch of the genitofemoral nerve. 3,29 The sheath is divided into three compartments by septa of connective tissue. The lateral compartment is occupied by the femoral artery and the femoral branch of the genitofemoral nerve. The femoral vein lies in the middle compartment. The medial area is called the femoral canal (Figs. 7.8, 7.16). It is conical and about 1.25-2 cm long, tapering to the apex at the approximate level of the fossa ovalis. 9.29 Its base is a rigid ring known as the femoral ring (or crural ring, between 0.5 and 1 cm in transverse diameter) (Figs. 7.1, 7.4, 7.9). According to different authors, the anterior border of the femoral ring is either the iliopubic tract or the inguinal ligament, or both. 3,8,9.29 Posteriorly, it is limited by the superior ramus of the pubis, the pectineus muscle and fascia, and Cooper's ligament. The lateral boundary is the femoral vein. The medial border has been considered by many authors to be the lacunar ligament. 3 Recently, however, some authors have stated that the reflected aponeurotic arch of the transversus abdominis onto the pecten pubis,8,38 or the fan-shaped medial insertion of the iliopubic tract onto the pubic tubercle, actually forms the medial border. 7•33 Cadaver dissections performed by us lead us to agree with this latter statement. The femoral canal is located in the most medial portion of the femoral sheath. It is clinically important because it is the outlet for femoral hernias. The proximal entrance to the femoral canal is the femoral ring. It is usually closed by the septum femorale, composed of fatty tissue. 45 The femoral canal contains some connective tissue, small lymph nodes, and lymphatic vessels. A large lymph node, known as the node of Cloquet, is commonly present inside the femoral triangle of the thigh at the end of the femoral canal.

nervation of the lower abdominal wall, the inguinal and genital region, the thigh and the leg, are found in the extraperitoneal space: the ilioinguinal, the iliohypogastric, the genitofemoral, the femoral and the lateral femoral cutaneous (Figs. 7.1,7.4A,B, 7.6, 7.I2B, 7.I3B,C). These nerves originate from the lumbar plexus (T12, Ll, L2, L3, and L4). The iliohypogastric nerve (Figs. 7.1, 7.8) appears at the lateral margin of the psoas muscle and crosses the quadratus lumborum obliquely, passes beneath the inferior pole of the kidney to pierce the transversus abdominis muscle, and then divides into two branches, the most important of which is the anterior hypogastric branch. This branch lies between the external and the internal oblique muscle at the level of the anterior superior iliac spine and reaches the suprapubic skin by piercing either the external oblique aponeurosis or the anterior rectus sheath. 7•20•29 It innervates the skin of the anterior abdominal wall above the pubis (Fig. 7.12). The ilioinguinal nerve (Figs. 7.1, 7.4, 7.5A, 7.8, 7.14B) follows a course similar to that of the iliohypogastric, but more inferiorly. It crosses the quadratus lumborum and the iliacus muscles before piercing the transversus abdominis just above the anterior portion of the iliac crest. Mter piercing the internal oblique, it runs along the inguinal canal, over the cremasteric muscle, and finally exits through the external inguinal ring to innervate the skin of the superomedial portion of the thigh, the root of the penis, the pubic region, and the scrotum or labium m,gus (Fig. 7.12).

iliohypogastric N. Femoral branch of genitofemoral N. - - Ilioinguinal N. - - - Genital branch of genitofemoral N.---~taral femoral cutaneous N. - - - - -

Saphenous N. -------,r-~~~

Innervation Mter removal of the peritoneum covering the lower portion of the posterior abdominal wall, five major nerves responsible for the in-

7.12. Areas of sensory innervation in the lower limb of interest to the laparoscopic herniorrhaphist.

FIGURE

R. Annibali et al.

FIGURE 7.13. Mter an accurate surgical dissection during a laparoscopic hernia repair, the femoral branch of the genitofemoral nerve and the lateral femoral cutaneous nerve have been identified as they approach and pass below the iliopubic tract: IP = iliopubic tract; LC = lateral femoral cutaneous nerve; FB = femoral branch of the genitofemoral nerve. The arrow indicates the enlarged deep inguinal ring, through which an indirect inguinal hernia found its outlet. (See color insert.)

The genitofemoral nerve (Figs. 7.1, 7.4, 7.5A, 7.8, 7.I4B) emerges between fibers of the psoas muscle at the level of the third or fourth lumbar vertebra, and crosses behind the ureter to divide into the genital and femoral branches at a variable distance from the iliopubic tract (Fig. 7.1). The genital branch is medial, traverses the iliac vessels to reach the internal inguinal ring, and runs along the inguinal canal together with the spermatic cord (Figs. 7.1, 7.4, 7.5A,B, 7.7A, 7.8, 7.9, 7.10, 7.14B, 7.15 [See color insert]). The genital branch of the genitofemoral nerve provides motor innervation to the cremaster muscle and sensory innervation to the skin of the penis and scrotum or labia (Fig. 7.12).7,10,20 The femoral branch lies usually on the lateral edge of the psoas muscle, beneath the psoas fascia. It is not constantly a single trunk, and may bifurcate before crossing the deep circumflex iliac artery to pass under the iliopubic tract just lateral to the testicular vessels (Figs. 7.1, 7.4, 7.5A,B, 7.7A, 7.8, 7.9, 7.10, 7.13, 7.14B, 7.15, 7.16). In the femoral sheath, it lies on the lateral side of the femoral artery. After piercing the anterior wall of the femoral sheath and the fascia lata, it reaches the superior portion of the femoral triangle in the thigh and supplies innervation to the femoral triangle and proximal part of the anterior thigh. It provides sensory innervation to the anteromedial surface of the upper thigh (Fig. 7.12). The lateral femoral cutaneous nerve emerges from the lateral margin of the psoas muscle, deep to the peritoneum and iliac fascia, through which it can often be seen (Figs. 7.1, 7.4, 7.5A,B, 7.7A, 7.8, 7.9, 7.10, 7.13, 7.14B, 7.15). It crosses the iliacus muscle obliquely toward the anterior superior iliac spine. Medial to the anterior superior iliac spine, it passes below the iliopubic tract to reach the thigh and divides into two branches. The anterior branch becomes superficial at a variable distance below the ante-

FIGURE 7.14. (A) A = area known as the "Triangle of Doom." B = triangular area where staples may cause nerve entrapment. (B) Cadaver preparation (right side) that shows the structures included within the Triangle of Doom (medial triangle) and the dangerous area beside it, bordered by the internal spermatic (testicular) vessels inferomedially and the iliopubic tract superolaterally (lateral triangle), where no staples or sutures may be placed: B = bladder (reflected posteriorly); CI = common iliac artery; VA = umbilical artery; CL = Cooper's pectineal ligament; PB = anastomotic pubic branch; AP = anterior pubic branch and iliopubic vein; RP =

retropubic vein; ES = external spermatic (cremasteric) vessels; IE = inferior epigastric vessels; VD = vas deferens; IV = external iliac vein; IA = external iliac artery; GN = genitofemoral nerve; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; IPA = iliopectineal arch; V = ureter; IS = internal spermatic (testicular) vessels; DC = deep circumflex iliac vessels; IP = iliopubic tract; FN = femoral nerve; LC = lateral femoral cutaneous nerve; IL = ilioinguinal nerve; PM = psoas major muscle; 1M = iliac muscle; LV = iliolumbar vessels. (See color insert.)

7. Surgical Anatomy of the Inguinal Region

FIGURE 7.15. Mesh correctly positioned and tacked with staples to cover the three weak areas corresponding to the deep inguinal ring, the inguinal triangle, and the femoral ring: VD = vas deferens; IS = internal spermatic (testicular) vessels; IV = external iliac vein; IA = external iliac artery; IP = iliopubic tract; IE = inferior epigastric vessels; RM = rectus abdominis muscle; TM = transversus abdominis muscle; 1M = iliacus muscle; PM = psoas major muscle; PB = anastomotic pubic branch; LS = linea semicircularis; IPA = iliopectineal arch; CL = Cooper's pectineal ligament; DC = deep circumflex iliac vessels; GN = genitofemoral nerve; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; LC = lateral femoral cutaneous nerve; U = ureter; B = bladder (reflected posteriorly) . (See color insert.)

rior superior iliac spine and innervates the skin of the anterior and lateral surfaces of the upper thigh as far as the knee (Fig. 7.16). The posterior branch pierces the fascia lata at a higher level and then runs posteriorly to reach the skin of the lateral aspect of the thigh. The innervated area extends from the greater trochanter to the midcalflevel (Fig. 7.12). The femoral nerve is the largest nerve originating from the lumbar plexus (Figs. 7.1, 7.4, 7.5B, 7.7A, 7.8, 7.9, 7.14B, 7.15, 7.16 [See color insert]). It emerges from the inferior aspect of the psoas muscle, passes along the lateral border, and then runs between the iliacus and pectineus muscles, covered by a layer of fascia. It passes below the iliopubic tract, reaches the femoral triangle within the lacuna musculorum, and finally divides into anterior and posterior branches. The anterior branch originates approximately 8 cm distal to the inguinal ligament and provides the intermediate femoral cutaneous and the medial femoral cutaneous nerves to innervate the skin of the lower anteromedial thigh. The saphenous nerve is the largest sensory branch of the femoral nerve, and continues to the leg to innervate the medial aspect of the leg and the great toe (Fig. 7.13). The posterior branch contains the muscular branches that provide motor innervation to the pectinus, sartorius, and quadriceps.

Anatomical Areas Critical in Laparoscopic Hernia Repair The term "Triangle of Doom," first introduced by Spaw, indicates the triangular area between the vas deferens medially and sper-

matic vessels laterallY; (Fig. 7.14A and B) . Its importance is related to the fact that the external iliac vessels form part of its floor, usually hidden by the peritoneum and the transversalis fascia. To avoid injury to these important structures, the common recommendation is that suturing or stapling be done only medial to the vas deferens or lateral to the spermatic vessels. 5 In our opinion, however, this could lead to the false belief that all m,yor dangers involved in laparoscopic herniorrhaphy are located in that triangular area. As a consequence, the inexperienced laparoscopic surgeon may acquire false confidence when placing the staples needed to hold the prosthetic mesh in place. We believe that the borders of the "dangerous area" should be extended and its contents thoroughly understood. For laparoscopic inguinal herniorrhaphy, the iliopubic tract is an extremely important landmark to identifY if staples are to be safely applied. In fact, lateral to the spermatic vessels and immediately below the fibers of the iliopubic tract, lie the genital and femoral branches of the genitofemoral nerve, the femoral nerve, and the lateral femoral cutaneous nerve. Consequently, staples placed caudal to the iliopubic tract and lateral to the femoral vessels can result in transient or permanent neuralgias involving one or more of the above mentioned nerves or branches. Pain in the groin or lower abdomen indicates injury to the ilioinguinal or the iliohypogastric nerve, whereas pain along the cord and scrotum occurs if the genital branch of the genitofemoral nerve has been damaged. 29 Injury to the iliohypogastric and ilioinguinal nerves is much less frequent during laparoscopic hernia repair than it is in conventional anterior inguinal herniorrhaphy,

FIGURE 7.16. Preparation of the femoral triangle to demonstrate the femoral sheath, iliopectineal arch, and the structures included in the lacuna vasorum and lacuna musculorum. 10 = internal oblique muscle; EO = cut edge of the external oblique muscle; IP = iliopubic tract; LC = anterior branch of the lateral femoral cutaneous nerve; P = iliopsoas muscle; FN = femoral nerve; PA = iliopectineal arch; FB = femoral branch of the genitofemoral nerve; FS = femoral sheath; IL = inguinal ligament (sectioned) ; FV = femoral vein; IS = internal spermatic (testicular) vessels; VD = vas deferens; ES = external spermatic (cremasteric) vessels. The arrow point~ to the opening of the femoral canal. (See color insert.)

since they lie in a plane superficial to the preperitioneal space. On occasion, however, they can be compromised when staples are deeply placed, especially if a vigorous bimanual technique is used. The genital branch of the genitofemoral nerve is not encountered commonly in the area in which staples are applied. It may be damaged, however, by the maneuvers used to reduce the sac of an indirect hernia. In addition, it is not unusual to observe the genital branch passing below the iliopubic tract in the vicinity of the deep inguinal ring to enter the inguinal canal from below. This anatomical variation can put the genital branch in jeopardy. The genital branch of the genitofemoral nerve is probably involved in the painful sensation known as "dysejaculation." This is a rare complication, described in 17 patients repaired by conventional anterior herniorrhaphy, and reported as a painful, burning, or searing sensation in the groin during ejaculation. The onset of the condition is noted at variable times after surgery.49 It may be triggered by distension of the vas deferens by the ejaculate. The femoral branch of the genitofemoral nerve and the lateral femoral cutaneous nerve are those at higher risk of being injured, since they are more superficial (they lie on the anterior surface of the psoas and iliacus muscles respectively) along the course where staples are usually applied to tack the inferior border and the outer corner of the mesh (Figs. 7.5B and 7.15). The femoral nerve is medial and in a relatively deeper position. Although less vulnerable, it may be iryured by staples placed medially and close to the iliopectineal arch, with possible sensory and/or functional consequences: pain in the anteromedial region of the thigh; inability to extend the leg; or quadriceps atrophy. To prevent damage to the nerves, as well as to the external iliac and deep circumflex iliac vessels, we recommend that, lateral to the vas deferens, staples should be placed only above and parallel to the iliopubic tract (Figs. 7.5B, 7.14A and B). In light of the dangers associated with improper placement of staples during herniorrhaphy, it seems appropriate to introduce a new triangular area in addition to the "Triangle of Doom." The boundaries of this second dangerous zone include the testicular vessels inferomedially and the iliopubic tract superolaterally. We recommend that no staples or sutures be applied in this triangle (Fig. 7.14A and B). Medial to the vas deferens, care should also be taken when tacking the inferomedial corner of the mesh. Staples should be applied on Cooper's pectineal ligament only, since staples placed too close to the deep inguinal ring and transversalis fascia sling could damage the terminal portion of the external iliac vein before it passes below the iliopubic tract (Fig. 7.15). Finally, when stapling the mesh to Cooper's ligament, it is important to avoid the anastomotic pubic branch, which usually lies on the lateral portion of the pectineal ligament (Fig. 7.l5).

Conclusion Laparoscopic hernia repair is a new and interesting surgical procedure. The operation is still under evaluation, however, to establish whether it can be considered a viable alternative to conventional hernia repair. More than ever, the words of Cooper are timely and topical: "No disease of the human body belonging to the province of the surgeon requires in its treatment a greater combination of accurate anatomic knowledge with surgical skill than hernia in all its varieties."23

R. Annibali et al.

Acknowledgment Figures 7.1, 7.2, 7.3, 7.4, 7.5, 7.6, 7.7, 7.8, 7.9, 7.lO, 7.12, 7.13, 7.14, 7.15 and 7.16 are reprinted from Annibali R, Fitzgibbons RJ]r., Filipi C, et al., Laparoscopic hernia repair. In Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.

References 1. Lytle W. The internal inguinal ring. Br] Surg. 1945;32:441-446. 2. Ravitch MM. Repair of hernias. Chicago: Year Book Medical Publishers; 1969:9. 3. Zimmermann L, Anson B. Anatomy and surgery of hernia, 2nd ed. Baltimore: Williams & Wilkins Co.; 1967:15. 4. Condon RE. The anatomy of the inguinal region and its relationship to groin hernia. In: Nyhus L, Condon R, eds. Hernia. Philadelphia: JB Lippincott Co.; 1978:14-78. 5. Gaster ]. Hernia: one day repair: Darien, CT: Hafner Publishing Co.; 1970:5-54. 6. Ponka]. Hernias of the abdominal wall. Philadelphia: WB Saunders Co., 1980: 18--39. 7. Skandalakis J, Colborn G, Gray S, et al. The surgical anatomy of the inguinal area-part I. Contemp Surg. 1991;38(1):20-34. 8. Thorek P. Anatomy surgery, 2nd ed. Philadelphia: JB Lippincott Co.; 1962:375. 9. Spaw AT, Ennis BW, Spaw LP. Laparoscopic hernia repair: the anatomic basis.] Laparoendosc Surg. 1991; 1 (5) :269-277. 10. Gullmo A, Broome A, Smedberg S. Herniography. Surg Clin North Am. 1984;64(2) :229-244. 11. Skandalakis J, Colborn G, Gray S, et al. The surgical anatomy of the inguinal area-part II. Contemp Surg. 1991;38(2):28--38. 12. Williams P, Warwick R, Dyson M, et al. Gray's anatomy, 37th ed. Edinburgh, London: Churchill-Livingstone; 1989:1123-1147. 13. Bouchet Y, Voilin C, \Ver R. The peritoneum and its anatomy. In: Bengmark, ed. The peritoneum and peritoneal access. London: Wright; 1989: 1-13. 14. Nomina anatomica: Revised by the International Anatomical Nomenclature Committee, approved by the 11th Congress of Anatomy. Mexico City: Williams & Wilkins Co., 1980. 15. Bendavid R. The space of Bogros and the deep inguinal venous circulation. Surg Gynecol Obstet. 1992;174:355-358. 16. Tobin CE, Benjamin CA, Wells JC. Continuity of the fasciae lining the abdomen, pelvis and spermatic cord. Surg Gynecol Obstet. 1946;83:575596. 17. Arregui ME, Navarrete J, Davis CJ, et al. Laparoscopic inguinal herniorrhaphy: techniques and controversies. Surg Clin North Am. 1993;513527. 18. Pfitzer W. Uber die ursprungverhOltnisse der arteria obturatoria. Anat Anz. 1889;4:504-533. 19. Poynter C. Congenital anomalies of the arteries and veins of the human body, with bibliography. Univ Studies. 1922;XXII:33-35. 20. Edwards EA, Malone PD, MacArthur JD. operative anatomy of abdomen and pelvis. Philadelphia: Lea & Febiger; 1975:44-47. 21. PickJW, Anson BJ, Ashley FL. The origin of the obturator artery. Study of 640 body halves. Am] Anat. 1942;70:317-344. 22. Esser M, Condon R. The surgical anatomy of the groin. Surg Rounds. 1987: (February) 15-27. 23. Read RC. Cooper's posterior lamina of transversalis fascia. Surg Gynecol Obstet. 1992;426-434. 24. Cooper A. The anatomy and surgical treatment of abdominal hernia. London: Longman and Co.; 1804. 25. Cleland J, MacKay JY, Young B]. The relations of the aponeurosis of the transversalis and internal oblique muscles to the deep epigastric artery and to the inguinal canal. In: Memoirs and memoranda in anatomy. London: Williams and Norgate; 1889:142-145.

7. Surgical Anatomy of the Inguinal Region 26. McVay CB, Anson BJ. Composition of the rectus sheath. Anat &c. 1940;77:213-225. 27. Anson BJ, McVay CB. Inguinal hernia. I: The anatomy of the region. Surg Gynecol Obstet. 1938;66:186-191. 28. Lampe EW. Experiences with preperitoneal hernioplasty. In: Nyhus LM, Condon RE, eds. Hernia, 2nd ed. Philadelphia: JB Lippincott; 1978:242-247. 29. Fowler R The applied surgical anatomy of the peritoneal fascia of the groin and the "secondary" internal inguinal ring. Aust N Z] Surg. 1975;45:8-14. 30. Cooper AP. The anatomy and surgical treatment of abdominal hernia. London: Longman and Co.; 1807. 31. Griffith CA. Inguinal hernia: an anatomic-surgical correlation. Surg Clin North Am. 1959;39:531-556. 32. McVay CB. The normal and pathologic anatomy of the transversus abdominis muscle in inguinal and femoral hernia. Surg Clin North Am. 1971;51 (6): 1251-1261. 33. Nyhus LM, Bombeck TC, Klein MS. Hernias. In: Sabiston DC Jr., ed. Textbook of surgery. Philadelphia: W.B. Saunders Co.; 1991:1134-1147. 34. Nyhus LM, Klein MS, Rogers FB. Inguinal hernia. Curr Probl Surg. 1991;6:401-450. 35. Griffith CA. The Marcy repair of indirect inguinal hernia. In: Nyhus LM, Condon RE eds. Hernia. Philadelphia: J.B. Lippincott Co., 1978: 137-162. 36. Lichtenstein IL, Amid PK, Shulman AG. The iliopubic tract. Is it important in groin herniorrhaphy? Contemp Surg. 1992;40:22-24. 37. Nyhus LM. The preperitoneal approach and iliopubic tract repair of

85 inguinal hernia. In: Nyhus LM, Condon RE, eds. Hernia. Philadelphia: J.B. Lippincott Co.; 1978:212-249. 38. McVay CB. The anatomic basis for inguinal and femoral hernioplasty. Surg Gynecol Obstet. 1974;139:931-945. 39. Lichtenstein IL, Amid PK, Shulman AG. The iliopubic tract. The key to inguinal herniorrhaphy? Int Surg. 1990;75:244-246. 40. Lichtenstein I, Shulman A, Amid P, et al. The pathophysiology of recurrent hernia. Contemp Surg. 1992;35:13-18. 41. Gilroy AM, Marks Jr SC, Lei Q, et al. Anatomical characteristics of the iliopubic tract: implications for repair of inguinal hernias. Clin Anat. 1992;5:255-263. 42. Ellis H. Clinical anatomy: a revision and applied anatomy for clinical students, 6th ed. Oxford: Blackwell Scientific; 1977:257. 43. Hollinshead WH. Anatomy for surgeons: the thorax, abdomen and pelvis. New York, NY: Hoeber-Harper; 1961:240--268. 44. Sorg J, Skandalakis JE, Gray SW. The emperor's new clothes or the myth of the conjoined tendon. Am Surg. 1979;45:588-589. 45. Skandalakis JE, Gray SW, Skandalakis LJ, et al. Surgical anatomy of the inguinal hernia. World] Surg. 1989;13:490-498. 46. Keith A. Human embryology and morphology. London: Arnold; 1923. 47. Russell RH. The saccular theory of hernia and the radical operation. Lancet. 1906;2:1197-1203. 48. Yeager VL. Intermediate inguinal ring. Clin Anat. 1992;5:289-295. 49. Bendavid R "Dysejaculation": an unusual complication. Postgrad Gen Surg. 1992;4(2):139-141. 50. Schaffer JP. Morris' human anatomy, 11th ed. New York: The Blakiston Co.; 1953:1348-1358.

8 Fascial Anatomy of the Inguinal Region Jonathan D. Spitz and Maurice E. Arregui

Introduction The overwhelming majority of all hernias in humans occur in the area of the inguinal canal and the femoral canal. Approximately 750,000 inguinal hernias are repaired annually in the United States. In the past, most were repaired by an anterior approach. Consequently, most surgeons are familiar with the inguinal anatomy from the anterior perspective. As laparoscopic techniques were applied to inguinal hernia repair, it became important to understand the inguinal anatomy from a new and largely unfamiliar preperitoneal perspective. The recent literature on laparoscopy describes the musculoaponeurotic, vascular, and nervous structures of the inguinal area from a transabdominal or preperitoneal vantage point. However, there remains significant confusion regarding the transversalis fascia and the multilayered preperitoneal fascia. The etiology of inguinal hernia involves the transversalis fascia, the peritoneum, and the preperitoneal fascia. The latter two structures are especially important in the case of congenital indirect hernias that develop as a consequence of a patent processus vaginalis. There is also a general misunderstanding regarding the presence of the posterior rectus sheath below the level of the arcuate line. The purpose of this chapter is to describe the peritoneum and its landmarks, the preperitoneal fascial layers, and the importance of the posterior rectus space and posterior rectus sheath. The fact that the posterior rectus space is distinct from the true preperitoneal space is a key anatomic concept. The focus of this chapter will be to maintain clinical relevance for the practicing surgeon by using photographs taken at the time of laparoscopic surgery to illustrate important aspects of the inguinal anatomy.

Inguinal Preperitoneal Anatomy The authors' appreciation of the anatomy of the preperitoneal fasciae and spaces is derived from extensive experience with laparoscopic inguinal herniorrhaphy. During laparoscopic exploration, structures are magnified, and the multiple fascial planes are more clearly defined than with open preperitoneal surgery. In addition to detailed laparoscopic dissection, we have reviewed the literature, including anatomic textbooks and atlases. The author (M.E.A.) has limited experience with dissections in fresh cadavers,

86 R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

but has in any case found this approach suboptimal because of postmortem changes that obscure the subtle preperitoneal fascial tissue planes, making them more difficult to follow and distinguish.

Surface Characteristics of the Peritoneum in the Inguinal Region The peritoneal surface of the anterior abdominal wall in the lower abdomen has several prominent landmarks. These include the median umbilical ligament which is the obliterated embryonic urachus connecting the fundus of the bladder to the umbilicus, the paired medial umbilical ligaments which are the obliterated umbilical arteries, and the paired lateral umbilical ligaments which represent the prominence created by the inferior epigastric vessels and accompanying fat (Fig. 8.1).1 Just lateral to the epigastric vessels is the true internal ring which is identified by the convergence of the vas deferens and the spermatic vessels as they penetrate the transversalis fascia. The transverse vesicular fold can be seen superomedially to the internal ring and is a thickened band of peritoneum and subperitoneal fibrosis that extends from the posterior aspect of the bladder to the lateral abdominal wall (Fig. 8.2). 2 Between the median and medial umbilical ligaments lies the supravesical fossa in which the infrequent supravesical hernia may occur. A direct hernia is located between the medial umbilical fold and the lateral umbilical fold or epigastric vessels. The indirect hernia is located lateral to the inferior epigastric vessels at the site of the internal ring. A patent processus vaginalis is often seen as a dimpling of the peritoneum just anterior to the site of convergence of the vas deferens and the spermatic vessels. Occasionally, an indirect hernia will be identified lateral to the epigastric vessels, but medial to the internal ring. We have named this defect an acquired indirect hernia. The etiology of an acquired indirect hernia is from a weakness in the lateral aspect of the transversalis fascia (Fig. 8.3). This is in contradistinction to a congenital indirect hernia that develops because of a patent processus vaginalis. The magnified laparoscopic view of the anterior abdominal wall offers an excellent view of the peritoneal lining, its rich blood supply, and the shallow fossae created by the embryonic ligaments mentioned above. The vasculature of the peritoneum and the vas deferens is derived from the internal iliac artery, whereas the blood

8. Fascial Anatomy of the Inguinal Region

FIGURE 8.1. Laparoscopic view of the right groin in an elderly female. The small peritoneal indentation lateral to the inferior epigastric vessels is the site of the internal ring where the round ligament enters the inguinal canal: MUL = medial umbilical ligament; OU = obliterated urachus or median umbilical ligament; IE = inferior epigastric vessels or lateral umbilical ligament; 1VF = transverse vesicular fold; BL = bladder; CL = Cooper's ligament; IR = internal ring; RL = round ligament. (Reprinted from Annibali R., et al. Anatomical Considerations for Laparoscopic Inguinal Herniorrhaphy, in: Principles of Laparoscopic Surgery. New York: Springer-Verlag; 1995, with permission.)

supply to the anterior abdominal wall originates from the inferior epigastric vessels (Fig. 8.4). This fact is important to consider when developing the preperitoneal space during a laparoscopic extraperitoneal hernia repair, as this is a relatively avascular plane between the posterior rectus sheath and the umbilical prevesical fascia (Fig. 8.5). At the inferior aspect of the umbilicus, the umbilical ligaments converge and penetrate the transversalis fascia. In an identical manner, the falciform ligament exits the transversalis fascia at the

FIGURE 8.2. Laparoscopic view of the right groin in a male. There is a small patent processus vaginalis (arrow) that marks the site of the true internal ring: MUL = medial umbilical ligament; IE = inferior epigastric vessels or lateral umbilical ligament; 1VF = transverse vesicular fold; VD = vas deferens; SV = spermatic vessels. (Reprinted from Annibali R. , et al. Anatomical Considerations for Laparoscopic Inguinal Herniorrhaphy, in: Principles of Laparoscopic Surgery. New York: Springer-Verlag; 1995, with permission.)

FIGURE 8.3. An acquired indirect hernia. The etiology of this hernia is from a weakness in the lateral transversalis fascia rather than from a congenitally patent processus vaginalis. MUL = medial umbilical ligament; IE = inferior epigastric vessels; IR = internal ring.

superior aspect of the umbilicus. There is a condensation of transverse fibers that reinforce the umbilicus. These fibers have been called the umbilical fascia.1.3 If these fibers are absent or attenuated, then an umbilical hernia can develop. In the lower quarter of the abdominal wall there is a point of transition as the aponeuroses of the three flat muscles pass primarily anterior to the rectus muscle. However, this point of transition is not complete. There is a continuation of the posterior rectus sheath into the pelvis to the level of the pubis and Cooper's ligament. The point at which some of the aponeurotic fibers alter their course anteriorly is the arcuate line or the linea semicircularis. This line is clearly visible with the laparoscopic perspective. It is well demarcated if the change is abrupt, while it is less defined if there is a gradual change (Fig. 8.6A and B). Externally, the linea semicircularis corresponds to a line roughly 2 cm inferior to the transverse plane created by the umbilicus.

FIGURE 8.4. The rich vasculature of the peritoneum. These are branches of the vesical arteries originating from the internal iliac artery. A Foley catheter is in the bladder. (Reprinted from Annibali R., et al. Anatomical Considerations for Laparoscopic Inguinal Herniorrhaphy, in: Principles of Laparoscopic Surgery. New York: Springer-Verlag; 1995, with permission.)

J.D. Spitz and M.E. Arregui

FIGURE 8.5. The blood supply to the preperitoneal fascia and bladder is separate from the blood supply to the anterior abdominal wall. The plane between the umbilical prevesical fascia and the anterior abdominal wall is a bloodless plane. (Reprinted from Pernkapf Anatomy, Vol. 2, 3rd ed. Fig. 263. Urban & Schwarzenberg; 1989, with permission.)

Preperitoneal Fasciae When performing a laparoscopic extraperitoneal hernia repair, the surgeon's aim is to develop the plane superficial to the peritoneum and umbilical prevesical fascia within the true preperitoneal space. This space is in direct communication with the space of Retzius inferior to Cooper's ligament. 4 The posterior rectus space is distinct from this preperitoneal space, the two being separated by the posterior rectus sheath (Fig. 2.2 in Chapter 2). The former is easily entered just below the level of the umbilicus while the latter is intimately fused with the peritoneum at this level. During laparoscopic extraperitoneal hernia repair we initially enter the posterior rectus space. The rectus muscle and the inferior epigastric vessels are maintained anteriorly and the attenuated rectus

A FIGURE 8.6. (A) A well-demarcated arcuate line in a thin elderly patient. (B) The transverse fibers of the posterior rectus sheath are clearly seen extending below the arcuate (semicircular) line. These fibers become fewer and more attenuated toward the groin. (Reprinted from Arregui,

sheath posteriorly. By breaking through these attenuated fibers just above Cooper's ligament we enter the preperitoneal space. Because there remains significant confusion regarding the existence of the posterior rectus sheath caudal to the umbilicus, a description of the rectus fascia is appropriate here. The covering of the rectus muscle is composed of the aponeuroses of the external and internal oblique muscles and the transversus abdominis muscles. It was formerly widely held that the aponeuroses of the abdominal wall muscles were composed of only one lamina each. This lamina was thought to proceed unilaterally to the midline to contribute to either the anterior or posterior rectus sheath. The midline was the end-point of the aponeuroses as there was not thought to be significant crossing of fascial fibers at the linea alba. Furthermore, the posterior rectus sheath was considered absent

B M.E. Surgical Anatomy of the Preperitoneal Fascia and Posterior Transversalis Fasciae in the Inguinal Region, in: Hernias and Surgery of the Abdominal Wall, New York: Springer-Verlag; 1998, with permission.)

8. Fascial Anatomy of the Inguinal Region

below the arcuate line. All fascial fibers were thought to pass anterior to the rectus muscle, contributing only to the anterior rectus sheath. Our current understanding of the composition of the rectus sheath is largely the result of the work of Rizk and Askar. 5.6 These authors independently reported their anatomical observations of the anterior abdominal wall, and in doing so changed long held traditional concepts concerning the formation of the rectus sheath. They depicted a bilaminar composition of the abdominal wall flat muscles with each layer contributing fibers to the contralateral side. According to Rizk, the linea alba should be considered less the insertion of the abdominal muscles, but more the common area of decussation of their intermediate aponeuroses. 5 Consequently, the rectus sheath was recognized to be a trilaminar structure with decussating components from the external and internal oblique muscles and the transversus abdominis. They described a "plywood"-like arrangement of the rectus sheath. 5 Physiologically, this plywood arrangement explains the intimate approximation of the adjacent layers without actual fusion that would interfere with free mobility of the abdominal wall. The magnified laparoscopic view of the anterior abdominal wall has also revealed that while the arcuate line is a point of transition, it is not complete. There are transverse fibers of the posterior rectus sheath that continue to the pubis and Cooper's ligament. Supporting this observation, Anson, Morgan and McVay have described the low linea semicircularis that results from the posterior fibers of the rectus sheath. Frequently, some of the lower aponeurotic fibers of the transversus may pass posterior to the rectus, gaining attachment to the caudal part of the linea alba and to the pubis. 7 The sheath is of variable thickness, which likely accounts for the inconsistent anatomical descriptions in the literature. In summary, the arcuate line is not an absolute point of termination of the posterior rectus sheath. Rather, the posterior rectus sheath continues in an attenuated form to Cooper's ligament. It is typically multilayered and of variable thickness. Its existence below the level of the arcuate line is indisputable.

A FIGURE 8.7. (A) Preperitoneal view of the right groin. The transversalis fascia (TF) forms a theoretical sling around the cord structures at the internal ring. The umbilical prevesical fascia envelops the cord structures and continues as the internal spermatic fascia (SF). The internal spermatic fascia is distinct from the fibers of the transversalis fascia. IE = inferior epigastric vessels. (B) Opening the internal spermatic fascia (SF) permits

Superficial to the peritoneum are areolar tissue, vasculature, umbilical ligaments, and the preperitoneal fasciae. The preperitoneal fascia in this area is called the umbilical prevesical fascia, (UPF) which is discrete from the posterior lamina of the transversalis fascia discussed later. The space between the UPF posteriorly and the posterior lamina of the rectus sheath and transversalis fascia anteriorly is the preperitoneal space. The space between the peritoneum and the UPF contains a typically small, but variable amount of adipose tissue that surrounds the median umbilical ligaments, bladder, and blood supply. If this fascial layer is mistakenly entered medial to the medial umbilical ligament, there is risk of injury to the bladder. The UPF is the investing layer of the bladder medially and the spermatic cord laterally (Fig. 2.6 in Chapter 2). Contained within the umbilical prevesical fascia is the indirect hernia sac, if one is present. The UPF continues with the cord structures as they enter the inguinal canal, where it is called the internal spermatic fascia (Fig. 8.7A and B). Tobin pointed out that the connective tissue between the peritoneum and the body wall forms a continuous lining for the abdomen, pelvis, and spermatic cord. 8 This connective tissue is dissectable as three strata: an inner stratum associated with the digestive system, an intermediate stratum embedding the adrenals, urogenital system, the aorta, and vena cava, and an outer stratum, which is the intrinsic fascia of the components of the abdominal wall. 8 In the region of the kidney, the intermediate layer thickens and is known as Gerota's fascia. Caudally, this layer covers the spermatic vessels and ureters and is continuous with the connective tissue of the bladder (umbilical vesical fascia) . At the level of the internal inguinal ring, the intermediate stratum around the vas deferens and the indirect hernia sac continues as the innermost layer of the spermatic cord, the internal spermatic fascia. The spermatic fascia descends upon the spermatic cord or the round ligament of the uterus in the female as they emerge from the inguinal canal. In the male subject, this fascia descends to the lower part of the testicle, completely surrounding both it and the cord.g

B access to the indirect hernia sac if one is present, the vas deferens, and the spermatic vessels. (Reprinted from Arregui M.E., DulucqJ.L., Tetik C., et al. Laparoscopic Inguinal Hernia Repair with Preperitoneal Prosthetic Replacement, in: Bendavid R. , ed. Prostheses and Abdominal Wall Hernias. Austin: R.G. Landes Company; 1994.)

J.D. Spitz and M.E. Arregui

Posterior Lamina of the Transversalis Fascia Any attempt to clearly define the transversalis fascia based upon descriptions in the literature will convince the reader that this structure is many different things to many different people. This

_....... -_

fascia is the source of much disagreement in spite of the fact that Anson described it as the most effective barrier against direct herniation,7 and Condon states that a groin hernia is a defect in the transversus abdominis, the muscle covered by transversalis fascia.lO Cooper originally described the transversalis fascia as that structure covering the internal surface of the transversus abdominis muscle. ll He reported that it is a bilaminar structure composed

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C'.

8.8. (A) In this anatomical drawing, the layer continuous with the posterior rectus sheath caudad to the arcuate line is labeled the transversalis fascia. (Reprinted from Taylor A.N., ed. Atlas of Human Anatomy. Vol. 2, 11th English ed., Fig. 105. Urban & Schwarzenberg, 1990, with permission.) (B) In this anatomical drawing, the layer con· tinuous with the posterior rectus sheath caudad to the arcuate line is labeled the posterior rectus sheath. (Reprinted from Pernkopf Anatomy, Vol. 2, 3rd ed. Fig. 178, Urban & Schwarzenberg; 1989, with permission.) Both drawings demonstrate that this fascial layer is dis· tinct from the preperitoneal fascia covering the bladder and umbilical ligaments. FIGURE

8. Fascial Anatomy of the Inguinal Region

of a posterior and an anterior lamina. The inferior epigastric vessels course between these two laminae immediately after their takeoff from the external iliac vessels. 12,13 McVay criticized various attempts at herniorrhaphy by emphasizing the importance of the transversalis layer stating, " ... methods of hernioplasty are still used which fail to correct the defect in the transversus abdominis aponeurosis; or they utilize more superficial layers which are of only secondary importance."14 Condon gives further significance to the transversalis fascia by describing a fascial fold around the internal inguinal ring. This is the so-called transversalis fascia sling that provides the functional basis for the inguinal shutter mechanism. 10 Theoretically, with contraction of the transversus abdominis muscle as in coughing or abdominal exertion, the fascial sling is drawn laterally. By increasing the angle of egress of the spermatic cord, the sphincter mechanism is thought to protect against the forces of increased intra-abdominal pressure. 10,15 While the indirect inguinal hernia represents a persistence of the processus vaginalis through the internal inguinal ring with the protrusion of omentum or abdominal viscus into the preformed sac, direct and femoral hernias occur because of a weakness of the transversalis fascia in the region of the posterior inguinal wall. In contrast to the small indirect hernia, the problem here is the loss of suitably strong tissue. Certainly some of the controversy that surrounds precise definition of the posterior lamina of the transversalis fascia stems from the fact that, lateral to the medial umbilical ligaments, there is very little preperitoneal fat. Consequently, the peritoneum, preperitoneal fascia, and posterior lamina of the transversalis fascia are fused, making their individual distinction difficult. However, with the improved optics and magnification afforded by the laparoscope, we have seen, as mentioned earlier, that the posterior rectus sheath continues in a variably attenuated fashion below the arcuate line. We are also able to see that the posterior rectus sheath is comprised of more than one layer in this caudal location inferior to the umbilicus. The multilaminar constitution of this layer supports the contention that this is not only an attenuated rectus sheath, but also it contains the posterior lamina of the transversalis fascia. It has been our contention that this multilaminar fasciallayer is, in fact, the continuation of the posterior rectus sheath with the underlying posterior lamina of the transversalis fascia (Fig. 8.8A,B). Simply stated, in the inguinal area the interior lining of the transversus abdominis muscle has fascial contributions of transversalis fascia and posterior rectus fascia. 2

Conclusions The posterior dissection serving as the early model of the laparoscopic preperitoneal inguinal hernia repair can perhaps be first attributed to the work of Cheatle in 1920. 16 He proposed that by developing the preperitoneal space of Retzius, the surgeon could offer a definitive repair of femoral hernia. Unfortunately, Cheatle's approach gained little notoriety, and the preperitoneal dissection remained largely unknown for decades. The introduction of mesh in 195817 and the subsequent preperitoneal placement of the prosthesis by surgeons such as Stoppa, Wantz, and Nyhus,18,19,20 heralded a new era in the surgical management of inguinal hernia. The most recent development in the field of hernia surgery has been the application of laparoscopic techniques. The laparoscopic preperitoneal dissection and placement of mesh simulate the sutureless repair advocated by Stoppa. 18 However, because

most surgeons are unfamiliar with the fascial planes of the preperitoneal space from the laparoscopic perspective, the procedure has been difficult for most surgeons to perform. Consequently, there has been slow acceptance of this technique. Much of the confusion regarding the preperitoneal fascia, the posterior rectus fascia, and the transversalis fascia may stem from the erroneous anatomical preconception that all fibers of the rectus sheath pass anterior to the rectus muscle below the arcuate line. As comprehensive knowledge of the preperitoneal fascial anatomy becomes more widespread, there likely will be a broader application of the laparoscopic preperitoneal hernia repair.

References 1. Skandalakis]E, Gray SW, Skandalakis LJ, Colborn GL, Pemberton B. Surgical anatomy of the inguinal area. WurldJ Surg. 1989; 13:490-498. 2. Arregui ME. Surgical anatomy of the preperitoneal fascia and posterior transversalis fascia in the inguinal region. Hernia. 1997;1:101-110. 3. Chevrel JP. Anatomie clinique. le tronc. Springer-Verlag, Paris Berlin Heidelberg New York 1994;108-109. 4. Bogros JA. Essay on the surgical anatomy of the iliac region and description of a new procedure for the ligation of the epigastric and external iliac arteries. Translated by Bendavid RA. Postgrad Gen Surg. 1996;6:4-15. 5. Rizk NN. A new description of the anterior abdominal wall in man and mammals. ] Anat. 1980;131:373-385. 6. Askar OM. Aponeurotic hernias. Recent observation upon paraumbilical and epigastric hernias. Surg Clin North Am. 1984;64:315-333. 7. Anson BJ, Morgan EH, McVay CB. Surgical anatomy of the inguinal region based upon a study of 500 body-halves. Surg Gynecol Obstet. 1960;3:707-725. 8. Tobin CE, Benjamin JA, Wells JC. Continuity of the fasciae lining the abdomen, pelvis, and spermatic cord. Surg Gynecol Obstet. 1946;83: 575-596. 9. Morton T, Cadge W. Surgical anatomy of inguinal herniae. In: The surgical anatomy of the principal regions of the human body. London: Taylor, Walton and Maberly; 1850. 10. Condon RE. Surgical anatomy of the transversus abdominis and transversalis fascia. Ann Surg. 1971;173:1-6. 11. Cooper A. The anatomy and surgical treatment of abdominal hernia. London: Longman and Co.; 1804. 12. Read RC. Cooper's posterior lamina of transversalis fascia. Surg Gynecol Obstet. 1992;426-434. 13. CleiandJ, MacKay.JY, Young BJ. The relations of the aponeurosis of the transversalis and internal oblique muscles to the deep epigastric artery and to the inguinal canal. In: Memoirs and memuranda in anatomy, voL l. London: Williams and Norgate; 1889:142-145. 14. McVay CB. The normal and pathologic anatomy of the transversus abdominis muscle in inguinal and femoral hernia. Surg Clin North Am. 1971;51 :6: 1251-1261. 15. Spangen L. Shutter mechanisms in the inguinal canal. In: Arregui ME, Nagan RF, eds. Inguinal hernia: advances ur controversies? Oxford: Radcliffe Medical Press; 1994;55-60. 16. Cheatle GL. An operation for the radical cure of inguinal and femoral hernia. BrJ Surg. 1920;2:168. 17. Usher FC, Oschsner J, Tuttle LL. Use of Marlex® mesh in the repair of incisional hernias. Am Surg. 1958;24:653. 18. Stoppa R, Petit I, Henry X. Unsutured Dacron® prosthesis in inguinal hernias. Int Surg. 1975;60:411-412. 19. Wantz GE. Giant prosthetic reinforcement of the visceral sac. Surg GynecolObstet. 1989;169:408-417. 20. Nyhus LM. The preperitoneal approach and iliopubic tract repair of inguinal hernia. In: Nyhus LM, Condon RE, eds. Hernia, 3rd ed. Philadelphia: J.B. Lippincott Co. 1989;154-188.

9 The Ligaments of Cooper and Thomson J.P. Richer, J.P. Faure, M. Carre tier, and Jacques Barbier

Introduction The surgery of groin hernias can be considered in two stages: the handling of the hernial sac, which necessitates dissection, resection, and reduction, and the parietal reconstruction, which calls upon the existing anatomical structures. Prosthetic material may be required to bridge a defect when the dissection is completed and the structures identified to which a prosthesis might be anchored. In man, the inferior borders of the internal oblique and transversus muscles are far removed from the pubic ramus and its pectineal ligament of Cooper. There exists between them an area called the myopectineal orifice, covered by the transversalis fascia and its reinforcements. This is a zone of relative weakness, divided by the inguinal ligament into two parts, inferior (femoral) and superior (inguinal). On the posterior aspect of the inguinalligament, the transversalis fascia consolidates inferiorly into a tract, the iliopubic bandelette of Thomson. These substantial anatomic structures (the pectineal ligament of Cooper, the posterior portion of the inguinal ligament, the iliopubic tract of Thomson) are the key structures used in several herniorrhaphy procedures. "There cannot be any surgery of groin hernias without a close look at the anatomy of the inguinal area."l

History

The Pectineal Ligament In 1543, Vesalius 2 described the os coccyx, the abdominal wall and the inguinal area. In 1561, Franco,3 in his treatise on herniae, shows an interest in their treatment. It is to Sir Astley Cooper that we owe the first description, in 1804, of the ligament of the pubis: "The pubis is covered by a ligamentous expansion, which forms a remarkable strong ridge above the iliopectineal line, extending from the spine of the pubis outwards, jutting above the bone along that line. "4,5 This area of the groin has been particularly well studied because of its surgical importance, and the pectineal ligament of Cooper has been the subject of several descriptions. Its morphological significance and its origin remain nevertheless quite controversial. Charpy, in 1891, wrote: "The pectineal crest of the pubis is a con92 R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

fluence of several fibrous parts: the aponeurosis of the pectineus, and, behind, the ligament of Gimbernat, the posterior crus of the inguinal ring . . . and lastly, the transversalis fascia reinforced by the ligaments of Henle and Hesselbach .... "6-8 Testut, in 1911, identified elements arising from the "adminiculum linea alba."9 Bardeleben, in 1912, considered the ligament of Cooper to be a thickening of the pectineal muscle fascia reinforced by fibers from various origins: interfoveolar ligament, falx inguinalis, Colles' ligament, as well as fibers from the conjoined tendon, from the psoas minor, and elements from the adminiculum linea alba.l° The conception that the ligament of Cooper originates as a thickening of the fascia of the pectineus muscle along the bony crest of the pubis was taken up and further elaborated upon by Rouviere in France in 1924.n Seelig and Chouke, between 1914 and 1927, displayed an interest in the surgical anatomy of this area. 12 McVay and Anson, between 1938 and 1950, brought together all the known facts from the United States and Europe and confirmed that the fascia transversalis descended as far as the ligament of Cooper and the femoral vascular sheath.l3-18 Aubaniac and Fortessa, in 1952, recognized the contribution of fibers from the psoas minor in the constitution of this ligament. 19 Since then, all publications, particularly those of Mattson,20 Clark and Hashimoto,21 Donald,22 and Burton23 have underlined the solid adhesion of the ligament of Cooper and its remarkable strength. Fruchaud, in 1956, emphasized this solidity and the surgical interest of its morphology.1

The Iliopubic Tract (Bandelette of Thomson) Winslow (1732) and Gunz (1744) identified a bandelette or "strap" extending from the iliac crest to the pubic spine at the inguinal level of the external oblique aponeurosis. Allan Bums, in 1802, identified this bandelette as an extension of the fascia iliaca at the posterior border of the ligament of Poupart. Hesselbach (1806) provided the first description of the iliopubic tract as the most substantial fibers of the internal aspect of the inguinalligament. 24 It is to Alex Thomson, in his thorough treatise on the anatomy of the lower abdomen and hernias, that we owe the description of this fibrous structure. Interested in the "femorovascular-funnel," he wrote: "The inferior border of this portion of the pectineofemorovascular sheath is substantially beyond an inch in size and

9. The Ligaments of Cooper and Thomson

blends with the eccentric layers of the femoral vessels as far as the upper level of the saphenous vein. This tract is nearly parallel to the anterior aspect of the thigh. Its fibers fan out from outside-in from the midportion of the said sheath. The fibers of the bandelette are parallel to the superior border of the anterior vascular sheath, enlarging considerably posteriorly and superiorly to attach between two bundles of the ligament of Cooper on the internal third of the crest of the pubic bone and on the lateral half of the anterior border of the superior aspect of the body of the pubis. This bandelette, with its own fibers of the lateral half of the ilio-femoral-vascular fascia, is named the iliopubic tract. "24

The Ligaments of Cooper and Thomson in Hernia Surgery By the end of the 1800s, the iliopubic tract and pectineal ligaments were used in the surgical treatment of hernias. In 1888, Bassini proposed to suture the conjoined tendon to the iliopubic tract in the treatment of inguinal hernias. 25 .26 This technique is repeated by several authors throughout the world but modified by fixation not to the iliopubic tract, but to the shelving edge of the inguinal ligament. The ligament of Cooper was first used by Ruggi in 1892 in the treatment of a femoral hernia by approximating and suturing to it the inguinalligament. 27 In 1897, Lotheissen was the first to suture the conjoined tendon to the ligament of Cooper during the repair of recurrent hernia. 28 The classical and artificial description of the inguinal and femoral areas as two separate entities was abandoned by the beginning of the 20th century by modem authors who perceived a single anatomical and functional entity in this area. 1 Since then, McVay and Anson have promoted throughout the U.S. and Europe the technique whereby the conjoined tendon is sutured to the ligament of Cooper for all hernias of the groin. 15.16 Laparoscopic approaches, both extraperitoneal and transperitoneal, are being used with increasing frequency in abdominal surgery.29-32 Structures that are normally visible from the anterior viewpoint, such as the inguinal ligament, pubic tubercle, and lacunar ligament, cannot be seen laparoscopically.29,31 Laparoscopic dissection and hernia repair requires precise knowledge of the anatomic relationships. The surgeon is oriented by identifYing specific anatomic landmarks: the inferior epigastric vessels, the obliterated umbilical artery, spermatic vessels, Cooper's ligament, and the iliopubic tract. 31 .32

Comparative Anatomy The evolution of the pelvic girdle in mammals, and more particularly in primates, yields evidence of complex anatomical and functional factors: acquisition of an erect posture, support of abdominal viscera, functions of evacuation and parturition (the human newborn is oflarge size).1,33 In quadruped domestic mammals, the pelvic girdle is narrow transversely, but elongated in the craniocaudal direction. The iliac bone of these animals is formed parasagitally with its long axis almost parallel to the spinal cord. Its lower and ventral border is barely rounded, and the pectineal crest barely developed. The pubic symphysis, though protruding, is hidden between the roots of

the thighs. The abdominal wall presents a pronounced dorsoventral diameter and provides a hammock for the abdominal contents. The inguinal canal has a lengthy course within the muscles of the abdominal wall. The cord and the femoral vessels, small in size, are closely wrapped by the muscular fibers of the internal oblique and transversus abdominis, which compress them against the barely hollowed out anterior border of the iliac bone. The pectineal crest is very short. The small ring, closed off by a resistant fascia which joins the vascular sheath, narrows further yet during strains or increased abdominal pressure, by the contraction of the muscular arch formed by the internal oblique and the transversus. The aponeurosis of the external oblique is closely joined by the femoral aponeurotic sheath. 33 In primates, and in man especially, the erect posture is linked to functional and morphological modifications of the pelvis. In man, one can observe a ventral tilt, an increase in width, a lesser height and frontalization of the pelvis, a flaring of the sacral bones simulating a funnel for the abdominal viscera, a lengthening of the iliac crest accompanied by a widening of the iliac alae. The anterior superior iliac spine seems to project forward and downward, and the anterior border of the iliac bone, between the anterior superior iliac spine and the pubic spine, seems to shorten and hollow out. The muscles of the inferior limb are considerably developed: gluteus, psoas, quadriceps, and adductors. These insert on the iliac bone along with the abdominal muscles. 33 With the erect position of the pelvis on the thighs, the inguinal crease opens up. It becomes shallow, almost transverse, and short. On a deeper plane, the hollowed out sacral bone provides room for the well-developed psoas and the femoral vessels, the caliber of which has increased to accommodate the size and function of the inferior limb. The inferior borders of the internal oblique and transversus are more aponeurotic and situated on a higher plane. The pecten of the pubis lengthens inward. Stretched vertically and transversely, the inguinal region is therefore poorly adapted to resist increased abdominal pressure. The wide myopectineal orifice is sealed by connective tissue, the transversalis fascia, and its reinforcements. This fascia courses along the inferior border of the transversus to blend with the iliofemoral sheath. The aponeurosis of the external oblique, whose inferior border inserts into the anterior superior iliac spine and the pubic spine, does not entirely shield the myopectineal orifice and does not descend to the pubis. In man, this inguinofemoral region is weakened further yet by the aponeurotic and tendinous nature of the muscular margins. 33,34 Several phylogenetic hypotheses may be proposed for the ligament of Cooper. The pectineal ligament of Cooper, through its morphology and thickness, may playa protective role for the vessels, as it blunts the cutting edge of the bony pecten of the pubis (this bone-vessel juxtaposition is not unique to man). The ligament is present in several mammals, notably quadrupeds. From the phylogenetic viewpoint, it would seem that the pectinealligament is linked to the considerable development of the pectineus muscle, which plays a major role in maintaining equilibrium in the erect posture.

Surgical Anatomy The groin, classically divided into inguinal and femoral regions, is in fact a single anatomical and functional entity. The modem

anatomists, Anson,13,14 McVay,15-18 Fruchaud,l and Keith35 have shown that the groin must be visualized in the standing position, live and during strain. The weaker layer through which inguinal, and also femoral, hernias emerge, is delineated above by the inferior margin of the internal oblique; below, by the pecten of the pubis with its overlying ligament of Cooper; medially by the lateral border of the rectus and laterally by the psoas (Fig. 3.1). This myopectineal opening is partially covered superficially by the aponeurosis of the external oblique, the lower margin of which provides the inguinal ligament. The latter is far removed from the bony frame of the groin. Thus, the stretched aponeurotic cover does not extend to the bony structures nor to the pectineal ligament, and it is further weakened by the opening of the superficial inguinal ring. In fact, only the transversalis fascia covers the entire myopectineal orifice, closely adhering to the posterior margin of the inguinal ligament, and reaching inferiorly to the ligament of Cooper and the femoral vascular sheath. 17 The transversalis fascia is reinforced by additional fibers whose origin and substance vary. Some are peripheral, such as the aponeurosis of the transversus abdominis medially near the lateral edge of the rectus in the form of the wing-shaped falciform ligament of Henle. Below and deep to the inguinal ligament, recurrent fibers of the external oblique aponeurosis form the lacunar ligament of Gimbernat. Laterally, a thickening of iliac fascia from the inguinalligament to the pubic bone forms the iliopectineal bandelette. Other additions cross the transversalis fascia at its central portion. The ligament of Hesselbach is a thickening of connective tissue along the lateral border of the epigastric vessels. The transversalis fascia is weakened by the penetration of the femoral vessels, the spermatic cord in man and the round ligament in women (Fig. 3.2). Groin hernias are characterized by deterioration of the transversalis fascia. Since the transversalis fascia

J.P. Richer et al.

9.2. The myopectineal orifice as seen from inside: 1 = ligament of Cooper; 2 = iliopubic tract (bandelette) of Thomson; 3 = ligament ofHesselbach; 4 = iliopectineal bandelette; 5 = epigastric vessels. FIGURE

is inadequate, repair must consist of a musculoaponeurotic reconstruction, making use of the most substantial anatomic structures: the lower border of the internal oblique and transversus, classically referred to as the conjoined tendon; the iliopubic tract, the shelving edge of the inguinal ligament; and above all, the pectineal ligament of Cooper, whose solidity has been acknowledged by all.

The Pectineal Ligament of Cooper

9.1. Superficial view of the myopectineal orifice: 1 = ligament of Cooper; 2 = iliopectineal bandelette; 3 = inguinal ligament; 4 = fascia transversalis; 5 = internal oblique; 6 = rectus sheath; 7 = ligament of Henle. FIGURE

Macroscopically, the pectineal ligament covers the pecten of the pubis. It has a medial portion at the level of the pubic tubercle, where the ligament of Gimbernat inserts. Its lateral portion is, however, more difficult to define as it quickly thins out to blend with the periosteum and the iliopubic fascia that covers it. As it thins out laterally, the loss of solidity can be felt as one palpates periosteum. This point can be measured. On average, its length is between 45 and 65 mm. 32 Its thickness, astride the pecten, is between 2 and 5 mm, as measured by Fruchaud. 1 The thickness is most pronounced between the external iliac vessels and the pubic spine. 32 Its shape is crescentic (Fig. 3.3). McVay demonstrated that the normal insertion of the transversalis fascia and transversus abdominis was into Cooper's ligament, not Poupart's. He recommended a Cooper's ligament repair for direct, large indirect, and femoral hernias. 16 In laparoscopic repair of inguinal hernias, it is important to identifY Cooper's ligament, palpable medial to the obliterated umbilical artery.31 Branches of the obturator vein may overlie the pectineal ligament as they travel to empty into the external iliac vein (Fig. 3.2). Careful pectineal dissection is required. Cooper's ligament is used to anchor the medial comer of the prosthetic patch. 36 It is also used for the sutures in anti-incontinence surgery.37,38 In a cadaver model, bone anchor placed in the pubic

Color Plate I

Remnant of umbilical a. Medial umbilical ligament

Linea semicircularis

Urachus (median umbilical ligament)

Rectus abdom. m. Inferior epigastric a. and v.

ligament

Testicular artery and vein

Anastomotic pubic branches

Falx inguinalis (Henle's lig.)

Medial fossa

Aponeurotic arch

Lateral fossa Deep inguinal ring Femoral canal--t-!===-_~. . . . .. ,

Femoral ring Pectineallig. (Cooper's) Ex1ernal iliac a. and v. Psoas minor tendon Iliacus muscle

Superior and inferior crura (transversalis fascia sling) lIiopubic tract Deep circumflex iliac a. and v. Iliopectineal arch AnI. pubic branch and iliopubic vein Vas deferens Obturator foramen , nerve, artery, vein Femoral nerve Lateral femoral cutaneous nerve Ilioinguinal nerve Iliohypogastric nerve Genitofemoral nerve Genital branch + Femoral branch'

FIeURE 7.1. Drawing illustrating the anatomy of the internal surface of the lower abdominal wall, inguinal region and lower trunk. (Reprinted from Annibali R, Fitzgibbons RJ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

Color Plate II

B FIGURE 7.2. (A) View of the deep surface of the anterior abdominal wall in a cadaver preparation, which demonstrates the peritoneal folds and fossae. (B) The peritoneal fossae are better demonstrated with transillumination of the lower anterior abdominal wall: UM = umbilicus; FB = fundus of the bladder; U = median umbilical ligament; ML = medial umbilical ligament; LL = lateral umbilical ligament (inferior epigastric vessels); SF = supravesical fossa; MF = medial fossa; LF = lateral fossal; IS = internal spermatic (testicular) vessels; VD = vas deferens; EI = external iliac vessels; A = abdominal aorta. The arrow indicates the deep inguinal ring. (C) Exterior view of the anterior abdominal wall and inguinal region transiIIuminated; UM = umbilicus; RM = sheath of rectus muscle; AA = aponeurotic arch of transverses abdominis muscle; SC = spermatic cord; IR = area corresponding to the internal inguinal ring; IE = inferior epigastric vessels; LF = latral fossa; IL = inguinal ligament. Dotted outline indicates the weak areas included within the inguinal triangle through which direct hernias occur. (From Annibali R, Fitzgibbons RJ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH , eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

FIGURE 7.3. Peritoneal folds and fossae, as seen at laparoscopy. A direct hernia is visible bilaterally and appears as a circular defect included between the aponeurotic arch of the transversus abdominis muscle superiorly and the iliopubic tract inferiorly; U = median umbilical ligament; ML = medial umbilical ligament; LL = lateral umbilical ligament; AA = aponeurotic arch of the transversus abdominis muscle; IP = iliopubic tract; SF = supravesical fossa; MF = medial fossa; LF = lateral fossa; VD = vas deferens; IS = internal spermatic (testicular) vessels; EI = external iliac vessels; B = bladder with Foley catheter inserted. (From Annibali R, Fitzgibbons RJ Jr. , Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission .)

Color Plate III

FIGURE 7.4. Panoramic view of the internal surface of the anterior lower abdominal wall, inguinal regions, lower trunk, and pelvis in a cadaver dissection: UM = umbilicus; LS = linea semicircularis; RM = rectus abdominis muscle; HT = inguinal (Hesselbach 's) triangle; IE = inferior epigastric vessels; AP = anterior pubic branch and iliopubic vein; TS = transversalis fascia sling; U = urachus; CL = Cooper's ligament; UA = umbilical artery; AO = anomalous obturator artery; SV = superior vesical artery; PB = anastomotic pubic branches; IV = external iliac vein; IA = external iliac artery; VD = vas deferens; PA = iliopectineal arch; IP = iliopubic tract; DC = deep circumflex iliac vessels; GN = genitofemoral nerve;

A FIGURE 7.5. (A) Photograph of a cadaver preparation (right side) showing the pre peritoneal space at the level of the inguinal area, after removal of the peritoneum and preperitoneal adipose tissue (the urachus has been resected and the bladder retracted posteriorly). (B) Same view of (A) but in a different cadaver. Note the staples correctly positioned just above the ilipubic tract to tack the inferior border of the mesh. The internal spermatic (testicular) vessels have been moved slightly laterally to better show the external iliac vessels on the floor of the "Triangle of Doom." RM = rectus abdominis muscle; IE = inferior epigastric vessels; IP = iliopubic tract; CL = Cooper's pectineal ligament; IS = internal spermatic (testicular) vessels; ES = external spermatic vessels; VD = vas deferens; IA = external iliac artery; EI = external iliac vessels; IPA = iliopectineal arch ; GN = genitofemoral nerve; GB = genital branch of the ge nitofemoral

GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; LC = lateral femoral cutaneous nerve; IL = ilioinguinal nerve; 1M = iliacus muscle; PM = psoas major muscle; IS = internal spermatic (testicular) vessels; UR = ureter; A = abdominal aorta; LV = iliolumbar vessels. Thick black arrow indicated deep inguinal ring; white arrow, obturator foramen; short arrow, femoral ring. (From Annibali R, Fitzgibbons RJ Jr. , Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH , eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

B nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; LC = lateral femoral cutaneous nerve; IL = ilioinguinal nerve; DC = deep circumflex iliac vessels; V = seminal vesicles; UA = umbilical artery; PB = anastomotic pubic branches; AP = anterior pubic branch and accompanying iliopubic vein; RP = retropubic vein; LV = iliolumbar vessels; B = bladder; CI = common iliac artery; AA = aponeurotic arch of the transversus abdominis muscle; UR = ureter; 1M = iliacus muscle; PM = psoas major muscle; TF = transversalis fascia; IF = iliac fascia (reflected in part (B) ; TM = transversus abdominis muscle. (From Annibali R, Fitzgibbons RJ Jr. , Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission. )

Color Plate IV

FIGURE 7.6. Preperitoneal space seen laparoscopically during a hernia repair; PF = peritoneal flap reflected; IS = internal spermatic (testicular) vessels; VD = vas deferens; CL = Cooper's pectineal ligament; ML = medial umbilical ligament; PB = anastomotic pubic branch; PV = iliopubic vein; IE = inferior epigastric vessels; SC = superior crus of the transver-

A FIGURE 7.7. (A) Cadaver preparation of the inguinal region. Close-up of the area of the right deep inguinal ring. (B) Laparoscopic view of the left internal inguinal ring. TS = transversalis fascia sling; SC = superior crus of the transversalis fascia sling; IC = inferior crus of the transversalis fascia sling; IS = internal spermatic (testicular) vessels; VD = vas deferens; IV = external iliac vein; IA = external iliac artery; IP = iliopubic tract; IE = inferior epigastric vessels; GB = genital branch of the genitofemoral

salis fascia sling; IP = iliopubic tract; AA = aponeurotic arch of the transversus abdominis muscle. The arrow points to the deep inguinal ring. (From Annibali R, Fitzgibbons RJ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

B nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; PA = iliopectineal arch; AA = aponeurotic arch of the transversus abdominis muscle; DC = deep circumflex iliac vessels; 1M = iliacus muscle; PB = anastomotic pubic branch. (From Annibali R, Fitzgibbons RJ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

Color Plate V

PI... minor muscll - - - - - - : - - - - - - PIo.. rnaj .. muscle - - - - - - - - - : : : : ; OUOdllWS IumbotlJm muscll - - - - - - : :

em,,,,,1 oblique muIdo - - -- In ... 1111 obI~.. muscle ------;:---.

T'&l1svt.fIUS Ibdominis mulde moh)'poglS.1c neMI

------

lIIoinguln" neM - - - - - - -

---------==

IlIu». muscle

Genitofemoral ntNt - - - - - - - - -

1.1101,1 fem .... «I_out nerve

Inguillllligom."

-----~----

r.mor .. n...... - - - - - - - - - - lliopec~ne"

Irth

-------~

r.mer.. brarch - - - - - - - - - Genna. brooch - - - -- - - ' "

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FIGURE 7.S. Anatomy of the inguinal and femoral region. (From Annibali R, Fitzgibbons RJ Jr. , Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopy Surgery. © 1993 WB Saunders, with permission .)

FIGURE 7.9. The internal surface of the lo wer anterior abdominal wall prepared in a cadaver. The weak areas inside the inguinal triangles through which direct herniations occur, and included between the aponeurotic arch of the transversus abdominis muscle superiorly and Coope r's pectineal ligament inferiorly, are better demonstrated here by transillu-

mination of the lower anterior abdominal wall. The urachus and the bladder have been reflected posteriorly. (From Annibali R, Fitzgibbons RJ Jr., Filipi C, e tal. Laparoscopic hernia repair. In: Greene FL, PonskyJL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

Color Plate VJ

FIGURE 7.10. Same preparation as Fig. 7.9. Close-up of the area of the left inguinal (Hesselbach's) triangle: RM = lateral border of the rectus abdominis muscle; LS = linea semicircularis (of Douglas); IE = inferior epigastric vessels; ES = external spermatic (cremasteric) vessels; RV = rectusial vein; CL = Cooper's pectineal ligame nt; IP = iliopubic tract; UA = umbilical arteries; SV = superior vesical artery; HL = falx inguinal is (or Henle's ligament); AA = aponeurotic arch of the transversus abdominis muscle; VD = vas deferens; IS = internal spermatic (testicular) vessels; PB = anastomotic pubic branch; AP = anterior pubic branch and iliopublic vein; PV = iliopubic vein; RP = retropubic vein; AO = anom-

alous obturator artery; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; LC = late ral femoral cutaneous nerve; TS = transversalis fascia sling; CI = common iliac artery; IA = external iliac artery; IV = external iliac vein; PA = iliopectineal arch; FN = femoral nerve; PM = psoas major muscle; 1M = iliacus muscle; A = abdominal aorta. The thick arrows point to the deep inguinal ring. The thin arrow indicates the femoral ring. (From Annibali R, Fitzgibbons RJ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH , eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

FIGURE 7.13. Mter an accurate surgical dissection during a laparoscpic hernia repair, the femoral branch of the genitofemoral nerve and the lateral femoral cutaneous nerve have been identified as they approach and pass below the iliopubic tract: IP = iliopubic tract; LC = lateral femoral cutaneous nerve; FB = femoral branch of the genitofemoral nerve. The arrow

indicates the enlarged deep inguinal ring, through which an indirect inguinal hernia found its outlet. (From Annibali R, Fitzgibbons RJ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

Color Plate VII

A FIGURE 7.14. (A) A = area known as the "Triangle of Doom." B = triangular area where staples may cause nerve entrapment. (B) Cadaver preparation (right side) that shows the structures included within the Triangle of Doom (medial triangle) and the dangerous area beside it, bordered by the internal spermatic (testicular) vessels inferomedially and the iliopubic tract superolaterally (lateral triangle) , where no staples or sutures may be placed: B = bladder (reflected posteriorly); CI = common ilic artery; VA = umbilical artery; C1 = Cooper's pectineal ligament; PB = anastomotic pubic branch; AP = anterior pubic branch and iliopubic vein; RP = retropubic vein; ES = external speramtic (cremasteric) vessels; IE = infe-

8 rior epigastric vessels; VD = vas deferens; IV = external iliac vein; IA = external iliac artery; GN = genitofemoral nerve; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; IPA = iliopectineal arch; V = ureter; IS = internal spermatic (testicular) vessels; DC = deep circumflex iliac vessels; 1P = iliopubic tract; FN = femoral nerve; LC = lateral femoral cutaneous nerve; 1L = ilioinguinal nerve; PM = psoas major muscle; 1M = iliac muscle; LV = iliolumbar vessels. (From Annibali R, Fitzgibbons ~ Jr., Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

deep circumflex iliac vessels; GN = genitofemoral nerve; GB = genital branch of the genitofemoral nerve; FB = femoral branch of the genitofemoral nerve; FN = femoral nerve; LC = lateral femoral cutaneous nerve; U = ureter; B = bladde r (reflected posteriorly). (From Annibali R, Fitzgibbons ~ Jr. , Filipi C, et al. Laparoscopic hernia repair. In: Greene FL, Ponsky JL, Nealon WH, eds. Endoscopic Surgery. © 1993 WB Saunders, with permission.)

Color Plate VIII

cle; FN = femoral nerve; PA = iliopectineal arch; FB = femoral branch of the genitofemoral nerve; FS = femoral sheath; IL = inguineal ligament (sectioned); FV = femoral vein; IS = internal spermatic (testicular) vessels; VD = vas deferens; ES = external spermatic (cremasteric) vessels. The arrow points of the opening of the femoral canal.

FIGURE 23.2. Color Doppler ultrasound of testis, showing a patent intratesticular artery. Courtesy of R. Bendavid and P. Hamilton.)

FIGURE 23.3. Color Doppler ultrasound showing absence of circulation within the testicle but a pronounced flow to the scrotal skin. (Courtesy of R. Bendavid and P. Hamilton.)

9. The Ligaments of Cooper and Thomson

symphysis offers no structural advantage over Cooper's ligament fixation. 37 The best point to place the staples in a colposuspension seems to be at 4 cm from the medial origin ofthis ligament. 38 Since it was described by Cooper, the ligament's origin has been controversial. In our own dissections, we have appreciated its solidity. We have differentiated the pectineal ligament from the pectineus muscle fascia with great difficulty, from the periosteum with less difficulty, and more easily still from the lacunar ligament of Gimbernat. Laterally, the pectineal ligament is independent of all other ligamentous structures. As to the psoas minor, we have not identified any connection with the pectineal ligament. Cadaver studies were carried out on pubic bone sections every 5 mm from the pubic tubercle laterally.39 Macroscopic examination revealed a perfect continuity between the ligament and the periosteum posteriorly and the fascia of the pectineus anteriorly. Stain studies (hemalum, eosin, safran) revealed a dense collagenous formation arranged longitudinally and transversely, and in some areas a fibrohyaline appearance. The vascularization is relatively substantial. A few striated muscular fibers from the pectineus were identified. No arcuate periosteal fibers were noted, and the pectineus fascia blends without distinction into the ligament of Cooper.40 These anatomical and histological findings confirm the thesis of Rouviere that the ligament of Cooper is a thickening of the pectineus fascia rather than thickening of the periosteumY Fruchaud, 1 in 1956, wrote: "What is important surgically is to know that the fibrous strands of the ligament of Cooper present two sides: an anterosuperior side which juts from the pectineal crest, and a posteroinferior side which descends 2 mm on the upper part of the posterior aspect of the pubic ramus, that is to say, within the pelvic cavity." The morphology and solidity of this ligament allowed this writer to insert two rows of sutures, on the anterosuperi or and posteroinferior aspects of the ligament (Fig. 3.3).I

The Iliopubic Bandelette (Tract) of Thomson The iliopubic tract, by strengthening the transversalis fascia, contributes to the formation of the posteroinferior wall of inguinal canal. Poorly understood by many authors, the iliopubic tract is in effect hidden by the inguinal ligament. That is why some authors, Bassini included, mistook the tract for the posterior aspect of the inguinal ligament. 25 ,26 But the iliopubic tract exists and is an important landmark in laparoscopic surgery.32,41 Clark and Hashimoto (1946) suggested dissecting and resecting the inguinal ligament for better identification of the iliopubic tract. 21 This appears as an elongated band, surgically indistinguishable from transversalis fascia. 4 Certain authors have been able to observe, during anatomic dissection, easy cleavage laterally between the iliopubic tract and transversalis fascia, whereas, medially, cleavage was impossible due to its close association to the femoral vascular sheath. 24 Solid, of an aponeurotic appearance, the iliopubic tract is narrow near its midportion, but flares at its two extremities. Its medial extremity blends with the transversalis fascia and the transversus aponeurosis near the edge of the rectus, on the pubic tubercle and the medial portion of the ligament of Cooper. The lateral extremity is directed toward the anterior superior iliac spine, on the deep aspect of the transversus, its inferior border blending with the iliac fascia, leaving a small orifice only for the passage of the deep circumflex iliac vessels. In patients presenting with a weakness of this area, as noted by Burton, the iliopubic tract of Thomson is poorly developed and offers little support (Fig. 3.2).23 The lateral femoral cutaneous nerve is located 1.7 cm medial to the anterior superior iliac spine, along the iliopubic tract. 42 Nerve entrapment sequelae have been reported and appear to be more commonly associated with the laparoscopic approach. 3o ,42 As it courses medially, the iliopublic tract forms the inferior margin of the internal spermatic ring and the roof of the femoral canal. 31 It is an essential structure in the laparoscopic repair of both direct and indirect inguinal hernia. 31 ,32 All inguinal hernia defects lie anterior to the iliopubic tract, and femoral hernias lie posterior to the bandelette of Thomson. 31,32 In contrast to the inguinal ligament, the histological analysis of the iliopubic tract shows a high elastin-to-collagen ratio. 32

Conclusion

9.3. Pubis and pectineal ligament of Cooper: Cooper: 2 = pubis; 3 = iliac ala; 4 = obturator foramen.

FIGURE

1 =

ligament of

Despite the protective mechanisms of the transversalis fascia and the angled course of the inguinal canal, all groin hernias (inguinal and femoral) cross the myopectineal orifice through the transversalis fascia. However, the breakdown of the fascia and the weakness of its reinforcements do not constitute the only pathophysiological mechanism. In addition to acquired or congenital causes, several authors have suggested alterations in collagen metabolism. 43 ,44,45 Stoppa et al. recognize an imbalance due to the increase in intra-abdominal pressure seen in certain diseases and the weakening of musculoaponeurotic structures seen in some pathophysiological states. 46 Anatomical factors as well will promote the appearance of hernias, such as a high lower border of the internal oblique and transversus as they insert into the rectus sheath; this leaves the medial angle of the floor of the inguinal canal unprotected. Repair of this area must include not only the transversalis fascia, but the more substantial neighboring tissues, and perhaps the addition of prosthetic material.

References l. Fruchaud H. Anatomie chirurgicale des hernies de l'aine. Paris: G. Doin; 1956. 2. Vesalius A. De humani corporis fabrica. J Oporinus Ed.; 1543. 3. Franco P. Traite des hernies, par Pierre Franco, de Terriers-ffl-Provence demeurant a present a Orange. A Lyon, par Thibault Payon; 156l. 4. Cooper A. The anatomy and surgical treatment of inguinal congenital hernia. London: JT Cox; 1804. 5. Cooper A. Oeuvres completes de Sir Astley Cooper, traduites par Chassaignac et Richelot-Bechet jeune. Paris: Librairie de la Faculre de Medecine de Paris; 1835. 6. Charpy A. La gaine des muscles droits et la cavite prevesicale. Rev Chir. 1888;8:116 etEtudes d'anatomie. Toulouse: Imprimerie Cassan Fils; 189l. 7. Charpy A. Sur les sillons du bas-ventre et de la cuisse. Arch Med Toulouse. 1910;17:49. 8. Charpy A. Le pli de l'aine. Arch Med Toulouse. 1910;17:337, 36l. 9. Testut L. Traite d'Anatomie Humaine, 6th ed. Paris: G. Doin; 1911. 10. Bardeleben. Handbuch der Anat der Menshen muskeln der stammes bearbeitet bei P. Eisler. lena; 1912 Bd 2; 64l. 11. Rouviere. Anatomie Humaine, descriptive et topographique. Paris: Masson; 1924. 12. Seelig, Chouke. A fundamental factor in the recurrence of inguinal hernia. Arch Surg. 1923;7:553. 13. Anson BJ, McVay CB. The anatomy of the inguinal and hypogastric regions of the abdominal wall. Anat Rec. 1938;70:211. 14. Anson BJ, McVay CB. Inguinal hernia. The anatomy of the region. Surg Gynecol Obstet. 1938;66:186. 15. McVay CB. Inguinal and femoral hernioplasty: anatomic repair. Arch Surg. 1948;57:524. 16. McVay CB. The anatomic basis for inguinal and femoral hernioplasty. Surg Gynecol Obstet. 1974;139:931-945. 17. McVay CB, Anson BJ. Fascial continuities in the abdominal, perineal and femoral regions. Anat Rec. 1938;71:4Ol. 18. McVay CB, Anson BJ. Aponeurotic and fascial continuities in the abdomen, pelvis and thigh. Anat Rec. 1938;76:213. 19. Aubaniac F. L'insertion inff:rieure du petit psoas. Travaux du Laboratoirer d'Anatomie de la Faculte de Medecine d'Algerie (Professeur de Ribet). Algerie: Imprimerie Imbert; 1952. 20. Mattson. Use of the rectus sheath and superior pubic ligament in direct and recurrent inguinal hernia. Surgery 1946;19:498. 2l. Clark, Hashimoto. Use of Henle's ligament, ilio-pubic tract, transversus abdominis aponeurosis, and Cooper's ligament in inguinal herniorrhaphy. Surg Gynecol Obstet. 1946;82:480. 22. Donald. The value derived from utilizing the component parts of the transversalis fascia and Cooper's ligament in the repair of large indirect and direct inguinal hernia. Surgery 1948;14:662. 23. Burton. The criteria, classification and technique of iliopectineal (Cooper's) ligament hernioplasty. Surg Gynecol Obstet. 1949;89:227.

J.P. Richer et al. 24. Thomson A. Ouvrage complet sur l'anatomie du bas ventre et sur les hernies. Paris: Imprimerie Lange Levy; 1838. 25. Bassini E. Sopra 100 casi di cura radicale dell'ernie inguinale, operata con metodo dell'autore. ltal Chir Congr. 1888. Arch Soc Med ltal. 1888; 5:315. 26. Bassini E. Uber die Behandlung des Leistenbruches. Arch Kin Chir. 1890;40:429. 27. Ruggi G. Metodo operativo nuovo per la cura radicale dell'ernia crurale. Bull Sci Med. (Bologna) 1892;7(3):223. 28. Lotheissen G. Zur radikaloperation der schenkelhernien. Zentralhl Chir. 1898;25:548. 29. Ger R, Mishrick A, HurwitzJ, Romero C, Oddsenn R Management of groin hernias by laparoscopy. World] Surg. 1993;17:46-50. 30. Marks SC Jr, Gilroy AM, Page DW. The clinical anatomy of laparoscopic inguinal hernia repair. Singapore MedJ 1996;37:519-52l. 31. Spaw AT, Ennis BW, Spaw LP. Laparoscopic hernia repair: the anatomic basis.] Laparoendosc Surg. 1991;1:269-277. 32. Teoh LS, Hingston G, Al-Ali S, et al. The ilio-pubic tract: an important anatomical landmark in surgery.] Anat. 1999;194:137-14l. 33. Grasse P. Traite de zoologie. Anatomie, systematique, biologie. Tome XVI: Mammiferes, teguments, squelette. Premier fascicule. Paris: Masson; 1967. 34. Schultz AH. The life of primates. Weidenfeld and Nicolson; 1969. 35. Keith. On the origin and nature of hernia. Br] Surg. 1923-1924;11: 455. 36. Felix E, Scott S, Crafton B, et al. Causes of recurrence after laparoscopic hernioplasty. A multicentric study. Surg Endosc. 1998;12:22623l. 37. Klutke lJ, Bullock A, Klutke CG. Comparison of anchors used in anticontinence surgery. Urology. 1998;52:979-98l. 38. Perdu M, Darai E, Goffinet F, et al. Etude anatomique du ligament de Cooper. Interet dans la cure chirurgicale de l'incontinence urinaire de la femme.] Gynecol Obstet Biol &prod. 1998;27:52-54. 39. Rousseau MA, Perdu M, Ledroux M, et al. Ligament pectineal de Cooper. Etude micromorphometrique. Morphologie. 1999;83:67-69. 40. Barbier J, Carretier M, Richer JP. Cooper's ligament repair: an update. World] Surg. 1989;13:499-505. 4l. Lichtenstein IL, Amid PK, Shulman AG. The iliopubic tract: the key to inguinal herniorrhaphy? lnt Surg. 1990;75:244-246. 42. Dibenedetto LM, Lei Q, Gilroy AM, et al. Variations in the inferior pelvic pathway of the lateral femoral cutaneous nerve: implications for laparoscopic hernia repair. Clin Anat. 1996;9:232-236. 43. Condon RE, Carilli S. The biology and anatomy of inguinofemoral hernia. Semin Laparosc Surg. 1994;1:75-85. 44. Ponka JL. Hernias of the abdominal wall. Philadelphia: Saunders; 1980: 82-87. 45. Read RC, White HJ. Inguinal herniation 1777-1977. Am]Surg. 1978; 136:651-654. 46. Stoppa R, Verhaeghe P, Marrasse E. Mecanisme des hernies de l'aine. ] Chir. 1987;124:124-43l.

The Transversalis Fascia: New Observations Robert Bendavid

The transversalis fascia is the least understood of all the structures tendons that close the opening are those of the internal oblique that make up the inguinal region. From the standpoint of anatomy and the transversalis [sic] muscles." The use of the word "transand physiology, little is known about this tissue layer, which was versalis" for the transversus abdominis muscle appears often in the first described and named by Astley Cooper nearly two centuries older literature: this may have been partly responsible for the conago. l fusion about what "transversalis" means exactly. Robert Condon writes: "The transversalis fascia is merely a porAnother interesting observation by Anson, McVay, and Morgan 5 tion of the continuous layer of endoabdominal fascia ... in the was the presence of "slit-like gaps between divergent bundles of groin it tends to be a little thicker and a little stronger than else- fibers ... masses of adipose tissue frequently filled the gap ... where in the abdominal cavity."2 Lichtenstein has written that "the herniations of adipose preperitoneal tissue passed through the transversalis fascia bridges the space bounded by the transversus transversus layer to occupy the defects." Are we here looking at abdominis arch superiorly and the inguinal ligament and Cooper's degenerative changes of muscle fibers with fatty infiltration, as well ligament inferiorly."3 These descriptions certainly do not apply to as degeneration of the aponeuroses of the internal oblique and children, young adults, females and most adults who do not have transversus abdominis? One feature of the anatomy of the groin which raised my cua hernia. Through thousands of inguinal repairs, I have always been impressed by the muscular or musculotendinous makeup of riosity and stimulated my quest for an answer was the depiction in the posterior inguinal wall of these patients, who usually have an all illustrations of the directions of the fibers within the ligament indirect hernia. of Gimbernat. They are shown to be vertical to the ligament of McVay, however, describes the posterior inguinal wall as "the fu- Cooper. In the operating room, close examination reveals those sion of the transversalis fascia to the transversus abdominis aponeu- fibers to be horizontal and parallel to the iliopectineal eminence rosis and their insertion on the pubic ramus."4 This is not easily and the ligament of Cooper. demonstrated in the operating room, although I have seen it on One last puzzling observation of anatomy that has not been satoccasion, and if the transversalis fascia is part of the endoabdom- isfactorily answered is the ultimate fate of the external oblique inal fascia, why is it inserting on the iliopectineal ridge? unless it aponeurosis after it becomes recurved inward in the fold of the happens to be a "thickening" at that level and then goes on to the groin, where it is then called the inguinal ligament. From the level of the femoral vessels laterally toward the anterior superior iliac pelvis as the endopelvic fascia. Anson, Morgan, and McVay observed that "the internal oblique spine, one can see the fibers of the external oblique aponeurosis extended to the level of the inguinal canal in only 2% of the 500 continue in a horizontal fashion anterior to the iliac vessels. Mebody-halves. In 75% of cases, the fleshy part covered somewhat dial to the vessels, however, the horizontal fibers continue inward more than 75% of the inguinal area."5 Chandler and Schadewald6 over the rim of the pubic ramus to become the lacunar ligament, presented similar findings: the internal oblique covered the in- with horizontal fibers, as can be confirmed in the operating room. guinal area completely in only 21 % of cases, at least half of the in- This is the only possible way to clearly understand the origin and guinal area in 46%, while in 33% of cases it failed to cover the insertion of the ligament of Gimbernat, which has never been inguinal area at all! quite clearly explained in the groin. It has also been my experience that not only muscular fibers of Certainly, a logical and teleological construction of the groin the internal oblique are present through the inguinal area, but that would be approved by a structural engineer can be seen in also an internal oblique aponeurosis which, on several occasions, Fig. 10.1, where the aponeurosis of the external oblique curves could easily be separated from a deeper and equally substantial under the spermatic cord to join the aponeurosis of the internal transversus abdominis aponeurosis and, deeper still, a diaphanous oblique and transversus abdominis to become the lacunar ligalayer: the transversalis fascia proper. ment inserting on the ligament of Cooper. The transversalis fasWhen Astley Cooper demonstrated that the superficial and deep cia is simply lining the inner surface of the transversus abdominis inguinal rings were not superimposed, he went on to say that "the aponeurosis. Peeling back the transversalis fascia (Fig. 10.2), one R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

R. Bendavid 10.1. View of the posterior inguinal wall from the preperitoneal space. The lower border of the transversalis fascia in fact joins the endoabdominal fascia. FiGURE

In emal obhque Transversus abdomlnls Transversal s faSCIa AponeurOSIS 01 ext mal oil,. ue

Deep Inguinal ring

ligament ' >-II ... rltv

pubic ramus

10.2. Transversalis fascia reflected, showing, as in most textbooks, an absent posterior inguinal wall below the conjoined tendon and vertical fibers to the lacunar ligament. FIGURE

Posterior view

Transversalls faSCIa

-11--

Stpem18bC 00fd

at deep Inguinal nng n

nng 10.3. A more accurate depiction of the posterior inguinal wall after the transversalis fascia has been reflected. Note the aponeurosis of the transversus abdominis as well as the horizontal fibers of the lacunar ligament. FiGURE

10. The Transversalis Fascia

Skin

--l'ransversus abdomiOis Superloal 'a5CIII-~H!fM1l~1

Round ligamenl

Of spermatic coed

IngUlnalllgament--II-U~;t; ·

~I~--I~~~~~

~-.~--·u.~~~meM

r:o..--- PecIJneaIll!}8Il18f1t (Coopers)

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01 pubis

ramus

FIGURE 10.4. Three-layered structure of the posterior inguinal wall in an individual without "hernia diathesis," and therefore without degeneration of the aponeurosis of the internal oblique and transversus abdominis muscles.

sees the traditional-but inaccurate-depiction of the lacunar ligament as vertical fibers and an arch, the "transversus arch" or "conjoined tendon," which is rarely the case. A more accurate reflection of the anatomy is seen in Figure 10.3, where the aponeurosis of the transversus abdominis extends inferiorly and its own horizontal fibers form the lacunar ligament inserting into the iliopectineal ridge and contributing to the ligament of Cooper. Parasagittal sections (Figs. 10.4 and 10.5) reveal how the external oblique aponeurosis joins the combined aponeuroses of the internal oblique and transversus abdominis. They show the relative thicknesses of the posterior inguinal wall in males and females and underline the trilaminar nature of this wall. It was logical to attempt proof of this macroscopic observation with microscopic evidence. Segments of the posterior inguinal wall

FIGURE 10.6. Histological appearance of the posterior inguinal wall. The transversalis fascia is distinct, separate, and of marked cellularity. The internal oblique and transversus abdominis aponeuroses are separated by loose areolar tissue. Above, some cremaster muscle fibers. Magnification = 100X.

were excised and analyzed by a histologist. 7 The results can be clearly seen in Figure 10.6, Figure 10.7 and Figure 10.8. The transversalis fascia is a distinct structure with marked cellularity compared to the aponeurotic layers, which show a more fibrous and collagenous pattern.

---Inleirnal oblique ---'rlBl~sy,_C1S

abdom

FIGURE 10.5. Three-layered and muscular appearance of the posterior inguinal wall in children, females, and most adult males when "hernia diathesis" is not present.

FIGURE 10.7. Histologic appearance of the aponeuroses of internal oblique and the transversus abdominis, cleanly separate. The transversalis fascia is markedly thinned out but still distinct. Magnification = 100X.

R. Bendavid

100

The French mathematician Fermat left us a theorem that took more than 300 years to prove. Let us hope we will not wait that long with Cooper's transversalis fascia.

Acknowledgment All figures reprinted from Bendavid R, The transversalis fascia: new realities, in Surgical Anatomy and Embryology, edited by SkandalakisJE and FlamentJB. Surgical Clinics of North America, February 2000. © 2000 WB Saunders Co., with permission.

References 10.8. Histological appearance at higher magnification. Again, the three layers are easily discerned. The transversalis fascia is strikingly separate and easily identified. Magnification = 250x.

FIGURE

To appreciate the anatomy and its variations in the inguinal region, the surgeon must perform thousands of herniorrhaphies. Few surgeons have that opportunity. It is also important to appreciate the new direction of pathology in terms of metabolic disease as the etiology of hernia formation. The fact that females show a lessened incidence of primary hernias, recurrent hernias, and incisional hernias may imply a sex-linked transmission as well in the manifestation of hernia diathesis.

1. Cooper A. The anatomy and surgical treatment of inguinal and congenital hernia. London: T. Bensley, Printers; 1804:5-6. 2. Condon R. The anatomy of the inguinal region and its relation to groin hernia. In: Nyhus LM, Condon RE, eds. Hernia, 4th ed. Philadelphia: Lippincott; 1995:35. 3. Lichtenstein IL. Hernia repair without disability, 2nd ed. St Louis, Tokyo: Ishaku Euroamerica, Inc; 1986:26-29. 4. McVay CB. The pathologic anatomy of the more common hernias and their anatomic repair. Springfield: Charles C. Thomas, Publisher; 1954:16. 5. Anson Bj, Morgan EH, McVay CB. Surgical anatomy of the inguinal region based upon a study of 500 body-halves. Surg Gynecol Obstet. 1960;III:707-725. 6. Chandler SB, Schadewald M. Studies of inguinal region; conjoined aponeurosis versus conjoined tendon. Anat Rec. 1944;89:339-343. 7. Bendavid R, Howarth D. The transversalis fascia: new realities. Surg Clin North Am. In press.

11 The Space of Bogros and the Interparietoperitoneal Spaces J. Hureau

Since Vesalius, l research in human anatomy, whether applied or fundamental, has had the objective of enhancing medical knowledge. Historically, surgeons have been the main petitioners for that knowledge. For several decades, investigators with a particular technique of morphological investigation have pressed for accurate anatomical awareness, often in areas that coincided with their interests. Too often has it been said that all aspects of anatomy have been described. Nothing is further from the truth. As soon as a new surgical technique appears or a new tool of morphological investigation is designed, our level of understanding appears suddenly deficient. The human mind is such that it truly seeks only that of which it has an immediate need. Ambroise Pare has stated, "The arts are not so accomplished that nothing may be added."2

Did Bogros Describe the Space that Bears His Name? In 1823, the leading investigations centered on a search for surgical approaches to arterial ligation in the limbs (Fig. 11.1) . Wounds and aneurysms of the inferior epigastric and external iliac arteries, near or above the inguinal ligament, have given rise to three techniques, among others that were extensively discussed in surgical manuals of the 19th century:3 the procedures of Bogros, of Astley Cooper, and of Abernethy. In this era before antisepsis, the major concern was to avoid entering the peritoneal cavity where suppuration was reputed to be far less "desirable" than in the inferior limbs.

What Did Bogros Write? "Injury to the epigastric artery is, with just cause, a great fear of surgeons every time an operation is performed near its course. Especially during debridement of inguinal and femoral hernias or ligation of external iliac artery . . . My aim is to put forth an approach for the ligation of the epigastric artery.... As the new procedure which I propose is based on the study of the relationship of these arteries to their neighboring structures, it is indispensable that I commence by an accurate and perhaps detailed anatomical description of the relative as well as the absolute site of these vessels ... "4 Such was the dedication and frame of mind with which Bogros R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

applied himself to the description of what would be later called the "space of Bogros." Detailing his reports of the anterior aspect of the external iliac artery, he stated, "the caecum on the right, the sigmoid on the left, as well as the peritoneum on the iliac fossa demarcate that aspect. This segment of the peritoneum, extending from the anterior abdominal wall to the iliac fossa, defines underneath it an interval of 4.5 to 6.5 mm, where the iliac artery terminates without cover by this serious layer. . . ." A little further on, writing on the origin of the epigastric artery, he states: "A loose layer of cellular tissue separates it from the transversalis fascia. Behind, a thicker layer of the same tissue separates it from the peritoneum, shortly beyond its origin." Moreover" ... the external iliac artery and the first segment of the epigastric artery course through the iliac portion of the abdominal wall. These vessels are so placed that they are separated from the lower abdominal cavity by only the peritoneum and a more or less thick cellular layer." Further study, layer by layer, of the "anterior wall of the iliac area" (inguinal or inguinoabdominal area), Bogros described successively, from the superficial to deep (a surgical approach): • • • •

the skin; the superficial fascia; the external oblique aponeurosis; the muscular layer made up by the internal oblique and transversus muscles; • the fascia transversalis;

and immediately behind the transversalis fascia: " . . . near the bladder, as well as about the abdominal apertures to the inguinal and femoral canals, one finds a thicker cellular layer than in the rest of this area. The first portion of the epigastric artery, which is found in this cellular layer, is closer to the fascia transversalis than to the peritoneum. . .. The peritoneum, which lines the abdominal cavity, covering the anterior aspect of the iliac and hypogastric areas, is elevated by the umbilical arteries and the urachus, then is reflected about these fibrous cords, forming about them a peritoneal fold. Medially, this serous membrane (peritoneum) descends within the pelvic cavity and lines the walls of this cavity as well as many of the contained organs. Laterally, it is reflected from the iliac area of the abdominal cavity, the caecum on the right, the sigmoid colon on the left, and forms behind the intestines, an extensive meso-iliac fold. The peritoneum, extend101

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FIGURE

ing from the iliac portion of the anterior abdominal wall to the iliac fossa, leaves in front a space 13.5 to 15.5 mm wide, where the external iliac artery terminates." Summarized in this last sentence is the description which Bogros gave of the interparietoperitoneal space in the inguinoabdominal area.

The Concept of the Space of Bogros The concept of the space of Bogros is not readily appreciated. U ntil the end of the 19th century, surgical manuals simply made mention of the ease with which, in this suprainguinal prevascular space,

the distal peritoneum can be reflected to allow an extraperitoneal vascular ligation. One cannot deny that the advent of antisepsis and asepsis has facilitated the opening of a peritoneum and at the same time, took away from the interest of extraperitoneal surgery. The term "space of Bogros" appeared for the first time in 1912, penned by Rouviere in his treatise of human anatomy in Poirier and Charpy. 5 An excellent description, similar to that of Bogros, is taken up by Rouviere in all the subsequent editions of his treatise. 6 He stated: "The peritoneum, which lines the deep aspect of the abdomino-inguinal wall, is reflected from the abdominal wall toward the iliac fossa, creating a fold of peritoneum on the shape of a gutter concave above and behind. This fold of peritoneum is such that, from the abdominal wall to the iliac fossa, the outer layer of the peritoneum is in contact with the soft tissues of the iliac fossa from 1 to 1.5 cm above the inguinal ligament. The peritoneum thus demarcates, with a dihedral angle formed by the fascia transversalis and the fascia iliaca inferiorly, a triangular, prismatic interval, filled with preperitoneal adipose tissue, called the space of Bogros" (Fig. 11.2). Testut and LataIjet7 underline the continuity of the preperitoneal (anterior interparietoperitoneal space) tissue layer between the peritoneum and transversalis fascia, as did Paturet,8 who studied the vascular and neural relationships of this space, and who pointed out as well that it is through the space of Bogros that preperitoneal hernias will emerge.

The Space of Bogros Is Part of a Whole: The Interparietoperitoneal Spaces The recognition of the interparietoperitoneal spaces as greater channels of diffusion is not recent. Couinaud9 has urged the reexamination of the work of Delbet at the end of the 19th century on the spread of pelvic abscesses in women. He sums up the theses of DrouetlO and Mathis ll on the extraperitoneal spaces. These studies, again, were born out of a need to know the precise modes of spread in the extra- and retroperitoneal spaces. Drouet's study was avant-garde; Mathis's work had more immediate applications

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11.2. Sagittal paramedian sections of the abdominoinguinal region. (A) Lateral to the internal inguinal ring; (B) medial to the internal ring; = transversus abdominis; 2 = anterior parietal peritoneum; 3 = fascia transversalis; 4 = iliopubic bandelette; 5 = space of Bogros; 6 = iliac fascia; 7 = deep circumflex iliac vessels; 8 = psoas muscle; 9 = fascia superficialis; 10 = superficial inguinal nodes; 11 = inguinal ligament; 12 = subcutaneous adiposocellular layer; 13 = fascia superficialis; 14 = internal oblique muscle; 15 = external oblique aponeurosis; 16 = subcutaneous fat; 17 = interfoveolar ligament; 18 = sheath of external iliac vessels; 19 = femoral vein; 20 = vascular sheath of femoral vessels; 21 = cribriform fascia; 22 = falciform border of the cribriform fascia (ligament of Hey and Allan Burns); 23 = long saphenous vein; 24 = spermatic cord; 25 = femoral septum; 26 = deep inguinal lymphatics; 27 = co~oined tendon; 28 = pectineus muscle; 29 = deep inguinal lymphatic vessel; 30 = lowermost node of the middle lymphatic. FIGURE

103

11. The Space of Bogros

(1959), at a time when the technique of retropneumoperitoneography was being developed. Not until the late 1970s and the appearance of computer tomography (CT) scans did we realize the inadequacies of out knowledge of anatomy as revealed by this new method of medical imaging in the normal subject as well as in retroperitoneal pathology. This was the object of our publications at that time (1978-1981).1 2- 14

The Space of Bogros and the Posterior Pararenal Space The posterior pararenal space is formed by, anteriorly and medially, the posterior layer of the perirenal fascia and its lateral extension (the lateroconal portion of the fascia propria) and, posteriorly and laterally, the fascia parietalis (Figs. 11.3 and 11.4). The space therefore, exists only between the Spigelian line and the lateral border of the psoas. It contains the pararenal fat pad (Gerota), which thickens from back to front and is largest between the posterior leaf of the perirenal fascia (the retrorenal layer of Zuckerkandl) and the anterior aspect of the quadratus lumborum covered by the parietal fascia. In regards to the diaphragm, this space disappears with the leaf of Zuckerkandl as it mingles with the parietal fascia. Inferiorly, the fatty layer, which is an extension of the pararenal fat pad, forms an anteromedial partition to a potential space of cleavage situated on the medial aspect of the iliac fossa. The posterolateral partition of this space is represented by the iliac muscle covered by a homogeneous fatty layer. It is limited superiorly by the adhesion of the parietal fascia to the iliac

11.3. Right lateral parasagittal section through the midportion of the kidney. Note the inferior extension of the posterior pararenal fat pad of Gerota, the space of Bogros, and its inferior inguinal extension. 9 = peritoneal cavity; 11 = ascending colon; 13 = iliac crest; 14 = diaphragm; 15 = duodenum (2nd portion); 16 = space of Bogros; 17 = anterior pararenal space; 18 = posterior pararenal space; 19 = anterior perirenal space; 20 = posterior perirenal space; 22 = fascia of Toldt; 24 = predUGdenopancreatic fascia; 25 = fascia of Treitz; 29 = interadrenal-renal fascia; 30 = parietal fascia; 31 = perirenal fascia (anterior leaf); 32 = perirenal fascia (posterior leaf); 34 = liver; 37 = pararenal posterior fat pad; 38 = right coronary ligament of the liver; 40 = mesocolon; 43 = iliac muscle; 44 = peritoneum; 45 = right kidney; 47 = right adrenal; 61 = quadratus lumborum; 62 = transverse colon; 63 = gall bladder.

FIGURE

11.4. Left parasagittal section through the midportion of the kidney, pancreas, splenic angle of the colon, and descending colon. 1 = colon (splenic angle); 9 = peritoneal cavity; 12 = descending colon; 13 = iliac crest; 14 = diaphragm; 16 = space of Bogros; 17 = anterior pararenal space; 18 = posterior pararenal space; 19 = anterior perirenal space; 20 = posterior perirenal space; 21 = stomach; 23 = Toldt's fascia (left); 26 = retropancreatic fascia (Toldt's); 27 = iliac fascia (in front of iliacus); 29 = interadrenal-renal fascia; 30 = parietal fascia; 31 = perirenal fascia (anterior leaf); 32 = perirenal fascia (posterior leaf); 37 = posterior pararenal fat pad; 40 = mesocolon; 41 = mesogastrosplenic; 42 = mesopancreaticosplenic; 43 = iliac muscle; 44 = peritoneum; 46 = left kidney; 48 = left adrenal; 54 = pancreas; 55 = spleen; 57 = renal fossa; 61 = quadratus lumborum; 68 = pancreatic duct (of Wirsung); 70 = greater omentum; 73 = rest of transverse mesocolon; 75 = omental bursa (lesser peritoneal sac).

FIGURE

crest, posteriorly and medially by the dihedral angle of the psoas and iliac muscles. Inferiorly and anteriorly, at the level of the innominate line of the pelvis and the iliac vessels, it is poorly defined but extends to the deep recesses of the inguinal and femoral regions. This constant space, empty of all structure, easily cleavable, is not bordered by any fascial structure about its walls. This space, within the internal aspect of the iliac fossa and without its own fascial layer, is an extension of the cleavage plane situated behind the posterior fatty pararenal pad of Gerota which originates beneath the diaphragm. It projects inferiorly to blend with the retroinguinal space described by Bogros. In the same fashion, the pararenal fat pad is in continuity with the anterior preperitoneal fat pad which fills the space of Bogros. Through the space of Bogros, beneath the inferior reflection of the peritoneal fold within the lower abdominal cavity, there is continuity between the anterior and posterior interparietoperitoneal spaces.

The Space of Bogros and the Retropubic Space The studies of Mathisll under the direction ofCouinaud and confirmed by the research of Agossou-Voyeme15 in our department, have shown that anteriorly and inferiorly, the interparietoperitoneal space communicates with the retropubic space (Fig. 11.5). The umbilico-prevesical aponeurosis is seen as a thickening of the fascia propria of Cloquet (visceral fascia of Couinaud and Mathis) .

J. Hureau

104

The space of Bogros is hence in continuity with all of the neighboring parieto-visceroperitoneal spaces: • with the posterior space through the medial iliac fossa space posteriorly and superiorly; • with the anterior parietoperitoneal space of the abdominal wall; • with the retropubic space near the midline; • with all the pelvic potential spaces, as demonstrated in women particularly, by Delbet near the end of the 19th century. Furthermore, as pointed out by Couinaud, "In the deep inguinal area, the space of Bogros extends anteriorly inside the spermatic fascia in men, hence toward the scrotum, and the round ligament in women, that is, toward the labia mcyora."9 The tunica of the spermatic cord on the parietal segment of the round ligament of the uterus is formed by an evagination of the fascia transversalis, a thickening of the parietal fascia. All these communicate with the potential cellular spaces which belong to a same system of interparietoperitoneal spaces anteriorly and posteriorly. This accounts for the seemingly paradoxical extension toward the scrotum, the labia mcyora, and the potential spaces within the true pelvis of pathological events, namely: • • • •

purulent or necrotizing collections of pancreatic origin; pancreatico-biliary effusions; retroperitoneal hematomas; tumor extension from the abdominal wall or retroperitoneum.

In the normal subject, a good illustration was provided by precoccygeal insufflation for a retropneumoperitoneum, a practice that has now been abandoned.

The Content of the Space of Bogros The space of Bogros is a cleavable space, devoid of any real structure but for a scant amount of adiposocellular tissue in continuity above and behind with the inferior portion of the Gerota pararenal fat pad; above and in front with the thin fatty layer of the anterior interparietoperitoneal space; and medially with the prevesical fat. Vessels, nerves, and other elements run along the walls of the space of Bogros, covered by a peritoneal reflection and separated from it by a thin layer of adipose tissue. The importance of the structures is of interest to the surgeon who is about to insert a prosthesis in the peritoneal space. A large prosthetic sheet, well splayed, occupies the deep aspect of the space of Bogros, ascending above and in front in the interparietoperitoneal of the inguinoabdominal area, behind the inguinal floor, and extending in front of the urinary bladder to the midline in the retropubic space, covering above and behind the external iliac vessels, the separate elements of the spermatic cord in man, ascending laterally to the dihedral iliopsoas angle in the direction of the iliac fossa, and up to the femoral nerve. The "parietalization" of some of these elements, necessary to the proper laying down of a prosthesis, will be that much easier, since these structures already have a parietal course and do not cross the space of Bogros (Fig. 11.8). It is sufficient, during dissection, to allow these elements to remain parietally placed, as is the normal course for them. The femoral nerve is not included in these extraperitoneal spaces. It can only be injured by careless suturing of a prosthesis. The elements down to the inguinal floor warrant particular mention here.

11.5. Sagittal paramedian section of the abdominoinguinal region through the lacunar ligament. 1 = superior pubic ramus; 2 = pectineal ligament; 3 = lacunar ligament; 4 = spermatic cord; 5 = anterior interparietoperitoneal space; 6 = peritoneum; 7 = transversalis fascia; 8 = transversus abdominis; 9 = internal oblique; 10 = external oblique aponeurosis; 11 = skin; 12 = subcutaneous adiposocellular layer; 13 = inguinal skin fold; 14 = pectineus muscle; 15 = internal obturator muscle; 16 = external obturator muscle; 17 = urinary bladder; 18 = space of Bogros; 19 = retropubic space; 20 = obturator nerve and vessel; 21 = superficial fascia. (Mter Testut and LataIjet7.) FIGURE

The Arteries The external iliac artery, in its vascular sheath, courses along the medial border of the psoas. The external iliac vein is medial to the artery and slightly posterior. At this level, the epigastric and the deep circumflex iliac arteries arise (Fig. 11.6). The inferior epigastric artery originates on the anteromedial aspect of the external iliac artery, between 5 and 20 mm above the inguinal ligament. It follows a curved course with a superolateral concavity deep to the inguinal floor, circumventing the deep inguinal ring medially. Then, in an oblique superomedial course, it penetrates the rectus muscle near the inferior border of the semiarcuate line. Near its origin, the inferior epigastric artery gives rise to three main branches: • the cremasteric artery, which takes off from the lateral concavity of the inferior epigastric artery, crosses the interfoveolar ligament of Hesselbach on its posterior aspect, entering the inguinal canal through the deep inguinal ring; • the anastomotic branch of the obturator artery originates from the convex aspect of the inferior epigastric artery, coursing obliquely down to the inguinal floor, down to the inguinal ligament, and the free border of the lacunar ligament of Gimbernat where it constitutes a real threat when dissecting free a strangulated femoral hernia. Behind the pubis, the anastomotic branch of the epigastric artery joins the obturator artery as the latter enters the obturator foramen; • the subpubic branch of the inferior epigastric artery courses transversely, medially on the deep aspect of the fascia transversalis, 1.5 cm above the inguinal ligament and the pubic symphysis. Its branches terminate in the adiposocellular interparietoperitoneal space, hence into the retropubic space, as well as in the pyramidalis and the rectus muscles; • the internal and external terminal branches reach the rectus, pyramidalis, and the flat abdominal muscles (Fig. 11.8). The deep circumflex iliac artery arises from the lateral aspect of the external iliac artery, less than 1 cm above the inguinal lig-

105

11. The Space of Bogros

FIGURE 11.6. Parietal arterial network at the level of the space of Bogros. Posterior view of the inguinal floor. 1 = semiarcuate line of Douglas; 2 = rectus muscle and sheath; 3 = inferior epigastric artery; 4 = interfoveolar ligament of Hesselbach; 5 = deep circumflex iliac artery; 6 = iliopsoas muscle; 7 = femoral nerve; 8 = inguinal ligament-posterior reinforcement, the iliopubic tract; 9 = iliopectineal bandelette of Thomson; 10 = external iliac artery; 11 = external iliac vein; 12 = pectineal ligament of Cooper; 13 = femoral septum; 14 = obturator artery; 15 = anastomotic branch (inferior epigastric to obturator); 16 = infrapubic branch of inferior epigastric artery; 17 = ligament of Henle; 18 = transversalis fascia; 19 = cremasteric artery; 20 = deep inguinal ring; 21 = conjoined tendon; 22 = muscular branch.

ament which it accompanies to the level of the anterior superior iliac spine. Situated in a dihedral angle formed by the fascia iliaca behind and the transversalis fascia in front, it courses along the lower aspect to the space of Bogros, from medial to lateral. It provides along its way 4 to 5 ascending branches to the deep aspect of the inguinoabdominal region.

The Veins16,17 The external iliac vein ascends medially and deeply to its homologous artery. Within the space of Bogros, it receives two veins which parallel the arteries: the inferior epigastric vein and the circumflex iliac vein, both initially paired but joining to become a single trunk prior to entering the external iliac vein. Both of these veins receive tributaries that are parallel to the smaller arteries described above. There are two veins per artery, which give this parietal venous system a plexiform aspect, particularly when the anastomoses are observed and especially with the simple or paired voluminous anastomoses between the obturator and deep epigastric veins (see Fig. 11.7). These anastomoses are parallel to the corresponding arterial anastomosis, a branch of the inferior epigastric artery. It must be remembered that the obturator vein often bifurcates into a superior and an inferior branch, each of which has no arterial equivalent. They themselves remain distal from the space of Bogros. Some of these branches, however, represent the distal parietal terminals of the external iliac vein: • a vertical anastomosis situated behind the pubic ramus connects the superior obturator vein to the external iliac vein. It is often parallel to the anastomosis which joins the obturator vein to the deep inferior epigastric vein;

FIGURE 11.7. Parietal venous channels at the level of the space of Bogros. Posterior view of the inguinal canal. 1 = semiarcuate line; 2 = rectus muscle and sheath; 3 = inferior epigastric vein; 4 = interfoveolar ligament; 5 = deep circumflex iliac veins; 6 = iliopsoas muscle; 7 = femoral nerve; 8 = inguinal ligament and posteriorly, the iliopubic tract; 9 = iliopectineal bandelette of Thomson; 10 = external iliac artery; 11 = external iliac vein; 12 = pectineal ligament of Cooper; 13 = superior obturator vein; 14 = anastomosis (between external iliac vein and obturator vein); 15 = inferior obturator vein; 16 = confluent obturator veins; 17 = dorsal vein of the penis; 18 = internal pudendal vein; 19 = retropubic venous plexus; 20 = anastomosis (inferior epigastric vein and obturator vein); 21 = anastomotic branch with the retropubic plexus; 22 = suprapubic veins; 23 = cremasteric veins; 24 = ligament of Henle; 25 = venous plexus of the rectus muscle; 26 = deep inguinal ring; 27 = corUoined tendon; 28 = muscle venous branches.

• a retropubic branch corresponds to the homologous arterial branch from the epigastric artery; • anastomosis with the retrosymphyseal network within the retropubic space. The venous network within the space of Bogros is of major concern during inguinal herniorrhaphies through the anterior or suprapubic preperitoneal approaches, and when inserting prosthetic meshes. Concern stems from the fact that these veins are fragile and show stasis; they are more numerous than arteries although they are not necessarily parallel to the arteries; they exhibit marked variations; they are richly anastomosed between themselves and neighboring networks within the retropubic space and the rectus muscle. Although parietal in position, these veins are often described within the thickness of the transversalis fascia and receive numerous branches from fat pads, especially in the retropubic space. They can be cut or tom during cleavage of these interparietoperitoneal spaces, even as they seem empty. This underlines the necessity of careful dissection and hemostasis when preparing the site for prosthesis implant.

The Lymphatics 18 To be identified in the lower part of the space ofBogros (Fig. 11.8) are the following lymphatic nodes: • the lowermost node of the external iliac lateral chain of nodes. It is situated on the anterior aspect of the artery, immediately

106

J. Hureau

internal iliac fossa, in front of the external iliac vessels, between the urinary bladder and the deep aspect of the space of Bogros along the line leading from the internal iliac fossa to the deep inguinal ring. None of the above structures cross the space of Bogros (see Fig. 11.8).

Conclusion

11.8. The space of Bogros (right side). 1 = anterior parietal peritoneum; 2 = deep inguinal ring; 3 = cremasteric artery; 4 = testicular vessels; 5 = inferior node (lateral chain, external iliac); 6 = deep circumflex iliac artery; 7 = genitofemoral nerve; 8 = external iliac artery; 9 = external iliac vein; 10 = parietal peritoneum in internal iliac fossa; 11 = vas deferens and deferens artery; 12 = inferior node (middle chain-external iliac); 13 = inferior node (medial chain-external iliac); 14 = node of Cloquet; the uppermost deep inguinal node; 15 = inguinal ligament; 16 = suprapubic vessels; 17 = transversalis fascia; 18 = inferior epigastric vessels; 19 = interfoveolar ligament; 20 = vessels to rectus and pyramidalis; 21 = vessels to flat muscles of the abdomen; 22 = ascending branch of the deep inferior epigastric artery. (Mter Lambert, in Paturet. 8 ) FIGURE

above the inguinal ligament, near the origin of the inferior epigastric and the deep circumflex iliac arteries; • the lowermost node of the external iliac middle chain of nodes. It is often absent; • the lowermost node of the external iliac medial chain of nodes. It must not be confused with the lymph node of Cloquet, the uppermost node of the deep inguinal chain of lymph nodes found at the upper end of the femoral canal, between the femoral vein laterally and the lacunar ligament of Gimbernat medially. This node of Cloquet may show its upper pole at the very medial portion of the space of Bogros, through the femoral septum which it displaces. All the lymphatic chains are parietally situated with respect to the space of Bogros.

Other Parietal Elements of the Space of Bogros

Nerves The femoral nerve is far laterally situated, deep to the iliac fascia in front of the psoas muscle. The genitofemoral nerve descends in front of the psoas muscle within a split of the iliac fascia, and bifurcates into a femoral branch which accompanies the external iliac artery and a genital branch which enters the inguinal canal behind the spermatic cord or the round ligament of the uterus. The vas deferens and its vascular pedicle can be parietalized at the

The space of Bogros is but a widening of the interparietoperitoneal space in the dihedral angle between the wall of the internal iliac fossa and the deep aspect of the inguinoabdominal wall, above the inguinal ligament, and below the peritoneal reflection. It is a crossroad that joins the posterior pararenal space, the anterior interparietoperitoneal space, the retropubic space, the extraperitoneal pelvic spaces and goes through the inguinal canal, the cellular and potential spaces of the scrotum or labia majora. The space of Bogros is empty and cleavable. It is situated in a zone of transition between the lower limit of the abdomen and the upper thigh, a vulnerable area of the human body. Man, a biped with a soft abdomen, walks erect, and as such, exposes the neurovascular axes of his lower limbs, making for a fragile abdominal wall. This is the source of a genuine "pathology of the erect position" in which groin hernias have achieved preeminence.

References I. Vesalius A. De humani ecrrparis fabriea. Basel: J. Oporinus Edit; 1543. 2. Pare A. Les oeuvres d 'Ambroise Pare, eonseiller et premier ehirurgien du Roy. Paris: Gabriel Buon, Edit.; 1585. 3. Chassaignac E. Traite clinique et pratique des operations ehirurgieales ou traite de tooapeutique ehirurgical. Paris: Victor Masson et Fil; 1861. 4. Bogros AJ. Essais sur I'anatomie chirurgicale de la region iliaque et description d'un nouveau procede pour faire la ligature des arteres epigastriques et iIiaque externe. These Mid, Paris. W 153,29 Aout 1823. Paris: Didot Ie jeune Edit.; 1823. 5. Poirier P, Charpy A. Traite d'Anatomie Humaine. Vol. 2, Fasc. I. Paris: Masson Edit.; 1912. 6. Rouviere H, Delmas A. A natomie humaine descriptive, topographique et fonetionnelle. Vol. 2. Paris: Masson et Cie, Edit.; 1974. 7. Testut L, Latarjet A. Traite d'Anatomie Humaine, Vol. I. Paris: G. Doin et Cie, Edit.; 1948. 8. Paturet G. Traite d'Anatomie Humaine. Vol. I. Paris: Masson et Cie Edit.; 1951. 9. Couinaud C. Anatomie de l'abdomen. Paris: G. Doin et Cie, Edit.; 1963. 10. Drouet T. Le tissu sous-peritoneal. Montpellier: These Medecine; 1941. II. Mathis C. Le retroperitoine, essai anatomo-c1inique. Paris: These Medecine; 1959. 12. Hureauj, Agossou-Voyeme AI(, Germain M, PradelJ. Les espaces interparieto-peritoneaux posterieurs ou les espaces retroperitoneaux: anatomie topographique normal. ] Radiol. (Paris) 1991;72:101-116. 13. Hureau j, Pradel j, Agossou-Voyeme AI(, Germain M. Les espaces interparieto-peritoneaux posterieurs ou les espaces retroperitoneaux: anatomie tomodensitometrique pathologique. ] Radiol. (Paris) 1991; 72:205-227. 14. Hureau j, Pradel J. Tomodensitometrie du trone-anatomie normale et pathologique. Padova: Piccin Edit.; 1988; 342. 15. Agossou-Voyeme AK. Les espaces interparietoperitoneaux. Etude topographique. Donnes anatomotomodensitometriques. Memoire de DERBH (3rd cycle). Universite Rene-Descartes, Paris. 16. Bendavid R. The space of Bogros and the deep inguinal venous circulation. Surg Gyneeol Obstet. 1992;174:355-358. 17. Farabeuf LH. Les vaisseaux sanguins des organes genitourinaires de pCrinee et du pelvis. Paris: Masson et Cie, Edit.; 1904. 18. Rouviere H. Anatomie des lymphatiques de l'homme. Paris: Masson et Cie, Edit.; 1932.

Part III Epidemiology

Epidemiology of Inguinal Hernia: A Useful Aid for Adequate Surgical Decisions Alejandro Weber, Denzil Garteiz, and Salvador Valencia

Hernias of the abdominal wall constitute an important public health problem and often pose a surgical dilemma even for the most skilled surgeon. l In most countries, hernioplasty and cholecystectomy are the most common forms of elective surgery. In the United States alone, between 500,000 and 750,000 patients are operated on for inguinal hernia each year. 2 Yet, in spite of its great incidence, precise epidemiological data about inguinal hernia are difficult to obtain. Collection of reliable statistical information depends upon implementation of appropriate methodology, the clarification of ambiguities of terminology and other areas of uncertainty, widespread agreement on consistent classification practices, and so on. Table 12.1 gives examples of factors influencing the reliability of statistics on inguinal hernia. A practical example of these difficulties appears in the figures of the National Center for Health Statistics of the United States (NCHS), which compiles data on the surgery carried out annually in that country. In 1979, this study registered 421,000 inguinal hernia repairs, and in 1991 only 143,000. 3 This large difference is explained by the exclusion of outpatient procedures. Another important bias factor is purely medical: a significant percentage of patients with hernias are asymptomatic, or a hernia may go undetected by the physician. Physical examination, even when performed by experienced surgeons, has a diagnostic certainty of only 69% in differentiating between direct and indirect hernias. 4 In addition, the investigation may be complicated by the sheer variety of inguinal hernias (indirect, direct, pantaloon, multiple, and so on) and conditions with which they can be confused. Although there are many thousands of publications about inguinal hernia, only a few focus on the epidemiological aspects of this entity. Among the earliest of these studies are those by Arnaud in the pre-Bassini era (1748), who reported that one-eighth of the population under 30 years of age was "ruptured." One hundred years later, Malgaigne was the first to use mathematical reasoning to estimate a total rate of prevalence for inguinal hernia of3.2%.5 Contrary to what one would expect, there are relatively few reliable modem epidemiologic studies concerning the percentage of the general population affected and the total number of patients who have had surgical hernia repairs. For this reason, the true incidence and prevalence of inguinal hernias has not yet been determined. However, there are surgeons and investigators who recognize the importance of epidemiologic data about hernia. Perhaps one of the most complete and reliable studies to date is the

recently published article by Rutkow, which compiles the information of large series from the National Hospital Discharge Survey (NHDS) and the National Survey of Ambulatory Surgery (NSAS).2 As in other diseases, the study of the different statistical aspects of inguinal herniation can be crucial to understanding of such matters as the magnitude of the problem and its socioeconomic implications, the significance of risk factors, and the treatment approach with the best chance of success in each individual case. A clear perception of the different epidemiological aspects of inguinal hernia, such as frequency, age, and sex distribution, clinical presentation (unilateral, bilateral, or multiple), occurrence of recurrent or complicated hernias, hereditary patterns, and predisposing factors, makes us reflect that a hernia is much more than a "rupture" to be sutured or patched. For a clear understanding of the epidemiology of inguinal hernia, the terms "incidence" and "prevalence" should be defined. Incidence is the rate of occurrence of new cases of hernia in the population studied, often expressed as number of cases per thousand per year; prevalence is the total number of persons affected by hernia at any given time, expressed as a percentage of the population studied.

Epidemiological Aspects of Inguinal Hernia Inguinal hernia is the most frequent of all abdominal wall hernias. Its prevalence is difficult to establish, however, because it depends upon the age group and sex distribution of the general population. One of the most complete statistical analyses was made by lason in 1941 in New York, showing an estimated prevalence of 4.6%.6 In 1979, three-fourths of the abdominal wall hernias operated on in the United States were inguinal. From a total of 686,000 hernias operated on, 500,000 were inguinal (73%), 65,000 umbilical (9.5%), 43,000 incisional (6.2%), 19,000 femoral (2.7%), and 59,000 were other types of hernias (8.6%).3 Rutkow's most recent review combined the results of the two most important centers of health data concentration in the United States in 1996. He found approximately the same proportions: inguinal hernia 65.6%, umbilical 15.6%, incisional 9.1 %, femoral 2.3%, and the remaining 7.1 % were other hernias (Spigelian, epigastric, and so on).2 An interesting consideration is that in the near future, we 109

R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

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A. Weber et al. TABLE 12.1. Factors influencing the reliability of statistics on inguinal hernia Data recollection methods

Lack of diagnostic certainty

Insurance company survey vs. review of medical records Surgical records of inpatient vs. outpatient hospitals Lack of international hernia classification Patient questionnaire vs. physical examination Different names for the same thing (hernioplasty, herniorrhaphy, inguinal hernia repair) Different eponymic terms for surgery

may see a reduction in incisional hernias due to the advent oflaparoscopic surgery. This may, however, lead to a new class of hernias when trocar site hernias are included as an epidemiological category.

Sex Distribution It is a very well-known fact that the male population is more com-

monly affected with inguinal hernias than the female, but the true proportion is still unknown. The first statistical report about the distribution of inguinal hernia in the general population according to sex was done by Malgaigne in 1841. 5 He considered that while 7.7% of men had inguinal hernia, only 1.9% of women were affected, a frequency almost 4 times greater in men. Recently, elQaderi in Jordan reported a difference twice that of Malgaigne, stating that men are affected 8.2 times more than women. 7 Other reports, such as that by Wantz, registered a difference of up to 25 times greater. s It is interesting to observe the variations in sex distribution of primary inguinal hernia reported by large and small series throughout time (Table 12.2). The large differences among these series, with respect to the male-to-female ratio, probably reflect the difference in the number of patients, as well as the various racial, genetic, nutritional, and other differences in the populations studied. Primatesta and colleagues from the Department of Public Health and Primary Care of Oxford University reviewed more than 30,000 operated hernias and estimated that the lifetime risk for requiring an inguinal hernia repair in men was 27%, while for women it was only 3%, a 9 to 1 proportion. 9 These lower figures, when comparing the operated cases to the reported prevalence of hernia between men and women (9:1 compared to 19:1), may reflect the fact that that in some countries women are operated on more expeditiously than men. Ponka,1O on the other hand, carried out a study which compared the distribution of the several types of inguinal and femoral hernia according to sex, and concluded that for indirect inguinal hernias the frequency in men is almost double, while for direct hernias this relationship is 13 times greater. In the case of femoral hernia, the frequency is almost four times greater in women that in men (Table 12.3). TABLE 12.2. Distribution of inguinal hernia according to sex Year

Series

Number of patients

Male

Female

Ratio

1910 1993 1998

Coley Shouldice Rutkow

70,090 29,313 2,861

75.7% 95.5% 95%

24.3% 4.5% 5%

3:1 19:1 19:1

Lack of examiner experience Clinically undetected inguinal hernia Inguinal hernia vs. inguinal mass Indirect vs. direct inguinal hernia Inguinal hernia vs. femoral hernia Unexplainable chronic inguinal pain

Age Distribution Inguinal hernia in children is generally treated more promptly than in adults. Children are regularly examined by pediatricians, who recognize and detect the problem earlier and guide the parents to take the child to surgery to avoid complications. Parents, in tum, take their affected child to the surgeon as soon as possible, as they usually take care of their children's health and wellbeing very conscientiously; adults would do well to pay similar attention to their own health. The overall incidence of inguinal hernia in children less than 18 years old has been reported in ranges from 0.8% to 4.4%.1l It is believed that the origin of indirect inguinal hernia is related to the presence of a patent processus vaginalis (PPV). According to some authors, PPV exists in approximately 80% of the newborn children, but there is evidence that not all indirect inguinal hernias develop from a ppV.I2 The mechanism and the timing of the obliteration of the processus vaginalis is not known exactly, but it has been determined that 40% are obliterated in the first months of life and another 20% by the second year. The rest of the children will have a patent processus vaginalis for the rest of their lives. I3 Despite this high incidence, only 15 to 20% of them will develop an inguinal hernia.I 4 When the hernia is associated with a PPV, it usually is unilateral and indirect. It is more frequent in boys than in girls, due to the testicular migration from the abdomen to the scrotum during the fetal period. In boys, right-sided hernia is more common because the left testicle reaches the scrotum first, and the left processus vaginalis obliterates earlier. In neonatal intensive care units, a high incidence of inguinal hernia has been noted, especially in premature infants. In a review of more than 1,000 low birth weight survivors, it was found that 17% of males and 2% of females had hernias, giving a total cumulative prevalence of 9.2%. Added to the high frequency of PPV in these patients, it has been found that low birth weight, male sex, neonatal intravenous feeding and other factors that increase abdominal pressure contribute to this high herniation rate. 15 TABLE 12.3. Distribution of inguinal hernia according to sex and type Type of hernia

Male

Female

Ratio

Indirect Direct Combined Femoral

54% 27% 8% 3%

33% 2% 3% 11%

1.6:1 13.5:1 2.6:1 1:3.6

Source: Ponka,]L. Hernias of the Abdominal Wall. Philadelphia: WB. Saunders; 1980, p. 84.

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12. Epidemiology of Inguinal Hernia TABLE

12.4. Bilateral hernia reported in different studies

Author

Number of hernias

Ekberg (25) Abramson (17) Weber (unpublished) el-Qaderi (7) Akin (16) Rutkow (2) Weber (26) Phillips (28) McKernan (27)

313 459 259 1722 27,408 696,000 313 379 296

Method

% of bilaterality

Herniography Open surgery Open surgery Open surgery Open surgery Open surgery Laparoscopic surgery Laparoscopic surgery Laparoscopic surgery

20-29% 6.2% 22% 5% 6.2% 25.2% 36% 64% 36%

only 7%.22 This risk may be increased in patients with other congenital anomalies or collagen diseases like Marfan's or Ehlers-Danlos syndrome,23 and in children whose mothers smoked more than 20 cigarettes daily during pregnancy.24 EI-Qaderi found only 5% bilaterality in 1,722 patients of all ages, which correlates with the report of 27,408 healthy young men between 20 to 22 years that was carried out in Istanbul. Of those men, the incidence of bilaterality was 6.2%.7 Herniography has been very useful in detecting bilateral or multiple hernias, especially in cases with chronic inguinal pain and without palpable mass. With herniography, the presence of unilateral hernia has been reported from 18 to 28%, multiple ipsilateral hernias from 6.9 to 7.2% and bilateral hernias from 20 to 29%, much larger ftgures than those reported from clinical examinations on the asymptomatic population. 25 In a retrospective study carried out in a Mexican general hospital, we found that, in a total of 259 open inguinal repairs in adults, 22% had obvious bilateral hernias. Until the advent of laparoscopic surgery, bilaterality of inguinal hernia in adults was not considered as important as in children. In a case when only one side with hernia was clinically evident, a contralateral exploration was not even considered. The existence of a bilateral hernia was underestimated by the surgeon, and the patient would most probably refuse the procedure. Laparoscopic observations of the inguinal region have begun to prove that bilateral hernia is more frequent than previously suspected. Routine exploration of the inguinal region during procedures such as cholecystectomy or antireflux surgery sometimes reveals previously unsuspected bilateral defects. In addition, during the repair of a clinically evident unilateral hernia, a contralateral asymptomatic Bilateral Inguinal Hernia and clinically undetectable defect can be diagnosed. In a report The ongoing controversy among pediatric surgeons regarding the of more than 300 patients treated by laparoscopy, 13% presented convenience of exploring both inguinal regions in a boy with a with multiple hernia and 36% with bilateral hernia. Among these, hernia has encouraged the study of the incidence of bilaterality 60% had indirect bilateral hernia, 23% direct bilateral hernia, and in congenital inguinal hernia in recent years. The percentage of 17% combined defects. 26 Other authors in large multicentric studbilaterality in male infants is 15%,18 with a higher proportion in ies as Tetik,27 Phillips,28 and Woodward29 have found percentages female infants, but it may be as high as 40% in premature babies. 19 that go from 20 to 40% bilaterality (Table 12.4). Usually, pediatric surgeons perform contralateral inguinal explcr ration when a left inguinal hernia is detected because the chance of ftnding a coexisting, though asymptomatic, hernia on the right Complex Inguinal Hernia side can be up to 60%.20 Laparoscopic studies in the pediatric population have detected a contralateral PPV in 27% of the cases,21 It is important that surgeons acknowledge that although the most but the incidence of children who have undergone a contralateral common ftnding in a patient with hernia is the presence of a sinrepair in a subsequent surgery has been reported to range from gle defect, there are certain conditions which should arouse suspicion the case may be more complex, either because of the 4 to 34%. In a recent meta-analysis, Miltenburg reported that the risk of presence of a bilateral or multiple hernias, or because the recurdeveloping a metachronous hernia in patients under 18 years is rence risk is greater.

The frequency of inguinal hernia in the young male population has been the easiest to record because most studies are conducted in military and other closed group populations, where explorations can be performed on a regular basis by the same medical staff.I 6 For example, in Turkey, an epidemiological study of 27,408 healthy men from a military academy, ranging from 20 to 22 years of age, revealed that 3.2% had inguinal hernia. About ftfty-four percent of these were right-sided, 39.7% on the left side and 6.2% bilateral. 16 This correlates with the previous observations of inguinal hernia during childhood. Abramson determined that the current prevalence rate in men over 25 years in a community of Jerusalem, excluding those operated upon, was 18%, but when he included those who had had surgery, the lifetime prevalence rate went up to 24% (much higher than the previously reported prevalence in other studies). In this study, the prevalence rate of inguinal hernia increased markedly with age. In the group of 65-74 year oIds, it was 40%, while in the group aged over 75 years, the ftgure reached 47%. Because of these ftndings, he reasoned that if men lived long enough, one-third to one-half of them would eventually develop a herniaP Consistent with the previous ftndings, when considering the percentage of patients who undergo a hernioplasty, the frequency also increases with age. For instance, out of the total repairs performed in the U.S. in 1996, 18% were on patients under 15, 29% in the 15-44 group, 23% in the 45-64 group and 30% in the over 65 group.2

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Felix, in his 1,000 patient laparoscopic surgery series, reported that 14% of the primary hernias and 27% of the recurrent cases had a pantaloon defect. 30 In addition, 11 % of the patients had a femoral defect, a surprisingly high incidence, compared to open surgery controls. 31- 35 For this reason, he referred to these as complex defects, concluding that the laparoscopic approach to the posterior inguinal wall was responsible for the more objective evaluation. We also have found multiple defects in 17% of our laparoscopic hernia repairs. One of them had bilateral pantaloon and femoral defects combined with umbilical and epigastric hernias, which obviously cannot be considered a coincidence. In these patients with multiple defects, the surgeon must make a special effort to treat all possible sites of herniation. Expanding Felix's definition, we speak of complex hernias when one or more of the following conditions are present: family history of bilateral hernia, recurrent familial hernia, bilateral or recurrent hernia in the patient himself, or multiple defects. In these cases, special consideration must be given to the use of a mesh to protect the posterior inguinal wall and to repair simultaneously all possible hernia sites to avoid recurrences or to prevent new herniations. These complex hernias are more frequent than expected, and we consider that they could be related to an alteration in collagen metabolism, as will be discussed below. 2

Recurrent Inguinal Hernia Recurrent hernia is an unpleasant situation for both patient and surgeon. For that reason, for many years surgeons have been in relentless, but so far unsuccessful, pursuit of a zero recurrence technique. Every surgeon should be acquainted with the failure rate of current techniques to insure the best choice for the patient. We will not discuss the recurrence rate of each individual technique, since they are discussed elsewhere. Often, the surgeon does not know his own true rate of failure, for in many patients recurrence is never detected: patients are lost to follow-up, another surgeon may treat the recurrence, or the surgeon may have left medical practice by the time the hernia recurs. The overall recurrence rate of hernia repair is of approximately 10% and ranges from 0.2% to 15%.36-37 A significant number of patients have repeated recurrences, as shown in the study of Ijzermans, who found a cumulative percentage of repeated recurrent hernia of 23%. The repeated recurrence rates reported by others range from 8 to 33%, according to the repair technique used. The risk of repeated recurrent hernia seems to decrease with age.ljzermans reported that patients less than 50 years old had a recurrence rate of 33% after 5 years; those from 50 to 70 had a rate of 22%, and the ones over 70 years only 14%. Almost all of these recurrences are of the direct type. It is also important to consider that the risk of repeated recurrent hernias after the last operation is reduced significantly when the former procedure was done more than 5 years earlier. Other factors such as the number of previous recurrences, site, increase in intra-abdominal pressure, obesity and the method of anesthesia employed, appear to have no effect on this recurrence rate. 32 It would appear that if repeated recurrences take place more than 1 year after hernia repair, most likely these late recurrences cannot be explained by failure of the hernioplasty; more probably, they are local manifestations of a generalized defect in collagen metabolism. 38-39 Surgeons must consider these facts when deciding which oper-

A. Weber et aI.

ation to offer a patient with a recurrent or repeatedly recurrent inguinal hernia, to minimize the risk of yet another recurrence.

Risk of an Emergency and Complications Inguinal hernia repair is most commonly performed on an elective basis, and the morbidity and mortality rates of the procedure are usually very low. The same is not true for herniorrhaphy performed as an emergency procedure, when it is associated with strangulation or intestinal obstruction, especially in the elderly, in whom these emergency procedures are more frequent. Strangulation occurs in 1.3 to 3% of groin hernias. s It has been reported that while the mortality rate for elective surgery is less than one death per 10,000 operations, for emergency surgery the figure may rise to 5%.40 It is thus important for the surgeon to recognize the risk factors associated with these complications so that prompt surgical management can be provided. Epidemiological studies which address these points draw interesting conclusions. Oxford University, for example, reviewed more than 30,000 cases of inguinal hernia repair and found significant risk factors related to age and sex. 9 More than 90% of these repairs were performed on males. Approximately 9% were emergency procedures, and patients over 50 years of age were most likely to fall into this category. This group also had higher emergency readmission rates and significantly higher mortality than those who underwent elective repairs. Mortality during the first year after the surgery was consistently higher, probably because of associated illnesses. However, it was exceptionally high during the first 30 days after the surgery, which would appear to be related directly to the hernia itself or its complications. TheJawaharlal Institute of Postgraduate Medical Education and Research of India reviewed the specific risk factors for strangulation and intestinal obstruction in groin hernias. 41 The results are summarized in Table 12.5. The cumulative probability of strangulation for inguinal and femoral hernias has also been shown to be high in a study by Gallegos, with a proportion approximately 10 times greater for femoral hernias. While for inguinal hernia the probability was 2.8% at 3 months and 4.5% at 2 years, for femoral hernia it was 22% and 45%, respectively.42 The complication rate for pre term or otherwise seriously ill newborns has been reported as high as 31 %, with the potentially life-

TABLE 12.5. Risk factors for strangulation and intestinal obstruction 1. Complicated groin hernias occurred most commonly in patients aged 45-50 years. 2. In children, the incidence of complicated hernia was higher in the group of less than 2 years. 3. The male:female ratio for complicated hernia was 12:1, and for uncomplicated hernia 25: 1. 4. The right:left ratio for strangulated hernia was 3:1, and for simple hernia 2:1. 5. 27% of femoral and 19% of inguinal strangulated hernias had gan-

grenous contents. 6. Recurrent inguinal hernias were more frequently strangulated than primary hernias. 7. 65.8% of the patients with complicated hernia had the hernia for less than one year. Source: Rai S, Chandra SS, Smile SR. A Study of the Risk of Strangulation and Obstruction in Groin Hernias. Aust N Z] Surg. 1998;68:650-654.41

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12. Epidemiology of Inguinal Hernia

threatening consequences of incarceration, intestinal obstruction, and gonadal infarction. 19 From these results, it can be seen that the highest risk of hernia complication and the need for emergency surgery occurs among older males with any type of hernia, or in children of less than two years, and in femoral hernias (especially in females with hernia on the right side). Other facts to consider are that the male to female ratios decrease in emergency cases, that approximately one-fourth of strangulated hernias may have gangrenous contents, and that complications are more likely to occur in recurrent hernias. All of these risk factors are increased with hernias of short duration. So, in general, a hernia should be operated on as soon as it is diagnosed, especially when it has a short history, to avoid complications. Obviously, the mortality rate due to complicated hernia is also affected by the presence of concomitant medical illness, so patients with comorbid conditions should be considered as a higher risk.

Etiologic Aspects of the Epidemiology of Inguinal Hernia

Risk Factors Throughout history, several risk factors have been associated with the development of inguinal hernia. Unfortunately, most of these associations have been purely observational, and few have been studied for statistical significance. Genetic pattern of transmission, bipedalism, increased abdominal effort, previous surgery, obesity, constipation, chronic cough, prostatism, and ascites are all examples of these alleged risk factors. It seems however, that the risk of developing an inguinal hernia depends on different conditions, and this has been confirmed by some interesting epidemiologic studies. Abrahamson studied a population of young male subjects in a community in Jerusalem and found an increased prevalence of inguinal hernia in men with varicose veins and prostatic hypertrophy. An association was also found in thin men with hemorrhoidal disease and inguinal herniaP Although no mention is made in his article about the possible cause of these associations, all of these disorders may be indirecdy associated with increased abdominal pressure or connective tissue abnormalities. On the other hand, he found a lower prevalence of hernia in overweight patients, suggesting that obesity may be a protective factor against inguinal herniation. In his study, chronic cough, constipation, and physical effort were not statistically related to inguinal hernia. A similar epidemiologic study in a female population has been reported by Liem. 43 The only statistically significant factors associated with hernia were a positive family history of this entity and constipation. It is interesting to note that, in females also, obesity was found to be a probable protective factor against herniation. Females who performed exercise on a regular basis also had a lower prevalence of hernia in this study. Regular exercise activities must be differentiated from actions that involve lifting heavy objects. While one probably reinforces the abdominal wall and inguinal region, the other contributes to increased abdominal pressure and hernia formation. Flich demonstrated that both the weight of the lifted objects and the number of years of lifting contribute to the presence of inguinal herniation. 44

The observation that patients who smoke have a higher probability of developing inguinal hernia has long been reported. Initially, it was believed to be due to the chronic cough in smokers and the consequent abrupt increases in abdominal pressure. Although this may be a contributing factor, there are studies that show a metabolic basis for the association. The theory of "metastatic emphysema" was first proposed by Cannon and Read,45 who showed that smokers have higher elastolytic activity in their tissues due to an imbalance between protease and antiprotease elements in the blood. They found specifically that smokers have lower aI-antitrypsin activity that affects not only the lung, but also the tissues of the inguinal region. Another interesting study by these authors showed an association between smoking, abdominal aortic aneurysm, and inguinal herniation. 46 Other studies have shown altered healing patterns and collagen synthesis in surgical wounds of patients who smoke. 47 According to Read, this effect of smoking on wound healing is reflected not only in the occurrence of inguinal hernia, but also in the recurrence rate of smokers who have had a hernia repair.48 Finally, an increased prevalence of congenital inguinal hernia has been reported in babies of mothers who smoked more than 20 cigarettes a day during pregnancy.24 It is clear that smoking is an important risk factor for the development of inguinal hernia.

Hereditary Factors Review of the literature shows that predisposition to the development of an inguinal hernia may be hereditary. Some of the most interesting examples are reports of familial inguinal hernia by Kindon, Ashley, Mayo, Warren, Smith, and others. 49-53 Other evidence of genetic influence appears in a cohort study of 885 patients with inguinal hernia, which showed that 20.9% had affected first degree relatives and 16.6% second degree relatives. Unfortunately, the inheritance pattern has not yet been clearly identified. 15 One recent epidemiologic study of more than 2,000 cases of congenital hernia found that a girl with an affected sister was at a higher risk of developing a hernia than a girl or a boy with an affected brother. According to these results, the authors concluded that the pattern of transmission for inguinal hernia must be multifactorial and probably not sex linked. 54 On the other hand, a study of 280 families with more than one member affected by inguinal hernia found a frequent vertical transmission pattern. To these authors, the results reflect an autosomic dominant pattern with incomplete penetrance and sex influence. 55 Although it is clear that familial predispositions exist, there is no conclusive evidence to date of a specific pattern of transmission for inguinal hernia.

Metabolic Factors Hippocrates was the first to observe that inguinal hernia in the adult is probably associated with a metabolic defect. He noticed that during times of famine, people who ingested a certain type of peas, Lathyrus odoratus or Lathyrus sativus, which we now know contain an active component (beta-aminoproprionitrile) that interferes with collagen synthesis, had a tendency to develop giant hernias in many locations, as well as alterations in bones and tendons. 56 Up until 1922, most surgeons believed mainly in the saccular

A. Weber et al.

114 TABLE 12.6. Disorders of connective tissue associated with inguinal hernia 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

Ehlers-Danlos syndrome Williams syndrome Androgen insensitivity syndrome Robinow syndrome Serpentine fibula syndrome Alport's syndrome Marfan's syndrome Tel Hashomer camptodactyly syndrome Leriche's syndrome Testicular feminization syndrome Rokitansky-Mayer-Kuster syndrome Goldenhar syndrome Morris's syndrome Hurler-Hunter syndrome Gerhardt syndrome Menkes disease Kawasaki disease Pfannenstiel syndrome Wiedermann syndrome Rubenstein-Taybi syndrome Alopecia-photophobia syndrome

theory of hernia development. Harrison was the first to refute this theory and to suggest, more than 70 years ago, the possible involvement of connective tissue changes. 57 But it was not until 1970 that Read and his colleagues first observed and recorded changes in the rectus muscle sheaths of patients undergoing hernia repair. 39 He sampled rectus sheaths of healthy persons versus hernia patients and found a significant difference in the weight of the samples: rectus sheaths from patients with inguinal hernia were much lighter. Further studies by Wagh later demonstrated that this difference was due to a deficiency in hydroxyproline (and therefore of polymeric collagen) in these patients.58,59 This same author later proved, in an interesting study, that patients with hernia had a lower rate of fibroblast proliferation in their tissues and that incorporation of proline into their collagen was defective. 60 All of these studies suggest that patients with direct inguinal hernia have ultrastructural and biological alterations in their tissues. The results of other studies, such as those by Peacock, have also found structural abnormalities in tissues from indirect and recurrent hernias. In one of his publications, he even proposes that the terms "direct" and "indirect" hernia should be abandoned, since structural abnormalities are found in tissues on both sides of the epigastric vessels. 38 Finally, the most recent evidence of altered tissue structure in hernia patients is reported by Bellon. 61 He used immunohistochemical studies to demonstrate the presence, in tissue samples taken from direct inguinal hernias, of a metalloproteinase that may precipitate this condition. It must also be mentioned that many connective tissue disorders are associated with increased rates of inguinal herniation; these are undoubtedly related to the weakened structure of the abdominal wall in these patients (Table 12.6).

References 1. Wexler MJ. Herniorrafia inguinallaparosc6pica. In: American College of Surgeons' Scientific American Cirugia. New York: Scientific American; 1995; Sup.5:1-3. 2. Rutkow I. Epidemiologic, economic, and sociologic aspects of hernia

surgery in the United States in the 1990s. Surg Clin Nurth Am. 1998; 78:941-951. 3. Rutkow 1M, Robbins AW. Demographic, classificatory, and socioeconomic aspects of hernia repair in the United States. Surg Clin Nurth Am. 1993;73:413-426.

4. Ralphs DNL, Brain AJL, Grundy DJ, Hobsley M. How accurately can direct and indirect inguinal hernias be distinguished? Br Med J 1980; 280;1039-1040. 5. MalgaigneJ: Le.;:ons c1iniques sur les hernies. Paris: Bailliere; 1841:19, 174. 6. lason A. The incidence of hernia in man. In: Hernia. Philadelphia: Blakiston; 1941:156-179. 7. el-Qaderi S, Aligharaibeh Kl, Hani IB, et al. Hernia in northern Jordan. Some epidemiological considerations. Trap Geogr Med. 1992;44: 281-283. 8. Wantz GE. Abdominal wall hernias. In: Schwartz SI, Shires GT, Spencer FC, et al., eds. Principles of surgery. New York: McGraw-Hill, Inc.; 1999: 1585-1611. 9. Primatesta P, Goldcare MJ. Inguinal hernia repair: incidence of elective and emergency surgery, readmission and mortality. Int] Epidemiol. 1996;25:835-839. 10. Ponka JL. Hernias of the abdominal wall. Philadelphia: W.B. Saunders; 1980:82-89. 11. Bronsther B, Abrams MW, Elboim C. Inguinal hernias in children. A study of 1000 cases and review of the literature.] Am Med Wom Assoc. 1972;27:522-535. 12. Snyder WH, Greany EM. Inguinal hernia. In: Mustard WT, Ravitch MM, Snyder WH, et al., eds: Pediatric surgery, 2nd ed. Chicago: Medical Year Book; 1969:692. 13. Chin T, et al. The morphology of the contralateral internal inguinal rings is age-dependent in children with unilateral inguinal hernia. ] Pediatr Surg. 1995;30:1663-1665.

14. Miltenburg DM, et al. Laparoscopic evaluation of the pediatric inguinal hernia-a meta-analysis.] Pediatr Surg. 1998;33:874-879. 15. Powell TG, Hallows JA, Cooke RWl, et al. Why do so many small infants develop an inguinal hernia? Arch Dis Child. 1986;61:991-995. 16. Akin ML, Karakaya M, Batkin A, et al. Prevalence of inguinal hernia in otherwise healthy males of 20 to 22 years of age.] R Army Med Corps. 1997;143:101-102. 17. Abramson JH, Gofin J, Hopp C, et al. The epidemiology of inguinal hernia. A survey in western Jerusalem. ] Epidemiol Community Health. 1978;32:59-67. 18. CoxJA. Inguinal hernia of childhood. Surg Clin Nurth Am. 1985;65: 1331-1342. 19. Rescorla FJ, Grosfeld JL. Inguinal hernia repair in the perinatal period and early infancy: clinical considerations.] Pediatr Surg. 1984; 19: 832-837. 20. Rodriguez RI, Flores PLC, Dominguez GF}, et al. Hernia inguinal unilateral: ~exploraci6n quirurgica contralateral sistematica? Cir Gen. 1993;15:2-5. 21. Holcomb GW 3rd, et al. Laparoscopic evaluation for a contralateral patent processus vaginalis. ] Pediatr Surg. 1994;29:970-973. 22. Miltenburg DM, Nuchtern J, Jaksic T, et al. Meta-analysis of the risk of metachronous hernia in infants and children. Am]Surg. 1997;174:741-744. 23. Moss RL, Hatch EI. Inguinal hernia repair in early infancy. Am] Surg. 1991;161:596-599. 24. Christianson RE. The relationship between maternal smoking and the incidence of congenital anomalies. Am] EpidemioL 1980;112:684-695. 25. Ekberg 0, Lasson A, et al. Ipsilateral multiple groin hernias. Surgery 1994;115:557-561. 26. Weber A, Garteiz D, Cueto J. Stoppa-type laparoscopic repair of complex groin defects. Surg Laparosc Endosc. 1999;9:14-16. 27. Tetik C, Arregui ME, DulucqJL, et al. Complications and recurrences associated with laparoscopic repair of groin hernias. A multi-institutional retrospective analysis. Surg Endosc. 1994;8:1316-1323. 28. Phillips EH, Arregui M, Carroll BJ, et al. Incidence of complications following laparoscopic surgery. Surg Endosc. 1995;9:16-21.

12. Epidemiology of Inguinal Hernia 29. Woodward AM, Choe ED, F1int LM, et al. The incidence of secondary hernias diagnosed during laparoscopic total extraperitoneal inguinal herniorrhaphy.] Laparoendosc Adv Surg Tech A. 1998;8:33--38. 30. Felix EL, Michas CA, Gonzalez MH. Laparoscopic hernioplasty: why does it work? Surg Endosc. 1997;11:3~1. 31. Schapp HM, Van de Pavoordt HD, Bast 1]. The preperitoneal approach in the repair of recurrent inguinal hernias. Surg Gynecol Obstet. 1992;174:460-464. 32. Ijzermans J, Wilt H, Hop W, et al. Recurrent inguinal hernia treated by classical hernioplasty. Arch Surg. 1991;126:1097-1100. 33. Marsden AJ. Recurrent inguinal hernia-a personal study. Br] Surg. 1988;75:263--266. 34. Rutledge R Cooper's ligament repair: a 25-year experience with a single technique for all groin hernias in adults. Surgery. 1988;103:1-10. 35. Postlethwait RW. Causes of recurrence after inguinal herniorrhaphy. Surgery. 1971;69:772-775. 36. Halverson K, McVay cv. Inguinal and femoral hernioplasty: a 22-year study of the author's method. Arch Surg. 1970;11:127-135. 37. Thieme ET. Recurrent inguinal hernia. Arch Surg. 1971;13:238-24l. 38. Peacock EE, Madden JW. Studies on the biology and treatment of recurrent inguinal hernia: II. Morphological changes. Ann Surg. 1974; 179:567-57l. 39. Read RC. Attenuation of the rectus sheath in inguinal herniation. Am ] Surg. 1970;120:610. 40. Schumpelick V, Treutner K-H, Arlt G. Inguinal hernia repair in adults. Lancet. 1994;344:375--378. 4l. Rai S, Chandra SS, Smile SR A study of the risk of strangulation and obstruction in groin hernias. Aust N Z] Surg. 1998;68:650-654. 42. Gallegos NC, Dawson J, Jarvis M, et al. Risk of strangulation in groin hernia. Br] Surg. 1991;78:1171-1173. 43. Liem MS, van der Graaf Y, Zwart RC, et al. Risk factors for inguinal hernia in women: a case-control study. The Coala trial group. Am] Epidemiol. 1997;146:721-726. 44. F1ich J, Alfonso JL, Delgado F, et al. Inguinal hernia and certain risk factors. Eur] Epidemiol. 1992;8:277-282.

115 45. Cannon DJ, Read RC. Metastatic emphysema. A mechanism for acquiring inguinal herniation. Ann Surg. 1981;194:270-273. 46. Cannon DJ, Casteel L, Read RC. Abdominal aortic aneurysm, Leriche's syndrome, inguinal herniation, and smoking. Arch Surg. 1984;119:387-389. 47. Jorgensen LN, Kallehave F, Christensen E, et al. Less collagen production in smokers. Surgery. 1998;123:450-455. 48. Read RC. Cigarette smoking, herniation, and recurrence. Surgery. 1998;124:942. 49. Kindon JA. On the causes of hernia. Roy Med Chir Trans Lond. 1864; 47:295-32l. 50. Ashley M. A case of familial inheritance of oblique inguinal hernia. ] Hered. 1942;33:355. 5l. Mayo C. Congenital hernia in three boys of the same family. Proc Staff Meet Mayo Clin. 1930;5:103. 52. Warren LF, Atleson F. Inheritance of hernia in a family of HolsteinFriesian cattle.] Hered. 1931 ;22:345. 53. Smith MP, Sparkes RS. Familial inguinal hernia. Surgery. 1968;57: 809-812. 54. Jones ME, Swerdlow AJ, Griffith M, et al. Risk of congenital inguinal hernia in siblings: a record linkage study. Paediatr Perinat Epidemiol. 1998;12:288-296. 55. Gong Y, Shao C, Sun Q, et al. Genetic study of indirect inguinal hernia.] Med Genet. 1994;31:187-192. 56. Hippocrates. Quoted by Selye, H. Lathyrism. Can Bioi. 1957;16:1. 57. Harrison PW. Inguinal hernia: a study of the principles involved in the surgical treatment. Arch Surg. 1922;4:680-689. 58. Wagh PV; Read RC. Collagen deficiency in rectus sheath of patients with inguinal herniation. Proc Soc Exp Bioi Med. 1971;137:382. 59. Wagh PV; Read RC. Defective collagen synthesis in inguinal herniation. Am] Surg. 1972;124:819-822. 60. Wagh PV, Leverich AP, Sun CN, et al. Direct inguinal herniation in men: a disease of collagen.] Surg Res. 1974;17:425-433. 6l. Bellon JM, Bujan J, Honduvilla NG, et al. Study of biochemical substrate and role of metalloproteinases in fascia transversalis from hernial processes. Eur] Clin Invest. 1997;27(6):510-516.

13 Occult Hernias in the Male Patient Sam G.G. Smedberg and Leif Spangen

Introduction The following presentation will focus on the understanding of the origin of groin pain in occult hernia and its differential diagnoses, the physical and radiological examination of the patient, and a discussion of the results of studies. Hernias may be symptomatic before they are clinically evident. Pain and discomfort, not the bulging of the hernia, are the most frequent first symptoms of hernia. 1 The pain caused by a nonpalpable hernia may be intense and disabling, preventing the patient from working or taking part in sports activities. However, there are several conditions that cause similar symptoms. A careful history of the pain and a thorough investigation demonstrating or excluding the presence of a hernia are necessary before surgery is decided upon. An abdominal wall hernia is "the protrusion of some internal body structure through the abdominal wall." The clinical problem of occult hernias includes not only the diagnosis and treatment of nonpalpable peritoneal sacs but also the protrusion of other tissues, of which preperitoneal fat (the so-called hernia lipoma or lipoma of the cord) is the most frequent. Asymptomatic occult hernias are of clinical interest for prophylactic treatment at the same time as repair of hernia in the same groin or on the contralateral side. The transabdominal preperitoneal (TAPP) laparoscopic procedure has made it possible to find these hernias, and some authors have recommended the TAPP operation for this reason. 2 In pediatric practice in North America, the contralateral side is often explored to find and treat an asymptomatic hernia. Unnecessary operations should be avoided, however. Negative findings necessitate a more extensive dissection with increased risk of damaging the cord. Selective exploration of the asymptomatic side has been suggested and can be performed after an examination before or during the operation to confirm the presence of hernia. Different techniques may be used, such as herniography,3 ultrasonography,4 intraoperative pneumoperitoneum,5 and even laparoscopy through the hernia opening on the symptomatic side. 6

Epidemiology In an adult male population examined by surgeons, one out of four had a hernia or had been operated on for hernia. 7 The same R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

investigation found that, over the age of 75, almost half of the male population had a hernia or had been operated on for hernia. Similar results were found in a Swedish epidemiological study of men aged 54 years (22%) and 62 years (30%).8

Indirect Hernia A patent processus vaginalis is present in all males in the perinatal period as part of the descent of the testicles to the scrotum. Pediatric studies show that the obliteration of the processus vaginalis takes place during the first two years of life, but as many as 40% remain patent. 9,10 Half of these develop into clinical hernias, and in 20% of males, a patent but undilated processus vaginalis is dormant for the remaining lifetime. 9 ,1l The highest incidence of hernia occurs during the first year of life, and a second peak incidence of indirect hernia is found in young adults. However, indirect hernias continue to appear in all age groups. Not until the seventh decade does the incidence of direct hernia match the incidence of indirect hernia in the male.

Direct Hernia Impaired collagen quality12 and accelerated breakdown of collagen in the inguinal region 13 have been demonstrated in hernia patients. Collagen studies show that hereditary factors predispose to these conditions.I 4 Repetitive increase in intra-abdominal pressure, as occurs in sports activities, overloads the thin supportive structures in the inguinal area. In patients with a predisposition for hernia, this may accelerate the development of a hernia. A high incidence of occult direct hernias, not expected until later in life, was demonstrated by herniography in young athletes. 15

Femoral Hernia The high incidence of femoral hernia in females is found predominantly in multiparous women. 16 Femoral hernias are more frequent in females than in males in a ratio of 2.5:1. The ratio of inguinal to femoral hernias is between 10:1 and 8:1.1 6 Preperitoneal fat may appear not only as lipomas of the cord in the inguinal canal, but also as fatty tabs in the femoral canal and in the

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13. Occult Hernias in the Male Patient obturator foramen. By herniography combined with femoral phlebography, Gullmo demonstrated fatty tabs in the femoral canal compressing the femoral vein during straining, imitating femoral hernias. I7 In elderly women with substantial weight loss, these fatty tabs disappear and may be replaced by small femoral and obturator hernias.

Localization Pain caused by a hernia is inguinal in the majority of cases. Lower epigastric pain (the location of the mesenteric root) may be caused by omentum trapped in the hernia sac. Scrotal pain or referred pain along the ilioinguinal nerve are less common. The differential diagnostic possibilities are, however, numerous, as may be seen in Table 13.1.

Diagnosis and Differential Diagnosis Radiation

History The history of symptoms in patients with obscure groin pain is of great importance. The history should be explored before the physical examination is performed or any other investigations are decided upon. The interpretation may be difficult, however, since there are several conditions causing similar symptoms. Furthermore, chronic pain tends to become more uniform over time irrespective of its origin. For this reason, a systematic analysis of the symptoms is valuable. Pain can be classified according to its evolution, exact localization, radiation, intensity and character, duration, and reproducibility. Factors that provoke and relieve the pain are of importance.

Evolution The very first symptom is often diagnostic, though sometimes difficult for the patient to recollect. Pain will often become dull and more difficult to localize and characterize after a long period of symptoms. The first symptom of hernia may be sudden and caused by (for example) lifting a heavy object. However, there is often a gradual onset of the symptoms provoked by activities that increase intra-abdominal pressure. Information about a sudden onset related to trauma gives the suspicion of a muscular or tendinous rupture or tear. The onset of overuse i~uries is often related to a change in the pattern of muscular activities, for example, the training in athletic sports. The onset of pain could also be related to previous operations in the lower abdomen and inguinal area such as herniorrhaphy, appendectomy, and gynecological operations through Pfannenstiel incisions. In these cases, the pain is most often caused by postoperative neuralgia, if not a recurrent hernia. Laparoscopic trocars may also cause nerve damage and pain.

TABLE

When there is radiation of pain in cases of inguinal hernia, it is often caused by nerve involvement. The pain radiates mainly along the ilioinguinal nerve, caudally to the upper medial part of the thigh or laterally toward the iliac crest. Genitofemoral nerve pain radiates to the scrotum·, while pain caused by an obturator hernia may radiate to the lower medial part of the thigh. Omentum trapped in an occult hernia may cause abdominal pain. Radiation of pain from the inguinal area to the iliac fossa or even higher up on the abdomen may be caused by tendinitis of the rectus abdominis muscle. Radiation in a downward direction on the medial side of the thigh may be caused by adductor muscle tendinitis. Compression of the lateral femoral cutaneous nerve causes pain radiating from the lateral part of the inguinal area to the lateral side of the thigh, so-called meralgia paresthetica. Pain radiating from the groin to the knee or in the opposite direction may be caused by hip joint arthrosis. In half of patients with ischial lumbago, pain radiates to the groin.

Intensity and Character The parietal pain related to hernia is most pronounced in the early development of the hernia due to dilation of the hernia sac. IS When the hernia grows and becomes manifest, this type of pain often disappears. Acute sharp pain may be neuralgic or caused by traumatic ruptures of muscles and tendons. Sharp pain in the chronic condition is most likely caused by nerve entrapment. Burning sensations are also related to nerve involvement. Intermittent pain of the neuralgic type is sometimes seen in cases with occult indirect hernias. Dull pain occurs in a variety of conditions. In long-standing pain it can be difficult to discriminate different conditions from one another. Overuse injuries such as tendinitis and

13.l. Differential diagnosis in obscure groin pain

Musculoskeletal disorders

Urogenital disorders

Other disorders

Hip arthrosis Symphysitis Pelvospondylitis Spinal disorders Chronic overuse injuries tendinitis tenoperiostitis stress fracture of pubic bone Acute overuse injuries musculotendinous tears and ruptures avulsion fracture

Prostatitis Chronic cystitis Ureteral obstruction Varicocele Hydrocele

Intra-abdominal adhesions Intra-abdominal tumor Constipation and other functional bowel disease Nerve entrapment, primary and postoperative ilioinguinal nerve iliohypogastric nerve femoral branch of genitofemoral nerve lateral femoral cutaneous nerve anterior branches of lower intercostal nerves Varicose veins Hip claudication Hernia; inguinal, femoral, obturator, Spigelian

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tenoperiostitis may cause moderate symptoms during the exercise itself. However, at rest a couple of hours after the sports activities, the pain often increases and may continue until the next day or longer. Elderly patients with groin pain both related to physical activity and causing discomfort in the night may suffer from arthrosis of the hip joint.

Duration The duration of pain caused by a hernia is often limited to the duration of the strain that increases intra-abdominal pressure. The pain often disappears in a short period of time if the patient can relax. Prolonged pain after physical activities suggests a musculotendinous origin. In patients with continuing pain varying in intensity, sometimes correlated to straining and sometimes without an obvious explanation, other causes such as nerve involvement, inflammatory conditions or hip arthrosis should be sought.

Reproducibility Hernia pain is often provoked by Valsalva maneuvers. In the relaxed supine position, hernias seldom cause pain. The understanding of the symptoms can be improved by relating them to daily life activities such as getting out of bed (rectus abdominis muscle), walking upstairs (iliopsoas muscle), stepping into or out of a car (adductor muscles), lifting heavy objects, laughing, straining (hernia, spinal disorder), and so on.

Physical Examination The physical examination should cover the most common differential diagnoses. Provided a thorough history has been obtained, the physical examination can focus on the most probable diagnoses. At inspection, with the patient standing, irregularities in the groin area should be noticed as well as the shape of the lower back. A leg length difference and muscular atrophies should be noted. Palpate for hernias on the standing patient, but without trying to provoke pain at this stage of the examination. Through the invaginated scrotal skin, you will reach the external inguinal ring and sometimes into the inguinal canal depending on the width of the ring. The patient is asked to strain and cough. A small indirect hernia can be detected as a soft swelling along the spermatic cord and an incipient direct hernia will compress the inguinal canal from behind. A weakness of the posterior inguinal wall should also be evaluated with the patient at rest in the supine position. Femoral hernias are searched for below the line between the pubic tubercle and the anterior superior iliac spine and medial to the femoral vessels. With the patient in the supine position, before pain is provoked, start the examination by testing the sensitivity of the skin of the lower abdomen and the thighs. When there is nerve involvement of any kind, you will often find numbness in the area of the nerve and hypersensitivity to pin pricking in the same area. Sometimes these findings are associated with a trigger point, the point of the injury, along the course of the nerve. The dermatomes of the ilioinguinal, the iliohypogastric and the genital branch of the genitofemoral nerves are easily separated. At the end of the examination, verification of nerve involvement is made by diagnostic

S.G.G Smedberg and L. Spangen

nerve blocks. Injecting an anaesthetic in the area of the pain gives only limited information. A nerve block should be done at a distance from the area of the pain, with a long acting drug such as bupivacaine. Three to 4 ml just under the external oblique aponeurosis medial and cranial to the anterior superior iliac spine is sufficient to block the ilioinguinal and the iliohypogastric nerves. Numbness of the skin verifies the correct location of the injection, and banishment of the pain verifies that the nerve is involved in the symptoms of the patient. If the latter is incomplete, however, the nerve may still be involved at a more central level. This can be verified by a central nerve block using epidural or spinal anaesthesia. An abdominal examination is performed searching for tenderness and palpable masses. Small indirect hernias may cause radiation of pain 3 to 4 cm along the Spigelian aponeurosis, the semilunar line cranial to the internal inguinal ring. The testicles and spermatic cords are palpated. Hydrocele, spermatocele, and varicocele are excluded. At rectal examination, the prostatic gland should be evaluated. If there is a suspicion of obturator nerve involvement, the obturator foramen can be reached with the examining finger through rectal examination. Tenderness of the symphysis pubis can easily be evaluated by bimanual examination. The musculoskeletal component of differential diagnosis in groin pain may necessitate an extensive examination. The main points of interest, however, are passive and active provocation tests of the rectus abdominis, iliopsoas, rectus femoris, and adductor muscles and tendons, overuse injuries of the adductor muscles being the most common. The lower thoracic and lumbar spine, sacroiliac joints, symphysis pubis, and the hip joints should be evaluated. Hip arthrosis can be found in middle-aged patients, not only in the elderly. Simple laboratory tests such as an erythrocyte sedimentation rate and urine microscopy may be of value.

Radiological Examinations Normally, the decision to operate on a hernia is based on clinical findings alone. No other confirmation is necessary. However, when the physical examination fails to reveal the presence of a hernia, there are radiological techniques available to aid diagnosis. Exploratory operations without a preoperative diagnosis should be a last resort in elective surgery. An inguinal operation is not harmless, and in a patient with a pain syndrome, the condition may be exacerbated after an operation. On the other hand, to wait for physical signs to appear while the patient suffers is an out-of-date strategy and no longer necessary, thanks to improved investigative techniques.

Herniography A positive contrast examination of the peritoneal lining of the inguinal region and the pelvis was introduced in adult patients in the early 1970sP·19 Its use has become widespread in the investigation of groin pain. The technique is not difficult, but since it is an invasive procedure, the indications should be restricted mainly to the investigation of occult hernia. With the patient in the supine position, the abdominal wall is punctured below the umbilicus on the left side with a mandrin-equipped catheter or in the midline with a fine needle, and the contrast medium is injected under flu-

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13. Occult Hernias in the Male Patient

oroscopy control into the abdominal cavity. The patient is turned to the prone position, and the head of the table is elevated. The contrast medium will pool in the inguinal region, and during Valsalva maneuvers hernias and irregularities of the peritoneal lining will be clearly demonstrated on tangential exposures. 20 Equipment that allows tilting of the tube is required (Fig. 13.1). Additional oblique exposures will facilitate the interpretation of the radiological findings. The groin side being investigated is tilted some 20° down to place the inguinal fossae at right angles to the beam and minimize the overlapping of hernias seen on the radiogram. Both sides are investigated in the same manner, irrespective of the location of symptoms. The patient should void before the investigation. Atropine may be administrated to prevent vasovagal reactions. No other preparation of the patient is necessary. Complications are few and relatively harmless. 21 Occasionally, the bowel is punctured. The needle is withdrawn and a new puncture can be performed, and the investigation continued. Bleeding from punctures of intra-abdominal vessels or from the abdominal wall are rare. Peritoneal reactions to the contrast media described in early reports are no longer a problem with the isotonic contrast media now available. The accuracy of herniography concerning the presence of hernia is generally reported to be high.17.22-24 False positive and false negative investigations are rare,25 though not unknown.26 The accuracy is the same whether the hernia is occult or clinically manifest25 (Fig. 13.2). The interpretation of the type of hernia, however, is more difficult, and may be misjudged even by an experienced investigator. Incipient stages of direct hernias may be difficult to distinguish from deep peritoneal fossae, and direct hernias emanating lateral to the medial umbilical fold may be difficult to differentiate from broad and shallow femoral hernias. The usefulness of herniography in occult hernia cases is encouraging. The Swedish series published in the 1980s22- 24 was followed by presentations of results from other countries. 27- 32 In a series of 73 patients with obscure groin pain, Ekberg and coworkers found hernias on the symptomatic side in 26 patients by

13.2. Herniography in a 30-year-old athlete with right-sided groin pain and no palpable hernia. A right-sided direct hernia was discovered.

FIGURE

herniography. Relief of groin pain was registered in 16 out of 17 patients who subsequently underwent operation. 22 In another series of 250 patients with obscure groin pain without previous surgery on the symptomatic side, hernias judged to be the cause of the pain were found by herniography in III patients. 24 Ninetyseven were operated on, all of whom had hernias. In 84 patients (87%) the pain was relieved. In the remaining cases, whether operated on or not, workup revealed a number of different diagnoses. Following this and two further publications, one on groin pain in patients with previous surgery33 and the other on athletes with groin pain,1 5 the differential diagnostic (Table 13.1) was put together.34 In more recent publications, similar results have been reproduced. 29 ,3o The technique is being adopted in an increasing number of countries. Many reports include herniographic findings of asymptomatic occult hernias on the contralateral side. The clinical significance of these findings is not obvious. In a series of 90 male patients with a symptomatic unilateral indirect hernia, herniography was performed. Contralateral asymptomatic findings were recorded. The patients were followed up for 3 to 7 years.35 Thirty had no contralateral hernia, and among these, no hernias developed during the follow-up. Nineteen had a patent processus vaginalis or a small, diverticular, slightly dilated indirect protrusion, one of which (5%) developed into a manifest hernia after 4 years. Occult indirect hernias located within the inguinal canal were detected in 9 patients (10%). A clinically manifest hernia developed in 50fthese (56%). Six out of 27 patients (22%) with direct or combined hernias became clinically manifest. In 1 of 5 patients with an incipient femoral hernia, a direct hernia developed. On the basis of risks of complications, the patient with an occult indirect hernia other than nondilated processus vaginalis on the asymptomatic side should be offered an operation.

Ultrasonography

13.1. Herniography: positioning of the patient and direction of the X-ray beam.

FIGURE

The use of ultrasonography in diagnosing occult hernia in adults has been limited. The supine position commonly used at the examination makes it difficult to demonstrate small hernias which are normally detectable only in the upright position during straining. Direct hernias may, however, bulge during straining in the

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supine position. Posterior wall deficiencies were demonstrated accurately by dynamic ultrasound examinations in Australian Rules footballers with chronic groin pain.36 An indirect sign of occult hernias shown by ultrasonography was reported in pediatric patients. The size of the internal inguinal ring on the asymptomatic side was measured in boys; in more than 95% of those with widened internal inguinal rings (over 4 mm), hernias were found. 37 The hernia sac in femoral hernia can be demonstrated by ultrasonography. Ultrasonography has also been valuable in the differential diagnosis of Spigelian hernias. 38 Reports in the literature on ultrasonography and hernia, however, mainly concern the identification and clarification of lumps in the inguinofemoral region.

Computed Tomography (CT) Like ultrasonography, CT is at its best in distinguishing between different kinds of lumps in the groin and abdominal wall. The experience of use of CT for the diagnosis of uncertain findings is limited. A positive finding of an abdominal wall hernia was considered reliable, while a negative finding did not exclude the diagnosis. 39 The use of the Valsalva maneuver increased the diagnostic accuracy. The use of CT in the diagnosis of abdominal symptoms has improved the preoperative diagnosis in rare conditions like obturator hernias. A study of 36 cases showed that an accurate preoperative diagnosis was improved from 39% before the introduction of CT to 78% after CT was introduced. 40 This had, however, no impact on patient outcome.

Magnetic Resonance Imaging (MRI) MRI has been used to verify the diagnosis in patients with clinically evident groin herniations. 41 The experience of MRI for differential diagnostic purposes in the groin area is limited. It has been used to confirm uncertain diagnoses in chronic pelvic pain.42 In one study including 10 patients with groin pain without physical signs, an indirect hernia was found in 1 patient and a direct hernia in 1. 43 The dynamic MRI was performed with the patient supine, kneeling at rest and during a Valsalva maneuver. A high signal indicating musculotendinous injury but no signs of hernia was found in 7. In one case, no abnormality was found.

Laparoscopy The use of the laparoscopic technique for hernia repair is well established, though there is some controversy about learning curves and costs. Laparoscopy can be used for the diagnosis of nonpalpable hernias, particularly indirect hernias. Contralateral asymptomatic hernias are quite often found at laparoscopy. In a randomized study comparing the TAPP and the Lichtenstein techniques, the authors found that the laparoscopic technique's ability to expose otherwise occult defects was an advantage, tending to eliminate the risk of recurrences due to missed hernias. 2 However, the comparably low pressure in the abdominal cavity at laparoscopy compared to the pressure obtained by the Valsalva maneuver makes the diagnosis of direct hernias difficult. Preperitoneal fat will in many cases hide direct hernia defects, and such a hernia may be missed. It is questionable whether a major pro-

S.G.G Smedberg and L. Spangen

cedure is indicated just for diagnostic purposes. The more preferable totally extraperitoneal (TEP) operation reduces the diagnostic value of the laproscopic operation in occult hernias even more. However, there are reports of laparoscopic hernia operations in groin pain cases using the TAPP technique. 44,45 These reports include athletes with groin pain and no palpable hernia. In one, 6 athletes with unilateral groin pain had small hernias on the symptomatic side and also a hernia on the contralateral side. 44 Surgery was successful in all. In the other series of 28 athletes, 30 hernia operations were performed, 14 conventional and 14 laparoscopic (two bilateral).45 All were operated on without a preoperative diagnosis. Hernia findings were not reported. All could return to full sports activities 1 to 9 weeks postoperatively. There were 2 neuralgias settled within 2 months, 1 recurrent pain after 5 months, and 1 recurrent hernia 22 months after conventional repair.

Comments Dealing with occult hernias is quite different from treating manifest hernias. The latter is mainly a matter of surgical repair with as few complications and recurrences as possible. In occult hernia cases, the diagnosis must first be established. Several questions arise. Do the symptoms justify an invasive investigation like herniography or is a less sensitive investigation warranted? Does a hernia discovered at the investigation have anything to do with the symptoms? The concern is that surgeons dealing with occult hernia cases have thorough knowledge of differential diagnosis. When a hernia has been diagnosed, the patient should be examined a second time to confirm the relation between the hernia and the symptoms before an operation is decided upon. There are, however, pitfalls in the judgment of symptoms: overuse injuries 34 due to pain avoidance strategies, or abdominal pain and neuralgia secondary to analgesic drug use. The diagnostic process, though timeconsuming, is an exciting challenge.

References 1. Ljungdahll. Inguinal and femoral hernia. An investigation of 502 operated cases. Thesis. Acta Chir Scand. 1973; Suppl 439:1. 2. Sarli L, Pietra N, Choua 0, et al. Confronto prospettica randomizzato tra ernioplastica laparoscopica ed ernioplastica tension-free secondo Lichtenstein. Acta Biomed Ateneo Parmense. 1997;68:5-10. 3. Ducharme jL, Bertrand R, Chacar R. Is it possible to diagnose inguinal hernia by x-ray? ] Can Assoc RadioL 1967;18:448-452. 4. Erez I, Rathaus V, Werner M, et al. Preoperative sonography of the inguinal canal prevents unnecessary contralateral exploration. Pediatr Surg IntL 1996;11:487-489. 5. Harrison CB, Kaplan GW, Scherz HC, et al. Diagnostic pneumoperitoneum for the detection of the clinically occult contralateral hernia in children. ] UroL 1990;144:510-511. 6. Kaufman A, Ritchey ML, Black CT. Cost-effective endoscopic examination of the contralateral inguinal ring. Urolog;y. 1996;47:566-568. 7. AbramsonJH, GofinJ, Hopp C, et al. The epidemiology of inguinal hernias. ] Epid Com Health. 1978;32:59-67. 8. Romanus R, Tisell L, Kral J. Om inguinalbni.ck. Sammantriide 197301-17. GOteborgs Liikaresiillskaps Forhandlingar, 1973, 59-63. 9. Rowe MI, Copelson LW, Clatworthy HW. The patent processus vaginalis and the inguinal hernia. ] Pediatr Surg. 1969;4:102-107. 10. Jewett TC, KuhnJP, AllenJE. Herniography in children. ] Pediatr Surg. 1976;11:451-454. 11. Keith A. On the origin and nature of hernia. BrJ Surg. 1924; 11:455-475.

13. Occult Hernias in the Male Patient 12. Wagh PV, Read RC. Defective collagen synthesis in inguinal herniation. Am] Surg. 1972;124:819-822. 13. Peacock EE. Biology of hernia. In: Nyhus LM, Condon RE, eds. Hernia, 2nd ed. Philadelphia: ].B. Lippincott; 1978, 79-92. 14. Friedman DW, Boyd CD, Norton P, et al. Increases in Type III collagen gene expression and protein expression in patients with inguinal hernias. Ann Surg. 1993;218:754-760. 15. Smedberg SGG, Broome AEA, Gullmo A, et al. Herniography in athletes with groin pain. Am] Surg. 1985;149:378-382. 16. Devlin HB, Kingsnorth A. Management of abdominal hernias. 2nd ed. London: Chapman & Hall;1998, 44. 17. Gullmo A. Herniography. The diagnosis of hernia in the groin and incompetence of the pouch of Douglas and pelvic floor. Thesis. Acta RadioL 1980;Suppl 361:l. 18. Lichtenstein IL. Hernia repair without disability. Saint Louis: C.v. Mosby; 1970,63. 19. Thompson W, LongerbeamJK, Reeves C. Herniograms. An aid to the diagnosis and treatment of groin hernias in infants and children. Arch Surg. 1972;105:71-73. 20. Gullmo A, Broome A, Smedberg S. Herniography. Surg Clin North Am 1994;64:229-244. 21. Ekberg 0. Complications after herniography in adults. Am]&entgenoL 1983;140:491-495. 22. Ekberg 0, Blomquist P, Olsson S. Positive contrast herniography in adult patients with obscure groin pain. Surgery. 1981;89:532-535. 23. Magnusson J, Gustafsson T, Gullstrand P, et al. Herniography-a useful diagnostic method in patients with obscure groin pain. Ann Chir et Gyn. 1984;73:91-94. 24. Smedberg SGG, Broome AEA, Elmer 0, et al. Herniography in the diagnosis of obscure groin pain. Acta Chir Scand. 1985;151:66~67. 25. Smedberg SGG, Broome AEA, Elmer 0, et al. Herniography in primary inguinal and femoral hernia. An analysis of 283 operated cases. Contemp Surg. 1990;36:48-5l. 26. Loftus 1M, Ubhi SS, Rodgers PM, et al. A negative herniogram does not exclude the presence of a hernia. Ann R Coll Surg EngL 1997; 79:372-375. 27. Fenn K, Keller G, Kuhn R Die Peritoneographie zum Nachweiss nicht tastbarer Hernien. Radiologe. 1982;22:166--169. 28. Verhaar JAN, PotJH. De waarde de herniografie bij onbegrepen pijn in de lies. Ned Tijdschr Geneeskd. 1985;129:359-362. 29. Makela JT, Kiviniemi H, Palm J, et al. The value of herniography in the diagnosis of unexplained groin pain. Ann Chir GynaecoL 1996;85:300--304.

121 30. Yilmazlar T, Kizil A, Zorluoglu A, et al. The value of herniography in football players with obscure groin pain. Acta Chir Belg. 1996;96: 115-118. 3l. Hall C, Hall PN, Wingate JP, et al. Evaluation of herniography in the diagnosis of an occult abdominal wall hernia in symptomatic adults. Br] Surg. 1990;77:902-906. 32. Estes NC, Childs EW, Cox G, et al. Role of herniography in the diagnosis of occult hernias. Am] Surg. 1991;162:608-610. 33. Smedberg SGG, Broome AEA, Elmer 0, et al. Herniography: a diagnostic tool in groin symptoms following hernial surgery. Acta Chir Scand. 1986;152:273--277. 34. Roos H, Smedberg S. Symptomatic non-palpable inguinal hernias. Postgrad Gen Surg. 1992;4:131-134. 35. Smedberg S, Broome A, Elmer 0, et al. The contralateral asymptomatic groin in adults with indirect hernia. In: Smedberg S, ed. Herniography and hernial surgery. Thesis, 1996. Bulletin No. 59 from the Department of Surgery, Lund University, Lund, Sweden. 36. OrchardjW, ReadjW, NeophytonJ, et al. Groin pain associated with ultrasound finding of inguinal canal posterior wall deficiency in Australian Rules footballers. Br] Sports Med. 1998;32:134-139. 37. Chen KC, Chu CC, Chou IT, Wu C]. Ultrasonography for inguinal hernias in boys.] Pediatr Surg. 1998;33: 1784-1787. 38. Spangen L. Ultrasound as a diagnostic aid in ventral abdominal hernia.] Clin Ultrasound. 1975;3:21l. 39. Hojer AM, Rygaard H, Jess P. CT in the diagnosis of abdominal wall hernias: a preliminary study. Eur RadioL 1997;7:1416--1418. 40. Yokoyama Y, Yamaguchi A, Isogai M, et al. Thirty-six cases of obturator hernia: does computed tomography contribute to postoperative outcome? World] Surg. 1999;23:214-216. 4l. van den Berg JC, de Valois JC, Go PM, et al. Groin hernia: can dynamic magnetic resonance imaging be of help? Eur RadioL 1998;8: 270--273. 42. Carter JE. Surgical treatment for chronic pelvic pain.] Soc Laparoendosc Surg. 1998;2:129-139. 43. Gould SWT, Lamb G, Vaughan N, et al. Dynamic magnetic resonance imaging: a new diagnostic modality for groin pain? Br] Surg. 1998; Suppll:35. 44. Azurin DJ, Go LS, Schuricht A, et al. Endoscopic preperitoneal herniorrhaphy in professional athletes with groin pain.] Laparoendosc Adv Tech A. 1997;7:7-12. 45. Ingoldby CJH. Laparoscopic and conventional repair of groin disruption in sportsmen. Br] Surg. 1997;84:213--215.

14 Quality Control and Scientific Rigor Erik Nilsson and Staffan Haapaniemi

Introduction The word "quality" occurs with increasing frequency in the medicalliterature and now appears in the titles of several journals. In one dictionary, quality is defined as "degree or standard of excellence,"1 and in the ISO (International Standardization Organization, Geneva, Switzerland) 9000 it is understood as the inherent properties of an object or a procedure that satisfY explicit or implicit requirements. In accordance with the principles of beneficence and nonmaleficence of biomedical ethics,2 quality may be translated into common language as a measure of our capacity to relieve health problems without causing new ones. As demands exceed resources in all health care systems, we have to include the concepts of justice and rationing in the discussion of quality. In cost-utility terms, quality might thus be considered to be the cost of a procedure in relation to the health improvement it generates. 3 In the quality control of hernia surgery, we have to define endpoints, outline goals with respect to these endpoints, and measure to what extent we reach our goals, with cost as a denominator. Quality control is related to audit, which refers to an initiative aimed at improving the quality of outcome by examining practices and results against agreed standards. 4 Both quality control and audit are components of evidence-based medicine, the aim of which is to integrate the best available evidence with clinical practice.5 Research seeks to extend scientific knowledge; quality control and audit examine whether practice keeps pace with that knowledge. 6 It has been emphasized that an intrinsic gap exists between clinical research and clinical practice. 7 Surgical dexterity and skills such as the ability to select the right procedure for the right patient may reside in this gap. Quality control reports the outcome of practice.

Endpoints in Hernia Surgery

Recurrence Recurrence rate has been considered the most important endpoint in hernia surgery. It is still the "acid test" of hernia repair. 8 In analyses of defined populations, the percentage of operations performed for recurrent hernia may be used as a crude index of past surgical quality. 9 In one of the few studies to address the question, the majority R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

of patients considered rate of recurrence more important than speed of recovery as outcome measure.I° Marsden ll described recurrence as a weakness in the operation area necessitating a further operation or the provision of a truss. He wrote, "It is a failure of the operation and does not include slighter degrees of weakness-the significance of which is still controversial." On the other hand, recurrence was defined as an expansile cough impulse by Shuttleworth and Davies,12 who added: "Asymptomatic recurrences make reviews which are not based upon physical examination liable to error." The difference between these two concepts is of considerable practical importance, the more so when followup examinations are undertaken at frequent intervals and when the recurrence rate is high. If follow-up is undertaken frequently enough, most recurrences will be asymptomatic and hence not detectable through questionnaire and selective follow-up. In a recent study, only 50% of all recurrences were detected by this method as compared to physical examination of all patients. 13 This has a great impact upon quality control in cohorts with recurrence rates exceeding, say, 10%, but may be of minor importance with recurrence rates of 2% or less five years after surgery. In routine quality control in a busy district hospital, it is difficult to allocate resources for physical examination of all hernia patients on a yearly basis when the predictive value of a negative questionnaire answer is 95% or higher (the chance being at least 95% that the patient at physical examination has no recurrence if the questionnaire answer indicates no bulge and no pain in the operated groin). Provided case-mix is unaltered and the same follow-up technique with questionnaire and selective physical examination is used, it is reasonable to assume that any observed outcome changes reflect variations in surgical quality. Whatever the control method used, it should be stated clearly in reports and in quality control documents. The importance of completeness of follow-up becomes obvious if we assume that all nonresponders to follow-up invitations have recurrences. Whereas the time course of appearance of recurrences following musculoaponeurotic repairs is well known,8,14 corresponding data for newer methods (open plug and laparoscopic techniques) are inadequate or lacking. Cumulative incidence of reoperation following registration of all hernia repairs has been suggested as a surrogate endpoint for recurrence. 15,16 Recurrence rate according to Marsden's definition ll was determined by Kald and coworkers with questionnaire and selective follow-up of patients who

123

14. Quality Control and Scientific Rigor answered questions about pain or bulge in the operated groin. The authors found that recurrence rate measured in this way exceeded reoperation rate three years after surgery by 40% .15

Complications, Including Mortality, in the Immediate Postoperative Period The frequency of postoperative complications reported after hernia surgery, whether in randomized controlled trials or in case series, is inversely related to the degree of scrutiny of the postoperative investigation. Whatever method is used for quality control or audit, postoperative complications observed by the operating unit should be recorded and followed over time. Rare and serious complications, particularly those that are procedure related, should be considered central indicators needing individual detailed assessment. This position should also be applied to postoperative mortality after elective hernia repair. According to the Swedish Hernia Register, the observed 30-day mortality for men following elective inguinal hernia repair was significantly lower than the expected mortality in the general Sweedish population, indicating a preoperative selection of patientsP On the other hand, a six to tenfold increase in standardized mortality rate was observed after emergency surgery, and, when bowel resection was undertaken, it exceeded that of the background population by 13 to 17 times.

Postrepair Pain and Groin Function All hernia surgeons recognize the importance of late (four to six months after surgery) and chronic pain after hernia repair. However, hard data on the incidence of this condition are scarce. In an often-quoted study based upon follow-up of 276 out of 818 patients who underwent open herniorrilaphy, postrepair moderate or severe pain was recognized two years after surgery in 11 %. Of 17 patients referred to a pain specialist, 7 recovered completely or had pain less frequently than once a week. Nine of the remaining 10 patients were judged to have a somatic ligamentous syndrome, and 2 of these had, in addition, a concurrent and less severe pain of neuralgic character. From this study, it might be concluded that neuralgia after herniorrhaphy is an uncommon cause of disabling pain. Chronic pain was also asked about in a recent Swedish cohort study based upon physical examination of 219 out of 230 eligible patients four years after conventional hernia repair.18 Twenty-four patients had moderate or severe pain, and in 4 patients (1.8%), the pain was of a neuralgic character. More information is needed both from epidemiological studies and from randomized controlled trials concerning postrepair pain following hernia surgery.19

Patient Satisfaction Validated techniques for obtaining information concerning changes in quality of life of patients undergoing surgical procedures are now readily available. The Short Form 36A (SF-36A) is a comprehensive health survey questionnaire that consists of eight multi-item dimensions. 20-22 It has been utilized in several randomized trials of hernia repair. 10,23,24 The Nottingham Health Profile Questionnaire (NHPQ) has received attention as a tool in the

analysis of quality of life following hernia repair.25 EuroQol is a simplified questionnaire in which five items can be combined in a common index. 26 ,27 It has been developed for and widely used in health economy studies, including hernia surgery.lO However, for many purposes, analogue or rating scales may be adequate for estimating patient satisfaction. 28 In hernia surgery, information for patients concerning the normal postoperative course, including instructions for activity and self-treatment, is particularly important. 29 If pain is to be treated by analgesics, the patient should be told how much of the drug should be taken, how often and for how long. Anticipation may influence outcome of surgical procedures. 30 ,31 The expectations of patients have been measured in a randomized hernia trial,25 but they are rarely considered in the discussion of outcomes. 32

Cost The cost of surgery receives increasing attention. This applies not only to direct, but to indirect costs such as compensation for sick leave. It has been repeatedly reported that both socioeconomic factors 33- 35 and the advice given to patients have a great impact on the duration of convalescence and sick leave. 29 ,36 Costs of postoperative complications should be included in the overall cost. The expertise of health economists is required for hernia surgeons who pursue analyses in this field. 3 Although international variations in hernia repair rates have been demonstrated,37 epidemiological data in the field of hernia surgery are inadequate. Finally, it is fair to recall that allocation of resources to the health care sector differs widely between industrialized and developing countries,38 and that the major problem confronting health policy makers in the industrialized world may be to define in operational terms what is meant by a decent minimum. 2

Problems and Challenges in Quality Control Eponyms The problem of eponyms has been clearly stated by Bendavid. 39 "No one does a Bassini, a Shouldice, or a Stoppa. Instead surgeons do a modified Bassini, a modified Shouldice or a modified Stoppa." In articles comparing repair techniques, a detailed description of the authors' modification(s) should be given.

Benchmarking Today, no technique or modification of a technique of hernia repair can be considered a gold standard. However, we still need benchmarking to establish goals for our own units. In this process, we need randomized controlled trials, epidemiological studies, analyses of administrative databases and registers, and well-controlled series from specialized centers. The randomized controlled trial is considered the most trustworthy comparison, the outcome of which is taken as the strongest evidence. 40 ,41 However, in a recent systematic review, the external validity (generalizability) and power (sample size) of most randomized controlled trials in the field of hernia surgery were rated as poor. In three other assessment categories (reporting, bias, and confounding), the studies

E. Nilsson and S. Haapaniemi

124

1997 24.7

A Shouldice

% ...-~~------------l B Conventional open

14.9 C Mesh. groin incision 42.3 o Mesh. abdominal incision 3.2

B...........

'~"~'~":'r.... 0

E'" " "

FIGURE 14.1. Methods of repair. (From the Swedish Hernia Register.)

~ ~~~P

~:!

...............

" .----- ......

~.:.~

--~~

"".

o,co

"". :x' . . . ._

..................•

... - - - -

"". .............. .

o~~~~~~~==~----~-=~~ Hernia repairs

1992

1993

1994

1689

1645

2285

1995

3324

1996

1997

4054

5872

ranged from poor to good. 42 One interesting and neglected question concerns the consequences of the trial for the participating units. What happened at these units one year after the trial?

The Swedish Hernia Register Prerequisites and Aims The register has been described previously.16,43 The use of each individual's Person Number makes it possible to follow patients over time and to adjust life tables for death of patients. The aim of the register is to describe and analyze hernia surgery in participating units and to support local audit programs. It is not its function to produce ranking lists, and it has not been used in that way.

Results The number of hospitals included has gradually increased from eight in 1992 to 29 in 1997. By the end of 1997, 18,869 herniorrhaphies had been recorded; 15,091 (84.3%) primary and 2,968 (15.7%) recurrent hernia repairs; 17,471 unilateral and 699 bilateral operations had been done within the frame of the register upon 17,061 patients, 91.6% of whom were men and 8.4% women. The methods of repair used changed greatly over the 6 years covered by this audit. The most remarkable changes were the reduction in traditional open pure tissue techniques from 68% in 1992 to 15% in 1997, and the increased use of mesh (open and laparoscopic) methods from 6% to 61 % (Fig. 14.1). At 5 years, mean and 95% confidence intervals of cumulative incidence of reoperation was 5.7% (4.9-6.4%) and 10.1 % (8.2-12.0%) for primary

Cumulative incidence 0.12 r;:::======:::::=::::;-7"",-:---;,--;-,--;---;-,-;-,----:'1 .. 7...... .. :........ 7...... -:- ...... i ...... -:- ...... f ...... -:0.11 - Primary hernias Recurrent hernias' '" 0.10 ___ J ____ ___ l ____ ___ J, ____ ,I ____ " , J __ _ 0.09 , 0.08 0.07 0.06 0.05 0.04 0.03 0.02 0.01 ~

•

0.00 ....=0........l000l0.I.I0................................''''''''''''".................'''''''''''........''''''''''''''.............''''''''''''''''''''"'...............,..,,, o 6 12 18 24 30 36 42 48 54 60 66 72 Time after surgery (months)

14.2. Cumulative incidence of reoperation, 1992-1997; 18,869 hernia repairs. (From the Swedish

Primary hernias

n = 15 901

5-year: 5.7%

95% CI (4.9 - 6.4%)

FIGURE

Recurrent hernias

n = 2 968

5-year: 10.1%

95% CI (8.2 - 12.0%)

Hernia Register.)

125

14. Quality Control and Scientific Rigor TABLE 14.1. Variables associated with increased relative risk for reoperation due to recurrent hernia; adjusted for methods of repair, multivariate Cox analysis I, 1992-1997, 18,869 hernia repairs!

Recurrent operation vs. primary operation Absorbable suture vs. nonabsorbable suture Direct hernia vs. other hernia types Postoperative complication vs. no complication Period 1992-1995 vs. 1996--1997

Number of operations

Relative risk

95% CI

2968 3634 8163 1774 8993

1.87 1.43 1.70 2.36 1.66

1.53-2.29 1.15-1.78 1.42-2.02 1.89-2.96 1.27-2.17

!Relative risk was estimated with the Cox proportional hazards model, first performing univariate analysis of assumed risk variables, and then selecting variables with the highest "univariate" relative risk for multivariate analysis. The proportional hazards assumption was exanIined as part of the Cox analysis. Interaction between risk factors was also introduced and examined in the multivariate analysis. (From the Swedish Hernia Register.)

and recurrent hernias respectively (Fig. 14.2). Since the register was established, a reduction in reoperation rate has been observed.

From Table 14.1, it is evident that an operation carried out between 1992 and 1995 was 1.66 times more likely to be followed by a reoperation than an operation performed in 1996 or 1997. The relative risk of the various methods used during the whole period from 1992 to 1997 is illustrated in Table 14.2. It must be added that these data demonstrate the effectiveness of the methods used with learning curves included, but not their efficacy. Effectiveness of the methods used (i.e., outcome in routine practice with learning curves included) is distinct from efficacy (i.e., results produced by experts under optimal conditions).44 Data from the Swedish Hernia Register may be supplemented by follow-up studies, such as the longitudinal study of outcome quality from a single hospital. 45

which from 1999 onward will collect data for all hernia repairs per hospital, whether ambulatory or inpatient procedures.

Quality Control and Cost-Utility

A quality control program must itself be audited. Data in the Swedish Hernia Register were validated in 1996. 16 This was repeated in 1998, and we have plans to do this on a yearly basis. Further validation of the Swedish Hernia Register may also be obtained by comparison with data from the Hospital Discharge

For 1998, the Swedish Hernia Register received approximately $50,000 (in United States dollars) from its sponsors, the Department of Health and Welfare and the County Councils of Sweden, for running the register. As over 8,000 hernia repairs were registered that year, the cost per operation registered would amount to approximately $6. For secretarial assistance at the participating hospital, an amount of $4 has to be added for each operation. Hence, a rough estimate of the overall cost of quality control through a register of this type would be $10 per operation. Does register participation benefit those most concerned, the hernia patients? To answer this question, reoperation rates for 1992 and 1995-1996 were compared between hospitals that joined the register in 1995, and hospitals that had participated in register work since its start in 1992. Reoperation rates after hernia repairs performed in the two groups in 1992 were almost identical. But reoperation rates following hernia repairs done in 1995-1996 were significantly lower in units that had been involved in the register since its start in 1992, compared to hospitals that joined the reg-

Database at the National Board of Health and Welfare in Sweden,

ister in 1995. This seems to indicate that register participation,

A udit of the Audit

TABLE 14.2. Relative risk of operation-methods of repair; adjusted for factors in I, multivariate Cox analysis II, 1992-1997, 18,869 hernia repairs!

Shouldice Conventional open2 Mesh, groin incision Mesh, abdominal incision Transabdominal preperitoneal (TAPP) Totally extraperitoneal (TEP)

Number of operations

Relative risk

95% CI

5,578 5,379 4,189 730 1,796 1,197

1.00 1.44 0.93 1.13 0.94 1.91

reference 1.14-1.82 0.65-1.34 0.70-1.81 0.66--1.33 1.21-3.02

!Relative risk was estimated with the Cox proportional hazards model, first performing univariate analysis of assumed risk variables, and then selecting variables with the highest "univariate" relative risk for multivariate analysis. The proportional hazards assumption was examined as part of the Cox analysis. Interaction between risk factors was also introduced and examined in the multivariate analysis. (From the Swedish Hernia Register.) 2Bassini, Marcy, McVay, et al.

126

with its associated aim of improving work, might benefit outcome quality.43 However, as all units increase their outcome quality, such differences can be expected to fade away.

Where to from Here?

Improvement in Surgical Education Inadequate surgical education is the main obstacle to better outcome in nonspecialized units. 46 The motives of surgeons (best possible care to individual patients) and of society (best possible service for everybody at lowest possible cost) must coincide if quality control is to play its proper role in improving hernia surgery.

Consider the Care Chain Quality control and improvement interact. As surgeons, we should consider whether we have paid enough attention to the nonsurgical aspects of our hernia service: information and advice to patients, anaesthesia, recovery room atmosphere, and so on. "Every system is designed to get the results it gets. "47

Conclusions

Raise Questions Do you know the outcome of your unit, exactly what information you need, and how you can reach the data requested? Can these data be validated? Considering your own case-mix, where do you find your benchmarks? What are your goals, and how do you measure your progress toward them?

Define the Level of Ambition of Your Quality Control It might be better to know a few hard facts than to amass a lot of

unreliable data.

Use an Epidemiological Approach Quality control is the joint responsibility of all members of a team and must cover all activities within the field concerned. It is not enough to know the outcome of the impressive trial in which you and your coworkers have participated; you have to consider the great majority of patients treated outside the trial, often by your trainees and sometimes as emergency cases in the middle of the night.

Allocate Resources Quality control has a cost, but when properly performed, it is rewarding.

E. Nilsson and S. Haapaniemi

Acknowledgments In 1997, the following hospitals were enrolled in the register: Ersta sjukhus Stockholm; Falkoping; Falun; Huddinge sjukhus Stockholm; Hudiksvall; Kalix; Kalmar; Karolinska sjukhuset Stockholm; Lidkoping; Lindesberg; Linkoping; Ludvika; Lycksele; Mora; Motala; Norrkoping/Finspang; Norrtiilje; Pitea; Skene; St. COrans ~ukhus Stockholm; Skelleftea, Siiffle, Viirnamo; Viistervik/Oskarshamn; Uddevalla/Stromstad, Viistra Frolunda; and Ostersund. Financial support for the Swedish Hernia Register is received from the National Board of Health and Welfare and the Federation of County Councils, Sweden. The authors thank hernia surgeons in participating hospitals for their collaboration. Secretary Gunnel Nordberg and statistician Lennart Gustafsson, Ph.D., have provided invaluable help during the preparation of this manuscript.

References 1. Hanks P, Hill Long T, Urdang L. Collins dictionary of the English language. London: William Collins Sons & Co Ltd.; 1979;1194. 2. Beauchamp TL, Childress JF. Principles of biomedical ethics. Oxford: Oxford University Press; 1983. 3. Drummond MF, O'Brien B, Stoddart GL, et al. Methods fur the economic evaluation of health care programmes. Oxford: Oxford University Press; 1997. 4. National Health Service Executive, ed. Clinical audit in the NHS. Leeds; 1996. 5. Sackett DL, Rosenberg WMC, Gray JAM, et al. Evidence-based medicine: what it is and what it isn't. BMJI996;312:71-72. 6. Bull AR. Audit and research: complementary but distinct. Ann R Coll Surg EnglI993;75:308-311. 7. Tonelli MR The philosophical limits of evidence-based medicine. Acad. Med 1998;73:1234-1240. 8. Devlin HB, Kingsnorth AN. Management of abdominal hernias. 2nd ed. London: Chapman & Hall; 1998. 9. Johanet H, Cossa JP, Marmuse JP, et al. Cure de hernie de l'aine par laparoscopie. Resultats a quatre ans de la voie transpreperitoneale. Ann Chir. 1995;50:790-794. 10. Lawrence K, McWhinnie D, Goodwin A, et al. Randomised controlled trial of laparoscopic versus open repair of inguinal hernia: early results. BMJ 1995;311:981-985. 11. Marsden AJ. The results of inguinal hernia repairs: a problem of assessment. Lancet 1959;i:461-462. 12. Shuttleworth KED, Davies WH. Treatment of inguinal herniae. Lancet. 1960;i:126--127. 13. Vos PM, Simons MP, Luitse JSK, et al. Follow-up after inguinal hernia repair. Questionnaire compared with physical examination: a prospective study in 299 patients. Eur J Surg. 1998;164:533-536. 14. Hay J-M, Boudet M:J, Fingerhut A, et al. Shouldice inguinal hernia repair in the male adult: the gold standard? Ann Surg. 1995;222:719-727. 15. Kald A, Nilsson E, Anderberg B, et al. Reoperation as surrogate endpoint in hernia surgery: a three year follow-up of 1,565 herniorrhaphies. Eur J Surg. 1998;164:45-50. 16. Nilsson E, Haapaniemi S, Gruber G, et al. Methods of repair and risk for reoperation in Swedish hernia surgery 1992-1996. Br J Surg. 1998; 85:1686--1691. 17. Haapaniemi S, Sandblom G, and Nilsson E. Mortality after elective emergency surgery for inguinal and femoral hernias. Hernia. 1999;4: 205-208. 18. Haapaniemi S, Nilsson E. Is a postal questionnaire in combination with selective physical examination adequate as follow-up after groin hernia repair? Unpublished.

14. Quality Control and Scientific Rigor 19. Callesen T, Kehlet H. Postherniorrhaphy pain. Anesthesiology. 1997;87: 1219-1230. 20. Jenkinson C, Coulter A, Wright L. Short form 36 (SF-36) health survey questionnaire: normative data for adults of working age. Bl\lj1993; 306:1437-1440. 21. Ruta DA, Abdalla MI, Garratt AM, et al. SF-36 health survey questionnaire. I. Reliability in two patient based studies. Qual Health Care. 1994; 3:180-185. 22. Garratt AM, Ruta DA, Abdalla MI, et al. SF-36 health survey questionnaire. II. Responsiveness to changes in health status in four common clinical conditions. Qual Health Care. 1994;3:186-192. 23. WeliwoodJ, Sculpher MM, Stoker D, et al. Randomised controlled trial of laparoscopic versus open mesh repair for inguinal hernia: outcome and cost. BM]1998;317:103-110. 24. Liem MSL, HalsemaJAM, van der GraafY, et al. Cost-effectiveness of extraperitoneal laparoscopic inguinal hernia repair: a randomized comparison with conventional herniorrhaphy. Ann Surg. 1997;226: 668-676. 25. BarkunJS, Wexler MJ, Hinchey EJ, et al. Laparoscopic versus open inguinal herniorrhaphy: preliminary results of a randomized controlled trial. Surgery. 1995;118:703-710. 26. The EuroQol Group. EuroQol-a new facility for the measurement of health-related quality of life. Health Policy. 1990;16:199-208. 27. Kind P, Gudex C, Dolan P, et al. Practical and methodological issues in the development of the Euroqol. Adv Med Sociol. 1994;5:219-253. 28. Gunnarsson U, Heuman R, Wendel-Hansen V. Patient evaluation of routines in ambulatory hernia surgery. Amb. Surg. 1996;4:11-13. 29. Callesen T, Klarskov B, Bech K, et al. Short convalescence after inguinal herniorrhaphy with standardised recommendations: duration and reasons for delayed return to work. Eur] Surg. 1999;165:236241. 30. Beecher HK Surgery as placebo. A quantitative study of bias. ]AMA. 1961;176:1102-1107. 31. Johnson AG. Surgery as placebo. Lancet. 1994;344:1140-1142. 32. Leibl B, Diiubler P, Schwartz J, et al. Standardisierte laparoskopische

127 Hernioplastik vs Shouldice-Reparation. Ergebnisse einer randomisierten Vergleichsstudie. Chirurg. 1995;66:895-898. 33. Barwell :r-rr. Recurrence and early activity after groin hernia repair. Lancet. 1981;2:985. 34. Salcedo-Wasicek MC, Thirlby RC. Postoperative course after inguinal herniorrhaphy. A case-controlled comparison of patients receiving worker's compensation vs patients with commercial insurance. Arch Surg. 1995;130:29-32. 35. Thorup J, Joergensen T, Billesboelle P. Convalescence after inguinal herniorrhaphy. Scand] GastroenteroL 1994;29: 1150-1152. 36. Shulman AG, Amid PK, lichtenstein IL. Returning to work after herniorrhaphy: "take it easy" is the wrong advice. BM] 1994;309:216-217. 37. McPherson K Why do variations occur? In: Folmer Anderson T, Mooney G, eds. The challenge of medical practice variations. London: Macmillan; 1990:16-35. 38. Bergstrom S, Mocumbi P. Health for all by the year 2000? BM]. 1996; 313:316. 39. Bendavid R. Complications of groin hernia surgery. Surg Clin North Am. 1998;78:1089-1103. 40. Greenhalgh T. Papers that summarise other papers (systematic reviews and meta-analyses). BM] 1997;315:672-675. 41. Bero L, Rennie D. The Cochrane collaboration. Preparing, maintaining, and disseminating systematic reviews of the effects of health care. ]AMA. 1995;274:1935-1938. 42. Cheek CM, Black NA, Devlin HB, et al. Groin hernia surgery: a systematic review. Ann R Coli Surg Engl. 1998;80(Suppll):SI-S80. 43. Nilsson E, Haapaniemi S. Hernia registers and specialization. Surg Clin North Am 1998;78:1141-1155. 44. Institute of Medicine. Assessing medical technologies. National Academy Press, Washington, DC, 1985;71-75. 45. Sandblom G, Gruber G, Kald A, et al. Audit and recurrence rate after hernia surgery. Eur] Surg. 2000;166:154-158. 46 Wantz GE. Hernioplasty controversy.] Am Coli Surg. 1998;3:372-376. 47. O'Connor GT. Every system is designed to get the results it gets. BM] 1997;315:897-898.

15 Classification of Inguinal Hernias V. Schumpelick and K-H. Treutner

Introduction The results of inguinal hernia repair are related to the location of the hernial orifice and the size of the fascial defect. Recurrence rates after operation on a large direct hernia are about five times higher than those after repair of a small indirect hernia. Classification of inguinal hernias is a prerequisite for planning, conducting, and discussing clinical trials on this subject. Precise documentation of location and size of the defect of the abdominal wall is crucial information for critical analysis of recurrence rates when evaluating different surgical techniques. It serves the same purpose as the TNM classification of malignant tumors, making clinical studies reproducible and therapeutic regimens comparable. I The classification should include all types of inguinal hernias, and should work equally well for classical open surgery and laparoscopic repairs. Valid objective comparisons of the results, complications, and recurrences of the relatively new minimal access techniques with those of the traditional surgical methods depend upon the development and acceptance of such a classification. The classification should be clear and simple to allow unambiguous typing in a routine clinical setting. The surgeon must be able to assign each patient to one definite category with ease and reliability. The use of any classification with a multitude of parameters and subtypes will be restricted to a few centers specialized in hernia surgery. The aim, however, must be to gather and analyze the experience on large numbers of patients beyond the borders of single departments. 2 Accumulation of data on the relationship between different methods of hernia repair and the varying parameters of inguinal hernias will establish the most successful treatment for any given combination of the location and size of the fascial defect. These findings could be the solid ground for evidence-based surgery and quality control in the field of inguinal hernia.

Classifications A review of the literature reveals a number of classifications of groin hernias. None of them, however, had achieved widespread acceptance. Unlike the TNM system, no single system of classification has yet been accorded the consensus of the surgical community. The reasons for this lack of an international agreement R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

may be that proposals do not cover all types of inguinal hernias, the size of the fascial defect is not precisely measured, or the system is too complicated for clinical routine. The simple classification of "direct" and "indirect" hernias dates back to Cooper in 1844. 3 Hesselbach defined the inferior epigastric vessels as the reference point and used the terms "external" and "internal" hernia. 4 Casten presented a classification in 1967 based on functional anatomy and surgical repair. As stage 1, he describes an indirect hernia with a normal internal ring as seen in infants and children, treated by high ligation of the sac. Stage 2 encompasses those indirect hernias with an enlargement of the internal ring to be repaired by excision of the sac and reconstruction of the internal ring. All direct and femoral hernias were summarized under stage 3 with the indication of a Cooper's ligament repair.5 In 1970, Halverson and McVay published a classification based on a description of the fascial defect and the repair technique. Their categories included small indirect inguinal hernias, medium indirect inguinal hernias, large indirect and direct inguinal hernias, and femoral hernias. They recommend high ligation of the neck of the sac followed by reconstruction of the internal inguinal ring for the first entity. For all the other types they recommended the procedures known by their own names. 6 Gilbert presented a classification in 1989 which takes into account the anatomical and functional integrity of the internal ring and the tissue quality within Hesselbach's triangle. Types I to III are indirect hernias, types IV and V are medial defects of the inguinal canal; femoral hernias are not classified. In type I there is a hernial sac of any size passing through a small and firm internal ring. Types II and III show enlargement of the internal ring to admit one or two fingers, respectively. Hernias with a large defect of the canal floor are called type IV, whereas those with a small medial orifice are named type V (Fig. 15.1).7 Rutkow and Robbins added a type VI for hernias with both indirect and direct components, and a type VII for femoral hernias. 8 The classification published by Nyhus in 1993 differentiates among four types. It is based on the size of the fascial defect and the strength of the posterior wall of the inguinal canal. However, there is neither a clear separation between direct, indirect, and femoral hernias, nor precise measurements. In type I there is an indirect hernia with an internal abdominal ring of normal size, usually found in infants, children, and young adults. Indirect inguinal hernias with enlargement of the internal ring are catego-

15. Classification of Inguinal Hernias

129

TABLE 15.2. Aachen classification of groin hernias Localization of defect

Size of defect

L = lateral/indirect

1< 1.5 cm II 1.5-3.0 cm III> 3.0 cm

M = medial/direct

Mc = combined F = femoral

Discussion

FIGURE

15.1. The Gilbert classification.

rized as type II. The crucial factor in type III is a defect of the posterior wall of the inguinal canal summarizing all direct hernias (III A), indirect hernias with a large dilated ring (III B), and femoral hernias (III C). Type IV covers all recurrent groin hernias either direct (IV A), indirect (IV B), femoral (IV C), or a combination thereof (IV D) (Table IS.I).9 In 1993, Bendavid presented another system for the description of groin hernias. The TSD classification is based on three parameters: type (T), stage (S), and diameter (D). He differentiates among five types: anterolateral (formerly indirect) hernias (type I), anteromedial (formerly direct) hernias (type II), posteromedial (formerly femoral) hernias (type III), posterolateral (formerly prevascular) hernias (type IV), anteroposterior (formerly inguinofemoral) hernias (type V). All types are further categorized by three stages (S I to S III) denoting the extent of the protrusion of the hernial sac and the diameter of the fascial defect (D) measured in centimeters at the level of the abdominal wall. Further details can be registered by additional letters such as "R" for recurrence, "s" for slider, or "L" for lipoma. This allows for a very accurate description of all groin hernias. 1o In 1994, another classification of inguinal and femoral hernias was published by Schumpelick et al. This intraoperative categorization is based on the location ("M," medial/direct; "L," lateral/indirect; "F," femoral) and the transverse diameter (I < l.S cm, II l.S to 3.0 cm, III > 3.0 cm) of the hernial orifice. In cases of combined direct and indirect hernias, the diameters of both fascial defects is added up. Those hernias are classified according to the part of major importance for the development of recurrences, the medial defect, with the index "c." This classification can be applied to open as well as laparoscopic approaches. The diameter of the tip of the index finger or the length of the branch of standard endoscopic scissors (l.S cm), respectively, serve as references for measurement (Table IS.2) .1.2 TABLE 15.1. Nyhus classification (1991) Type I Type II Type III

Type IV

Indirect with normal internal ring Indirect with dilated ring, normal floor A. Direct inguinal hernia B. Large indirect inguinal hernia C. Femoral Recurrent hernias

Rational choice of the most effective method of repair for any type of hernia, and consequent improvement in results, must be based upon a functional classification system. This point of view is strongly supported by our own experience. Between 1986 and 1992, we performed 370 Shouldice repairs for recurrent inguinal hernias. The patients were followed up for S to 10 years. There were no re-recurrences after surgery for small and medium-sized lateral hernias (L I to II) or medial hernias less than l.S cm (M I). Recurrence rates for large indirect (L III) and medium direct (M II) hernias were l.9% and l.6%, respectively. Shouldice repair of recurrent inguinal hernias classified M III (2.4%) and Mc II (2.6%) resulted in slightly higher figures. Follow-up of hernioplasty for large combined hernias with a total fascial defect greater than 3 cm (Me III), however, revealed a re-recurrence rate of7.7% (Table IS.3).1I The analysis of this group of patients clearly demonstrates a relation between the type and size of the hernia and the long-term outcome. Those patients with large direct and combined hernias are considerably more prone to re-recurrence than those with small lateral and small to medium-sized medial fascial defects. We therefore introduced a new regimen for surgical treatment of recurrent inguinal hernias. Whereas those classified as L I to II and M I to II are still repaired by the Shouldice procedure, direct hernias with an orifice greater than 3 cm and all combined hernias are now operated on using mesh material. In another group of 380 patients with recurrent inguinal hernias operated on between 1994 and 1996, we performed a TIPP repair (transinguinal preperitoneal prosthesis) in 94 cases. All those hernias were intraoperatively classified either as combined type (Mc), large direct (M III), or indirect (L III) hernias. The latest follow-up of these patients revealed only two re-recurrences after 12 and 24 months, respectively (2.1 %). Modification of the treatment protocol according to classification of the abdominal wall defect resulted in lower recurrence rates. 12 Now, more than 100 years after the introduction of scientifically based hernia repair by Bassini, hernioplasties are the most common procedure in general surgery. The time has come for an evidence-based system for choice of technique. This calls for a joint effort to find a consensus on a clear and simple but valid and reliable classification of inguinal hernias. TABLE 15.3. Results of Should ice repair for recurrent inguinal hernia according to the Aachen classification of groin hernias (n = 370)

L M

0% 0%

Mc L

lateral/indirect; M = medial/direct; Mc

III

0% 1.6% 2.6%

1.9% 2.4% 7.7%

combined.

130

References 1. Schumpelick v, Treutner K-H, Arlt G. Inguinal hernia repair in adults. Lancet. 1994;344:375-379. 2. Schumpelick V, Treutner K-H, Arlt G. Klassifikation von Inguinalhernien. Chirurg. 1994;65:877-879. 3. Cooper A Anatomy and surgical treatment of abdominal hernia. 1st American ed from 2nd London ed. Philadelphia: Lea and Blanchard; 1844. 4. Marcy HO. The anatomy and surgical treatment of hernia. New York: D. Appleton and Co.; 1892:66. 5. Casten DF. Functional anatomy of the groin area as related to the classification and treatment of groin hernias. AmJ Surg. 1967; 114:894-899. 6. Halverson K, McVay CB. Inguinal and femoral hernioplasty. Arch Surg. 1970;101:127-135. 7. Gilbert AI. An anatomic and functional classification for the diagnosis and treatment of inguinal hernia. Am J Surg. 1989;157:331-333. 8. Rutkow 1M, Robbins AW. "Tension-free" inguinal herniorrhaphy: a preliminary report on the "mesh plug" technique. Surgery. 1993;114:3-8. 9. Nyhus LM. Individualization of hernia repair: a new era. Surgery. 1993;114:1-2. 10. Bendavid R. The TSD classification. A nomenclature for groin hernias. GREPA. 1993;15:9-12. 11. Treutner K-H, Arlt G, Schumpelick V. Shouldice repair for recurrent inguinal hernia-a ten-year follow-up. In: Schumpelick V, Kingsnorth AN, eds. Incisional Hernia. Berlin-Heidelberg-New York: Springer; 1999:359-366. 12. Arlt G, Schumpelick V. Transinguinal preperitoneal prosthesis placement under local anesthesia-management and follow-up of 100 patients. In: Schumpelick V, Kingsnorth AN, eds. Incisional Hernia. Berlin-Heidelberg-New York: Springer; 1999:389-395.

Commentary Robert Bendavid Discussions on the issue of hernia classification seem to have taken place in the Tower of Babel. Schumpelick and Treutner have been eyewitnesses to these discussions as well as active participants. For my part, my TSD classification, though complete, suffers from the same deficiency as all the other classifications: it has to be consulted, like a book of spells, before the correct designation can be

V. Schumpelick and K-H. Treutner

applied. Because they all tend to be similar in many ways, they are hard to remember individually. No classification can cover all abdominal wall hernias, nor should it. According to the 1997 statistics of the Shouldice Hospital, 7,273 abdominal wall hernia operations were performed. Inguinal and femoral hernias numbered 6,653 or 91.5%. Of all inguinal and femoral hernias, 60.98% were indirect inguinal hernias (4,057 patients); 36.98% direct inguinal hernias (2,460 patients) and 1.95% femoral hernias (160 patients); these accounted for 99.91 % of all groin hernias. The rare prevascular, paravascular, or Spigelian hernias made up 0.09% and should be excluded as statistically nonsignificant. Thus, it would be sufficient for a classification to cover indirect, direct, and femoral hernias, names that have been here for a long time and which appear with every attempt at classification: I = indirect, D = direct, and F = femoral. The widest dimension of the neck of a defect should be used to denote the size of a defect. A 2 em hernia will be an 12 or a D2 or an E2. If a direct and indirect hernia, each 2 em, are present, then the hernia would be denoted 12-D2. Whether a peritoneal sac or lipoma protrudes is not important for this purpose: only the size of the defect is. Recurrence should be designated R. Two previous attempts at surgery would be 2 X R, 3 attempts 3 X R, and so on. Since preoperative diagnosis is seldom accurate, the operative diagnosis must be the criterion on which communication and modality of treatment must rest. An indirect hernia 3 em in diameter at its neck, present with a direct inguinal hernia 4 em in widest dimension and a femoral hernia 1 em wide at its neck with 4 previous attempts at repair would be labeled at surgery and for the chart as "Right 4 X R-I3--D4-F1." IDF classification would always use the three letters, and if no hernia is present (zero), then 10 or DO or FO should be recorded. For the chart and computer entry, a simple grid could be devised, as in this sample: Recurrences

Indirect

Direct

Femoral

Right

Left

Part IV Pathology

16 Mechanisms of Hernia Formation Jack Abrahamson

Introduction Hernias emerge through preformed or acquired defects or weak areas of the abdominal wall unprotected by muscle or aponeurosis. These defects could be evolutionary, such as the myopectineal orifice of Fruchaud,I-3 or the superior and inferior lumbar spaces, or congenital, such as a patent processus vaginalis in the newborn or adult, or a patent umbilical defect at birth. The weakness could be an acquired scar such as the umbilicus, or a poorly healed abdominal incision or a scarred over defect resulting from loss of part of the abdominal wall through trauma, excision, or infection, or after disinsertion of the abdominal wall muscles from the iliac crest following harvesting of bone for grafting. Rarely, blunt trauma to the abdominal wall may cause disruption of the flat muscles and allow a hernia to pass through the tear. However, the development of a hernia is usually multifactorial with one or more factors applying in any particular case.

Hernias Occurring in Unprotected Areas These hernias include the groin hernias, all of which emerge through the myopectineal orifice of Fruchaud. They constitute by far the biggest group of hernias. Less common hernias through unprotected areas include epigastric and paraumbilical hernias passing through defects between the decussating fibers of the linea alba,4,5 Spigelian hernias through gaps between the microtendons of the aponeurosis of the transversus abdominis muscles along the semilunar line, lumbar hernias passing through the superior and inferior lumbar triangles, and subcostal hernias emerging through defects in the attachments of the flat abdominal muscles to the costal arch.

Groin Hernias Evolution Since groin hernias are the commonest of hernias, they will be discussed in detail. Fruchaud, when describing the myopectineal orifice that bears his name, urged a more holistic concept of groin hernias, all of which pass through the fascia transversalis and the myopectineal orifice, which is bounded above by the myoaponeurotic arch of the lower edges of the internal oblique and transR. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

versus abdominis muscles (the "conjoined tendon") and below by the pectineal line of the superior pubic ramus. This opening in the lower abdominal wall allows the passage of blood vessels, nerves, lymphatics, muscles, and tendons between the abdomen and the lower limb. The opening is divided into upper and lower halves by the lower free edge of the external oblique aponeurosis (the inguinal ligament) . The space is closed off posteriorly by the fascia transversalis, which is the only structure in this area separating the abdominal cavity from the lower limb, and which must resist the intra-abdominal pressure unsupported by muscles or aponeurosis. This situation, and the absence of the posterior rectus sheath below the arcuate line, is a surprising and unfortunate evolutionary defect, which is compounded in humans by the adoption of upright posture and bipedal locomotion. Bipedalism has opened up and stretched the groin region and changed its functional anatomy in such a way as to interfere with the mechanical efficiency of the shutter mechanisms of the abdominal wall, causing a greater tendency in man to develop groin hernias. 6 Most mammals that walk on all four limbs have a lower abdominal wall structure similar to that of humans and may even have a permanently patent processus vaginalis, yet they rarely develop inguinal hernias. The reason for this is that in mammalian quadrupeds, the thigh is flexed sharply forward, the groin structures are neither stretched nor under tension, and the inguinal canal runs in an upward direction. The groin is at a higher level than the abdomen so that the weight of the abdominal contents is directed cranially forward and downward, away from the inguinal region onto the anterior wall of the upper abdomen, which is structurally more suited to bear it and is also reinforced by the lower thoracic cage. Thus, the inguinal canal is not subjected to significant gravitational stress. In bipedal man, so the theory goes, the exact opposite has occurred. The upright posture causes the weight of the abdominal contents to be directed caudally downward so that the gravitational stress passes down onto the lower abdominal wall which evolution has inadequately adapted for its new role. When man is upright, the unsupported fascia transversalis is constantly exposed to this weight. This is thought by some to be a significant factor in weakening the transversalis fascia and causing groin hernias. 6 Groin hernias occur when the fascia transversalis fails to withstand the stresses of normal or increased intra-abdominal pressure. If one takes into account the anatomical factors discussed above, it may be surprising that less than 5% of the human race develops groin hernias. The factors that bring about failure of the 133

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134

fascia transversalis in the small number of humans who develop groin hernias must be studied as well as those that contribute to its integrity in over 95% of people.

Patent Processus Vaginalis The development of the processus vaginalis, its migration into the scrotum, and its final obliteration are intimately linked to the descent of the testis from the abdomen into the scrotum. These processes are initiated and controlled by the calcitonin gene-related peptide (CGRP) released by the genitofemoral nerve under the influence of fetal androgens. 7 The testis descends through the internal ring, across the primitive inguinal canal, out through the external ring, and into the scrotum between the 26th and the 40th week of gestation. It is preceded and guided by the processus vaginalis. Mter completion of testicular descent, the lumen of the processus vaginalis is obliterated between the internal ring and the upper pole of the testis. The mechanisms involved in the obliteration of the processus vaginalis are unknown. The entire processus vaginalis, or parts of it, may remain patent, sometimes becoming the site of an indirect inguinal hernia, a scrotal hydrocele, or an encysted hydrocele of the cord or of the canal of Nuck in the female. In the female fetus, the processus vaginalis and the round ligament descend into the labia majora, but the descent of the ovary is arrested at the rim of the true pelvis. 8 A patent processus vaginalis is the prime cause of indirect inguinal hernia in infants and children in whom it is cured by simple ligation at the internal ring: herniotomy.9 In adults as well, a completely patent or only partially obliterated processus vaginalis may be the basic cause of an indirect hernia. However, simple herniotomy in adults is followed by a high rate of recurrent indirect inguinal hernia, indicating that additional etiological factors are present which are not dealt with by simple herniotomy. On the other hand, the presence of a patent processus vaginalis does not necessarily indicate that an indirect inguinal hernia is present, nor does it mean that one will necessarily develop in the future. Hughson found a patent processus vaginalis in 20% of adult autopsy examinations, yet none of the subjects suffered from hernia during life. 10 Gullmo noted an open processus vaginalis in 5% of young women having hysterosalpingography, yet none had clinically detectable hernias. ll This finding has been confirmed by others.l 2- 14 So additional factors must be present to produce an indirect inguinal hernia even when a patent processus vaginalis is present.

spermatic cord. As these muscles contract, the fibers of the arch shorten, the arch straightens, and descends to lie close to or against the inguinal ligament anterior to the posterior wall of the inguinal canal. At the same time, the shutter passes down in front of the internal ring as well and counteracts the pressure on the ring from inside the abdomen. The fascia transversalis, which contributes to the border of the internal ring, is pulled up and tensed by the contracting transversus abdominis muscles, causing the ring to close like a sphincter snugly around the cord. Contraction of the external oblique muscle may also contribute to the shutter mechanism; its aponeurosis forms the anterior wall of the inguinal canal and, when tensed, presses on the internal ring, thus reinforcing the weak posterior wall of the canal by counterpressure against the intra-abdominal forces. The same contraction also pulls the inguinal ligament upward to some degree to meet the descending shutter. The acts of coughing, straining, or lifting which tend to blowout the internal ring and the fascia transversalis thus act simultaneously to bring into action the protective physiological mechanisms that oppose those tendencies.

Lipomas of the Cord These are usually not true lipomas (i.e., not new growth) but masses of varying sizes and amounts of extraperitoneal fat covering and adherent to the cord both in front of and behind the internal ring. Since they prolapse out of the abdominal cavity through a defect in the abdominal wall, they may be considered a type of hernia. However, it is rare to find a lipoma of the cord passing out of the abdomen without the presence of a hernial sac as well. This indicates that one is dealing with a hernia accompanied by prolapse of some extraperitoneal fat. It has been suggested that adiposity may be a protective factor against the development of an indirect inguinal hernia because extraperitoneal deposits of fat lie above the internal ring, plugging it. However, the contrary has also been suggested: due to the upright bipedal stance of man, the extraperitoneal fat at the internal ring is pressed down by the weight of the abdominal contents and the intra-abdominal pressure and acts as a bougie to dilate the internal ring and allow a hernia to develop.15 Some surgeons make a point of carefully dissecting off and excising all the fat around the cord when repairing a hernia. Others simply return the lipomas through the internal ring into the abdominal cavity with equally good results.

The Shutter Mechanism

Raised Intra-Abdominal Pressure

Extremely high intra-abdominal pressures are generated during normal daily activities such as coughing, straining, and lifting heavy weights, yet in the overwhelming majority of individuals, the naturally weak areas of the groin, such as the internal inguinal ring and the fascia transversalis, do not give way, and a groin hernia does not develop, even in those with an open internal ring and a patent processus vaginalis. This is due to the remarkable physiologic "shutter mechanism" that is automatically activated by the same contraction of the abdominal muscles that raises the intraabdominal pressure. The lower fibers of the internal oblique and transversus abdominis muscles form the myoaponeurotic roof of the inguinal canal, the "conjoined tendon," that arches over the

When the intra-abdominal pressure is actively raised, as in coughing, straining, or lifting, the countermechanisms are automatically activated and, together with the transversalis fascia, are usually sufficient to resist the increased pressure, and a hernia does not appear. However, when the intra-abdominal pressure rises passively and the abdominal muscles are relaxed, these mechanisms are not activated, and the fascia transversalis is left on its own to withstand the increased intra-abdominal pressure. If a patent processus vaginalis is present or if the fascia transversalis is not sufficiently strong or becomes attenuated by the prolonged pressure and stretching, it gives way. The internal ring will be stretched open, and an indirect hernia will appear.

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In the same way, attenuation and stretching of the fascia transversalis at the posterior wall of the inguinal canal will result in a direct hernia. In pregnancy, the abdominal wall is passively stretched and the intra-abdominal pressure rises, and a groin hernia may appear for the first time and may even "disappear" after the birth. This is usually an indirect hernia that appears in a patent processus vaginalis that has been present as a latent hernia, but direct and femoral hernias may also appear during pregnancy. Groin hernias and often umbilical hernias are produced by a similar mechanism in the presence of chronic ascites caused by liver cirrhosis,16 and in ventriculoperitoneal shunting and peritoneal dialysis, where the fascia transversalis together with the rest of the abdominal wall become passively stretched and thinned yet must withstand the weight of the large quantity of accumulated intraabdominal fluid and increased hydrostatic pressure.5,17-20 The appearance of a groin hernia caused by malignant ascites may be the first indication of intra-abdominal cancer. Excess body weight is no longer considered to be a factor in the development of groin hernias. In fact, adiposity may even have a protective influence against the development of a groin hernia. 21 The balance between the resistance of the abdominal wall and the intra-abdominal pressure may be upset even in a fit young man who is suddenly called upon to lift or to hold an extremely heavy weight to which he is not accustomed or trained; he immediately develops pain in the groin and a groin hernia even down to the scrotum. The hernia is usually indirect and the abdominal wall "rupture" probably occurs in the presence of a patent processus vaginalis, the opening up of which the countermechanisms have resisted until the overwhelming increase in pressure occurred. The probable presence of a preformed sac of patent processus vaginalis, as opposed to the sudden increased workload, is often the basis of workmen's compensation litigation. 5 A similar phenomenon occurs in older men where only a moderate effort seems sufficient to suddenly produce a groin hernia. Groin hernias, especially direct inguinal hernias, are most common in men over the age of 50 years. 22 ,23 Lack of physical fitness, the aging process, and the stresses of life appear to weaken the abdominal muscles, the shutter mechanism, and the fascia transversalis so that the usual counterforces fail. Consequently, an indirect inguinal hernia appears through a preexisting patent processus vaginalis or a direct hernia through a sudden tear or "rupture" of the fascia transversalis, or a bulging direct hernia may simply stretch and balloon the attenuated fascia transversalis in front of it.

The Integrity of the Fascia Transversalis The ability of the fascia transversalis to withstand physiological and pathologic elevations in the intra-abdominal pressure is dependent on the state of the collagen fibers that make up its tissues and give it its strength. Collagen is an active, live tissue maintained by a constant balanced state of production and absorption. Factors that interfere with this balance or cause production of abnormal collagen fibers will bring about attenuation and weakening of the fascia transversalis. These factors include certain congenital connective tissue disorders such as Marfan's, Ehlers-Danlos, and Hurler-Hunter syndromes, and certain mesenchymal metabolic defects that cause collagen deficiency and structural abnormalities of the collagen fibers. Heredity also plays a part as evidenced by higher incidence than that of the general population of hernias in several generations of a family. It is not clear whether in

these families there is a higher incidence of patent processus vaginalis, or a defect in the structure of the fascia transversalis, or both. The role of connective tissue pathology in the genesis of groin hernia has recently been further elucidated. The collagen framework of the transversalis fascia in patients with groin hernia was found to be disorganized and modified, with increased vascularization and cellularity. These changes were present mainly in patients with direct hernias in whom the fascia transversalis of the opposite, nonherniated side showed the same changes,24 findings reported also by Read and others. 25 ,26 A decrease in oxytalan fibers and an increase in the amorphous substance of the elastic fibers as a function of age may be responsible for alterations in the resistance of the transversalis fascia and the high incidence of groin hernias in older men. 27 Read has investigated the normal and abnormal metabolism of collagen and its relationship to the causation of hernia, especially in smokers. 28 ,29 He found that substances in cigarette smoke deactivate antiproteases in lung tissue. The integrity of the lung tissue depends on the balance of the protease/antiprotease system, and deactivation of antiproteases leads to its destruction and to emphysema. The free, unbound, and active protease and elastase compounds are also found in the serum of smokers, apparently discharged by the increased number of white blood cells circulating in the blood and lungs of smokers. These circulating unopposed enzymes upset the protease/antiprotease system in the blood and bring about destruction of elastin and collagen of the rectus sheath and fascia transversalis, and so cause their attenuation and a predisposition to herniation in cigarette smokers. 3o Read furthermore noted that, among smokers, the levels of circulating serum elastolytic and protease substances is higher in the blood of patients with hernias than in controls, in those with direct compared with indirect hernias, and still higher in those with bilateral direct inguinal hernias. An increase in the levels of circulating proteases and elastases occurs in many other conditions not associated with smoking, causing a disturbed protease/antiprotease balance and destruction of tissues leading to herniation. These conditions include many situations of stress and systemic illnesses that lead to an enhanced leukocyte response and the discharge of proteases and oxidants from the leukocytes, with a rise of elastase in the blood, leading to a relative decrease in antiprotease activity.25,29 These mechanisms may be partly responsible for attenuation of the fascia transversalis and hernia formation in nonsmokers in a fashion similar to smokers24 and may explain the appearance of hernias in patients recovering from surgical operations, infections, and systemic illnesses.

General Factors The ability of the abdominal wall in the groin and elsewhere to withstand the forces favoring herniation may be reduced by the weakening of the muscles and fasciae with advancing age, lack of physical exercise, adiposity, multiple pregnancies, and loss of weight and body fitness, such as may occur after illness, operation, or prolonged bedrest.

Surgical Incisions Certain "cosmetic" operative incisions, such as very low and unduly long transverse abdominal incisions for gynecologic or uro-

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logic procedures or "cosmetic" appendectomy incisions, may be followed by the appearance of a groin hernia caused by cutting into the myoaponeurotic arch of the lower fibers of the internal oblique and transversus abdominis muscles and/or cutting across the motor or sensory nerves of the groin, causing atrophy of the muscles. The consequent damage to the muscles of the groin region and their weakening and the postoperative fibrosis in the region interferes with the action of the shutter mechanism and promotes the development of a groin hernia.

Physical Activity Strenuous physical activity alone does not cause hernias: the incidence of groin hernia is the same in sedentary workers as in heavy manual laborers. However, it does bring about a rise in the intraabdominal pressure and so may cause an existing small and unnoticed groin hernia to expand and become clinically obvious. It may also be the final factor bringing on a hernia in those already predisposed to herniation by other more basic causes, as previously discussed.

Incisional Hernias Postoperative ventral abdominal incisional hernias develop by pathophysiological mechanisms different from those of the primary hernias discussed above. The many etiological factors involved will be briefly discussed in this section but further elaborated in Chapter 20. Many factors, singly or in various combinations, may interfere with satisfactory healing of the wound, resulting in the failure of the lines of closure of the abdominal wall following laparotomy and leading to the development of a postoperative hernia. The main causes are poor surgical technique and sepsis. Incisional hernias may be divided into early and late types.

Early Hernias These may appear within days, weeks, or months of the original laparotomy closure. They often involve the whole length of the wound, grow rapidly, and become large. They are mainly the result of technical failure on the part of the surgeon.

Surgical Incisions Nonanatomical incisions that cut across muscles, nerves, and blood vessels, cause atrophy of the muscles. The vertical pararectus incision along the outside of the lateral border of the rectus sheath is typical of this type of incision.

Layered Closures Layered closures are followed by a greater incidence of postoperative hernias than are wounds closed by the single layer mass closure technique. Many small sutures, closely placed and taking small

bites of each thin layer, often lead to tearing out of the sutures as well as necrosis of the tissues along the suture linep,31-36

Suture Material and Technique The use of inappropriate suture material, mainly absorbable sutures that do not support the wound for a sufficient length of time, will lead to separation and hernia formation. Approximately 80% of the final wound strength is reached after six months, so the wound must be supported for at least this time. Of the suture materials available today, only the synthetic nonabsorbable sutures can reliably give this support. Attention should be paid to the suturing technique. A fairly heavy thread of synthetic nonabsorbable suture material, at least four times the length of the wound, should be used for the single layer mass closure of the abdominal incision. The sutures should be about 1 cm apart and pass through the abdominal wall except for the skin and peritoneum,37-40 about 3 cm from the cut edge so as to avoid cutting out of the sutures. Tension is a potent cause of the failure of abdominal wound clasure. 41 The lateral pull of the abdominal muscles against the suture leads to progressive ischemic pressure necrosis at the point where the tissues meet the suture, until the sutured edges separate. 42 Tension is avoided by using an appropriately long length of suture as previously mentioned.

Sepsis Sepsis is the second major cause of early wound failure and is a contributing factor, if not the most important one, in more than 50% of postoperative hernias that develop within one year after the operation. It may range from frank acute cellulitis and necrosis of the tissues on each side of the incision, to low-grade chronic sepsis around sutures such as braided or twisted silk. The infection causes inflammation and edema of the tissues, which become so soft and weak that the sutures tear through and pull out under the strain of the intra-abdominal pressure.l7,43

Drainage Tubes Drainage tubes brought out through the wound leave a track of unsutured wound, and thus may act as a passage for organisms from the skin to go into the depths of the wound. They may also irritate the tissues, leading to edema and softening and tearing of the tissues.

Obesity Obesity is associated with a threefold increase in incisional herniation and recurrence of repaired incisional hernias. 5,28,36,44 Incisions through obese abdomens, with the forceful retraction needed, are associated with a higher rate of wound infection. The fatty tissues do not hold the sutures, especially against the enormous tension of the weight of masses of intra- and extra-abdominal fat. Furthermore, obese patients have a higher rate of postoperative complications such as paralytic ileus, atelectasis,

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pneumonia, and deep venous thrombosis that raise the incidence of incisional hernia.

General Condition The general condition of the patient influences the rate of postoperative ventral hernia. The factors are generally those that negatively influence the processes involved in wound healing and include age, generalized wasting, malnutrition and starvation, hypoproteinemia, avitaminosis, malignant disease, anemia,jaundice, diabetes mellitus, chronic renal failure, liver failure, ascites, prolonged steroid therapy, immunosuppressive therapy, and alcoholism.

Postoperative Complications Postoperative complications increase the incidence of postoperative hernias, especially prolonged postoperative paralytic ileus and intestinal obstruction. These are accompanied by abdominal distention, which can cause up to a 30% increase in the length of the wound, and this, together with the concomitant increase in the girth of the abdomen, causes enormous tension on the suture line, with necrosis and separation, and inevitably, a postoperative hernia. 45 Pulmonary complications also increase the incidence of postoperative hernia, especially in smokers. Postoperative wound dehiscence or "burst abdomen," whether covered by skin or with frank evisceration, is often followed by postoperative hernia whether resutured or treated by the open method. This is not surprising, since practically all the conditions mentioned previously are also causal factors in burst abdomen.

Late Hernias The etiology of the late occurring incisional hernias is not clear. The hernia develops in what apparently is a perfectly healed wound that has functioned satisfactorily for five, 10 or more years after the operation. 46 The incident is not related to the method used for closing the original incision and is presumably the result of the failure of the collagen in the scar, although there seems to be no obvious reason why mature collagen that has served well for a number of years should change its structure. Degenerative changes in the quality of collagen have been shown to be related to age 27 and may be a factor in decreased resistance of the abdominal wall scar tissue. Abnormal collagen production and maintenance in smokers may also be a factor in the late development of incisional hernia. There is a deficiency of collagen and abnormalities in its physiochemical structure, manifesting in reduced hydroxyproline production and in changes in the diameter of the collagen fibers associated with an imbalance between proteolytic enzymes and their anti-enzymes. 25

Conclusion The cause of primary groin hernia and the less common primary hernias of the abdominal wall is multifactorial. Evolutionary, hereditary, congenital and environmental aspects, and the general

state of health all play their part. Besides maintaining general body fitness and not smoking tobacco, there is little one can do to avoid this common affliction. On the other hand, incisional hernias are largely due to easily controllable human factors and can be avoided by choosing an experienced surgeon with a particular interest in and understanding of the anatomy and pathophysiology of the abdominal wall. He will choose the most suitable incision, which he will close in conformity with the highest standards, using the best materials and techniques to avoid tension and infection.

References 1. Fruchaud H. Du retentissement de la posluon debout propre a l'homme sur l'anatomie de la region de l'aine. Consequences chirurgicales. Les bases anatomiques du traitement chirurgical des hernies de l'aine. Mim Acad Chir. 1953;63:652-661. 2. Fruchaud H. Anatomie chirurgicale des hernies de l'aine. Paris: Doin; 1956. 3. Fruchaud H. Traitement chirurgical des hernies de l'aine. Paris: Doin; 1957. 4. Askar OM. Aponeurotic hernias: epigastric, umbilical, paraumbilical, hypogastric. In: Bendavid R, ed. Prostheses and abdominal wall hernias. Austin: RG. Landes Company; 1994:59-68. 5. Abrahamson]. Hernias. In: Zinner MJ, ed. Maingot's abdominaloperations. lOth ed. Stamford: Appleton and Lange; 1997:479-580. 6. McArdle G. Is inguinal hernia a defect in human evolution and would this insight improve concepts for methods of surgical repair? Clin Anat. 1997;10:47-55. 7. Clamette TD, HutsonJM. The genitofemoral nerve may link testicular inguinoscrotal descent with congenital inguinal hernia. Aust N Z] Surg. 1996;66:612-617. 8. Skandalakis JE, Colborn GL, Skandalakis L]. The embryology of the inguinofemoral area: an overview. Hernia. 1997;1:45-54. 9. Abrahamson]. Repair of inguinal hernias in infants and children: the approaches of a pediatric surgeon. Clin Pediatr. 1973;12:617-621. 10. Hughson W. The persistent or preformed sac in relation to oblique inguinal hernia. Surg Gynecol Obstet. 1925;41:610. 11. Giillmo A, Broome A, Smedberg S. Herniography. Surg Clin North Am 1984;64:229-244. 12. Jan TC, Wu CC, Yang CC, et al. Detection of open processus vaginalis by radionuclide scintigraphy. Kao Hsiung I Hsueh Ko Hsueh Tsa Chih. 1992;8:54-58. 13. Surana R, Puri P. Fate of patent processus vaginalis: A case against routine contralateral exploration for unilateral inguinal hernia in children. Pediatr Surg Int. 1993;8:412-414. 14. Surana R, Puri P. Is contralateral exploration necessary in infants with unilateral inguinal hernia? ] Pediatr Surg. 1993;28:1026-1027. 15. Stoppa R Hernia of the abdominal wall. In: ChevrelJP, ed. Surgery of the abdominal wall. Berlin: Springer-Verlag; 1985:155-224. 16. BelghitiJ, Panis Y Herniorrhaphy in cirrhotic patients with umbilical hernia. Postgrad Gen Surg. 1992;4:129-130. 17. Abrahamson]. Factors and mechanisms leading to recurrence. In: Bendavid R, ed. Prostheses and abdominal wall hernias. Austin: RG. Landes Company; 1994:138-170. 18. Brown MV, Hamilton DNH, Junor BJR Surgical complications in patients on continuous ambulatory dialysis.] R Coll Surg Edinb. 1983;28: 141-146. 19. GrosfeldJLI, Minnick K, Shedd F, et al. Inguinal hernia in children: factors affecting recurrence in 62 cases.]Pediatr Surg. 1991 ;26:28~287. 20. Tsai TC, Huang FY, Hsu JC, et al. Continuous ambulatory peritoneal dialysis complicating with abdominal hernias in children. Acta Paediatr Sin. 1996;37:26~265. 21. AbramsonJH, GofinJ, Hopp C, et al. The epidemiology of inguinal hernia: a survey in Western Jerusalem. ] Epidemiol Community Health. 1978;32:59-67.

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22. Wantz GE. Clinical crossroads. A 65-year-old man with an inguinal hernia. ]AMA. 1997;277:663-669. 23. Wantz GE. Letter.]AMA. 1997;277:1679. 24. Pans A, Pierard GE. Immunohistochemical study of the rectus sheath and transversalis fascia in adult groin hernias. Hernia. 1998;2(Suppll): 13. 25. Read RC. The metabolic role in the attenuation of transversalis fascia found in patients with groin herniation. Hernia. 1998;2 (Suppl 1):17. 26. Peacock EE. Reflections on hernias as a systemic disease. In: Bendavid R, ed. Prostheses and abdominal wall hernias. Austin: R.G. Landes Co., 1994:171-179. 27. Rodrigues-junior Aj, de Tolosa EM, de Carualho CA. Electron microscopic study on the elastic and elastic related fibres in the human fascia transversalis at different ages. Gegenbaurs Morphol]ahrb. 1990;136:

645. 28. Read RC, Yoder G. Recent trends in the management of incisional herniation. Arch Surg. 1989;124:485-488. 29. Read RC. Blood protease/antiprotease imbalance in patients with acquired herniation. Prob Gen Surg. 1995;12:41-46. 30. Lehnert B, Wadouh F. High coincidence of inguinal hernias and abdominal aortic aneurysms. Ann Vase Surg. 1992;6:134-137. 31. Abrahamson]. Epigastric, umbilical and ventral hernia. In: CameronjL, ed. Current Surgical TherafrY. Vol. 3. Toronto: Decker, Inc.; 1989:417-432. 32. Pollock AV. Laparotomy.] Roy Soc Med. 1981;74:480-484. 33. Richards PC, Balch CM, Aldrete jS. Abdominal wound closure. A randomised prospective study of 571 patients comparing continuous versus interrupted suture techniques. Ann Surg. 1983;197:238-243.

34. Ellis H, Coleridge-Smith PD, joyce AD. Abdominal incisions: vertical or transverse? Postgrad Med] 1984;60:407-410. 35. Chevrel]p. Postoperative complications. In: Chevrel jP, ed. Surgery of the abdominal wall Berlin: Springer-Verlag; 1987:83-91. 36. Manninen Mj, Lavonius M, Perhoniemi VJ. Results of incisional hernia repair. A retrospective study of 172 unselected hernioplasties. Eur ] Surg. 1991;157:29-31.

37. Ellis H, Heddle R. Does the peritoneum need to be closed at laparotomy? Br] Surg. 1977;64:733-736. 38. Ellis H. Internal overhealing: the problem of intraperitoneal adhesions. World] Surg. 1980;4:303-306. 39. Elkins TE, Stovall TG, Warren j, et al. A histologic evaluation of peritoneal injury and repair: implications for adhesion formation. Obstet Gynecol 1987;70:225-228.

40. Stark M. Suturing of peritoneum. World] Surg. 1993;17:419. 41. Abrahamson]. Factors and mechanisms leading to recurrence. Probl Gen Surg. 1995;12:59-67. 42. Bartlett LC. Pressure necrosis is the primary cause of wound dehiscence. Can] Surg. 1985;28:27-30. 43. Abrahamson j. Etiology and pathophysiology of primary and recurrent groin hernia formation. Surg Clin North Am. 1998;78:953-972. 44. Bucknall TE, Cox Pj, Ellis H. Burst abdomen and incisional hernia: a prospective study of 1129 major laparotomies. BM] 1982;284:931-933. 45. jenkins TPN. Incisional hernia repair: a mechanical approach. Br] Surg. 1980;67:335-336.

46. Ellisj, Gajraj H, George CD. Incisional hernias: when do they occur? Br] Surg. 1983;70:290--291.

Metabolic Aspects of Hernia Disease Raymond C. Read

Introduction

They are certainly alive, and the fact that hernias are so often multiple in middle-aged and old people leads me to suspect that a Modem herniology began during the golden age of anatomy pathological change in the connective tissues of the belly wall may (1750-1850), the underlying assumption then being that the tis- render certain individuals particularly liable to hernia." And fursues lining the various abdominal defects were normal and would ther, "It is most important that surgeons should form a just and stay that way. Causation was attributed to a mechanical disparity true opinion concerning the manner in which hernias arise. If between visceral pressure and the resistance of the musculature. they occur only in those who have hernial sacs already formed durCooperl (1804) not only described the transversalis fascia and its ing fetal life, then we must either excise the sacs at birth or stand role in preventing groin herniation, but listed factors which in- by and do nothing but trust to luck. But if . . . the occurrence of crease intra-abdominal pressure: cough, obesity, constipation, hernia is due to circumstances over which we have control, then pregnancy, ascites, and unusual exertion such as heavy lifting. The the prevention of hernia is a matter worthy of our serious study." strength of the abdominal wall was considered to be diminished Andrews (1924)6 followed, suggesting that atrophy of the conby congenital deficiency, debility, or aging. Rupture of the peri- joined tendon played a role. Little attention was paid to these pitoneum or abdominal musculature (Galen)la was disproved as a oneers. Thus, Zimmerman and Anson,7 in their 1967 textbook, significant factor by dissection and the fact that trauma, unless continued to state that inguinal herniation developed as a result massive, did not result in herniation. of a congenital anatomical predisposition. Indirect hernias were Even though it was well known that, at autopsy, persistence of a ascribed to the presence of a preformed sac; direct herniation was patent processus vaginalis did not equate with herniation (Clo- explained by the absence of the lowermost fibers of the internal quet, 1819),2 surgical thought regarding etiology came to be dom- oblique muscle, leaving the transversalis fascial floor of the ininated by Russell's saccular theory,3 "which rejects the view that guinal floor unsupported. It was not until 1964 that the first exhernia can ever be 'acquired' in the pathological sense ... the perimental evidence pointing to connective tissue abnormalities presence of a developmental diverticulum is a necessary an- as a possible cause of herniation in humans was made. Wirtschafter tecedent in every case," and "we may have an open funicular peri- and BentleyS cited an increased incidence of hernia in patients toneum with perfectly formed muscles: we may have congenitally with lathyrism coupled with the induction of herniation in animals weak muscles with a perfectly closed funicular peritoneum, and using lathyrogens. we may have them separately or together in infinitely variable graMy own interest in the role of metabolic factors in hernial caudations." Harrison (1922)4 was the first to question this dictum: sation was stimulated by a finding made in the late 1960s9 during "When we consider the dozens and hundreds of men who first the development of a modified McEvedy posterior preperitoneal show a hernia at 50 or 60, after their active life is over, the hy- approach to the repair of inguinal hernias. The rectus sheath, pothesis [saccular] becomes improbable to say the least. However, some centimeters above the defects, appeared thinner than northe main objection to the theory is that even if true, it gives us no mal lO and felt greasy. Samples of constant size weighed significantly useful guidance. In and of itself, the persistence of a more or less less than those taken from matched controls operated upon for elongated narrow processus vaginalis should not predispose to a other conditions. Patients with direct or bilateral hernias showed future hernia if all elements of strength present in the wall of the more attenuation than those with indirect defects. ll Atrophy was abdomen were also present in the wall of the processus ... the unrelated to age or muscle mass. 12 Hydroxyproline content and muscles, however, appeared to be normal. . . . The natural con- therefore collagen, which comprises 80% of the rectus sheath, was clusion is that the cause of an indirect hernia as of a direct her- strikingly decreased. Collagen showed altered salt precipitability nia is the failure of the transversalis fascia to withstand the and impaired hydroxylation with decreased amounts of mature inintra-abdominal pressure to which it is subjected." soluble (polymeric) collagen.I 3 Cultured fibroplasts proliferated The following year, Sir Arthur Keith 5 dealt another blow to the less and had reduced uptake of radioactive proline. Collagen fisaccular concept, stating, "We are so apt to look on tendons, fas- brils on electron microscopy showed irregular periodicity and varicial structures, and connective tissues as dead passive structures. able diameters, with some intracellular positioning. These changes R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

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in ultrastructure were later confirmed (1990) by Nikolov and Bettsher. 14 Similar findings were present in pericardial and skin biopsies. 15 Since, as McVay16 emphasized, the anterior rectus sheath is continuous with the transversalis fascia (as demonstrated historically by the success of relaxing incisions in the former to reduce suture tension after herniorrhaphy), the data reflected changes in the floor of the inguinal canal unaffected by scarring, secondary to the protrusion itself.

Hypothesis Veterans were presenting in late middle-age with a surprisingly high incidence of primary inguinal herniation, almost half having direct or bilateral defects. They showed evidence of widespread damage to connective tissue, different from that seen in lathyrism because cross-linking of collagen was unaffected. Almost all smoked heavily, having become addicted to nicotine when cigarettes were sent with the rations during World War II. Many had already suffered the consequences-emphysema, lung cancer, accelerated atherosclerosis, and so on. Since the collagen changes in their skin biopsies (similar to those in the groin) resembled those seen in the skin and lungs of patients with pulmonary emphysema, with or without deficiency of a-l-antitrypsin,l7 it seemed likely that smoke was damaging not only their lungs but, by a systemic effect, the abdominal wall. This allowed herniation through a locus minoris resistentiae, the inguinal canal. The conclusion was that long-term excessive exposure to tobacco smoke was a risk factor for groin herniation. To ascertain the mechanism involved, we first considered what was known about how smoking damages the lung. Prior to 1962, clinicians speculated that destruction of alveoli in this condition resulted from mechanical factors (cough and forced expiration against resistance) similar to those to which hernias were once ascribed. However, Laurell and Eriksson'sl8 report of predisposition to this disease secondary to an inherited deficiency of a-I-antitrypsin, coupled with its experimental production by Gross et aI., using tracheal instillation of proteolytic enzymes,19 led to the now accepted protease-antiprotease imbalance theory. Smoking stimulates a neutrophil-macrophage response. Their five- to-tenfold concentration in the lungs, with activation and release of zymogen elastase, is the prime mover. Further, oxidant combustion products of tobacco damage antiprotease defenses. 2o To explain the systemic effects of smoking, and in particular the effect on connective tissue, we envisaged that the chronic inflammatory response in the lungs was spilling over into the systemic circulation. Uninhibited proteolytic activity and large numbers of activated neutrophils and macrophages, along with products of tobacco combustion, were causing collagenolysis and inhibiting repair.21 The process (metastatic emphysema) would be analogous to distant damage to the lung and skin seen in acute pancreatitis or the secondary pulmonary effects of visceral or extremity ischemia. 22

Supporting Data Our patients with inguinal herniation, many of whom had associated pulmonary emphysema, had leukocytosis with elevated circulating elastolytic activity and a reduced antiproteolytic inhibitory

R.C. Read

capacity. Neutrophils showed enlarged zymogen granules and were primed for proteolysis. The changes were more marked in direct herniation and those with bilateral defects,23 suggesting that the presence of a preformed sac allowed indirect herniation with less attenuation of the transversalis fascia than was seen with direct protrusions. The age distribution of 2,500 hernia cases admitted to our surgical service resembled that of 500 patients treated for lung cancer and another 3,000 cases with cardiovascular diseases related to chronic smoking. The changes in collagen that we observed in our patients were described later (1984) by Berliner, who concluded that fascia and aponeuroses are dynamic, metabolically active structures characterized by an ongoing balance of collagen synthesis and enzymatic lysis. Basic concepts concerning the pathogenesis and repair of groin hernias revolve around this essential point. 24 In 1998, Pans and Pierard, using biomechanics and immunochemistry, concluded, "The collagen framework of the transversalis fascia was modified, mainly in the direct hernia group, associated with increased vascularity and cellularity. Similar changes were observed on the nonherniated sides, suggesting that connective tissue pathology plays a role in the genesis of groin hernias."25,26 This degeneration resembles that previously described in the skin of smokers (wrinkles).27 Peacock, while maintaining that the connective tissue changes in adults with groin herniation are restricted to the groin, also allowed that the pathology was present on the clinically normal side. 28 In 1988, the use of tobacco was reported to be significantly more common in patients presenting with hernia, especially women. 29 Ten years later, Scott found that the use of tobacco was twice as common in 130 patients operated on for recurrence, compared to those treated for primary herniation. 3o In the late 1980s, Weitz and his colleagues31 provided independent support for the metastatic emphysema hypothesis when they unequivocably recovered the "fingerprints" of free active neutrophil elastase (increased fivefold) from the plasma of cigarette smokers by measuring a specific fibronopeptide cleavage product of fibrinogen identified by radioimmune assay. They concluded, "Our findings raise the possibility that other systemic complications of cigarette smoking (for example, atherosclerotic disease) may be the result of uncontrolled neutrophil elastase activity." Most recently (1998), Jorgensen et al.,32 in an elegant prospective randomized study, matched young male and female volunteers, 19 smokers and 18 nonsmokers. Deposition of total protein and mature collagen was assessed in a wound healing model implanted subcutaneously for 10 days. Nonsmokers produced almost twice the amount of hydroxyproline in granulation tissue as their counterparts, who smoked an average of 20 cigarettes a day. Other proteins were unaffected. Thus, they were able to demonstrate that in humans, smoking specifically impedes collagen synthesis.

Proteolysis in Patients with Aneurysm Yet another abdominal protrusion, aortic aneurysm, was once blamed on mechanical factors, turbulence, and hypertension and aging abetted by atherosclerosis. Nevertheless, smoking was shown to be a risk factor in 1968. 33 Auerbach 34 later found nonsmokers with aortic aneurysm to be outnumbered eight to one, while Cronenwett35 determined that the presence of obstructive pulmonary disease was the best predictor of rupture. In 1980, Swanson et al. 36 for the first time invoked a metabolic factor, endogenous collage-

17. Metabolic Aspects of Hernia Disease

nase, in the pathogenesis of ruptured aneurysm. Busutill et al.,37 the same year, reported that elastase caused aneurysm, with its 70 to 80% loss of elastin, but prevented occlusive disease. They suggested the enzyme originated in neutrophils or monocytes. Two years later, we 38 reported that smokers with aortic aneurysm, but not Leriche's syndrome, demonstrated leukocytosis with elevated serum and leukocyte elastase activity (later to be confirmed, even after excision of the aneurysm 39 ) and reduced antiproteolytic capacity. Smoking was then experimentally shown to increase aortic elastase content. 40 Since these findings were similar to those previously described by us in patients with hernia, we investigated the possibility of an association between the two conditions. We found inguinal herniation to be twice as common in patients with aneurysm, compared to those having Leriche's syndrome thrombotic occlusion of the aorta. In addition, the former had more severe fascial attenuation with earlier and larger, mainly direct, recurrent or bilateral hernial defects. 23 This significant association was confirmed by Lehnert and Wadouh in 1992.41 They reported herniation affecting 1 of 3 patients with infrarenal aortic aneurysm. A similar relationship was later shown42 and repeatedly confirmed43 ,44 to hold true for incisional herniation after resection of an aneurysm, but not for occlusion with aortofemoral prosthetic interposition. In 1984, Brown et al. 45 reported increased serum monocyte derived circulating elastase activity persisting long after the aneurysm was excised, proving that these proteases do not originate in the smooth muscle cells of the aneurysmal wall. Rizzo et al.,46 in 1988, described inflammatory infiltrates permeating the wall of aneurysms. Cigarette smoking has also been correlated with the formation, expansion, and rupture of saccular aneurysms arising in the intracerebral arteries, previously thought to be congenital. 47 The fact that pancreatic trypsins and elastase have been identified in the blood of smokers and may contribute to the development of abdominal aortic aneurysm emphasizes the damage inflicted by tobacco use on protective circulating antiprotease mechanisms. 48 Thus, in smokers, aneurysm, like herniation, has to be considered the result ofa systemic protease-antiprotease imbalance. This conclusion is supported by a reported eightfold increase in the incidence of cerebral aneurysm in patients with a-I-antitrypsin deficiency correlated with a similar change in plasma elastase. 49

Genetic Influences Smoking does not always lead to death from lung cancer or a heart attack. Similarly, not all smokers develop aneurysms or hernias. Further, these latter may arise in patients who have never used tobacco. For example, many hernias occur soon after birth, especially if premature. Such congenital defects have been ascribed to a delay in normal development, that is, closure of the processus vaginalis. However, herniation may be multiple, familial, or part of various connective tissue disorders, including osteogenesis imperfecta, Marfan's or Ehlers-Danlos syndromes, congenital elastolysis (cutis laxae) or more commonly, hip dislocation of childhood. Recently (1997), autosomal dominant polycystic kidney disease, which is known to involve an abnormality of basement membrane or extracellular matrix production, has been added to the list. Up to 43% of adult patients with this abnormality have abdominal herniation. 50 Most of the congenital conditions described above have been shown to arise from genetic mutations.

141

In 1992, Deak et al. 51 demonstrated abnormal synthesis (collagen gene expression) in cultured skin fibroblasts taken from two patients with multiple aneurysms, suggesting sporadic mutation. However, a number of individuals with single aneurysms showed no such change despite a positive family history. The following year, this group studied nine men, 17 to 67 years of age, with either indirect or direct inguinal herniation. Few smoked, some had a familial history, and a third demonstrated joint hypermobility. Isotopically labeled skin fibroblasts secreted twice as much type III collagen (one of the two most common among the 29 different forms) as controls. This altered ratio with the usually predominant type I collagen, led to a decrease in insoluble (polymeric) fibrils, confirming our original observations. Thus the proportion of collagen types regulates fibrillogenesis, fibril diameter, and bundle architecture. They commented, "An increase in type III collagen, (a metabolic abnormality of production) may predispose certain individuals to the development of inguinal herniation and recurrence after corrective surgery. "52 Genitourinary prolapse in women was shown53 in 1990 to be similarly associated with hypermobility, suggesting an underlying connective tissue disorder. In 1996, collagen deficiency with increased cross-linking and decreased solubility associated with collagenolysis was identified54 in this condition.

Conclusion In infancy, herniation is known to relate to prematurity or known connective tissue disorders. In adults, cigarette smoking has been shown to damage connective tissue, causing attenuation of the transversalis fascia, thus leading to inguinal and incisional herniation (metastatic emphysema). Genetic mutation can also interfere with collagen type I and III synthesis, thereby playing a role in herniogenesis. Thus, Keith's suggestion 75 years ago that a pathological change in connective tissue could cause herniation has been confirmed by a number of investigators. These findings support the increasingly widespread use of prostheses in the repair of abdominal herniation, as well as the need to widely encompass Fruchaud's myopectineal orifice.55

References 1. Cooper AP. The anatomy and surgical treatment of inguinal and congenital hernia. London: Longman; 1804. 1a. Stoppa R, Wantz GE, Munegato G, Pulchinotta A. Hernia Healers: An Illustrated Histmy. Arnette: France, 1998;8-9. 2. Cloquet J. Recherches sur les causes et l'anatomie des hernies abdominales. Paris: Mequignon-Marvis; 1819. 3. Russell RH. The saccular theory of hernia and the radical operation. Lancet. 1906;3:1197-1203. 4. Harrison PW. Inguinal hernia: a study of the principles involved in the surgical treatment. Arch Surg. 1922;4:680-689. 5. KeithA. On the origin and nature of hernia. BrJSurg. 1924;11:455-475. 6. Andrews E. A method of herniotomy utilizing only white fascia. Ann Surg. 1924;80:225-238. 7. Zimmerman LM, Anson BJ. Anatomy and surgery of hernia. 2nd ed. Baltimore: Williams & Wilkins Co., 1967. 8. Wirtschafter ZT, Bendey JP. Hernias as a collagen maturation defect. Ann Surg. 1964;160:852. 9. Read RC. Preperitoneal exposure of inguinal herniation. Am] Surg. 1968;116:653--658.

142 10. Read RC. Attenuation of the rectus sheath in inguinal herniation. Am ] Surg. 1970;120:610-614. 11. Wagh PV, Read RC. Collagen deficiency in rectus sheath of patients with inguinal herniation. Proc Soc Exper BioI Med. 1971;37:382-384. 12. Wagh PY, Read RC. Defective collagen-synthesis in inguinal herniation. Am] Surg. 1972;124:819-822. 13. Wagh PY, Leverich AP, Read RC, et al. Direct inguinal herniation in men: a disease of collagen.] Surg Res. 1974;17:425-433. 14. Nikolov VSP, Beltschev B. Some ultrastructural features of fascia transversalis in direct inguinal hernias in senile men. Anat Anzeiger lena. 1990;170:265-272. 15. Sun CN, White HJ, Read RC, et al. Alteration of collagen fibrils in direct inguinal herniation in men. In: Eighth International Congress on Electron Microscopy, Canberra. 1974. Vol. II; 482-483. 16. McVay CB. "The normal and pathologic anatomy of the transversus abdominis muscle in inguinal and femoral hernia." Surg Clin North Am, 1971 ;51: 1251. 17. Read RC. Presidential address: systemic effects of smoking. Am] Surg. 1984;148:706-711. 18. Laurell CB, Eriksson S. The electrophoretic alpha-l-globulin pattern of serum alpha-I-antitrypsin deficiency. Scand] Clin Lab Invest. 1963; 15:132-140. 19. Gross PE, Pfizer EA, Tokler E, et al. Experimental emphysema and its production with papain in normal and silicotic rats. Arch Environ Health. 1965;11:50-58. 20. Wewers MD, GadekJE. The protease theory of emphysema (editorial). Ann Intern Med. 1987;107:761-763. 21. Cannon DJ, Read RC. Metastatic emphysema: a mechanism for acquiring inguinal herniation. Ann Surg. 1981;194:270-278. 22. Lee PC, Howard JM. Fat necrosis. Surg Gynecol Obstet. 1979; 148:785-789. 23. Cannon DJ, Casteel L, Read RC. Abdominal aortic aneurysm, Leriche syndrome, inguinal herniation and smoking. Arch Surg. 1984;119: 387-389. 24. Berliner SD. An approach to groin hernia. Surg Clin North Am 1984; 64(2):197-213. 25. Pans A, Pierard GE, Albert A, et al. Adult groin hernias: new insight into their biomechanical characteristics. Eur] Clin Invest. 1997;27:1-6. 26. Pans A, Pierard GE. Immunohistochemical study of the rectus sheath and transversalis fascia in adult groin hernias. Hernia. 1999; 111:45-51. 27. Kadunce DP, Burr R, Gress R, et al. Cigarette smoking: risk factor for premature facial wrinkling. Ann Intern Med. 1991;114:84()-.844. 28. Peacock EEJr. Biology of hernia. In: Nyhus LM, Condon RE, eds. Hernia. 2nd ed. Philadeiphia:J.B. Lippincott Company; 1978:3. 29. Bielecki K, Puawski R. Is cigarette smoking a causative factor in the development of inguinal hernia? Pol Tyg Lek. 1988;43:974-976. 30. Scott JS. Causes of groin hernia recurrence following open repair. Presented at the First Annual Scientific Meeting of the American Hernia Society, Miami Beach, FL, Feb. 1998. 31. Weitz JI, Crowley KA, Landman SL et al. Increased neutrophil elastase activity in cigarette smokers. Ann Intern Med. 1987;107:680-682. 32. Jorgensen LN, Kallehave F, Christensen E, et al. Less collagen production in smokers. Surgery. 1998;123(4):450-455. 33. Hammond E, Garfinkel L. Coronary heart disease, stroke and aortic aneurysm. Arch Environ Health. 1969;19:167-182.

R.C. Read 34. Auerbach 0, Garfinkel L. Atherosclerosis and aneurysm of the aorta in relation to smoking habits and age. Chest. 1980;78:805--809. 35. Cronenwett J, Murphy T, Zelnock G, et al. Actuarial analysis of variables associated with rupture of small abdominal aortic aneurysms. Surgery. 1985;98:472-483. 36. Swanson RJ, Littooy FN, Hunt TK, et al. Laparotomy as a precipitating factor in the rupture of intra-abdominal aneurysms. Arch Surg. 1980; 115:299-304. 37. Busuttil RW, Abou-Zamzam AM, Machleder HI. Collagenase activity of the human aorta. A comparison of patients with and without abdominal aortic aneurysms. Arch Surg. 1980;115:1373-1378. 38. Cannon DJ, Read RC. Blood elastolytic activity in patients with aortic aneurysm. Ann Thorac Surg. 1982;34:10-15. 39. CohenJR, Faust G, Tenenbaum N, et al. The calcium messenger system and the kinetics of elastase release from human neutrophils in patients with abdominal aortic aneurysms. Ann Vasc Surg. 1990;4(6): 570-574. 40. CohenJR, Sarfati I, Wise L. The effect of cigarette smoking on rabbit aortic elastase activity.] Vasc Surg. 1989;4:580-584. 41. Lehnert B, Wadouh F. High coincidence of inguinal hernias and abdominal aortic aneurysms. Ann Vasc Surg. 1992;67:134-137. 42. Stevick CA, Long]B, Jamasbi B, et al. Ventral hernia following aortic reconstruction. Am Surg. 1988;51:287. 43. Hall KA, Peters B, Smyth SH, et al. Abdominal wall hernias in patients with abdominal aortic aneurysmal versus aortoiliac occlusive disease. Am]Surg.1995;170:572. 44. Holland AJ, et al. Incisional hernias are more common in aneurysmal arterial disease. Eur] Vasc Endovase Surg. 1996;12:196-200. 45. Brown SL, Buckstrom B, Busuttil, RW. A new serum proteolytic enzyme in aneurysm pathogenesis.] Vase Surg. 1985;2:393-399. 46. Rizzo RJ, McCarthy~, Dixit SN, et al. Collagen types and matrix protein content in human abdominal aortic aneurysms.] Vase Surg. 1989; 10:365-373. 47. Misra BK, Whittle IR, Steers AJ, et al. De novo saccular aneurysms. Neurosurgery. 1988;23: 10-15. 48. Dubick MA, Hunter GC, Perez-Lizano E, et al. Assessment of the role of pancreatic proteases in human abdominal aortic aneurysms and occlusive disease. Clin Chern Acta. 1988;177:1-10. 49. Baker Cj, Flore A, Connolly ES Jr, et al. Serum elastase and alpha-lantitrypsin levels in patients with ruptured and unruptured cerebral aneurysms. Neurosurgery. 1995;37(1):56-61. 50. Morris-Stiff G, Coles G, Moore R, et al. Abdominal wall hernia in autosomal dominant polycystic kidney disease. Br] Surg. 1997;84:615617. 51. Deak SB, RicottajJ, Mariani 1J, et al. Abnormalities in the biosynthesis of type III procollagen in cultured skin fibroblasts from two patients with multiple aneurysms. Matrix. 1992;12:92-100. 52. Friedman DW, Boyd CD, Norton P, et al. Increases in type III collagen gene expression and protein synthesis in patients with inguinal hernias. Ann Surg. 1993;218(6):754-760. 53. Baker NP, Baker J, Sharp H, et al. Genitourinary prolapse: relationship with joint mobility. Neurourol Urodyn. 1990;9:321-322. 54. Jackson SR, Avery NC, Tarlton]F, et al. Changes in metabolism of collagen in genitourinary prolapse. Lancet. 1996;347:1658-1661. 55. Fruchaud H. Traitement ehirurgieal des hernies de l'aine. Paris: Doin; 1957.

18 Pathological Tissue Changes and Hernia Formation Alain Pans

Introduction Classically, inguinal hernias are considered the result of a multifactorial process linking predisposing anatomical and dynamic factors: intra-abdominal pressure acting on a weak area, the myopectineal orifice, which is sealed by the transversalis fascia. All groin hernias are therefore characterized by the displacement of this fascia by a peritoneal sac. There are individual anatomical variations that aggravate the fragility of the inguinal region, enlarging the weak area and rendering less effective the physiological protective mechanisms of the inguinal region. l To these are added histobiochemical factors, which are unquestionably the least known at present, but very likely playa key role in the genesis of inguinal hernias. In the light of the work of Peacock and Madden2 and Wagh, Read, and Cannon,3-6 it appeared that hernia formation was actually based on much more fundamental metabolic collagen anomalies. Hence, inguinal hernia could be considered a local manifestation of systemic collagen pathology. This aspect has, however, been studied very little up to now. This is why we undertook a detailed study of the transversalis fascia and the sheath of the rectus abdominis muscle in control groups and in patients with inguinal hernias. We first analyzed the macroscopic biomechanical properties of these structures, then proceeded to the microscopic level in an attempt to clarify them by means of their histologic characteristics.

Biomechanical Characteristics of the Transversalis Fascia and the Anterior Rectus Sheath We have at our disposal very little information concerning the mechanical properties of the transversalis fascia. Minns and Tinckler7 have studied the mechanical characteristics of the transversalis fascia of inguinal hernia patients. The ultimate tensile strength of these tissues was lower than that of controls. All the patients in our study underwent bilateral inguinal hernia repairs, whether the condition was itself bilateral or whether it was decided, with the patient's consent, to treat the unaffected side preventively. The technique used was a midline suprapubic approach with placement of a prosthesis on each side in the R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

preperitoneal space. Once the preperitoneal dissection was accomplished, good exposure of the posterior wall of the inguinal canal was obtained. Biopsies of constant surface area were taken from the transversalis fascia, on the left and right sides, as well as from the anterior rectus sheath. Analogous samples were taken from a control group made up of autopsy subjects within 24 hours of death and of organ donors. The study included 63 patients (89% men) with 88 groin hernias. Mean age of patients was 57.7 years. The hernias were indexed according to the classification of Nyhus. s Eligible for the study were 38 fascias from nonherniated groins, 32 from indirect hernias (type II), 40 from direct hernias (type IlIa). The mean age of the 30 control subjects (63% men) was 59.5 years. The biomechanical properties of these tissues were evaluated using a commercially available apparatus, the Cutometer® SEM 474 (C&K Electronics, Cologne, Germany) equipped with an aspirator probe 2 mm in diameter. The deformation of the tissue in the opening of the probe was registered by computer. Three cycles of 5 seconds of traction under negative pressure of 50 and 200 millibars, separated by periods of relaxation of 5 seconds, were successively applied to each specimen. The application of the first cycle of suction resulted in an immediate elastic distension (ED 1) , recorded at 0.15 s, followed by a delayed viscoelastic distension and ending with measurement of the maximum distension (MDl) of the tissue obtained after 5 s of traction (Fig. 18.1). When traction was discontinued, the tissue tended to return to its initial shape. During that phase, the immediate elastic retraction (ERl) after 0.1 s of relaxation and the resilient distension (RDl) after a 5 s relaxation time were recorded. The differential distension (DD) was calculated as the difference in maximum distension between the third (MD3) and the first (MDl) cycles. Calculated in addition were the viscoelastic ratio (VER), the biological elasticity (BE), the elastic function (EF), and the relative elastic recovery (RER) (Table 18.1). The indicator 50 or 200 was added to each biomechanical variable to indicate whether the measure was performed at 50 or 200 millibars respectively. Our study is original in that it employs in hernia pathology recent evaluative technology developed for pathologies of the skin. Actually, the Cutometer was initially intended to identify the mechanical properties of healthy and pathological skin in vivo. The suction levels of 50 and 200 mb correspond to physiological pressures exerted upon the transversalis fascia, at rest and while coughing respectively. 9 143

144

A. Pans

0.5 0.4

E S c:

0.3

~ > Q) iii

0.2 0.1 0.0

Time (5) FIGURE 18.1. Biomechanical parameters recorded during the elevation of the transversalis fascia over time. Pressure: 200 mbar. ED1, elastic (immediate) distension (0.15 s); MD1, maximum distension at the end of the first traction (5 s); ER1, elastic (immediate) retraction (5.1 s); RD1, resilient distension at the end of the first cycle (10 s); MD3, maximum distension at the end of the third traction (25 s).

In the study of the mechanisms contributing to the creation of an inguinal hernia, it seems to us important to sample the transversalis fascia at the level of the posterior wall of the inguinal canal itself, the quintessential "critically weak" area, forming the bed of future direct hernias. As for the rectus sheath, it is considered an indicator of systemic pathology of connective tissue. The mechanical behavior of the transversalis fascia was markedly different from that of the rectus sheath, a thicker and more solid structure macroscopically. The fascia showed much less elasticity, a clearly increased viscoelasticity, and increased deformability during successive applications of mechanical stress. Overall, we did not observe any important difference in the mechanical characteristics of the rectus sheaths of patients and controls. This would seem to not support a major systemic pathology of connective tissue. Nevertheless, the transversalis fascias from direct hernia patients showed an extensibility (MD, ED-50 and -200) and elasticity (BE50) very significantly higher than those of controls. This difference in elasticity leveled off at 200 mb. The same characteristics were seen, to a slightly lesser extent, in the fascias from non hernia sides, regardless of the type of hernia (direct or indirect) on the affected side. MD and ED-50 and -200 were significantly higher, whereas the significant elevation of BE disappeared at 200 mbar. We may conclude that the fascia, presumed healthy at the time of the intervention, also showed pathological characteristics. Thus, the observed changes appear to be the cause, rather than the consequence, of hernia. Although fascias from indirect hernias alone showed an increase TABLE

18.1. Biomechanical parameters

Extensibility parameters

Elasticity parameters

BE = 102 (MD1 - RDI)MDI-I (%) MD (mm) EF = 102 (MD1 - ER1)EOl- 1 (%) ED (mm) RER = 102 (MOl - ER1)MD- 1 (%) DD = MD3 - MD1 (mm) VER = 102 (MD1 - ED1)EOl-I (%)

in maximum distension at 200 mbar compared to controls, they constituted nevertheless an entirely separate pathological group, as we have shown in an earlier work. IO Two highly significant correlations appeared entirely characteristic of direct hernias: at 200 mbar, as MD and ED increased, EF diminished. This means that the more the fascia is stretched out, the less readily it springs back to its original position. One may therefore suspect that there is an impediment to the immediate rebound of the fascia, in keeping with an architectural disorganization of the collagen lattice. We have also demonstrated that in the herniated fascias, as well as in those from nonhernia sites, the difficulty in returning to their initial position was proportional to the importance of the stress to which they had been submitted. This is in good agreement with the clinical history of hernias whose volume increases progressively with time, evidence that the transversalis fascia returns less and less to its original state.

Analogy with Skin at 50 mbar The fascias of direct hernias and of nonhernia sites show an increase in extensibility (MD and ED) and of elasticity (BE and RER). Such biomechanical characteristics were observed in the skin of patients with Ehlers-Danlos syndrome, mainly of types I and nY

Analogy with Skin at 200 mbar The fascias of direct hernias and of nonhernia sites show above all an increase in extensibility (MD and ED). The increase in elasticity is significant only for direct hernias and to a degree 20 times less than that at 50 mbar. This comes closer to the biomechanical characteristics of stretch marks following childbirth. 12 However, in that cutaneous pathology, the elasticity parameters are no different from those of healthy skin.

Influence of in vivo and ex vivo Conditions It is also necessary to take into consideration the fact that our mea-

surements were made on loose excised samples, hence the elimination of tensions transmitted to them by neighboring tissues. As far as skin is concerned, the biomechanical properties of normal skin ex vivo appear identical to those of the skin in vivo. 13 By contrast, this is not the case with stretch marks. Extensibility remains increased, but the elasticity of stretch marks ex vivo is significantly reduced, while it does not appear to be altered in vivo. This is probably due to the presence of traction in situ which maintains stretch marks under relative tension. From the sum total of these comparisons, it appears once more that the best correlation is observed between the biomechanical behavior of the fascias of direct hernias and nonhernia sites (at 50 mbar) and that of the skin of patients with type I and II EhlersDanlos syndrome. The etiology of these two types of Ehlers-Danlos syndrome is not yet known; however, the gene coding for the al chain of type V collagen appears to be implicated. 14 Recently, a mutation in the C-propeptide of the pro-al chain of type V collagen was demonstrated, which carries with it a diminished synthesis of type V col-

18. Tissue Pathology and Hernia Formation

145

lagen and in this way causes an anomaly in the fibrillogenesis of type I collagen.15

Immunohistological Characteristics of the Transversalis Fascia and the Rectus Sheath There are only a few histologic studies of the anatomical structures of the inguinal region. Berliner16 observed in certain cases a scarcity and fragmentation of the elastic fibers as well as degenerative changes (unspecified) in the transversalis fascia taken from the site of a hernia. Weinstein and Roberts l7 have studied the external oblique aponeurosis in 20 patients operated on for inguinal hernia, among whom the age varied between 3 and 80 years. They noted the same relative proportion of collagen fibers and elastic fibers in all the age groups, with a predominance of collagen fibers and few blood vessels. Panou de Faymoreau l8 carried out, during hernia treatment, the removal of samples containing transversalis fascia and the aponeurotic structures of the region. He observed a predominance of fatty tissue, abundant and congested vascularity, disorientation of aponeurotic fibers, and fragmentation of elastic fibers surrounded by sclerosis. None of these mainly qualitative studies makes reference to control tissues. On the samples obtained for the biomechanical study, we performed a histologic study. The detailed information on the histologic techniques used can be found in our original paper. l9 This study included 10 rectus sheaths of patients and controls, 15 control fascias, 15 direct hernia fascias, 15 indirect hernia fascias, and 21 fascias taken from nonherniated sites. The latter were subdivided into two groups according to whether the contralateral side showed a direct (n = 9) or indirect (n = 11) hernia. The sections were carried out in three spatial planes (coronal, transverse, and sagittal) , whenever the quantity of material allowed. They were stained with hematoxylin and eosin, with Masson's trichrome and the double stain of mixed picrosirius red and orcein. An immunohistochemical study was carried out in order to demonstrate the endothelial cells with the help of Ulex europaeus lectin and a polyclonal antibody. The enumeration of elastic fibers stained with orcein was done by a computerized system for analyzing images (analySIS®, Soft-Imaging Software GmbH, Munster, Germany).

FIGURE 18.2. Thick parallel collagen bundles packed in a control rectus sheath, with the fine collagen network connecting the subcutaneous tissue and sheath (XIO, transverse section, Masson trichrome) . We have not observed any architectural difference between the sheaths of controls and those of patients in relation either to the elastic fibers or to the bundles of collagen. Nor did the two groups present any significant difference in terms of the quantity of adipocytes, of cellularity, or of the number of vessels per field.

Fascias Smooth Muscle Fibers It is necessary to note the presence of smooth muscle fibers (SMF) within the fascia itself, in the same amount in both controls and

Rectus Sheaths Sections of the anterior rectus sheath from control subjects were characterized by a regular three-dimensional structure of collagen bundles. This consisted of thick bundles always arranged parallel among themselves, usually transversely (that is to say, perpendicular to the linea alba) or occasionally obliquely, depending on the location (Fig. 18.2). Consistently, there was a fine network of interwoven collagen fibers insuring the connection of subcutaneous tissue and the sheath (Fig. 18.3). This network was observed much less often between the sheath and the muscle. Elastic fibers within the sheath itself were few, regularly distributed, sometimes cut crosswise, sometimes lengthwise in the same plane. They were much more abundant in the fine subcutaneous, preaponeurotic lattice of collagen fibers. Their plane of section was similarly variable, depending on location (Fig. 18.4) .

FIGURE 18.3. Fine collagen network connecting the subcutaneous tissue and sheath (X20, picrosirius red in polarized light).

A. Pans

146

same way that striated muscle fibers come to be inserted in their tendon. It is therefore not impossible that these smooth muscle fibers confer a certain contractile function on the transversalis fascia, enabling it to participate in the protection of the inguinal region against abdominal pressure.

Adipocytes The proportion of adipocytes observed in the control fascias (0: 4 cases; +: 6 cases; + +: 4 cases; + + +: 1 case) did not differ significantly from that observed in the different groups of pathology. We did not think, therefore, that the phenomenon of fatty degeneration was an essential element of hernia disease.

FIGURE 18.4. Elastic fibers (in black) in the preaponeurotic network (X20,

orcein and picrosirius red) .

patients. These fibers were grouped in bundles and formed an integral part of the supporting tissue of the transversalis fascia, as shown in Fig. 18.5. To our knowledge, this has never been described in the literature. Of course, insertion of the cremaster into the transversalis fascia is mentioned. 2o By analogy, we have searched for smooth muscle fibers in the spermatic cord, an anatomical structure in close contact with the transversalis fascia. To do this, we harvested a spermatic cord together with the transversalis fascia of the inguinal floor of an autopsy subject 45 years of age. The same appearance of smooth muscle fibers, not forming part of a vascular wall or the vas deferens, was identified in the cord. The smooth muscle nature of these fibers was confirmed by an immunohistochemical stain with the aid of murine monoclonal antibodies against a-actin of smooth muscle (Fig. 18.6). The literature makes no mention of the presence of smooth muscle fibers within the spermatic cord,21 although they are described in the round ligament. 22 However, some 10 cases ofleiomyoma of the spermatic cord, a very rare smooth muscle tumor, have been reported in the literature. 23 One may consider that the smooth muscle fibers of the spermatic cord come to be inserted in the transversalis fascia in the

Number of Vessels and Cells per Field The number of vessels and cells per field was significantly increased in the group of direct hernias. No inflammatory infiltrate was observed in any of the fascias. This agrees with the observations of Panou de Faymoreau 18 describing abundant, congested vascularity in inguinal tissues taken from a hernia site. However, the mean diameter of the vessels observed in our study was 50 /-Lm. The vascular walls were normal. It is thus not a matter of newly formed vessels, such as one might see in granulation tissue. Two hypotheses may explain this observation and could in any case coexist. The first is that an actual increase in vascularization came into being well before the development of the hernia. But, in that case, it would be a very early phenomenon in the genesis of the hernia, as the same normal mature vessels are observed on the nonhernia side. In essence, our earlier biomechanical study and the histological considerations which follow argue for the fact that the non hernia side is already at a preclinical stage of hernia development. The second hypothesis would move mainly in the direction of relative growth of the vascularization in direct hernias. It is in fact logical to think that the vessels of the transversalis fascia are stretched by the volume of the actual underlying hernia. Once the fascia is excised, this extrinsic tension disappears, and it is possible that the vessels then take a more tortuous form due to their relatively excessive length. From a histologic point of view, this would mean that the plane of section could cut across a winding vessel many times, leading to an apparent increase in the number of vessels per field. The latter hypothesis seems to us likely. As for the increase in the cellularity per field in the direct hernia group, it is probably due in part to the increase in the number of vessels per field. We have not observed any inflammatory infiltrate.

Elastic Fibers

FIGURE 18.5. Smooth muscle fibers (S.M.F.) in the thickness of a control

transversalis fascia

(X 10,

frontal section, Masson trichrome) .

Elastic fibers were present throughout the thickness of the transversalis fascia. Their configuration was sometimes longitudinal, sometimes fragmented depending on the plane of section. The elastic fibers of the fascias of patients presented a morphology and a distribution similar to those of controls (Fig. 18.7). There was no difference in terms of percentage of surface area occupied by elastic fibers .

147

18. Tissue Pathology and Hernia Formation

FIGURE 18.6. Spermatic cord (autopsy). The side of the transversalis fascia is stained in black by India ink. (A) Striated cremasteric muscle fibers (C.M.) and smooth muscle fibers (S.M.F.) (X4, Masson trichrome).

(B) Smooth muscle fibers stained by antismooth muscle antibodies. The cremasteric muscle is not stained. Reprinted from Hernia 1999;3:45-51 , with permission.

We confirm, therefore, the fragmented appearance of elastic fibers, according to location, observed by Berliner 16 and Panou de Faymoreau. 18 But this fragmentation is also seen in control fascias. Consequently, we think that it is rather a case of a characteristic linked to the plane of section through the elastic fibers. In a particular plane, elastic fibers can be sectioned transversely, obliquely, or longitudinally according to their arrangement. By analogy with skin,24 it is also necessary to take into consideration the fact that fragmentation of elastic fibers can also be a result of aging.

The transversalis fascia was characterized by an architectural organization much more heterogeneous than that of the rectus sheath. In general, it was a weave of bundles of collagen presenting, according to the plane of section, a preferential orientation. The quantity of bundles, fascicles, and fibers of collagen was estimated in a semiquantitative manner according to the score 0, +, ++, +++ (Fig. 18.8). We observed a tendency toward diminution of the number of fascicles in the three categories of patho-

logical fascias and to augmentation of the number of fibers in direct hernias and in nonhernia sites. The proportion of cases showing zones of architectural disorganization was significantly more elevated in the direct hernia group and the nonhernia sites of which the other side was also a direct hernia. These semiquantitative results were confirmed and refined by studying the number of interactions of the collagen lattice with a line traced perpendicular to the general orientation (Fig. 18.9). Three zones of the section were considered, the architectural zone most representative of the totality of the section, as well as two other zones as different as possible from each other on the architectural plane. The notion of variability was studied, calculating for each section the difference between the two most extreme values. The mean of these differences was then calculated. By comparison with the control group, a significant progressive increase in the number of intersections in the representative zone of each section was observed in the indirect hernia group, the nonhernia sites, and direct hernias respectively. This increase in the nonhernia group was observed independent of the type of hernia on the other side. This signifies, therefore, that if the number of

FIGURE 18.7. Elastic fibers in a control transversalis fascia (X20, longitudinal section, orcein and picrosirius red) .

FIGURE 18.8. Fibers, fascicles, and collagen bundles in a control fascia (Masson trichrome) . Reprinted from Hernia 1999; 3:45-51, with permission.

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FIGURE 27.18. The force to rupture (Newtons) of the implants plotted against implantation time (weeks). The values for carbon fiber (dashed line) and Mersilene® mesh (solid line) at each time interval are shown, together with the range of values (vertical bar). The upper shaded portion is the range of the force to rupture for strips of Mersilene mesh and the lower shaded portion for carbon fiber strips.

Weeks post implantation

Carbon fibre Mersilene Carbon fibre/Mersilene FIGURE 27.20.

The force at failure of the 3 implant constructs shown against implantation time.

carbon fiber strips, the force to rupture increased as the implantation time increased, although the intact carbon fiber was very weak in tension. This was in contrast to the force to rupture of the implanted Mersilene strips, which remained nearly constant and similar to the intact Mersilene material. The carbon fiber implants were stronger than the Mersilene implants after 8 weeks' implantation and continued to increase in rupture strength. The energy absorbed by both implanted materials was similar up to 6 weeks' implantation. Mter this, the carbon fiber implants showed a far greater increase in energy absorption than did the Mersilene (Fig. 27.19). When combined as a composite implant, the failure force is always greater than the Mersilene or carbon fiber individually (Fig. 27.20), as is the work to failure (area under the stress-strain curve) after 6 weeks' implantation (Fig. 27.21).

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Mechanical Test Results of the Clinical Carbon Fiber Material Although the tensile properties of the modified carbon fiber samples showed no significant improvement over the original material (Fig. 27.22), an unpaired "S" test on the data suggested that there was a highly significant (p < .001) improvement in the suture retention properties. There was no significant difference between the suture retention properties of the modified material and the Mersilene (Fig. 27.23).

Clinical Results of the Modified Carbon Fiber Material Immediately postoperatively, and at 6 months, there was no evidence of the sinus formation or infection that had been associated with previous prosthetic materials. One failure occurred 16 months postoperatively. At reoperation, a defect was found at the

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WEEKS POST IMPLANTATION

27.19. The variation of energy absorbed by the strips in tension with implantation time. The values for carbon fiber strips and Mersilene® mesh strips are shown with the range of values at each time (vertical bar). The dashed horizontal lines show the energy to rupture for intact carbon fiber and Mersilene strips before implantation.

Weeks post implantation

Carbon fibre Mersilene Carbon fibre/Mersilene

FIGURE

27.21. The work to failure (area under the stress-strain curve) for the three constructs examined.

FIGURE

218

RJ. Minns and M.I.A. Selmia

Tensile Tests (dumbbell-shaped specimens)

clinical results, as assessed by all the patients, were regarded as excellent.

Discussion

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FIGURE 27.22. Tensile properties of modified carbon fiber sample show no significant improvement over original material.

medial part of the repair between the patch and the inguinalligament where the suture appeared to have pulled through. The carbon fiber implant appeared extremely well infiltrated by fibrous tissue and was firm and supportive to probing. The mean preoperative visual analogue score for discomfort was 4.0, with a standard deviation of 2.7, and for pain the score was 1.8 with a standard deviation of 2.58. The scores at 5 years after operation were significantly reduced (paired Hest); for discomfort: mean 0.25, standard deviation 0.65, p < .001; and for pain: mean 0.11, standard deviation 0.53, p < .001. The clinical result as assessed by the patient was excellent in all but one case, in which it appeared that preoperative testicular pain was unaffected by hernia repair, but there was no evidence of recurrence in the clinically examined group. At the 13-year follow-up, there was no pain or discomfort, no evidence of recurrence, and no lymph node enlargement. The

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27.23. Suture retention properties of modified carbon fiber samples versus Mersilene®.

FIGURE

It appears that the strength of the transversalis fascia is related to the occurrence of inguinal hernias, the defective tissue having a lower rupture stress than normal fascia. However, what is of more interest is the area under the stress-strain curve, as this is related to the work done in breaking the specimen. Normal transversalis fascia has a greater curve area than herniated fascia and is consequently less easily ruptured. The resistance to rupture relates to the ability of the collagen fibers to withstand the repeated high loads that would be encountered physiologically. Any defect in the collagen framework reduces its resistance to rupture. Another factor that may be related to the failure of the transversalis fascia is its time dependence properties, which were low, according to the load relaxation tests conducted. This would mean that the transversalis fascia would have a low ability to absorb shock in the case of sudden loading, and local areas of high strain may consequently rupture weak. points in the collagen framework. The pliability of a synthetic mesh for hernia reinforcement allows for adaptation to the directional extensibility and loadings that are encountered in the body, especially in the area where the transversalis fascia has failed. However, excessive extension of the mesh in one direction or the other would tend to have a twofold effect on the integrity of repair. First, on loading, the mesh holes and interstices would be closed from the open weave of the mesh at rest. Second, and perhaps more important, when the mesh is positioned under load caused by the tension of the sutures, the load-extension properties in situ are dramatically modified. The mesh would appear very stiff and restrict the natural movement of the wound area if applied under tension or very lax if the mesh was applied loosely, allowing large relative movements between tissue and the reinforcement, thus having little value as a supportive prosthesis. With the information obtained from this study, it should be possible to design a suitable prosthesis that would be mechanically strong, with a stiffness and extension in all directions comparable to the surrounding fascia and with mesh pores or interstices that would allow tissue ingrowth.l1 The mesh fiber arrangement depends on weave and average fiber angle to give the desired mechanical properties. It appears that a knitted weave with interlocked fiber junctures is desirable in that slippage and unraveling of the mesh fibers will not occur, 2 and it has the required load-extension properties to evenly support the defective tissue at all stages of extension. In the area of the defective transversalis fascia, there is a mechanical weakness in patients who have undergone prosthetic herniorrhaphy. To reinforce this weakened area, three types of prosthetic material have been used clinically with various degrees of success: skin, woven meshes, and nonwoven sheets. However, on loading the prostheses, the interstices presented to and in contact with the fibrovascular tissue would alter, as would the amount of load and movement taken by the prosthesis and that taken by the sutures. How much the mesh or the sutures or both deform in situ would be related to the mechanical properties of the materials and sutures used. A stiff mesh and relatively elastic sutures applied tightly would mean that the prosthesis would restrict movement of the surrounding tissue and possibly allow a better chance of tissue ingrowth at the interface. What would be sacrificed would

27. Structure and Mechanics of Biomaterials

219

be the natural movement of the wound area. Any excessive pres- we saw no evidence of fragmentation or migration of carbon fibers sure would transfer load to the rather elastic sutures, and this either into the surrounding tissues or into the regional lymph nodes, would be the weak point of the prosthesis. This appears to be the this might be revealed in long-term experiments. Certain mineral fibers are known to cause carcinoma of the lung case of the stainless steel mesh. Skin wounds, although apparently well healed, remain weak and brittle structures through 150 days or mesotheliomas of the pleura and peritoneum when ingested, and have at that time only half the ability of uninjured tissue to re- but fibers greater than 3 #-tm diameter have difficulty penetrating sist rupture. 15 Therefore, for transversalis fascia, which is similar in the respiratory bronchioles. If carbon fibers and Mersilene fibers structure to skin, mechanical support for at least 150 days would are ingested, their diameters diminish the possibility of initiating fibrosis and reaching the pleural surfaces. However, long-term appear to be one requirement for a supportive prosthesis design. If it were possible to control the structural organization of col- studies of malignant changes induced by carbon fiber have not lagen during healing, and thus improve scar performance,12 a been carried out, and further investigations are obviously needed. prosthesis that had the ability to do this and provide mechanical The carbon fiber patches implanted in the experimental animal support in the first 150 days after operation would appear ideal. show a successful mechanical and structural repair after 8 weeks' Porcine skin certainly has the extension and load properties that implantation. Although mechanically weak in the early stages of are required at operation if employed correctly. That is, if the su- implantation, carbon fiber may, combined with a clinically actures are applied with little tension at rest, the scar tissue will then ceptable material such as Mersilene mesh as a composite, offer the be evenly supported, as shown by the extension properties deter- exciting possibility of being a superior reinforcing prosthesis for mined compared with transversalis fascia. However, one cannot abdominal defects and incisional hernias. depend on scar tissue to take over support of the prosthesis that In the clinical study of the new strengthened carbon fiber patch, fragments or disintegrates. Porcine skin is not absorbed before 150 there was a very low recurrence rate with a high patient satisfacdays, and, as it would appear that the scar tissue, which has be- tion rate 13 years after the implantation.1 2 In the one case of recome incorporated within the prosthesis, would be subjected to currence after 4 years, suture pullout seems to have been the cause low loads, no recurrence has occurred clinically. rather than a mechanical failure of the carbon fiber patch itself. We recommend that a prosthesis used as a supportive material The previous exprimental findings were borne out at the time of not under tension should be inert, have elasticity comparable to repair of the recurrence when excellent ingrowth of fibrous tissue the scar tissue formed, be easily manageable at operation, provide into the carbon patch was observed. an interface allowing chemically and structurally the incorporaIt may be argued that the recurrence rate after a standard election of repair tissue within the interstices, and provide supportive tive hernia repair should be low without the need to use prosthetic strength for up to 1 year after operation. Stainless steel appears materials. With good tissue available and good technique, this too stiff on its own, and its elasticity as a prosthesis depends on should certainly be the case. However, there are cases, especially suture elasticity. Also, the interstices are extremely large for in the elderly, where poor tissue quality may contribute to a reorganized tissue ingrowth. Mersilene mesh has adequate two- currence. The availability of a good biocompatible material such dimensional supportive strength and extension properties but suf- as carbon fiber with improved qualities compared to previous prosfers from large pore size, and the possibility of complete tissue in- thetic materials should prove to be of benefit in such circumcorporation is small. Porcine skin, when properly applied, appears stances. Long-term effects of carbon fiber on soft tissues appear to have adequate elasticity and extension properties in two di- not to present a problem. I6 mensions when sutured in position and provides an ideal interRecurrence rates after repair of recurrent inguinal hernias vary: face for tissue incorporation. It is clear from the mechanical testing in one series by one surgeon, it was 9%.4 George and Ellis6 rethat the Mersilene mesh is stronger in the initial stages of repair ported a recurrence rate after repair of incisional hernias of 46% than the carbon fiber patch in the experimental animal. However, and observed in their literature search that recurrence rates after that strength is overtaken by the incorporated tissue within the the use of Marlex mesh varied between 0 and 11.3%.8,17,18 carbon fiber patches after 8 weeks of implantation. This suggests Johnson-Nurse and Jenkins I9 demonstrated the benefit of fithat an appropriate design of prosthesis should incorporate the brous tissue ingrowth into the carbon fiber patch repairs of sheep advantageous features of both materials. Not only would the Mer- incisional hernias and the very low subsequent recurrence rate. silene mesh supply initial strength to the prosthesis immediately We suggest that the use of carbon fiber may have beneficial and after implantation, but it would also allow fixation by virtue of eas- wider applications not only in elective hernia repair, but also in ier suturing. Mersilene fails because knots within the mesh unravel recurrent inguinal hernia, and in the surgical management of the at the suture fixing locations, thus leaving the strength of the pros- difficult abdominal incisional hernia, as an alternative to Mersithesis dependent on the strength of the mesh rather than of the lene or Bard® mesh. 5 sutures. However, this failure strength appears quite adequate for the type of physiological loads likely to be encountered. Mersilene mesh positioned over the carbon fiber patch may decrease the likelihood of abrasion of the overlying skin. References Although both materials produce a connective tissue response, the carbon fiber patches produce a response of organized noninflam1. Adler RH, Pelecanos NT, Geil RG, Rosenzweig SE, Thorsell HG. A colmatory fibrous tissue that becomes quickly incorporated with the malagen mesh prosthesis for wound repair and hernia reinforcement. terial. No viscoelastic studies were performed. However, within the Surg FIlTUm. 1962;13:29-33. matrix of the tissue is a ground substance, which gives rise to the re2. Matheson AJM, James JH. A review of inguinal hernia repair using pair tissue having highly time-dependent properties. This may be a stainless steel mesh. J R GoU Surg Edinb. 1975;20:59-62. good thing for the distribution of load through the fibrous matrix 3. Forrester Je. Mechanical, biochemical and architectural features of during high rates ofloading that may occur physiologically. Although surgical repair. Adv Biol Med Phys. 1973;14:1-34.

220 4. Forrester jC, Zederfelot BH, Hayes TL, Hunt TK. Tape-closed and sutured wounds: a comparison by tensiometry and scanning electron microscopy. Br J Surg. 1970;57:729-737. 5. Tinckler LF. Preperitoneal prosthetic herniorrhaphy. Postgrad Med J 1969;45:665-667. 6. George CD, Ellis H. The results of incisional hernia repair: a 52-year review. Ann R Coil Surg Edinb 1996;68:185-187. 7. Minns Rj, Soden PD,jackson DS. The role of the fibrous components and ground substance in the mechanical properties of biological tissues: a preliminary investigation. I J Biomech. 1973;6:5S3-165. 8. Liakakos T, Karanikas I, Panayiotidid H, Dendrinos S. Use of Marlex® mesh in the repair of recurrent incisional hernia. Br J Surg. 1994;81: 248-249. 9. Edwards LC, Pernokas LN, Dunphy]E. The use of a plastic sponge to sample regenerating tissue in healing wounds. Surg Gynecol Obstet. 1957;105:303-309. 10. jenkins DHR, McKibbin B. The role of flexible carbon-fiber implants as tension and ligament substitute in clinical practice. A preliminary report. J Bone Joint Surg. 1980;62B:497-499. 11. Minns Rj, Stevens DC, Gore GM, Tinckler LF. The mechanical and structural properties of reinforcing materials used in prosthetic herniorrhaphy. Eng Med. 199;8:15-19.

RJ. Minns and M.I.A. Selmia 12. Ward R, Minns RJ. Woven carbon fiber patch versus Dacron® mesh in the repair of experimental defects in the lumbar fascia of rabbits. Biomaterials. 1990:1. 13. Minns Rj, Claque MB, Ward R, Cullen Pj, Dunstone GH. The repair of inguinal hernias using carbon fiber patches. A five-year follow-up. Clin Mat. 1993;14:139-144. 14. Selmia MIA, Minns Rj, Cullen PJ. The repair of inguinal hernia using carbon fiber patches. A thirteen-year follow-up. Cleve Med J 1999;3: 103-106. 15. Minns Rj, Denton~, Dunstone GH, SunterjP. An experimental study of the use of a carbon fiber patch as a hernia prosthesis material. Biomaterials. 1982;3: 199-203. 16. Tayton K, Phillips G, Ralis Z. Long-term effects of carbon fiber on soft tissues. J Bone Joint Surg. 1982;64B: 112-114. 17. Usher RC. Hernia repair with Marlex® mesh. Arch Surg. 1962;84:73-

78. 18. Molloy RG, Moran KT, Waldron RP, Brady MP, Kirwan WOo Massive incisional hernia, abdominal wall replacement with Marlex® mesh. Br J Surg. 1991;78:242-244. 19. johnson-Nurse C, jenkins DHR. The use of flexible carbon fiber in the repair of experimental large abdominal incisional hernias. Br J Surg. 1990;67:135-137.

Biomaterials Pathology Nir Kossovsky, Charles]. Freiman, and David Howarth

Introduction The modem era of biomaterials was born with the discovery of antibiotics in the mid-twentieth century. Antibiotics enabled surgeons to control the bacteria that invariably settled on a medical device from the operating room atmosphere immediately before implantation. Once bacteria were under control, differences among various materials and the biological responses they provoked became apparent, and the need to develop materials that exhibited improved "biocompatibility" emerged. In this chapter, we present a brief but comprehensive review of the essential factors contributing to biomaterials and their induced biological response, which we term bi(JTeactivity.

General Principles

Materials Principles It is useful to divide the physical properties of a medically im-

planted device into two broad categories: surface properties and bulk properties. Although there is some overlap, this division is useful in understanding the pathological phenomena associated with an implanted device, as well as the mechanisms underlying the pathophysiological responses of the body to that device. The science of biomaterials and medical device pathology exists because the materials from which medical devices are fabricated differ from the materials from which our bodies are fabricated. These differences in chemistry between biomaterials and our natural materials lead to both different surface properties and different bulk properties. Everything we touch, see, taste, or smell is matter. Generally, our experience with matter is superficial, with only the top few layers of molecules. It is these surface molecules that give materials many of their physical and chemical properties. Therefore, all of the principal chemical and biophysical interactions between implanted materials and the biological environment occur at surfaces. Surfaces are physically unique environments with special mechanical, chemical, and electrical properties. These properties are derived from the electron clouds of the atoms comprising the surface and are influenced significantly by the electrons of atoms comprising an opposing surface. R. Bendavid et al. (eds.), Abdominal Wall Hernias © Springer Science+Business Media New York 2001

In contrast, bulk properties are the features of a material that arise from the composition and microstructure of everything below the few molecules at its surface. These properties include operationally defined attributes such as elastic modulus, fatigue strength, tensile strength, ductility, fracture toughness, and hardness. Because degradation phenomena are closely related to a material's bulk properties, they are addressed in the bulk properties section although they are technically surface events.

Surface Properties Surface chemistry is the science of phase boundaries. In mathematics, the term surface refers to the geometric concept of area without thickness. However, in surface chemistry, it refers to the chemical concept of a phase boundary, a region where the physical properties vary from those of one phase to those of the adjoining phase. Because this transition occurs over distances of molecular dimensions, a "chemical surface" has a thickness. The boundary between phases, the interface, is a thin layer of material whose properties differ profoundly from those of the bulk phases it separates. For example, the state of (mechanical) energy of the surface is different from that of the underlying bulk so that, in a fluid interface, the difference manifests itself as a contractile tendency, which makes the interface act like an elastic membrane seeking the configuration of minimum area, a sphere. The chemical composition of the interface layer is generally different from that of the bulk phase. For example, the interface between a piece of metal such as iron and the air is extremely complex and bears little resemblance to either iron or air. The metal is likely to be covered with an oxide layer (rust), and the top layer of the oxide is probably hydroxylated from prolonged contact with water vapor in the air. The next layer may consist of tightly bound water, followed by a layer ofloosely bound water depending on the relative humidity. Finally, there is usually a layer of environmental "scum" consisting of airborne organic waste. The interface may also exhibit electrical charge separation, and consequently the interface between two neutrally charged bulk phases may appear to bear a charge. The unique energetic (mechanical), chemical, and electrical properties of interfaces often exert great and highly varied effects on the behavior of material systems. These may appear bizarre and contradictory if one at-

221

222 tempts to describe or explain them in terms of bulk phase behavior alone. At the molecular level of life, the chemical properties are determined by the shapes of molecules, as well as the sequence of atoms comprising those molecules. This phenomenon is demonstrated to all of us daily. For example, the egg white protein ovalbumin changes from a globular shape to a much more linear shape through the addition of energy by mechanical beating. Mter heat is added, the result of this changed shape (from beating) is a souffle in contrast to an omelet. When a device is implanted in the body, it is immersed in an aqueous solution with a high concentration of proteins, as well as other macromolecules. These proteins are highly surface active and tend to be drawn to the interface. The concentration of these proteins can be significantly higher at the interface than in the aqueous solution. In addition, the proteins at the interface can experience shape changes. The nature of the surfaces of materials from which the biomaterials are fabricated determines the type of interaction those surfaces are likely to have with the protein-rich aqueous environment. The interactions involving surface protein shape change may lead to the initiation of any of the four m.yor pathophysiological phenomena (inflammation, thrombosis, infection, and neoplasia). Finally, the sequelae of initiation of these pathophysiological phenomena range from clinical insignificance to major medical complications and device failure.

Bulk Properties Bulk properties are operationally defined attributes. One of the most critical properties of a material is its response to mechanical forces, such as tension, compression, shear, torsion, and bending. Materials tend to form in a manner that is both proportionally and directionally related to the magnitude of the applied forces; when the force is removed, materials may tend to return to their original shape. The relationship between the applied force and the resulting deformation can be quite complex. When the force to which a material is subjected is removed, a number of different events may occur. First, a deformed material may return to its original configuration, in which case the deformation will have been of the elastic type. Second, a deformed material may not return to its original configuration, and there will remain a permanent change in dimensions, or form, in the absence of an applied load. In this instance, the deformation will have been of the plastic type. Generally, materials will exhibit elastic deformations at lower forces and plastic deformations at greater forces. The ratio of the force to deformation, for the force range where a material exhibits elastic behavior, is known as the elastic modulus. As the force is increased, the deformation of a material progresses from elastic behavior to plastic behavior to catastrophic failure. The transition from elastic to plastic behavior is marked by the loss of the linear relationship between force and deformation. This transition is known as the yield strength and is expressed in units of force. The transition from plastic behavior to the beginning of the failure mode is marked by the point at which a material continues to undergo progressive strain in the absence of any additional force. This point is known as the material's ultimate strength.

N. Kossovsky et aI.

Ductility is the degree of plastic deformability. Brittle materials (nonductile) usually fail within the elastic range. In contrast, ductile materials exhibit plastic deformation within the elastic range. Tensile strength is the force that must be applied in opposing directions to cause the material to break completely. This is typically measured by placing clamps at opposing ends of a strip of material and using a tensiometer to gradually increase the force applied until there is complete separation of the material into two pieces. The tensile strength of an abdominal mesh prosthesis can be tested either simply with the material itself or after the material has been implanted. The tensile strength in the latter case includes the strength of any products of the bioreactive process, such as collagen deposition. In contrast, bursting strength is the degree of force that must be applied uniformly to cause a rupture. With an abdominal mesh prosthesis, this is typically measured by implanting the material and infusing the area of implantation with a fluid until an emanation of that fluid occurs. The study of wear and resistance to it is known as tribology and is formally defined as the study of the effects of friction on moving parts and the methods, such as lubrication, of obviating them. Wear is defined as the removal of material from a solid surface by another material as a result of relative motion between the two. This removed mass can be poorly adherent to the new surface and may be released. Thus, such wear causes two types of failure. The first is a "wear-out" mode occurring after long periods of wear, when significant amounts of material are ultimately removed. The second is a "seizure" mode, which occurs in systems where particles whose diameters are larger than the clearing space between the sliding surfaces are produced and ultimately jam the system.

Bioreactivi ty In discussing the potential pathological responses to an implanted medical device, perhaps the best way of viewing the body is as a collection of homeostatic systems. The implantation and presence of a given implanted medical device has the potential to introduce stress into these homeostatic systems. If this stress exceeds the adaptive capacity of the system, the system experiences irreversible injury, causing cells to die. The precise moment when reversible injury progresses to irreversible injury cannot at present be identified. A system exposed to persistent sublethal stress will show one of several adaptive responses. These responses may be identified either clinically or pathologically as evidence of cell injury. Generally, cells adapt to injury by conservation of resources. This may be accomplished by decreasing or ceasing their differentiated functions and reverting to ancestral unicellular characteristics, focusing solely on survival functions. A medical device (or the material that it is composed of) should not induce undue stress on the adjacent cells once implanted. However, meeting this requirement alone does not ensure a favorable clinical course. Various homeostatic mechanisms in the body may induce stress by initiating a "preemptive" reaction to the device. This is the reason that both cellular and organized systemic responses to stress are seen following device implantation. These responses constitute the elements of pathophysiology. Four major pathophysiological phenomena are examined. They are inflammation, thrombosis, infection, and neoplasia. These processes are not completely independent, and for any given de-

223

28. Biomaterials Pathology

vice they may not all be relevant. However, they represent the major biological responses that may greatly affect the clinical performance of a medical device.

Inflammation and Wound Healing In the pathology of abdominal mesh, perhaps the greatest concern, and hence the area that most research focuses on, is inflammation and wound healing. Inflammation is the reaction of vascularized living tissue to injury. It is the primary biological reaction to implanted medical devices. In addition, it is probably a component of the other three major pathophysiological responses: thrombosis, infection, and neoplasia. The inflammatory system has four arms that are related both temporally and hierarchically. The first arm of inflammation is usually the initial component to respond to injury, and thus it is known as the acute phase of inflammation. It involves primarily blood vessels. The hallmarks of acute inflammation include the accumulation of fluid and plasma components in the affected tissue. This is due to the dilation and increased permeability of blood vessels and intravascular stimulation of platelets in the presence of polymorphonuclear leukocytes. Polymorphonuclear leukocytes are the principal cellular mediators of the nonvascular element of the acute inflammatory reaction through engulfment of foreign agents or iJtiured cell material. In contrast to the polymorphonuclear leukocytes, the platelets, in conjunction with mast cells and basophils, mediate the vascular element by the liberation of the vasoactive substances and other inflammatory intermediates (Table 28.1). The second arm of inflammation is known as the chronic phase of inflammation. This arm is most active with persistent injury. When the acute inflammatory response is unable to eliminate the iJtiurious agent or restore injured tissue to its normal physiological state, there may be a progression to a state of chronic inflammation. The primary cellular components of the chronic inflammatory response are macrophages, plasma cells, lymphocytes, and, in certain conditions, eosinophils. Macrophages are the most important cells to consider in the chronic inflammatory reaction to an implanted material, for they play a pivotal role in material degradation and in potential imTABLE

mune activation. Macrophages are endowed with a broad spectrum of inflammatory and degradative biochemical systems, and their level of activity is clearly related to the chemistry of the biomaterial to which they are responding (Table 28.2). The third arm of inflammation, the immune response, is only slowly being recognized as a bioreaction associated with medical devices and biomaterials. The immune response is a specific and acquired reaction by the immune system to foreign material entering or coming into contact with the body. It is a very complex and sophisticated defense reaction involving antibodies, a variety of cells, and blood vessels. These are usually the same elements that mediate chronic inflammation, but the duration and intensity of the biological reaction in an immune response tend to be much more pronounced than in nonimmune chronic inflammation. The fourth arm of inflammation consists of the wound healing phase and characteristically follows any of the first three arms chronologically. This phase consists of the replacement of damaged tissues by various cells that specialize in secreting extracellular matrix materials to form scar. Especially with implanted medical devices, the terms acute and chronicinflammation usually are misnomers. Many materials evoke, at the onset, an inflammatory reaction characterized by the infiltration of macrophages. With certain materials polymorphonuclear leukocytes may appear at the site of implantation months after macrophages have been actively engaging an implant. Wound healing and scar formation follow the initiation of inflammation, but their progression and the magnitude of scarring may be affected by the degree of persistent inflammatory activity as well as by the severity of primary injury.

Thrombosis Of the four major pathophysiological phenomena, thrombosis is probably the least relevant to abdominal mesh. This is due to the traditionally extravascular location of these devices. However, it is possible, although perhaps not probable, that the device could, due to poor anatomical conformation or by contributing to the formation of fistulas, seromas, and so forth, have a thrombogenic effect. Poor anatomical conformation or the formation of seromas

28.1. Inflammatory mediators

Origin Cell derived Histamine Serotonin Lysosomal enzymes Prostaglandins Leukotrienes Platelet-activating factor Cytokines Plasma derived Complementary system Kinin system

Clotting/fibrinolytic system

Action Vascular leakage Vascular leakage Immobilization of neutrophils, vascular leakage, and chemotaxis Vasodilation, pain, fever, potentiation of other mediators Leukocyte adhesion, bronchoconstriction, vasoconstriction, vascular permeability, and chemotaxis Bronchoconstriction, vascular leakage, and chemotaxis Acute phase reactions, leukocyte adhesions, and chemotaxis Opsonization and lysis of microbial organisms, vascular leakage, and chemotaxis Dilation of blood vessels, contraction of smooth muscle, aggregation of polymorphonuclear leukocytes, and vascular leakage Converts fibrinogen to fibrin, vascular leakage, and chemotaxis

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TABLE 28.2. Macrophage products Group Neutral proteases

Chemotactic factors Arachidonic acid metabolites Reactive oxygen metabolites Complement components Coagulation factors Growth promoting factors Cytokines

Other agents Interferon

Specific products Collagenase Elastase Plasminogen activator Prostaglandins and leukotrienes O 2; HOCI, H 20 2 and OH-

Factor V and thromboplastin Interleukin-l, interleukin-6, and tumor necrosis factor Platelet activating Antiviral activity

Action Degrades connective tissue components Degrades connective tissue components Activates plasmin (fibrinolytic agent) Attraction of other leukocytes Vasodilation, vasoconstriction, vascular permeability, and chemotaxis Endothelial damage, tissue damage, inactivation of antiproteases, and vascular leakage Parenchymal damage, opsonization, vascular permeability, and chemotaxis Local conversion of fibrinogen to fibrin Fibroblasts, blood vessels, and myeloid progenitor cells Acute phase reactions, fever, leukocyte adhesion, chemotaxis, B cell differentiation, endothelial cell activation, and fibroblast stimulation Invokes inflammation, bronchoconstriction, vascular leakage, and chemotaxis

could cause pressure on blood vessels, thereby affecting the flow of blood and possibly giving rise to thrombi. Fistulization could expose the vasculature to infectious agents, against which an inflammatory reaction could promote thrombosis. Although some of the materials from which abdominal meshes are fabricated are used for vascular prostheses, there is a lack of research on the thrombogenic activities of the various abdominal meshes, and hence thrombosis is not reviewed for each type of mesh.

mental and immune defense factors that interact with biomaterial properties in what has been termed by Gristina as the "race for the surface" of the interface. 6 Prosthesis design and prevention of implant-associated infection must include consideration for the interaction of the biomaterial with the host tissue and the contribution of each to the microenvironment.

Infection

Over the years, medical researchers have discovered what appears to be an ever-increasing number of substances that possess carcinogenic potentials. It is curious, therefore, that little research has been done on the possible carcinogenic effects of abdominal mesh. This lack of research prevents us from reviewing the carcinogenic effects for each specific type of mesh. A neoplasm, or cancer, is an uncontrolled proliferation of cells that express varying degrees of fidelity to their precursors. The neoplasm is an abnormal mass of cells that persists after cessation of the stimulus that produced it, and, in general, it is irreversible. Its growth is, for the most part, autonomous. The structural resemblance of the neoplasm to its putative cell of origin makes specific diagnoses possible as to the source and potential behavior of the neoplasm. Although the causes of most cancers are not identified and the mechanisms of carcinogenesis remain obscure, considerable data on the biological attributes of neoplasia are available. A wide variety of human and experimental data suggest that the neoplastic process entails not only cellular proliferation but also a modification of the differentiation of the involved cell types. Several observations are important at this point. First, neoplasms are usually derived from cells that normally retain a proliferative capacity. Thus, mature neurons and cardiac myocytes do not often give rise to tumors. Second, a tumor may express varying degrees of differentiation, from relatively mature structures that mimic normal tissues to a collection of cells so primitive that the cell of origin cannot be identified. Third, the stimulus responsible for the uncontrolled proliferation may not be identifiable; in fact, it is not known for most human neoplasms. The experimental production of cancer by a chemical occurred

Infection is the second greatest concern with abdominal mesh, and, not surprisingly, in the available literature on abdominal mesh, infection is the second most studied of the four major pathophysiological phenomena. Infection is a pathological reaction to implanted medical devices because it is potentiated by the process of device implantation. This simple phenomenon was appreciated back in the fourteenth century when the French surgeon Guy de Chauliac noted that wound infections were easier to control if associated foreign bodies were extracted. 1 Elek and Cohen, in the 1950s, showed that 106 Staphylococcus pyogenes were required to produce a pus-forming clinical infection in human volunteers but that the addition of a foreign body reduced the necessary bacteria inoculum to 102.1a Several mechanisms have been postulated to play a role in prosthesis-associated infections. An implanted foreign body may produce tissue liquefaction and sterile abscess formation by inciting an acute inflammatory reaction when reactive materials, such as cobalt or copper, are implanted into soft tissue. 2 Tissue damage can be exacerbated by the release of enzymes and oxygen free radicals and other inflammatory mediators. Tissue reactivity can also be greatly increased by the production of particulate wear debris.3-5 Implants may alter local host immune defenses through the reduction of granulocyte and bactericidal capacity. Infection may also be enhanced due to sequestration of bacteria from phagocytes in the early postoperative period. The establishment of tissue integration of the implant or the development of bacterial colonization and subsequent deviceassociated infection is influenced by a number of host environ-

Neoplasia

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28. Biomaterials Pathology

in 1915, when Japanese investigators, using coal tar, produced skin cancers in rabbits. Since that time, the list of organic and inorganic carcinogens has grown exponentially. Yet, a curious paradox existed for many years. Many compounds known to be potent carcinogens are relatively inert in terms of chemical reactivity. The solution to that riddle became apparent in the early 1960s, when it was shown that most, although not all, chemical carcinogens require metabolic activation before they can react with cell constituents. For biomaterials, a process analogous to metabolic activation may be the free radical, oxidative, and hydrolytic reactions associated with inflammation. A number of different sarcomas have been induced in rodents by the implantation of materials such as plastic and metal films, various fibers, plastic sponges, glass spheres, and dextran polymers. In addition to the chemical nature of these implants, the critical features include size, smoothness, and durability of the implanted surfaces. Biomaterial-induced cancers appear to be highly species specific. With "physical" carcinogens, common factors of this class seem to be the need for the development of chronic fibrosis or, at least, an inflammatory response. 7 Foreign bodies once considered prototypic examples of "physical carcinogens" are being reevaluated as chemical carcinogensB as new data on the chemical properties of asbestos come to light. 7 In addition, there are numerous synthetic polymers that may release monomers or additives that might induce a chemical carcinogenic response at the site of implantation or in other parts of the body.9 However, an association between implanted devices and neoplasia has yet to be demonstrated in humans.

Specific Materials Having examined general principles applicable to all types of abdominal mesh, we turn our attention to specific types of clinically available abdominal mesh. When discussing specific devices, we have limited our research to data acquired solely through abdominal applications. In addition, we have confined our discussion to meshes that are clinically available.

Permanent Meshes Permanent meshes, also called nonabsorbable meshes, are devices that, barring a catastrophic event or surgical removal, remain essentially intact throughout the life of a patient. In contrast, the absorbable meshes that we examine are degraded by the body over time. The permanent meshes that we examine are Marlex® (C.R. Bard, Inc., Billerica, MA), Prolene® (Ethicon, Inc., Somerville, NJ), Gore-Tex® ePTFE Soft Tissue Patch (W.L. Gore & Associates, Inc., Flagstaff, AZ), and Mersilene® (Ethicon, Inc.).

Polypropylene In 1954 Italian scientist Giulio Natta, using Karl Ziegler's metalorganic catalyst technique, developed propylene, an ethylene with one small carbon methyl group attached. Propylene was unique in that, when polymerized, all the methyl groups faced in the same direction rather than the usual random fashion. Such "isotactic polymers" (the name was proposed by his wife) possess useful properties and can now be manufactured. Other isotactic polymer plas-

tics are polycarbonate, a tough flexible plastic (used in drinking straws), and polyvinyl chloride (PVC). Polypropylene, a thermoplastic polyolefin, can vary widely in mechanical properties, depending on its degree of crystallinity, as reflected in its density. The repeating monomer of the polypropylene polymer consists of two carbon atoms, one of which is saturated with two hydrogen atoms and the other of which is saturated with one hydrogen atom and one methyl group. The polymer is formed by free radical addition, and, because of its asymmetry, may exist in one of three forms depending on the spatial position of the methyl group. The name given to the polypropylene chain structure depends on whether the methyl groups are all in the same plane (isotactic), uniformly alternating planes (syndiotactic), or randomly distributed (atactic). The strength of the material correlates strongly with the degree of crystallinity and is maximal in the isotactic form and minimal in the atactic form. Polypropylene is extremely resistant to biological degradation. It has excellent environmental stress-cracking resistance and is relatively impermeable to water vapor. Polypropylene is not weakened significantly by the action of tissue enzymes. 10 In addition to the fabrication of surgical meshes for abdominal wall and hernia repairs, sutures are a major medical application of this material. Currently, there are several polypropylene meshes available, Marlex, Prolene, Trelex®, and Surgipro®. The latter is made of braided strands of polypropylene, while the other three are monofilament strands. Marlex and Prolene have been the subjects of most research and publications.

Marlex Marlex is currently the most widely used abdominal mesh. 11 Pioneered by Francis C. Usher in 1958,l2 it was originally fabricated from polyethylene,13,14 but it was later formulated in 1962 as a polypropylene mesh to overcome shrinking, stiffening, and distortion in autoclaving.I 5 Both the polyethylene mesh and polypropylene mesh are referred to as Marlex. However, because the polyethylene-formulated Marlex is no longer in use, we will confine our discussion to the current polypropylene formulation of Marlex and the term Marlexwill refer exclusively to the polypropylene mesh.I 2- 14,16-26 Marlex has enjoyed a favorable reputation. 15,22,25,27-31 It is known for being resistant to infection,15,IB,22,24,27,32-34 well tolerated,15,25,2B,30 and strong enough to allow a woman to have an uncomplicated, successful pregnancy and vaginal delivery.35 However, the mesh has been noted to cause bowel complications,10,25 seromas,23,33 sinus formation,ll,33 mesh migration ,11 buckling,36,37 and adhesions11 ,31,3B,39 that can make the device difficult or impossible to remove when necessary.38,39

Physical Characteristics Marlex is a monofllament mesh in which each filament has a diameter of 0.017 cm. The mesh is 0.065 cm thick, weighs 0.1522 g/10 cm2, and has a density of 0.23 g/cm3. The bursting strength is 68.9 ::!: 1.9 kg and 4.5 ::!: 0.12 kg/cm2. As to tensile properties, its breaking strength is 34.6 ::!: 1.1 kg (wale) and 16.5 ::!: 1.4 kg (course), and its breaking elongation is 74.3 ::!: 2.3% (wale) and 203.2 ::!: 3.9 (course). The pores of the mesh vary from 68 to 23 p,m X 23 p,m. 4O Marlex is radiolucent and does not compromise radiological diagnostic techniques. 34 It does not readily oxidize with age, either on the shelf or when implanted.

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Tyrell et al.,n using New Zealand white rabbits, found the tensile strength to be 2.66 kg 10 weeks after implantation (Fig. 28.1). In addition, they found that the tensile strength increased over 50% from weeks 2 to 10, but they note that the data were not normally distributed. Murphy et al.,41 using CD rats, recorded a tensile strength of 3.02 kg/em 15 to 20 weeks after implantation of the device. Jenkins et al.,42 using Sprague-Dawley rats, examined bursting strength and found that it increased by over 100% from the first week of implantation to the fourth week. Although there is wide variation in the data, at 1 week all ruptures were at the prosthesis/muscle interface, whereas at week 4 all ruptures occurred at the inguinal canal. Law and Ellis,19 using Sprague-Dawley rats, found that the abdominal wall breaking strength did not weaken over a 4-week interval after implantation in the presence of infection (S. aureus). Inflammation and Wound Healing-Lahoratory Studies Murphy et al. 41 graded mean adhesion formation after 15 to 20 weeks as moderate, requiring gentle dissection augmented with limited sharp dissection. Law and Ellis 17 found on average moderate adhesions freed by aggressive blunt dissection at both weeks 1 and 22. Jenkins et al. 42 characterized the average adhesion formation at week 1 as maximal, changing to moderate at week 4. The adhesion formation of the polypropylene mesh and the polytetrafluoroethylene patch was judged in a study by Hengirmen et al. 43 as moderate in abdominal wall defects in rats. Macrophage response to experimental implantation of polypropylene prostheses in New Zealand white rabbits diminished after the first 90 days, although foreign body granulomas increased. 44 Law and Ellis 19 conducted tensiometric studies of healing in abdominal wall defects created in Sprague-Dawley rats. At up to 22 weeks, Marlex mesh and Gore-Text Soft Tissue Patch provided a strong repair, but the fibrous response induced by Dexon® mesh was insufficient to produce a strong support. Bellon et al. 45 found no significant differences in degree of adhesion formation or integration between Marlex and Prolene in abdominal defects in

M Marlax

D Dexon

Gore-Tax

New Zealand white rabbits. Polypropylene's structure allows for its total integration with reparative tissue. 46 Hydrophobic polypropylene meshes were found to repel migrating connective tissue cells, which invaded the interstices of polyethylene terephthalate mesh in a unique three-dimensional organ culture matrix designed by Dasdia et al. 47 Adhesions and inflammation around the graft were found to be greater with polypropylene than with polytetrafluoroethylene in rats with abdominal wall defects. 48 Brown et al.,49 using Hartley guinea pigs, studied adhesion formation with five separate sets of conditions. They found that infection had little effect in slowing the formation of tenacious scar. Inflammation-Clinical Studies The pores of Marlex enable the penetration of fibrous tissue. 15,26,27,32 Wound seromas have also occurred,23,33 as have wound sinuses. 33 Molloy et al. 33 reported that in 50 patients seromas occurred in 2 (4%) and wound sinuses in 6 (12%). One of these had wound infection at the time of repair. Sinuses appeared during an interval of 6 to 18 months after surgery. The mesh was not removed in any of these cases. Patient follow-up ranged from 6 months to 10 years (mean = 3.75 years). Stone et al. 50 reported that in 23 patients studied over 20 years wound sepsis occurred in 12 patients (52%), intestinal fistulas in 12 patients (17%), and erosion into bowel/skin in 3 patients (13%). When a skin graft was attempted (15 patients), successful results (more than 80% take) occurred in 3 patients (20%). Difficult removal of the device was reported with 16 patients (Fig. 28.2). Infection-Clinical Studies Marlex has acquired a reputation for being resistant to infection,15,18,22,24-27,32-34 and, if infection does occur, it can be resolved without removal of the mesh. 22 ,25,27,33,39 However, chronic infection 18 and extrusion in the presence of infection 26 have been reported. The mesh itself can become infected if necrotic fascia and soft tissue are sewn into the mesh or if it is covered prematurely with grafts or flaps when large concentrations of bacteria have colonized the mesh surface. 37

Vicryl

2.5

G T

0.5

.'"

1.5

Weeks

12 FIGURE

28.1. Tensile strengths of four prostheses.

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28. Biomaterials Pathology FIGURE

28.2. Clinical data for Marlex and Prolene.

\_ Marlex

Prolene \

100% 90% 80% 70% 60% 50% 40%

30% 20% 10% 0%

Wound Sepsis

Molloy et al. 33 reported that in 50 patients the wound infection rate was 8% (4 patients). S. aureus occurred in 2, Staphylococcus albus in one, and a J3-hemolytic Streptococcus in one. All the infections responded to appropriate antibiotic therapy, and device removal was not required.

Prolene Physical Characteristics Prolene is also a polypropylene mesh. Prolene was first made clinically available in 1970, and the formulation has not changed since that time. 51 Among surgeons, it has a reputation for being easier to use than Marlex, being not as stifP°,52,53 and easier to remove. 50 Unlike Marlex, Prolene will not unravel when cut. 53 Prolene is reportedly 0.027 in thick and has a burst strength of 250 Ib/in 2.53 Inflammation and Wound-Heating-Clinical Studies Stone et al. 47 reported that in 101 patients studied over 20 years wound sepsis occurred in 25 patients (24%), intestinal fistulas in 3 (3%), and erosion into bowel/skin in 1 (1%). When a skin graft was attempted (29 patients), successful results (more than 80% take) occurred in 21 patients (72%). Difficult removal of the device was reported with seven patients (Fig. 28.2). Capozzi et al. 53 reported that in 485 patients (encompassing 651 repairs) 4 patients (0.8%) developed seromas that resolved with simple aspiration. The average follow-up period was 5.06 years. Infection-Clinical Studies Capozzi et al. 53 reported that in 485 patients (651 repairs) 7 patients (91.4%) developed subcutaneous wound infections. In two instances, the infection extended to the mesh layer. The removal of the device was not required, and the infections were resolved with simple drainage, packing, and other conservative measures. Prophylactic antibiotics were not used unless the hernia operation was done in addition to another procedure.

Polytetrafluoroethylene On April 6, 1938, young Roy Plunkett (born in New Carlisle, Ohio, in 1910) opened a tank of gaseous tetrafluoroethylene in hopes

Intestinal Fistula

Erosion into Bowel/Skin

Difficult Removal

Acceptable Skin Graft Take (>80%)

of preparing a nontoxic refrigerant. Much to the surprise of Dr. Plunkett and his assistant, Jack Rebok, no gas emerged. When Plunkett placed the tank on a scale, he found that it weighed what it should when full. Intrigued, Plunkett was determined to get to the bottom of this mystery. Instead of immediately discarding the tank, Plunkett and Rebok got a saw and hacked the tank in two. Inside, they found a white powdery wax that neither of them had ever seen before. It was (poly)tetrafluoroethylene or, as it is commonly known today, Teflon®. On taking a sample home for further analysis, Plunkett learned that it had some very remarkable properties. It was more inert than sand (not affected by strong acids, bases, or heat, and no solvent would dissolve it), but, unlike sand, it was extremely "slippery." Finally, finding it to be similar to polyethylene, Plunkett wrote up his notes and left a sample with DuPont's Plastics Group. Although Plunkett tried for several years to interest various factions at DuPont in his discovery, the patented formula, along with a half-pound of the expensive prototype, sat unused on a shelf for nearly 5 years before someone could think of a use for it. At that point, Teflon was valueless because (like the mythical universal solvent that would dissolve its own container) it could not be applied to any product without slipping right off. Today, polytetrafluoroethylene is the most commonly used fluorocarbon polymer in medical application. The monomer tetrafluoroethylene is structurally similar to ethylene. The polymer, formed by free radical addition, tends to be highly crystalline, with a density more than twice that of water at 2.2 g/ml. It has low tensile strength, low shear strength, low elastic modulus, low surface tension, and a low coefficient of friction. Because it is highly viscous even when melted, it is difficult to use industrially in applications other than medical textiles. As a textile, polytetrafluoroethylene, along with polyethylene terephthalate and polypropylene, dominate the medical textile field. Polytetrafluoroethylene is fabricated into filaments by mixing the melted polymer with cellulose-type fillers. Mter the thread filaments are spun, the fillers are oxidized. The now dark chocolatecolored fibers are cleansed of oxidized filler with strong acids or heat soaks. 54 Although polytetrafluoroethylene appears to adsorb oxygen fairly well, as do the fluorocarbons currently used as blood substitutes, it does not seem to bind the sterilizing agent ethylene ox-

228 ide. Thus, little aeration appears to be necessary for this material following gas sterilization. 55 Polytetrafluoroethylene is not known to be susceptible to any degradative biological process and is highly resistant to almost any form of corrosive oxidative attack. However, when abraded, polytetrafluoroethylene tends to flake, due to its low shear strength and despite its low friction coefficient and low surface tension. The earliest studies of the biological reaction to polytetrafluoroethylene arose from the clinical problems associated with the polytetrafluoroethylene acetabular cups. As Charnley noted in a controlled study in which he injected polytetrafluoroethylene particulates into his thigh, the polytetrafluoroethylene hurt much more than the ultrahigh-molecular-weight polyethylene. 56,57 The abrasive wear of polytetrafluoroethylene produced large numbers of particles that evoked an aggressive granulomatous inflammatory reaction. In addition to the typical chronic inflammatory cell infiltrate, which was judged to be relatively greater than the infiltrate evoked by any other common orthopedic material, both necrosis and a lymphoplasmacytic infiltrate were noted. 58,59 Similarly, when abraded materials from the early polytetrafluoroethylene DeBakey disc in cage mitral valve prostheses embolized to the heart and kidney, the inflammatory cellular reaction has been described as strikingly intense. 6o Even when used as a composite, continuous phase polytetrafluoroethylene has induced significant inflammation when the application has yielded particulates. Both the mica composite Fluorosint® and the alumina or carbon composite Proplast® have initiated aggressive and often destructive inflammatory reactions. 61 Unlike any other material used for biomedical application that we have seen, polytetrafluoroethylene particulates evoke both a late neutrophilic infiltrate and the formation of dense lymphoid aggregates. Curiously, the material is nevertheless used today in particulate form by injection for both vocal cord augmentation and ureteral orifice procedures. The principal uses of this material today are for meshes in abdominal hernia repair (Teflon mesh) and for vascular prostheses. Polytetrafluoroethylene (PTFE) is currently available in modified form as Gore-Tex Expanded Polytetrafluoroethylene (ePTFE) Soft Tissue Patch.

The Gore-Tex ePTFE Soft Tissue Patch The Gore-Tex ePTFE Soft Tissue Patch is not a mesh but rather a microporous sheet that appears to the unaided eye as a smooth, solid, nonporous sheet. ePTFE was first made clinically available in December 1981, and the formulation has not been changed. Some studies 21 ,26 have used experimental formulations that have never been available clinically. The research done by Lamb et al., 21 which has been widely cited,ll,18,33,62-M utilized a knitted polytetrafluoroethylene mesh that, while provided by the manufacturer of the clinically available ePTFE, has never been available for clinical use as an abdominal device. It is also worth noting that the widely cited41 ,65,66 research done by Sher et al. 67 also utilized an experimental formulation of ePFTE that has never been available clinically.68 Although this formulation was also provided to Sher et al. by the manufacturer of the clinical product, the formulation was an industrial membrane with a different pore size that was not designed for clinical use. 68 We will confine our discussion to the only polytetrafluoroethylene formulation that has been available for clinical use, the ePTFE Soft Tissue Patch. Satisfactory results have been obtained with ePTFE.62,65 It has a

N. Kossovsky et aI.

low rate of adhesion formation. 62 ,63,65 There have been reports that polytetrafluoroethylene exhibits incomplete host tissue fixation 15,63 and fibrous tissue ingrowth.63 In addition, there have been reports of ePTFE "wrinkling and curling on itself."15 There is concern that ePTFE can provide a nidus for bacteria, given the small size of its pores. 15,32 It has been reported that infection can necessitate removal of the device. 69 Evidence suggests that ePTFE can act as a physical barrier to neoplasia. 70

Physical Characteristics Tyrell et al. 11 found the tensile strength to be 1.565 kg 10 weeks after implantation (Fig. 28.1). In addition, they found that the tensile strength increased less than 4% from weeks 2 to 10. However, they note that the data were not normally distributed. Murphy et al. 41 recorded a tensile strength of 2.67 kg/ cm 15 to 20 weeks after implantation of the device. Law and Ellis19 found the abdominal wall breaking strength significantly weaker in the presence of bacterial contamination (S. aumus) 4 weeks after implantation. Inflammation and Wound-Healing-Laboratory Studies Murphy et al. 41 graded mean adhesion formation after 15 to 20 weeks as minimal, requiring only gentle gauze dissection. Law and Ellis 17 found, on average, minimum adhesions freed by gentle blunt dissection at both week 1 and week 22. Brown et al. 49 studied adhesion formation with five separate sets of conditions and found that, on average, infection or peritonitis had little effect in promoting the formation of adhesions. Preoperative or postoperative antibiotics seemed to have a very minor effect on the formation of adhesions where infection was present.

Polyethylene Terephthalate In 1941, two English fiber chemists, Whinfield and Dickson, patented the combination of terephthalic acid and ethylene glycol, "Terylene®." It was the first successful synthetic fiber to replace cotton and wool. Resistant to stain and impervious to destruction by moths or beetles, Terylene was an immediate hit in the textile industry. DuPont's version ofTerylene came to be known as Dacron® and, as the first waterproof, crease-resistant synthetic fiber, became DuPont's biggest selling product. In 1952, DuPont took a film version of Terylene (Mylar®) and produced magnetic tape from it, and it is used today in microfilm, magnetic audiofilm, and compact disks. Later in 1952, DuPont scientists came up with an artificial blood vessel made of Dacron polyester. The vessels were improved throughout the 1950s and 1960s with a coating of albumin, a protein found in especially high concentration in egg whites. Albumin was thought to reduce clot formation under certain conditions in certain prostheses. Polyethylene terephthalate is the most widely used polymer in the fabrication of textile components for medical devices. It is the predominant member of the textile family of medical device materials, which also includes polypropylene and polytetrafluoroethylene. Polyethylene terephthalate may be reinforced with fillers such as titanium dioxide and carbon or may be copolymerized. As in polypropylene, the raw material is melt extruded to produce fibers that may then be woven or bonded to produce threads or assembled sheets of material. Polyethylene terephthalate is the only material currently used to fabricate textile vascular graft prostheses. The material is also

229

28. Biomaterials Pathology used to create cardiovascular patches and wound repair meshes and as an anchoring component for many percutaneous devices. It is also used to fabricate the sewing rings for cardiovascular devices and for blood filters in extracorporeal circulation devices. Its brief use as an articulating component in hip prostheses was ended owing to its poor tribological properties and the consequent osteolytic inflammatory reactions induced by the wear debris.57 Some in vivo studies of suture material show little or no loss of strength of the textile in vivo. 71 Other studies show an early loss of 10 to 20% of the fiber strength following implantation.54 Studies of vascular grafts recovered from humans in the late 1970s show fairly convincing evidence of in vivo degradation. The measurement of diameter and cross-sectional area of filaments removed from explanted polyethylene terephthalate vascular prostheses showed swelling on the order of 5% during the first 30 months of implantation. Among the explanations for this observation were absorption of water and blood proteins or, alternatively, chain scission and molecular weight loss associated with the introduction of hydroxy and carboxy groups into the surface layers of the fibers. Devices recovered 30 months after implantation showed a fiber size decrease, which has been explained as complete dissolution of the degraded surface layers of the polymer.72 Reductions in bursting strength of 10 to 15% were associated with these physical changes. Chemical changes have also been reported. Polyethylene terephthalate fibers, as present in recovered arterial prostheses following human implantation, show loss in molecular weight and increases in carboxyl group concentration. The kinetics of chain scission approximate a logarithmic decay model, with 25% reduction in the initial average molecular weight at 10 years. 73 A 25% reduction in bursting strength was projected for 162 months. Working independently from in vitro simulations and extrapolated data, Guidon et al. 72 suggested a 4 to 7% annual loss of fiber tensile strength associated with fiber crazing, splitting, and cleavage. As noted earlier, polyethylene terephthalate does not wear well. Abrasive forces present in hip joints generate large numbers of particulates, which then lead to unacceptable levels ofinflammationP Polyethylene terephthalate has complement-activating properties. The material also has the propensity to swell and trap small molecules, which may result in the transfer of industrial processing solutions into the final anatomical site, where they may leach out over time and produce local injury.74 In fiber form, and especially in particulate form, the material evokes an aggressive macrophage mediated inflammatory reaction, coupled with a significant infiltrate of fibroblasts and neovascular tissues.

Mersilene Polyethylene terephthalate is currently available in the form of Mersilene mesh and has been clinically available since at least 1960. 75 The formulation has remained the same since its introduction. Contrary to general conception, this would make it the oldest abdominal mesh formulation that is still in use as the current polypropylene formulation of Marlex was not made clinically available until 1962. Satisfactory results have been obtained with Mersilene. 20 ,76,77 However, even proponents of Mersilene conceded that it has a poor reputation in the United States, and some American surgeons oppose its use. 76 It is thought by its proponents that the poor rep-

utation and opposition are based on unverified information. 76 Mersilene is widely used in France, Italy, and Belgium. Physical Characteristics Mersilene is a multifilament mesh. Each filament has a diameter of 0.0014 cm. The mesh is 0.023 cm thick, weighs 0.0432 gl10 cm2, and has a density of 0.19 g/cm3• The bursting strength is 19.9 ± 0.3 kg and 1.3 ± 0.02 kg/cm 2• As to tensile properties, its breaking strength is 12.2 ± 1.3 kg (wale) and 6.9 ± 0.9 kg (course), and its breaking elongation is 45.2 ± 3.0% (wale) and 103.9 ± 3.1 % (course). The pores of the mesh measure 120 X 85 /Lm, taking the two longest perpendicular axes of the pore. 40 Mersilene mesh is constructed of interlocked fiber junctions, which allow it to be cut to any shape without raveling. 78 Although it has been reported that Mersilene is "readily sterilized by standard steam pressure, "78 the manufacturer warns that "unused Mersilene which has been removed from the package may be resterilized not more than one time by a conventional steam autoclaving process at conditions of 250°F (121°C) for 20 minutes. Mersilene mesh may also be flash autoclaved not more than one time at conditions of 270°F (132°C) for 10 minutes. Resterilization under any other conditions or by any other means is neither recommended nor endorsed by Ethicon, Inc."79 (emphasis added). Inflammation and Wound Healing-Clinical Studies Advocates of Mersilene warn that contact with the stomach and bowel should be avoided due to possible fistulization, transmigration, and internal obstruction. 76 Its ability to produce adequate fibroblastic response is controversial among surgeons. There have been reports that it is "reactive enough to induce a rapid fibroblastic response to ensure fixation,"76 but it has also been reported that it "does not stimulate a marked fibroblastic infiltration."32 Pans and Pierard,8o in a study of the repair of abdominal muscular wall defects in rats, found the least amount of adhesions to omentum and gut with Mersilene compared with Gore-Tex and an experimental Vicryl®-Mersilene prosthesis.

Absorbable Meshes Absorbable meshes, in contrast to permanent meshes, are devices that the body dissolves over time. Although these meshes have been used for abdominal organ wrapping, the authors have excluded these data on the basis that they are outside the scope of this chapter. The absorbable meshes we will examine are Dexon (American Cyanamid Company) and Vicryl (Ethicon, Inc.) In a study by Mori et al.,8I 3-week-old Wistar KY strain male rats underwent a full-thickness abdominal wall excision with repair with nonabsorbable meshes (Prolene, Marlex, and Gore-Tex) and absorbable mesh (Vicryl). Vicryl mesh, although it has less strength, resulted in the fewest adhesions.

Polyglycolide Polyglycolic acid, either alone or copolymerized with lactic acid, is an extremely popular synthetic material for the fabrication of absorbable sutures. The homopolymer polyglycolic acid material has a repeating ester backbone consisting of two carbons and an oxygen, whereas the side chains of nonesterified carbon are two hydrogen atoms. The material is highly ordered and therefore

N. Kossovsky et aI.

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highly crystalline, with a high melting point. It is melt extruded into sutures. The copolymer, on the other hand, consists of nine parts glycolide with one part L-lactic acid. The copolymer induces a respectable amount of disorder to the polymer, thereby reducing both crystallinity and melting temperature. As degradable sutures, the copolymer seems to be absorbed more rapidly.82 The degradation mechanism seems to be hydrolysis of the ester linkages; both heat and alkaline conditions hasten the loss of strength of the sutures.

Dexon Polyglycolic acid is available in the form of Dexon mesh. Dexon was first made available in 1983, and that formulation is the only one that has been available in the United States. d3 However, other formulations, introduced after 1983, have been clinically available outside the United States. 83 Satisfactory results have been obtained with the device. 84.85 Physical Properties Dexon can be cut to any size without fraying.86 The device has been reported to be completely absorbed within 90 to 180 days.84.86-88 Tyrell et al. 11 found that the mean tensile strength decreased approximately 50% from weeks 2 to 10 of implantation. They note that the data were not normally distributed (Fig. 28.1). Inflammation and Wound Healing-Laburatury Studies Although the device is reported to cause adhesions, there is evidence to suggest that the adhesions fade as the mesh is absorbed. 85 It is controversial whether the fibrous ingrowth into the device is sufficient to accomplish a permanent repair. Although it has been reported that the ingrowth is sufficient to provide a permanent repair, other reports indicate otherwise. 87.89 Law and Ellis l7 found that, on average, adhesion formation changes from minimum adhesions freed by gentle blunt dissection at week 1 to moderate adhesions freed by aggressive blunt dissection at week 22.

Vicryl Polyglactin 910 mesh is polyglycolic acid copolymerized with lactic acid and is available as Vicryl. Vicryl is clinically available in two formulations, a knitted mesh and a woven mesh. Vicryl woven mesh was first made clinically available in 1985, and the formulation has not been changed. 90 Vicryl knitted mesh was first made clinically available in 1983 and then later recalled and re-released in 1985. 91 The reason for the recall is unclear. When possible, we will differentiate between the knitted and woven formulations. Satisfactory results have been obtained with Vicryl,92-94 and infections have been resolved without the removal of the device. 93 Physical Properties The Mullen burst strength of knitted Vicryl is in excess of 60 psi.93 Knitted Vicryl appears to be completely absorbed within 90 days.93 However, there is evidence to suggest that Vicryl's rate of absorption is more variable than Dexon's.ll The variable rate of degradation may explain why Tyrell et al. ll found that the tensile strength increased approximately 75% from week 2 to week 10. However, they noted that the data were not normally distributed (Fig. 28.1).

Similarly, Jenkins et al. 42 examined bursting strength and found an increase of approximately 50% from weeks 1 to 4. At week 1, all ruptures occurred at the prosthetic/muscle interface, whereas at week 4 ruptures occurred at both the prosthetic/muscle interface and the inguinal canal. Inflammation and Wound Healing-Laburatury Studies There is evi-

dence to suggest that granulation and fibrosis can form on the device, acting as a permanent reinforcement. 93 However, it has been reported that Vicryl invokes less collagen ingrowth than does Dexon.l l Jenkins et al. 42 studied adhesion formation and found that, on average, from weeks 1 to 4 there was a minor change in adhesions, with minimal adhesions at both week 1 and week 4.

Summary

Bioreactivity In reviewing the experimental data on the various abdominal mesh prostheses, we have encountered two recurrent problems. First, many papers fail to identify specifically the device being examined. Second, many papers report properties for one formulation of a device based on experiments with a completely different formulation. For example, in the case of Marlex, we have reviewed papers that justifY conclusions on the polypropylene formulation using data obtained from the polyethylene formulation, with no mention of this difference. The research on the ePFTE Soft Tissue Patch often justifies conclusions by utilizing research of experimental formulations that were constructed differently from the clinically available device, once again without noting the discrepancy. Many papers on Dexon simply do not specifY which of the many clinically available formulations were investigated. Likewise with Vicryl, many papers do not give any indication whether the data had been obtained from the knitted or woven formulation of the device. We have attempted to clarifY these incongruities in the sections on each device and have summarized our impressions in Table 28.3. However, we believe that it is incumbent on future researchers to take the following steps before disseminating their findings. First, contact the manufacturer of the device and obtain a clear understanding of the various formulations of the device and which of those formulations are or have been available clinically and when. Second, specifY the exact formulation that is being investigated and indicate whether it is an experimental or clinically available formulation, as well as whether there are other formulations available clinically. When reviewing other research on the device, note the date of the research and compare it with the date when the clinical formulation was made available, as this could indicate that the research was not based on the clinically available formulation.

Histology We compared the various histological parameters, in particular wound strength and collagen ingrowth, for the various materials as reported by individual investigators (Fig. 28.3). It appears that there is no direct relationship between the rate of collagen ingrowth and wound strength.

231

28. Biomaterials Pathology TABLE

28.3. Relative bioreactivity comparison* Fibrogenicity (collagen-rich chronic inflammation)

Anatomical confonnatioan Marlex Prolene ePTFE Mersilene Dexon and Vicryl

Resistance to infection

1 2 3 4 5

Resistance to degradation (hygroscopic and mechanical)

Extent of available data

5 5 4 3 1

5 3 4 2 1

5 5 4 3

*5 = greatest; 1 = least. tChronic inflammation, but generally macrophages with late fibrosis.

Marlex With long-tenn placement, Marlex consistently evokes a chronic inflammatory reaction characterized by a relative paucity of macrophages and giant cells, aggressive and rapid fibroblast infiltration through the pores of the mesh, in addition to dense collagen deposition. With regard to mesothelial cell growth over the mesh, evidence suggests that it largely regenerates and is morphologically unimpressive. This has not been demonstrated conclusively, however. In some wound infection models,19 the chronic inflammatory process with fibroblast proliferation and collagen deposition was not significantly altered in the presence of Marlex. In other experiments modeling acute peritonitis,49 the fibrinopurulent reaction in the short tenn was so severe that no significant wound healing occurred.

By almost all admissions, ePTFE's ability to encourage fibrous tissue proliferation in the setting of gross wound infection is significantly impaired.

Mersilene Histological studies of Mersilene as an abdominal mesh prosthesis are few. 64 In our experience, polyethylene terephthalate evokes an aggressive macrophage and giant cell rich inflammatory reaction that is followed by a dense fibrous ingrowth. The fibrous tissue matures over time and can become hyalinized after many years. Dexon With long-tenn use, the fibrils of the Dexon mesh are essentially fully absorbed by macrophages and the vacated volume is replaced by a moderately cellular fibrous ingrowth. The cellularity of the fibrous proliferation is greater than that associated with Marlex. Wound infection data with this material in the abdominal mesh setting are not available.

Gore- Tex ePTFE Soft Tissue Patch With long-term placement, ePTFE evokes a chronic inflammatory reaction that is different in many ways from the more extensively studied Marlex. First, fibrous tissue does not penetrate through the pores and thus the binding of ePTFE to the wound bed is substantially less intense. Second, the giant cell component of the inflammatory reaction is significantly greater. Third, in several reports, polytetrafluoroethylene has been shown to evoke a neutrophilic reaction in the absence of culturable bacteria. The mechanism for this late "acute" type of reaction is not clear, but in our own work we have suggested that macrophage-derived interleukin-8 may be the responsible chemotactic factor. 95

Vicryl With long-tenn use, the fibrils of the Vicryl mesh are essentially fully absorbed by macrophages and the vacated volume is replaced by a moderately cellular fibrous ingrowth. The cellularity of the fibrous proliferation is greater than that associated with Marlex. Wound infection data with this material in the abdominal mesh setting are not available.

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239

30. Suture Selection for Hernia Repair 30.3. Toughness, a measure of the energy absorbed by the suture (area under the stress-strain curve), before and after 6 weeks' incubation in vivo. Polyglycolic acid, polyglactin, and gut did not survive the 6 weeks' incubation. (Reprinted from Greenwald et al.,IO with permission.)

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Continuous Versus Interrupted Sutures Although there are no systematic prospective studies comparing continuous suture repairs with interrupted suture repairs of hernias, such data are available for midline and transverse abdominal closures. Absorbable sutures were used in each of the studies discussed here. Fagniez et al. 26 compared continuous absorbable polyglycolic acid suture closures with polyglycolic acid sutures placed in an interrupted fashion. The study randomized 3135 patients undergoing laparotomy. The patients were well matched for medical conditions, oncologic drugs, corticosteroid therapy, radiation, anemia, ventilator support, obesity, ascites, age, and male/female ratio. The dehiscence rate was 1.4% with continuous closures and 2.0% with interrupted ones (p = not significant). These are truly remarkable results, and they are highly reliable considering the large number of patients under study. Wissing and co-workers 27 compared four techniques for closing the midline fascia after laparotomy in a randomized prospective multicenter trial. The study included 1491 patients using the following methods: interrupted closure with polyglactin 910, continuous closure with polyglactin 910, continuous closure with polydioxanone-s, and continuous closure with nylon. The overall

2.0E+7

tension-free mesh repairs. He preferred polypropylene. For many years, Devlin and co-workers used stainless steel wire for Shouldice repairs. In 1986, they reported that they also had changed to using polypropylene for the same operation. 23 Recently, Nyhus et al. 24 stated that they "learned very early on that silk or cotton should never be used to sew polypropylene mesh. The suture and mesh must be made of the same material." This suggests that polypropylene sutures may be an ideal nonabsorbable suture for herniorrhaphy and virtually requisite for polypropylene mesh repairs, whereas a PTFE suure may be preferable with expanded PTFE patches. On the other hand, Robbins and Rutkow described the use of interrupted polyglactin sutures to secure their plug in mesh plug repairs. A 4-year follow-up study demonstrated a 0.7% recurrence rate in 2861 patients after primary repair and a 3.4% re-recurrence rate in 207 patients who had a previous repair. These data strongly support the use of absorbable sutures when the repair is not under tension.

-0

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-0

~ ~

-0

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'-0

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incidence of wound infection was 8.6%, and the incidence of wound dehiscence was 2.3%. Incisional hernias occurred in 16.9% of those closed with interrupted polyglactin 910 and in 20.6% of those with continuous polyglactin 910. These differences were not statistically significant. However, these rates of incisional hernia are unacceptably high and suggest problems with surgical technique. Trimbos and co-workers28 performed a rarIdomized trial to compare interrupted absorbable polyglactin 910 sutures with continuous absorbable polyglyconate sutures for closing the midline fascia following laparotomy. The polyglyconate sutures were begun at the two ends of the incision and advanced to be tied at the center. There were 172 patients assigned to the interrupted suture closures and 168 assigned to the continuous suture closures. The patients were evaluated 2 weeks after surgery and again after 1 year. Results were suture fistula: interrupted, 0%, continuous, 2%; wound pain: interrupted, 1%, continuous, 2%; incisional hernia: interrupted, 3%, interrupted, 4%. None of these paired differences were statistically significant. The authors recommended using continuous sutures to speed the surgery and leave less foreign material in the wound. Finally, Gislason and co-workers29 investigated the incidence of dehiscence and incisional hernia in 599 patients after closure of the abdominal aponeuroses. Patients were randomized to closure with one of three suture techniques: continuous mass closure with polyglyconate, continuous mass closure with polyglactin 910, or interrupted mass closure with polyglactin 910. The latter comparisons are of particular interest here. The overall rate of dehiscence was 2%, 4% occurring after continuous polyglyconate closure as compared with 2% after both continuous and interrupted polyglactin 910 closures. These differences were not statistically significant. The rate of incisional hernias depended on the presence of infection. In the absence of a wound infection, however, there were nine incisional hernias in the polyglyconate group, seven hernias in the continuous polyglactin 910 group, and six hernias in the interrupted polyglactin 910 groups. These were not significantly different from one another. Thus, none of the studies described above demonstrate a significant advantage to continuous or interrupted suture techniques for abdominal closure. This justified the use of a continuous suture technique that distributes the tension and reduces the

240

P.B. Dobrin

amount of foreign body in the wound. However, interrupted suture techniques may be preferable in the case of circular hernias such as umbilical and some epigastric defects. In this case, interrupted sutures may give greater security as the sutures lie in line with the radially applied forces about the circle. Unfortunately, there are no data comparing matched continuous and interrupted nonabsorbable sutures of the modem type currently used for herniorrhaphy or abdominal closures. There are, however, a number of nonrandomized, noncomparative studies using continuous polypropylene to close midline abdominal incisions. The results obtained are most encouraging. Shephard and co-workers3o evaluated the outcomes of 200 unselected patients who underwent midline incisions or laparotomy for gynecologic malignancy. Twenty-two percent had undergone preoperative radiation therapy, 18% were obese, and 15% had undergone prior bowel surgery. Thus, these patients were at increased risk for wound healing problems. Number two polypropylene was used in all cases. There was an 8.5% postoperative wound infection rate and, over a 2-year period, a 5% rate of postoperative incisional hernia. These numbers are satisfactory. Knight and Griffen31 reported the results of 1000 consecutive patients whose abdominal incisions were closed with continuous monofilament polypropylene suture. Wound dehiscence occurred in just 0.4%, and incisional hernias occurred in only 0.7%. These are remarkably low values, leading one to wonder how closely the patients were studied in the postoperative period. Although they did not compare polypropylene with any other suture, the authors suggested that polypropylene may be especially useful in contaminated wounds. Thus, although these are not comparative studies, they certainly argue that polypropylene is an effective and useful monofilament nonabsorbable suture.

Polypropylene Sutures Polypropylene sutures have certain properties that are particularly relevant to their use in surgery. They are strong when used in sizes that are appropriate for the load to which they are subjected. 32- 38 They are also resistant to oscillatory loads. 39 They resist deterioration in vivo,9,33,38,40 although they may be degraded by oxidation, certain chemicals, high energy radiation, and ultraviolet

24.0

light. 33,38,41-47 They pass through tissue with little friction,34,37,47 are not thrombogenic,48 and are relatively resistant to infection. 49 Examination of the mechanical characteristics of various sized polypropylene sutures demonstrates some remarkable features. The elastic modulus (a measure of stiffness) and tensile stress (a measure of resistance to breakage) correlate inversely with the cross-sectional area of the filaments but directly and linearly with the circumference of the filaments (Figs. 30.4, 30.5).50 This surprising finding suggests that the strength of the suture may lie in its shiny outer surface rather than in its core. Similar relationships were found for nylon, another monofilament suture, but not for silk, a braided suture. X-ray birefringence studies of melt-spun polypropylene and polyethylene fibers suggest that the crystalline elements of the skin are more highly oriented than those of the core. Although this orientation was found in melt-spun fibers, it was not observed in un extruded bulk material. 51 During manufacture, melt-spinning consists of extruding the material in a molten state and then extending the filaments longitudinally under load while they are waml and still extensible. 52 In this manner, the crystalline materials may be oriented in the direction in which the filaments are being pulled. The filaments usually are passed through a water bath filled with cool or room temperature water to harden them. Under these conditions, the skin must solidity first, orienting the crystals in the outer surface. As a result, the skin of the filament may bear most of the load, protecting the crystals in the core from being oriented. These observations have practical implications with respect to intraoperative handling of the suture. 53 Laboratory studies demonstrate that abrasion of the suture by the tom foil envelope in which it is packed, kinking or axially twisting the suture, and tugging on the suture to remove the accordion-like pleats, as often done by the scrub nurse, have no effect on suture strength. A stray knot, however, which tends to crease the suture skin, and pinching with surgical forceps both decrease suture strength. The latter perturbation causes injury in a graded fashion comparable with a pharmacological dose/response curve. 50 These observations emphasize the crtical importance of discarding sutures that have acquired a stray knot during surgery and the absolute prohibition against grasping the suture with any instrument. Handling with fingers seems the most prudent course. Of course, portions of the suture that are not to be incorporated in the repair, such as those near

7-0

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....I ::;)

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30. Suture Selection for Hernia Repair

FIGURE 30.5. Tensile stress, a measure of resistance to breakage, for three sizes of polypropylene sutures. Tensile stress is inversely related to crosssectional area (left) but is directly related to suture circumference (right). This suggests that strength is in the outer surface of the suture. (Reprinted from Dobrin,5o with permission.)

241

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CROSS-SECTIONAL AREA X 10

the needle, may be handled in any way that is convenient, as they will be discarded. Another way in which a suture may be made to break is by overloading it. Consider construction of a continuous suture line. If a suture line is constructed with a loose loop, the slack will be distributed among several loops on either side of the loose one. IT a suture line is constructed with one or more tight loops, however, suture-tissue friction will not permit redistribution of the excessive tension. 39 Excessive tension can easily be applied inadvertently as the surgical assistant "follows" the surgeon, pulling up on each loop. Finally, as a suture line is being constructed, continuous or interrupted, it is subjected to tension. This is probably greatest as the surgeon pulls up on the two strands and ties the knot. 36 This now remains as chronic tension on which additional acute loads may be applied, such as those resulting from coughing, from abdominal distention, or from a Valsalva maneuver associated with heavy lifting. Experimental studies of chronically loaded polypropylene sutures demonstrate that the filaments undergo gradual viscoplastic creep to greater length. Sutures subjected to heavy chronic loads tend to break at lower than usual acute loads within 48 hours of loading. 54 IT they do not break in the first 48 hours after chronic loading, they actually increase in strength, breaking at higher than normal acute loads (Fig. 30.6).55 This suggests that slow, gradual viscoplastic extension (creep) causes increased orientation of the crystals in the core of the suture. Whatever the mechanism, this increased resistance to breaking after chronic loading suggests that, if a polypropylene suture does not break soon after surgery, it will remain intact and actually will gain in strength during the postoperative period.

Sutures and Wound Infections Certain sutures seem to be associated with increased risk of infection. Cahill and co-workers56 compared two monofilament sutures with PTFE in performing hernia repairs. These included

4.5

'an2

400

500

100 200 300

800 700 800 900

CIRCUMFERENCE ICROSS-SECTIONAL AREA

anlal

nylon in 61 patients, polybutester in 61 patients, and PTFE in 69 patients. Polybutester is a unique, remarkably extensible suture. Ten percent of the patients had infectious complications, and four had deep infections, all of these occurring in the patients who had been closed with PTFE. Therefore, the authors concluded that PTFE sutures carried an increased risk of infection. Jones57 reviewed 256 consecutive Shouldice (77%) and Bassini (32%) herniorrhaphies performed without mesh at one hospital over a 15-month period. Sutures used included braided (linen, silk, polyester) or monofilament (nylon, polypropylene) materials. All were nonabsorbable sutures. Braided sutures were used in 68% of the repairs and monofilament sutures in the remaining cases. Wound infections occurred in 12 of the 175 operations in

CONTROL 400

375

ILl

350

CI ~

325

III

300

275

e ~II::

250

y r

= 0.6296 x + 255.33 = 0.9565

100

125

150

175

CHRONIC LOAD (gm)

FIGURE 30.6. Acute force required to break polypropylene sutures after they have been loaded chronically. Chronic loading increases the strength of the suture in response to subsequently applied acute forces. (Redrawn from Dobrin and Mrkvicka. 55 )

242

P.B. Dobrin

which braided sutures were used (6.8%) but in only 1 of the 81 operations in which monofilament sutures were used (1.2%). This difference was highly significant (p < .01). These findings are supported by experimental work by Bucknall,58 who compared monofilament sutures with multifilament nonabsorbable sutures in infected wounds in rats. Electron microscopy detected bacteria in the interstices of the infected multifilament sutures. These findings are supported by several clinical and experimental studies that show that braided and naturally occurring material such as silk, as well as nonbraided catgut, have higher rates of infection than monofilament sutures. 59-62 Osther and co-workers63 studied fascial closures in 204 consecutive patients with suspected wound healing problems with monofilament polyglyconate or multifilament polyglycolic acid sutures. These investigators found more than twice the incidence of

wound infections (16% versus 7%) when the fascia had been closed with multifilament sutures. This difference was statistically significant (p < .05). Figure 30.7 illustrates the surface structure of various monofilament and multifilament sutures. It should be emphasized that the presence of any suture, a foreign body, compromises the host's ability to cope with infection. Patterson-Brown and co-workers 64 compared the incidences of infection in inoculated pouches in guinea pigs in the presence of different suture materials. The pouches were inoculated with Escherichia coli and Bacteroides fragilis. The following proportions of pouches were infected: polypropylene, 52%; polyglactin 910, 53%; polyglycolic acid, 41 %; PTFE, 51 %; polydioxanone, 52%; no suture present, 26%. It is evident that the presence of suture material doubled the risk of infection. Following his experimental studies, Bucknell58 recommended using a synthetic monofilament

FIGURE 30.7. Different suture materials. Absorbable: (A) Chronic catgut (2/0 surgical gut). (B) Dexon. (C) Monocryl®. Nonabsorbable monofilament: (D) ePTFE (Gore-Tex®). (E) 2/0 Prolene. (F) Nylon (2/0 Ethilon®). Nonabsorbable multifilament: (G) Silk. (H) Nylar (2/0 Nurolon). (I) Poly-

ester (2/0 Mersilene) . (Reprinted from Chu CC, von Fraunhofer JA, Greisler HP. Wound closure biomaterials and devices. Boca Raton: CRC Press; 1997;67-68, with permission.)

30. Suture Selection for Hernia Repair

nonabsorbable suture for operating in an infected field. Polypropylene wound be such a candidate. Often one can use a polyglycolic acid or polyglactin mesh with absorbable sutures for infected fields that must be closed to retain abdominal contents. 65 Most patients will develop new incisional hernias as the mesh degrades, but, once the infection is controlled and the field is clean, the fascia may be closed with polypropylene mesh and polypropylene sutures.

Suture Granulomas of the Urinary Bladder

243

nylon sutures. When the suture/incision length ratio was greater than 4:1, there was a 9.0% incidence of incisional hernia. When the suture/incision ratio was less than 4:1, however, there was a 21.5% incidence of incisional hernia. Thus, using a sufficient suture length avoids the need for excessive tightening of the suture and should prevent the "cheese knife" effect of the suture on the native materials. With prosthetic repairs, the bilaminar prosthesis described by Bendavid77 should avoid cutting of the ePTFE. Of course, another way to avoid this complication is to use an absorbable suture, but this makes little sense in the presence of a patch composed of foreign material.

Conclusions

An unusual delayed complication of sutures for herniorrhaphy is the development of a paravesical suture granuloma66-68 or a suture granuloma of the bladder. 69 •7o These present clinically and histologically as a chronically inflamed pseudo tumor. Most often suture granulomas develop around a nonabsorbable suture, usually silk. Surgical excision reveals a mass with chronic inflammation and giant cells. In some cases, the mass may be mistaken for a rhabdomyosarcoma because it is covered with normal urotheHum. 67 In one case, a boy had undergone herniorrhaphy at 8 months of age. At 2 years of age, he presented with an umbilical fistula running between the umbilicus and the herniorrhaphy site. Excision of the fistula revealed inflammation surrounding the silk suture. 71 Silk, a braided, naturally occurring protein, seems to be especially predisposed to the formation of suture granulomas. In a study of abdominal incisions, Kronborg72 found suture granulomas 12 times more frequently with silk sutures (12/163) than with polyglycolic acid sutures (1/163). This difference was statistically significant. Clearly, suture granulomas of the bladder and paravesical area would be less likely if one avoided silk sutures and used an absorbable or synthetic monofilament suture instead.

Review of published evidence suggests that surgeons may use absorbable as well as nonabsorbable sutures, the use of one having little advantage over the other. Similarly, surgeons may use continuous as well as interrupted sutures, again with little demonstrable advantage on either side. Monofilament sutures are preferable to braided or multifilament sutures to reduce the risk of infection. Based on the rate of wound healing and the rate of degradation of absorbable sutures, it would seem wise to use a nonabsorbable suture, especially if the repair will be under continued tension. With all of these considerations, it seems that polypropylene fulfills most or all of these requirements. The foreign body represented by the suture may be considered negligible in light of the large amount of foreign material present in mesh and ePTFE patches. The suture material used should match the mesh or patch, so polypropylene should be used for polypropylene meshes, but PTFE suture should be used for ePTFE patches. All sutures, especially polypropylene, should be handled with care to avoid injuries to suture surfaces.

Buttonhole Incisional Hernia

References

Another unusual complication of sutures is the development of a slit-like "buttonhole" incisional hernia. This results from the sawing effect of a permanent suture through native tissues or expanded PTFE (ePTFE). It is a unique case of incisional hernia and usually does not manifest itself until several years after surgery. Krukowski and Matherson 73 and Pollock74 have reported sporadic cases of this complication. Krukowski and Matherson attribute this complication to the presence of nonabsorbable sutures. It also has been seen with sutures sawing through ePTFE patches. 75 •76 Bendavid77 has described a bilaminar ePTFE and polypropylene mesh patch that, because of the toughness of the mesh, should prevent this complication. Buttonhole hernias are comparable with most early postoperative dehiscences of midline abdominal closures. These are most often seen due to the suture cutting through the fascia, not to breakage of the suture. One of the ways to avoid both acute cutting of the fascia by suture and also chronic cutting to form a "buttonhole" hernia is to avoid excessive tension on the suture. In a classic investigation, Jenkins 78 demonstrated that, for a continuous suture line, the length of the suture should be approximately four times as long as the incision to avoid excessive tension. This has been evaluated clinically. Israelsson andJonsson 79 studied 813 patients whose midline incision was closed with polydioxanone or

1. Witte MB, Barbul A. General principles of wound healing. Surg Clin North Am. 1997;77:509-528.

2. Tera H, Aberg C. The strength of tissue against individual sutures in structures involved in the repair of inguinal hernia. Acta Chir Scand. 1976;142:309-314.

3. Read RC, McCleod PC. Influence of a relaxing incision on suture tension in Bassini's and McVay's repairs. Arch Surg. 1981;116:440-445. 4. Wantz GE. Suture tension in Shouldice's hernioplasty. Arch Surg. 1981; 116:1238-1239. 5. Douglas DM. The healing of aponeurotic incisions. Br J Surg. 1952; 40:79-84. 6. Postlethwait RW. Polyglycolic acid surgical suture. Arch Surg. 1970;101: 489-494. 7. Postlethwait RW. Polyglycolic acid suture. AmJSurg. 1974;127:617-619.

8. Bourne RB, Bitar H, Andreae PR, et al. In vivo comparison of four absorbable sutures. Vicryl, Dexon plus, Maxon and PDS. Can J Surg. 1988;31:43-45.

9. Carlson MA, Condon RE. Polyglyconate (Maxon) versus nylon suture in midline abdominal incision closure: a prospective randomized trial. Am Surg. 1995;61:980-983. 10. Greenwald D, Shumway S, Albear P, et al. Mechanical comparison of 10 suture materials before and after in vivo incubation. J Surg Res. 1994;56:372-377.

11. Baltazar N, Johnston DW. Dexon versus conventional sutures in hernia repair. CanJSurg. 1976;19:341-342.

244 12. Anderson JR, Burcharth F, Larsen HW, et al. Polyglycolic acid, silk, and topical ampicillin. Their use in hernia repair and cholecystectomy. Arch Surg. 1980;115:293-295. 13. Burcharth F, Hahn-PedersenJ, Andersen B, AndersenJR Inguinal hernia repair with silk or polyglycolic acid sutures: a controlled trial with 5-years follow-up. WQTldj Surg. 1983;7:41&-418. 14. Dorflinger T, Kiil J. Absorbable suture in hernia repair. Acta Chir Scand. 1984; 150:41--43. 15. Solhaug JH. Polyglycolic acid (Dexon) versus Mersilene in repair of inguinal hernia. Acta Chir Scand. 1984;150:385-387. 16. Dick AC, Deans GT, Irwin ST. A prospective study of adult inguinal hernia repairs using absorbable sutures. j R CoU Surg Edinb. 1997; 42:428--429. 17. Leeper DL, Pollock AV, Evans M. Abdominal wound closure: a trial of nylon, polyglycolic acid and steel sutures. Br j Surg. 1977;64:603-606. 18. Pollock AV, Greenall MJ, Evans M. Single layer mass closure of major laparotomies by continuous suturing. j R Soc Med. 1979;72:889-893. 19. Donaldson DR, Hall TJ, Zoltowski JA, et al. Does the type of suture material contribute to the strength of the lateral paramedian incision? Br j Surg. 1982;69:163-165. 20. Krukowski ZH, Cusick EL, EngesetJ. Polydioxanone or polypropylene for closure of midline abdominal incisions: a prospective comparative clinical trial. Br j Surg. 1987;74:828--830. 21. Gys T, Hubens A. A prospective comparative clinical study between monofilament absorbable and non-absorbable sutures for abdominal wall closure. Acta Chir Belg. 1989;89:265-270. 22. Lichtenstein IL. Polyglycolic acid (PGA) sutures (C). JAMA. 1970; 214:760. 23. Devlin HB, Gillen PHA, Waxman BP, et al. Short stay surgery for inguinal hernia: experience of the Shouldice operation 1970-1982. Br j Surg. 1986;73:123-124. 24. Nyhus LM, McKernan JB, Phillips EH, et al. Symposium: operative repair of inguinal hernias. Contemp Surg. 1999;54:368-333. 25. Robbins AW, Rutkow 1M. Mesh plug repair and groin hernia surgery. Surg Clin North Am 1998;78:1007-1023. 26. Fagniez P-L, Hay]N, Lacaine F, et al. Abdominal midline incision closure. A multicentric randomized prospective trial of 3,135 patients comparing continuous vs. interrupted polyglycolic sutures. Arch Surg. 1985;120:1351-1353. 27. WissingJ, van Vroonhoven 1], Schattenkerk ME, et al. Fascia closure after midline laparotomy: results of a randomized trial. Br j Surg. 1987;74:738-741. 28. Trimbos JB, Smit IB, Holm JP, et al. A randomized clinical trial comparing two methods of fascia closure following midline laparotomy. Arch Surg. 1992;127:1232-1234. 29. Gislason H, Gronbech JE, Soreide O. Burst abdomen and incisional hernia after major gastrointestinal operations-comparison of three closure techniques. Eur j Surg. 1995;161:349-354. 30. Shephard JH, Cavanagh D, Riggs D, Praphat H, Wisneiwski BJ. Abdominal wound closure using a nonabsorbable single-layer technique. Obstet GynecoL 1983;61:248-252. 31. Knight CD, Griffen FD. Abdominal wound closure with a continuous monofilament polypropylene suture. Experience with 1,000 consecutive cases. Arch Surg. 1983;188:1305-1308. 32. Lee S, Hailey DM, Lea AR. Tensile strength requirements for sutures. j Pharm PharmacoL 1983;35:65--69. 33. Chu CC. Survey of clinically important wound closure biomaterials. In Szycher M (ed): Biocompatible polymers, metals and composites. Lancaster, PA: Technomic Publishing; 1983;477-523. 34. Yu Gv, Cavatiere R Suture materials, properties, uses. jAm Podiatr Med Assoc. 1983;73:57--64. 35. Landymore RW, Marble AE, Cameron CA. Effect of force on anastomotic suture line disruption after carotid arteriotomy. Am j Surg. 1987;154:309-312. 36. Dobrin PB. Polypropylene suture stresses after closure of longitudinal arteriotomy. j Vase Surg. 1988;7:423--428.

P.B. Dobrin 37. Von Fraunhofer JA, Story RJ. Masterson BJ. Tensile properties of suture materials. Biomaterials. 1988;324-327. 38. Chu CC, Kisil Z. Quantitative evaluation of stiffness of commercial suture materials. Surg Gynecol Obstet. 1989;168:233-238. 39. Dobrin PB, Gosselin C, Kang S, et al. Effect of pulsatile pressure on the breaking strength and movement of Prolene sutures. j Vasc Surg. 1997;26:1029-1035. 40. Nilsson T. Mechanical properties ofProlene and Ethilon sutures after three weeks in vivo. Scand j Plast Reconstr Surg Hand Surg. 1982; 16: 11-15. 41. Blais P, Carlsson DJ, Wiles DM. Surface changes during polypropylene photo-oxidation: a study by infrared spectroscopy and electron microscopy. j Polymer Sci Part A-I. 1972;10:1077-1092. 42. Blais P, Carlsson DJ, Clark FRS, et al. The photo-oxidation of polypropy1ene monofilaments. Part II: physical changes and microstructure. Texas Res) 1976;46:641--648. 43. Garton A, Carlsson DJ, Sturgeon PZ, et al. The photo-oxidation of polypropylene monofilaments. Part III: effects of filament morphology. Texas Res) 1977;47:423--438. 44. Schnabel W. Polymer degradation. Principles and practical applications. Munchen, Germany: Hanser International; 1981. 45. Drews RC. Polypropylene in the human eye. Am Intra-Ocular Implant Soc) 1983;9:137-142. 46. Barish L. Sunlight degradation of polypropylene textile fibers: a microscopical study. j Text Inst. 1989;80:107-199. 47. Gupa BS, Wolf KW, Postlethwait RW. Effect of suture material and construction on frictional properties of sutures. Surg Gynecol Obstet. 1985; 161:12-16. 48. Dahlke H, Docin N, Thurau K Thrombogenicity of different suture materials as revealed by scanning electron microscopy. j Biomed Mater Res. 1980;14:251-268. 49. Mouzas GL, Yealdon A Does the choice of suture material affect the incidence of wound infection? Br j Surg. 1975;62:952-959. 50. Dobrin PB. Some mechanical properties of polypropylene sutures: relationship to the use of polypropylene in vascular surgery. j Surg Res. 1988;45:568-573. 51. Fung PY-F, Carr SH. Morphology and deformation of melt-spun polyethylene fibers. j Macromol Sci-Phys. 1972;B6:621--634. 52. Ahmed M. Polypropylene fibers: science and technology. New York: Elsevier; 1982:169-218. 53. Dobrin PB. Surgical manipulation and the tensile strength of polypropylene sutures. Arch Surg. 1989;124:665--668. 54. Dobrin PB. Chronic loading of polypropylene sutures: implications for breakage after carotid endarterectomy. j Surg Res. 1996;61:4-10. 55. Dobrin PB, Mrkvicka R Chronic loading and extension increases the acute breaking strength of polypropylene sutures. Ann Vasc Surg. 1998;12:424--429. 56. Cahill J, Northeast AD, Jarrett PE, et al. Sutures for inguinal herniorrhaphy-a comparison of monofilaments with PTFE. Ann R Col Surg Eng. 1989;128-130. 57. Jones DJ. Inguinal hernia repair: which suture? Ann R Col Surg Eng. 1986;68:323-325. 58. Bucknall TE. Factors influencing wound complications: a clinical and experimental study. Ann R Col Surg Eng. 1983;65:71-77. 59. Blomstedt B, Osterberg B. Suture materials and wound infection. Acta Chir Scand. 1978;144:269-274. 60. McGeehan D, Hunt D, Chaudhuri A, et al. An experimental study of the relationship between synergistic wound sepsis and suture materials. Br j Surg. 1980;67:636--638. 61. Katz S, Izhar M, Mirelman D. Bacterial adherence to surgical sutures. A possible factor in suture induced infection. Ann Surg. 1981;194: 35-4l. 62. Kapodia CR, Mann JB, McGeehan D, et al. Behavior of synthetic absorbable sutures with and without synergistic enteric infection. Eur j Surg. 1983;15:67-72. 63. Osther PJ, qjode P, Mortensen BB, et al. Randomized comparison of polyglycolic acid and polyglyconate sutures for adominal fascial clo-

30. Suture Selection for Hernia Repair

64.

65.

66.

67.

68.

69. 70.

sure after laparotomy in patients with suspected impaired wound healing. Br] Surg. 1995;82:1080-1082. Paterson-Brown S, Cheslyn-Curtis S, BiglinJ, et al. Suture materials in contaminated wounds: a detailed comparison of a new suture with those currently in use. Br] Surg. 1987;74:734-735. Dayton MT, Buchele BA, Shirazi SS, et al. Use of an absorbable mesh to repair contaminated abdominal wall defects. Arch Surg. 1986;121: 954-960. Daniel Wl, Aarons BJ, Hamilton NT, et al. Paravesical granulomas presenting as a late complication of herniorrhaphy. Aust NZ ] Surg. 1973;43:38-40. Lynch TH, Waymont B, Beacock Cj, et al. Paravesical suture granuloma: a problem following herniorrhaphy.] Urol. 1992;147:460-462. Carroll KM, Sairam K, Olliff SP, et al. Case report: paravesical suture granuloma resembling bladder carcinoma on CT scanning. Br] RadioL 1996;69:476-478. Helms CA, Clark RE. Post-herniorrhaphy suture granuloma simulating a bladder neoplasm. Radiology. 1977;124:56. Jackman SV, Schulman PG, Schoenberg M. Pseudotumor of the bladder: a late complication of inguinal herniorrhaphy. Urology. 1977;50: 609-611.

245

71. Okuyama H, Fukuzawa M, Nakai H, et al. Acquired umbilical fistula after repair of inguinal hernia: a case report.] Pediatr Surg. 1998;33: 737-738. 72. Kronborg O. Polyglycolic acid (Dexon) versus silk for fascial closure of abdominal incisions. Acta Chir Scand. 1976;142:9-12. 73. Krukowski ZH, Matherson NA. Buttonhole incisional hernia: a late complication of abdominal wound closure with continuous nonabsorbable sutures. Br] Surg. 1987;74:824-825. 74. Pollock AV. "Buttonhole" incisional hernia [letter]. Br] Surg. 1988; 75:187. 75. van der Lei B, Bleichroot RP, Simmermacher RK. e-PTFE patch for the repair of large abdominal wall defects. Br] Surg. 1989;76:803-805. 76. Monaghan RA, Meban S. e-PTFE patch in hernia repair. A review of clinical experience. Can] Surg. 1991;34:502-505. 77. Bendavid R Composite mesh (polypropylene-e-PTFE) in the intraperitoneal position. A report of 30 cases. Hernia. 1997;1:5-8. 78. Jenkins TPN. The burst abdominal wound: a mechanical approach. Br] Surg. 1976;63:873-876. 79. Israelsson LA,Jonsson T. Closure of midline laparotomy incisions with polydioxanone and nylon: the importance of suture technique. Br] Surg. 1944;81:1606-1608.

31 Use of Fibrin Glues in the Surgical Treatment of Incisional Hernias J.P. Chevrel and A.M. Rath

In the 1900s the advantages of the adhesive properties of fibrin were investigated in the form of a blood clot applied to a wound for hemostasis and adhesion. l An autologous plasma glue, rich in fibrinogen and thrombin, was used in 1940 for nerve anastomosis. 2 The fibrinogen was not sufficiently concentrated, however, and normal fibrinolysis destroyed the glue. It was only in 1972, in Vienna, that Matras et al. 3 used a very concentrated cryoprecipitated fibrin glue for nerve anastomosis in an animal model and in humans. Its safety and effectiveness made it attractive for a wide variety of surgical indications, and new generations of fibrin sealants quickly developed in response to these demands.

Why Does Fibrin Glue Improve

Wound Healing? In normal wound healing, fibrin formation is important during the first hours after injury and in the first stage of wound healing, for it constitutes the matrix into which collagen fibers will grow to enhance wound strength. The two mechanisms that contribute to the generation of the wound extracellular matrix are leakage of plasma proteins, such as plasma fibronectin and fibrinogen, and synthesis of variants of fibronectin by cells in the wound vicinity. 4 It was proved that defibrinogenation delays collagen accumulation and strengthening in skin wounds. 5 Fibrin deposition also precedes new blood vessel formation. It was demonstrated that fibrin gels themselves can induce an angiogenic response, even in the absence of platelets, which normally produce a growth factor inducing angiogenesis. 6 Fibrin acts as a scaffold for migrating fibroblasts. Fibrin and its degradation products are chemotactic for leukocytes, macrophages, and circulating monocytes. Platelets and fibrin initiate the healing process and ensure its continuity by attracting cells that produce angiogenic growth factors. 7 The fibrinogen concentration in fibrin glues seems to playa role in fibroblast migration and angiogenesis. Pandit et al. s showed that a fibrinogen concentration of 60 mg/ml significantly increases the volume fraction offibroblasts and the number of blood vessels in fibrin glue-treated rabbit ear ulcers.

Fibrin Glue Composition Fibrin sealant has been used clinically in many surgical applications, although a Food and Drug Administration approved commercially available product does not yet exist in the United States. 9 Two fibrin glues commercially available in France (Tissucol®, Immuno; and Biocol®, Laboratoire Franc;:ais de Fractionnement et Technologie) are bi-compound biological products. The first compound consists of a solution of highly concentrated fibrinogen, fibronectin, and Factor XIII. The second compound is composed of thrombin and, for Biocol, calcium chloride. To reconstitute the lyophilized compound 1, a protease inhibitor, aprotinin, is used. Compound 2 reconstitution is achieved by the use of water for Biocol and a solution of calcium chloride for Tissucol. All the constituents are of human origin except aprotinin, which is bovine (Table 31.1). To obtain the fibrin glue, the two compounds must be mixed together. Several reactions then occur (Fig. 31.1): The thrombin transforms fibrinogen into monomers of fibrin, which make a gellike aggregate; it also activates the Factor XIII to Factor XIIIa, as calcium is present. Factor XIIIa then polymerizes the monomers of fibrin and the fibronectin. lO It has been shown that Factor XnIa catalyzes covalent link formation between the fibronectin of the glue and the host collagen; this would explain the good adhesion of fibrin glue. l1 Time for reconstitution (solubility) depends mainly on the temperature. For Tissucol it was found to be 19 minutes at 37°C, but it can be shortened by the use of a heating mixer to 7 minutes. Addition of electrolytes, NaCI for example, can significantly shorten this reconstitution time, but at the cost of seriously compromising fibrin polymerization and cellular vitality. In fact, the strong ionization of such a product suppresses fibroblast proliferation. 12,13 Time to coagulation depends on the thrombin concentration. Tissucol and Biocol have comparable thrombin concentrations, 500 and 670 IU/ml, respectively. Adhesion occurs within 20 seconds. Fibrin glue is resorbed completely, mainly by proteolysis, but fibrinolytic activity depends on the type of tissue glued and is highly variable. Aprotinin inhibits such degradation and one can prolong the action of the glue by increasing its aprotinin content. Optimal

247

31. Fibrin Glues in the Surgical Treatment of Incisional Hernias TABLE 31.1. Composition of biological glues for 1 ml of fibrin glue

Lyophilisate 1 Fibrinogen Fibronectin Factor XIII Lyophilisate 2 Thrombin CaCl2 Reconstitution solution of lyophilisate 1 Aprotinin Reconstitution solution of lyophilisate 2

Biocol®

Tissucol®

127 mg 11 mg

75/115 mg

19 IV

10/50 IV

670 IV/ml

500 IV/ml

2/9mg

Bmg

10,000 KID/ml

3000 KID/ml

Water

CaCl2 40 mmol

KID, kallidogenose inactivation units.

aprotinin concentration is difficult to estimate for a particular tissue. Ideally, the fibrinolysis resistance of the glue should last long enough to prevent early separation but wear off by the time the wound healing process has taken over that task. In practice, it is considered that 3000 kallidogenose inactivation units (KIU)/ml of aprotinin is correct. lO Tissucol has this concentration, whereas Biocol has 10,000 KIU /1.

Quality Criteria A biological glue must satisfy the criteria of efficacy, biocompatibility, safety, and ease of utilization. Efficacy is evaluated by measuring fibrin clot tensile strength and adhesive power after coagulation of the compounds. Ten minutes after application, the fibrin glue clot reaches the tensile strength of 1200 g/cm 2. Its adhesive power is 214 g/cm2.I 4 Time to coagulation is 20 seconds. Tissucol also exists as a "slow glue," which sets in 1.5 to 2 minutes, at a thrombin level of 4 IU/ml. Stability of the fibrin clot depends on aprotinin concentration. Biocol has three times more aprotinin than Tissucol: 10,000 KIU/ml, which is only necessary in a urokinase-rich milieu,

Component 1

Fibrinogen

Factor XlII

whereas 3000 KIU /ml is a sufficient concentration for current uses of fibrin glues. The persistence of fibrin aggregates may lead to local inflammatory reactions. As far as cytocompatibility is concerned, these physiological fibrin sealants are well tolerated and do not impair the healing process. The addition of salts to speed reconstitution is cytotoxic, for it increases osmolarity and conductivity, avoiding fibroblast proliferation. Biocol and Tissucol are human plasma and bovine serum derivatives. Safety controls must handle two different problems: viral disease transmission and bovine spongiform encephalopathy (BSE) transmission. Biocol is manufactured from plasma derived from French blood transfusion centers, whereas Tissucol uses plasma coming exclusively from officially licensed plasmaphoresis centers in central Europe. Both products are carefully screened at different stages in their preparation.I 5 Biocol is tested for hepatitis B surface antigen, anti-hepatitis B core antibody for hepatitis B, antivirus antibody for hepatitis C, anti-human immunodeficiency virus (HIV)-1 and HIV-2 antibodies for HIV, anti-human T-celllymphotropic virus (HTLV)-1 and HTLV-2 antibodies, alanine aminotransferase level, and syphilis. Furthermore, during the manufacturing process, a specific viral inactivation stage is introduced in which a solvent detergent procedure destroys the envelope of the viruses (HIV, canine herpes virus, HBV, cytomegalovirus, and EBV); the product is pasteurized at 60°C for 10 hours and then incubated at 37°C for 22 hours at pH 4 in the presence of pepsin, which accelerates the process of viral inactivation. Purification procedures and testing for the absence of viral markers in the finished products complete this battery of precautions. The manufacture of Biocol has received approval from the Institut Pasteur and from the New York Blood Center. For Tissucol, the selection of donors is equally strict. The search for viral contamination uses the same tests and, in addition, since January 1996, the polymerase chain reaction (PCR) , which is a genetic amplification technique allowing early screening of the viruses for hepatitides B, C, and D, HIV, papilloma virus, herpesvirus, and HTVL, particularly during the incubation period. These tests are carried out at the time the sample is obtained and then repeated on the donor on the 90th day. During manufacture, viral thermoinactivation is carried out by steam heat for 10 hours.

component 2 Thrombin Ca++ Aggregated fibrin r-----: monomers FXIII'- Factor XIIIa

Fibronectin

Fibrin reticulated

Soluble degradation products

fibronectin

Aprotinin Plasminogen

FIGURE 31.1. Reactions and mechanisms after fibrin glue application. (Modified from Seelich.I°)

i Tissular plasminogen activators

Plasmin

248

J.P. Chevrel and A.M. Rath

A new problem may have arisen with the recognition of the risk of transmission of BSE to humans. The aprotinin in these fibrin glues is of bovine origin. It is at present made in Germany (HoechstBehring for Biocol, Bayer and Pentapharm for Tissucol) from bovine lungs from countries deemed free of BSE (Argentina, Uruguay). In the absence of any known case of BSE in these countries, the risk seems to be nil. Bovine lungs are considered by the World Health Organization to be only weakly infectious, and the methods of obtaining aprotinin are in agreement with the principles laid down by the European Drug Agency. The two laboratories manufacturing aprotinin are at present working simultaneously toward development of a synthetic product. Finally, some rare cases of anaphylactic reactions to fibrin glues have been published,I6-18 most of them due to an antibovine thrombin reaction or to an undetected immunity problem in the donor, in the case of a fibrin glue made from homologous fresh frozen plasma from a patient. Manufactured glues such as Biocol and Tissucol should not provoke such problems. Medically treated allergy due to the aprotinin has been described 19 and is a caution listed in Biocol inserts. Fibrin glue utilization is easy. Solubility must be achieved thermomechanically and not by the addition of salts in the composition, as it was stated earlier. Biocol, which is cryodehydrated, reconstitutes in 5 to 10 minutes at room temperature, whereas Tissucol needs to be heated at 37°C and is soluble in 7 to 15 minutes. Both compounds are mixed in a mixing device before spraying. One milliliter of glue covers 25 to 100 cm 2 with the adapted spraying device. The glued surfaces must be held in contact for 2 minutes after fibrin glue application.

Why Use Fibrin Glues in

Incisional Hernia Repair? The main principle of incisional hernia repair is to re-establish a physiological abdominal wall in order to restore its respiratory and postural functions. In other words, it is mandatory to reconstruct the linea alba into which the flat muscles insert through the rectus sheath. When this insertion is lost, as is the case in midline incisional hernias, flat muscles retract, become sagittate, and tend to enlarge the hernial orifice. A vicious circle is created, modifying the physiological mechanisms in which abdominal wall is involved: respiratory mechanics (paradoxical respiration, studied by Rives et al.20 ), posture (lumbar lordosis), abdominal cavity integrity (abdominal organ protrusion), and skin integrity (trophic alterations of the skin over the hernia). In the case of large incisional hernias, closure of the defect can be difficult or made only under tension. To achieve a tension-free suture, it is necessary to perform relaxing incisions in the anterior

FIGURE

31.2. Glue application.

rectus sheath (Gibson, Clotteau-Premont). These incisions allow plasty of the linea alba (Welti-Eudel, Chevrel) at the cost of weakening the abdominal wall at the site of the relaxing incisions over the rectus abdominis muscles. A prosthetic reinforcement is necessary: An onlay mesh may be sutured in front of the abdominal wall, fixed laterally to the external oblique fascia with a nonalr sorbable running suture. Spraying of fibrin glue (Fig. 31.2) over the mesh attaches it immediately to the musculofascial surface, creating a new tendon of insertion of the flat muscles into the reconstructed linea alba. At the end of the operation a physiologically reinforced abdominal wall is thus restored. Fibrin glues can be used to eliminate dead space that may lead to seroma formation and/or infection. Fibrin glue is also a hemostatic agent. Its properties as a wound healing accelerator make it suitable for complete prosthesis fixation in the repair of lateral or parastomal hernias.

Results of Fibrin Glue Fixation of a Reinforcement Prosthesis for Incisional Hernia Repair From June 1979 to June 1998, 422 incisional hernias were operated on in the Department of General Surgery of the Avicenne Hospital, Bobigny, France. At the beginning of the experience, 153 patients underwent rhaphy or plasty without a prosthesis, and 273 patients had a plasty reinforced by an onlay mesh. In 143 of these, a spray of fibrin glue completed prosthesis fixation. Tissucol was employed in 72 cases and Biocol in 71. At first, 4 to 5 ml of glue was sprayed, but it was seen that this could lead to seroma

TABLE 31.2. Comparative results Rhaphy or plasty (n = 153) Morbidity Hematomas Seromas Sepsis Recurrence rate

26 8 5 13 42

(16.9%) (5.2%) (3.26%) (8.49%) (27.40%)

Rhaphy or plasty plus onlay prosthesis (n = 130) 30 3 9 18 17

(23%) (2.3%) (6.92%) (13.84%) (13.07%)

Rhaphy or plasty plus prosthesis and fibrin glue (n = 143) 15 2 9 4 7

(10.48%) (1.39%) (6.29%) (2.79%) (4.89%)

31. Fibrin Glues in the Surgical Treatment of Incisional Hernias 50

~40 S I! 30

! 20 ~

o rhaphy or plasty

FIGURE

rhaphy or plasty + prosthesis

rhaphy or plasty + prosthesis + fibrin glue

31.3. Recurrence rate: comparative results.

formation. We reduced the volume to 2 ml, which is enough to achieve good results with significantly fewer seromas. It was found that patients with fibrin glue had fewer hematomas than the other two groups, the sepsis rate was impressively decreased, and seroma formation increased with the use of a prosthesis regardless of whether fibrin glue was used or not (Table 31.2). In the group in which fibrin glue was used, seroma formation was statistically related with the absence of suction drains: In fact, 15.8% of the patients without suction drains developed a seroma, whereas only 3% of the 100 patients drained had this complication. There was no difference in morbidity between Biocol and Tissucol. Recurrence rates closely depend on the technique used. It is unacceptably high when a simple herniorrhaphy or a hernioplasty without mesh reinforcement is used: 27% in our series. When an onlay mesh is used, recurrence rate falls to 13%. The use offibrin glue dramatically improves this figure: 4.8% recurrence rate (Fig. 31.3). Here again, no relationship was found between recurrence rate and type of fibrin glue used. Mter reoperation, we obtained good results in 98.6% of cases. Fibrin glue spraying seems to be a safe, easy to perform, and effective method to complete an onlay mesh incisional hernia repair.

References 1. Bergel S. Uber Wirkungen des Fibrins. Dtschr Med Wochenschr. 1909; 35:63~65.

249 2. Seddon ~, Medawar PB. Fibrin suture of human nerves. Lancet. 1942;2:87-92. 3. Matras H, Dinges HP, Mamoli B, Lassmann H. Non-sutured nerve transplantation. ] Maxillofac Surg. 1973;1:37. 4. Van der Water L. Mechanisms by which fibrin and fibronectin appear in healing wounds: implications for Peyronie's disease. ] UrnL 1997; 157(1):306-310. 5. Brandstedt S, Olson PS. Effect of defibrinogenation on wound strength and collagen formation. A study in the rabbit. Acta ChiT Scand. 1980; 146(7):483-486. 6. Dvorak HF, Harvey VS, Estrella P, Brown LF, McDonagh J, Dvorak AM. Fibrin containing gels induce angiogenesis. Implications for tumor stroma generation and wound healing. Lab Invest. 1987;57 (6) :67~86. 7. Schlag G, Redl H, Turnher M, et al. The importance of fibrin in wound repair. In Schlag G, Redl H (eds): Fibrin sealant in operative medicine, vol 2. Berlin: Springer; 1986;3-12. 8. Pandit AS, Feldman DS, Caulfield J. In vivo wound healing response to a modified degradable fibrin scaffold. ] Biomater AppL 1998;12(3): 222-236. 9. Spotnitz WD, Falstrom JK, Rodeheaver GT. The role of sutures and fibrin sealant in wound healing. Surg Clin North Am. 1997;77(3): 651-659. 10. Seelich T. Tissucol® (Immuno, Vienna): biochemistry and methods of application. ] Head Neck PathoL 1982;3:65-69. 11. Duckert F, Nyman D, Gastpar H. Factor XIII, jilrtin and collagen. Collagen platelet interaction. Stuttgart: Schattauer; 1978:391-396. 12. Seelich T. A propos des criteres de qualite d'une colle biologique. Lyon ChiT. 1988;84:259-260. 13. Schlag G, Redl H. Fibrin sealant: efficacy, quality and safety. In Waclawiczek HW (ed): Progress in fibrin sealant. Heidelberg: Springer; 1989:3-17. 14. Bagot d'Arc M. Colle de fibrine: efficacite, qualite, securite. Symposium International "Actualitis en chirurgie des nerft pmphiriques. "Nancy, France, November 1990. 15. Chevrel JP, Rath AM. The use of fibrin glues in the surgical treatment ofincisional hernias. Hernia. 1997;1(1):9-14. 16. Mitsuhata H, Horiguchi Y, SaitohJ. An anaphylactic reaction of topical fibrin glue. Anesthesiology. 1994;81:1074-1077. 17. Berguer R, Staerkel RL, Moore EE, et al. Warning: fatal reaction to the use of fibrin glue in deep hepatic wounds. Case reports. ] Trauma. 1991;31:408-411. 18. Milde LN. An anaphylactic reaction to fibrin glue. Anesth Analg. 1989;69:648-686. 19. Gandon P, RatJP, Larregue M. Allergie au Tissucol. La lettre du GERDA. 1988;5:1. 20. Rives], Lardennois B, Pire]C, et al. Les grandes eventrations. Importance du volet abdominal et des troubles respiratoires qui lui sont secondaires. Chirurgie. 1073;99:547-563.

32 Collagen-Based Prostheses for Hernia Repair P.B. van Wachem, T.M. van Gulik, MJ.A. van Luyn, and Robert P. Bleichrodt

Introduction

Autologous and Homologous Implants

Closure of abdominal wall defects is still a major surgical problem. The usual methods have significant disadvantages.! If the defect is bridged by prosthetic material, nonabsorbable prostheses have produced the best results. However, the presence of prosthetic material may lead to eventual complications due to foreign body reaction, lack of fixation to the surrounding host tissues, or erosion of the viscera and overlying skin. Moreover, synthetic meshes require skin cover, are prone to infection, and cannot be used in a contaminated environment. 2 Reconstructions with autologous material such as free dermal, fascial, or musculofascial flaps are also unsatisfactory. Transplant harvesting is time consuming and frequently followed by functional deficits at the donor site. The results of such reconstructions are often disappointing because of bulging of denervated muscles and reherniation rates of up to 20%.! Ideally, prosthetic material acts as a scaffold for the ingrowth of fibrocollagenous tissue and supports the abdominal wall or diaphragm until the newly formed host tissue can resist intraabdominal pressure. The use of a collagen prosthetic mesh for hernia repair is based on this concept. Collagen is the m.yor supportive component of connective tissue and constitutes about 30% of the total body protein in mammals. Existing as stress-resisting fibers with a characteristic structural organization, collagen imparts strength to skin, fascia, dura, bone, tendon, ligaments, and the gut wal1. 3 For application as prosthetic devices, collagen is available as a reconstituted product or, in its naturally occurring form, as a fibrous collagen matrix. Reconstituted collagen is manufactured from solubilized collagen, usually from animal skins, reconstituted into filaments, sheets, tapes, sponges, or tubing. 4 The advantage of reconstituted collagen is that it consists of highly purified collagen that can be molded into any shape, but major disadvantages are its low physical strength and its relatively poor resistance to biodegradation. Fibrous collagen is available as fascia, dura mater, and dermis, providing a naturally woven, biological fabric. Because fibrous collagen retains its structural integrity, it maintains its original stress-resisting mechanical properties. Clearly, as a prosthetic device for the repair of hernia, fibrous collagen is the preferable material.

Dermal Implants

In 1913, Otto Loewe was the first to report the use of autodermoplasty for hernia repair.5 With good results, he implanted dermal grafts in nine patients with abdominal wall defects. Both Loewe 5 and Rehn 6 advised removal of the epidermal layer and the subcutaneous fat to prevent infection and cyst formation. However, the method was not widely accepted because removal of the epidermal layer was difficult and time consuming. In Russia, the method became popular after Janov7 perfected a method of removing the epidermal layer while sparing the papillary layer. His method involved submersion of the skin graft in boiling normal saline. 7,8 Whether the epidermis needs to be removed remains controversial because good results have also been reported from implantation of unprocessed skin under tension. 9- 11 Mter implantation, the dermis is incorporated in the fibrocollagenous tissue of the host, as shown in experimental studies.!2-14 In the first days after implantation, fibrin is deposited on the skin graft, followed by infiltration by granulocytes and macrophages. With the formation of granulation tissue, capillaries infiltrate the graft within 3 to 4 days. Mter 14 days, the graft is fully vascularized. The new vessels are the center of tissue repair, with outgrowth of fibroblasts and formation of collagen. Within 2 months, the graft is transformed into a cell-rich fibrocollagenous tissue. If the graft is implanted under tension, hair follicles and sebaceous glands disappear within 6 days.!3 In clinical practice, several techniques of autodermoplasty have been applied in hernia repair. The graft can be a strip that is threaded through the fascia like a shoelace, supporting its primary closure. 6,9,15 The material may be implanted as an underlay, inlay, or onlay graft. Encouraging results of autodermoplasty were found in observational studies. Korenkov et al.I 4 reviewed three studies involving 160 patients in whom hernias were repaired with autologous full-thickness skin grafts and three studies involving 458 patients in whom corium grafts were used. The reherniation rates were 3.2 to 12% and 0 to 7.6%, respectively, after a follow-up of 2 to 5 years. However, bulging of the abdominal wall was a common finding.

251

32. Collagen-Based Prostheses for Hernia Repair

Fascial Implants

Human Dura Mater

The theoretical advantages of autologous fascial grafts compared with nonbiological substitutes are that they are easily accepted by the host and incorporated into the fibrocollagenous tissue without eliciting a foreign body response and that fascia induces collagen synthesis and remodeling of fibrocollagenous tissue. The most frequently used graft is fascia lata. This is a strong and versatile graft of dense fibrocollagenous tissue, strong enough to resist intraabdominal pressure. The collagen fibers are ideally oriented and woven to resist longitudinal slipping of fibers and fibrils and are molecularly organized to ensure maximum inter- and intramolecular cross-linking. 16 Initially, fascia lata strips were used as living sutures. 17,18 Kirschner introduced the use of fascia lata as a sheet to bridge fascial defects.I 9 From experimental and clinical studies it is known that fascial grafts remain viable after implantation. The grafts are revascularized, as shown angiographically in experimental studies. 20 ,21 Moreover, Gallie and Le Mesurier18 found that the fascial implants were enveloped in newly formed vascular tissue within 3 weeks. Several case reports and experimental studies confirmed these observations. 21 - 24 In contrast to scar tissue, which responds to physical stress by becoming thin and elongated, fascia lata retains its shape, with parallel orientation of fibrils as seen on electron micrography.16 The anchorage of fascia lata to the adjacent myoaponeurotic tissues around the edges of the defect has proved to be better than that of synthetic prostheses, while the tensile strength of the grafts remains constant for 1 year after implantation. 25 Stimulation of synthesis and net deposition of collagen is another advantage of fascial grafts. 16 In clinical practice, free fascia lata grafts are used for the repair of abdominal hernias and abdominal wall defects. In many reported series, the grafts were used for reconstruction in a contaminated or infected environment. In earlier reports, reherniation rates of 6 to 15% were found after hernia repair with fascia lata. 26,27 Peacock16 used free fascia lata as onlay grafts after primary closure of ventral hernias to reinforce the myoaponeurotic wall and to stimulate the synthesis of collagen. He found reherniation in only 1 of the 17 patients after a follow-up of 2 to 5 years. Recently, two larger series of patients with ventral hernias repaired with free fascia lata grafts were reported. 21 ,28 Williams et al. 28 reconstructed 12 ventral hernias, of which 7 were done in a contaminated field. Postoperative complications included two cases of soft tissue dehiscence (intact fascia), two patients with graft breakdown, and one patient with a recurrent bowel fistula. Reherniation occurred in 1 of the 12 patients. The fate of the patients with graft breakdown and recurrent fistula is not mentioned. Disa et al. 21 performed abdominal wall reconstructions with autologous fascia lata in 32 patients of which 30 were performed in a contaminated field. Postoperative local abdominal wall complications included cellulitis in three, seroma in two, and skin dehiscence with exposed fascia grafts in seven patients. In five of the seven patients with a wound dehiscence, the wound healed by secondary intention; in two patients the graft was covered with a split skin graft. Donor site complications occurred in 12 to 18% of the reported series; no cases of knee instability were found.

Human dura mater has been used in surgery since 195529 and for hernia repair since 1958. 30 Since then, human dura mater has been used with success in the reconstruction of abdominal wall hernias, congenital abdominal wall defects, and diaphragmatic hernias. The dura mater is a strong structure that contains several layers of dense fibrocollagenous tissue. In each layer the collagen fibers run parallel, but the collagen fibers in the different layers cross each other, forming a strong and elastic structure with an average breaking strength of 4.2 N/m2.30 Freeze drying (lyophilization) and chemical dehydration are the most frequently used methods to process dura mater. Preparation of freeze-dried dura mater allografts has been described in detail by Jarrel et al. 31 In brief, dura mater is removed within 24 hours from selected human cadavers. Mter being tailored, washed, and sterilized in ethylene oxide, the grafts are freeze dried, sealed in sterile glass containers under vacuum, and stored at room temperature. Dehydration by organic solvents followed by gamma-irradiation is another frequently used method to preserve dura mater. Processing destroys and removes all cells and noncollagen proteins, thus diminishing immunogenicity. Both methods preserve the collagen fibers in their natural multidirectional pattern, although gamma-irradiation is known to interact with cross-links. Concern exists about the transmission of human immunodeficiency virus and viral hepatitis. A review of 664 dura mater allograft implantations by surgeons throughout the United States found no documented cases of infection among implant recipients. 32 Since then, four cases have been documented of iatrogenic Creutzfeldt:Jakob disease acquired after implantation of lyophilized dura mater grafts, all of which originated in one German firm.33-36 No cases ofCreutzfeldt:Jakob disease have been reported from grafts from authorized banks in the United States, probably as a result of strict selection criteria and screening of donors, serological testing, postmortem examinations, bacteriological surveillance, and specialized treatment to inactivate viruses and the Creutzfeldt:Jakob disease agent. 37,38 Pesch and Stoss39 implanted solvent dehydrated, gamma-irradiated human dura grafts in abdominal wall defects in rats. In the first week after implantation, an inflammatory response was found. Within 3 hours the graft was infiltrated by granulocytes, which disappeared within 1 week. Macrophages started to infiltrate the graft after 36 hours, and their number increased tremendously in the following days, accompanied by degradation of collagen fibers. Granulation tissue was formed around the patch, and capillaries and fibroblasts infiltrated it from the outside to the center, slowly replacing the graft with fibrocollagenous tissue. Mter 1 year a layer of fibrocollagenous tissue replaced the graft. Similar observations were made by Wojtyczka. 40 Mechanical investigations demonstrated a 75% reduction of the tensile strength until the 12th week and a slight increase afterward. Mter 30 weeks, bulging of the abdominal wall was a common finding. Dura mater has been successfully used for repair of abdominal wall defects and diaphragmatic hernias in children. The short-term results of repair of congenital abdominal wall defects are remarkably good.4l-44 However, in corroboration of experimental studies, reherniation and bulging of the abdominal wall are frequently mentioned complications in the long term. In a series of Klein et al.,43 secondary abdominal wall reconstructions were required in

252 56% of the patients after reconstruction of a congenital defect with dura mater. Several reports have been published about the usefulness of human dura mater for the repair of abdominal hernias in adults under clean and contaminated circumstances.

Heterologous Implants To overcome the drawbacks of autologous grafts, interest has focused on the modification of allogeneic and xenogeneic fibrous collagenous tissues as potential commercially available devices. Commercially available examples of these devices are the abovementioned allografts and dermal and skin xenografts. 45 ,46 In many of these devices, the cellular components have been eliminated to reduce the immunogenic potential of the collagen bioimplant. Collagen by itself has low immunogenicity, and this is further reduced during the modification processes to which it is subjected. 47

Dermal Grafts Approximately 40% of the total collagen content of the body resides in the dermis of the skin. 48 The dermis combines optimal flexibility with high physical strength in all directions due to its unique three-dimensional, fibrous architecture. A certain hierarchy in the collagen fibrous system in the dermis can be distinguished. Under the light microscope, dermal fiber bundles (10 to 50 #Lm) can be observed that are composed of collagen fibers (2 #Lm). These fibers are formed by bundles of still thinner units, the fibrils (0.1 to 0.2 #Lm). The fibrils in turn are made up of bundles of polypeptide chains termed filaments (0.01 to 0.02 #Lm).49,50 As a device to bridge defects, as in the closure of abdominal wall defects or in hernia repair, dermal tissue would seem to provide an ideal biological mesh prosthesis. For use as a surgical device, the collagen substance needs to be purified and preserved, a process rendering the collagen protein resistant to decay. Several methods can be applied to preserve proteinaceous substances. The most commonly used techniques to stabilize collagen are tanning and lyophilization. Tanning is a time-honored process in which animal skin, that is, animal dermal collagen, is transformed into leather. The mechanism underlying the tanning process is the artificial introduction of intermolecular cross-links within the collagen matrix. 51 For implantation purposes, collagen is usually cross-linked by treatment with aldehydes, such as formaldehyde or glutaraldehyde.52 A common feature of collagenous implants is that they are liable to degradation and absorption by the host. This process involves an inflammatory response, subsequent enzymatic degradation, and gradual absorption by phagocytosing macrophages. The sequence of events leading to absorption of a collagen device is quite similar to the chronic inflammatory reaction observed in relation with foreign bodies. 53 Collagen can be to some extent rendered resistant to degradation and absorption by cross-linking the collagen molecules. The higher the degree of cross-linking, the more persistent the collagen device will be after implantation. 54

P.B. van Wachem et al.

Klopper.54 Sheepskin was used because it has a remarkable structure, featuring a loose and essentially porous dermal architecture. The dermal fiber bundles (Fig. 32.1A) interweave at a low angle, combining flexibility and extensibility with high tensile strength. 50 During pre tanning processes, all the cellular and nonfibrous components of the skin are removed by treatment with a lime-sodium sulfide solution and proteolytic enzymes. The skin is subsequently split in a horizontal plane to separate the papillary layer, containing most appendages, from the regularly woven dermal layer. The latter layer is then tanned, that is, cross-linked with a glutaraldehyde (G) solution, after which the collagen mesh, now referred to as GDSC, is allowed to dry. The resulting GDSC patches are eventually sterilized by gamma-irradiation (2.5 Mrad). The degree of cross-linking can be gauged by determination of the shrinkage temperature. 55,56 In a series of experiments in the rat, the host tissue response and the fate of GDSC grafts were studied. GDSC patches were implanted subcutaneously as an onlay graft in rats with ventral hernia. 54 The patches elicited a foreign body type of tissue reaction, which gradually decreased over time. Although subject to absorption, the GDSC grafts persisted for more than 36 weeks after implantation. By that time, newly formed host collagen had been deposited as layers of fibrous tissue associated with the graft. Clinical application of the GDSC grafts as a dressing for split skin graft donor sites resulted in sound healing with no untoward effects. 57 In a feasibility study in humans in whom abdominal incisional hernias too large for primary closure were repaired with GDSC grafts, absorption of the grafts was apparently too rapid and resulted in recurrences. Thus, although the xenogeneic GDSC grafts had theoretically provided an attractive biological material for the repair of hernia, the degradation and absorption rate after implantation were far too high to allow permanent repair. Further research was focused on the cause of failure and on the development of methods to improve collagen cross-linking techniques to produce a more persistent type of dermal collagen.

Cytotoxicity and Biocompatibility To test the cytotoxicity of GDSC, a sensitive test system with human fibroblasts, called the methy1cellulose (MC) cell culture,58,59 was developed. The test can be used as an indirect system for materials testing for up to 7 days without the culture medium needing to be refreshed, thus without running the risk of removing possible toxic leachables or compounds. With this method, GDSC was found to induce a cell growth inhibition of approximately 77% (Fig. 32.1B). Both primary (leachables) and secondary (enzymatically released) cytotoxic compounds originating from the graft were found to be responsible for cell growth inhibition. 60 ,61 Biocompatibility was studied in a subcutaneous rat model. The results confirmed the in vitro results. GDSC showed increased infiltration of polymorphonuclear neutrophils with extensive intracellular lipid formation, cell degeneration, and death. 62 The grafts were degraded by giant cells within 15 weeks.

Cross-Linked Dermal Sheep Collagen

Cross-Link Modifications and Tissue Engineering

The application of a purified dermal sheep collagen (DSC) graft as an abdominal wall substitute was examined by Van Gulik and

To reduce cytotoxicity and improve biocompatibility, processing of GDSC was modified in three ways. First, cross-linking procedures

253

32. Collagen-Based Prostheses for Hernia Repair

FIGURE

32.1. (A) Scanning electron micrograph (X 140), showing that DSC matrices consist of thinner and thicker collagen bundles. (B) Light micrographs (X625). (Top) Cell proliferation of the control at day 7 in MC cell culture. Spread cells are present in mono and double layer. (Bottom) Cell growth inhibition and deviant cell morphologies during culture in the presence ofGDSC. (C) Light micrograph (X400), showing a good cell

distribution in between DSC collagen (C) bundles at 4 hours after seeding. (D) Light micrograph (XI000), showing one myotube (M) with two nuclei adhering to a collagen (C) bundle at day 7 after seeding. (C and D reprinted from van Wachem et al. 68 ©1996 John Wiley & Sons, Inc., with permission.)

with glutaraldehyde were modified63 to bring about a significant increase in shrinkage temperature. Second, a switch was made to sterilization with ethylene oxide because gamma-irradiation was known to interact with cross-links. Third, new cross-linking agents such as hexamethylenediisocyanate (H) and carbodiimide (C) were examined. 65 ,56 The resulting DSCs are further referred to as HDSC and CDSC. Mechanical properties of modified GDSC, HDSC, and CDSC were examined during in vitro degradation. 67 Carbodiimide cross-linking resulted in the highest shrinkage temperature when used in combination with an activator of carboxyl groups.65 Probably this is related to an increased formation of in-

trinsic cross-links (that is, within collagen fibrils). Ethyleneoxide sterilization further increased the resistance of the grafts. These modifications dramatically reduced cytotoxicity. The in vitro growth inhibitions of modified GDSC, HDSC, and CDSC were 15%, 10%, and 0%, respectively.68 In vivo, only modified GDSC showed a slight tissue incompatibility. In contrast to HDSC and CDSC, modified GDSC showed extensive calcifications, accompanied by less ingrowth of giant cells and fibroblasts and poor formation of rat collagen in between the modified GDSC bundles. 68 ,69 HDSC was found to induce formation of rat collagen in between the DSC bundles. Both modified

FIGURE 32.2. (A) Macrograph of a large defect of oval form (2 by 4 cm) in the abdominal wall of a rat. It was repaired with RDSC and sutured with

Maxon®. (8) Macrograph of a herniation as observed by bulging of the belly (arrow) at 5 weeks after implantation ofRDSC. (C) One of the CDSCimplanted rats at week 20 after implantation. The shaved belly of the anesthetized rat (arrow) showed no herniation. (D) Light micrograph (X63) showing growth of muscle tissue at week 5. At the anchorage site with the

A FIGURE 32.3. (A) Micrograph (XlOO), showing the seeded CDSC disc at

week 3. Locally, at the edge of the implant (i), a specific immune reaction with lymphocyte (L) accumulation is observed. (8) Micrograph (XIOO), showing the nonseeded control disc with an overview of the implant (i) and overlapping muscle. Most muscle fibers are cross sectioned (M), and

implant (i = CDSC), muscle cells (arrows) are sprouting in the fibrous tissue, which also contains many blood vessels (V) . The sprouting is limited to a first rim. Muscle cells were never found to grow spontaneously into the implant, which had induced a foreign body reaction with giant cells and fibrous tissue. (See color insert). (Reprinted from van Wachem e t al.71 ©1994 Wichtig Editore, with permission.)

B one is longitudinally (L) sectioned; the latter shows the typical striation, which was not found inside the implant even myoblast seeded. (See color insert). (Reprinted from van Wachem e t al. 73 ©1999 Elsevier Science Ltd., with permission.)

255

32. Collagen-Based Prostheses for Hernia Repair

CDSC and HDSC degraded within 15 weeks. CDSC degraded at a much slower rate and showed formation of rat collagen and vascular sprouting, which made it the optimal rat collagen scaffold compared with modified CDSC and HDSC.68 Degradation of the patches resulted in reherniation 70 ,71 (Fig. 32.2A). In addition, extensive adhesion formation between the patch and bowel was found. To prevent adhesion formation, we modified the HDSC patch by plasma polymerization with polytetrafluoroethylene. This resulted in a patch with a hydrophobic (TFE) and a hdyrophilic side. The patches were used to repair full-thickness abdominal wall defects in rats, with the TFE-plasma polymerized side of the patch facing the intraabdominal viscera. During a follow-up of 6 weeks, the TFE-HDSC ~showed fewer bowel adhesions, fewer herniations, and delayed degradation than the control HDSC.70 However, degradation proceeded rapidly. Mter 4 and 6 weeks, HDSC implants were about half their original thickness, which resulted in reherniation or bulging of the abdominal wall (Fig. 32.2B). With CDSC, the degradation time could be increased to at least 20 weeks (Fig. 32.2C). CDSC promoted new collagen formation and functioned as guidance for a small rim of muscle overgrowth. However, muscle cells did not grow into the DSC matrix (Fig. 32.2D; see color insert). To improve the properties of the patches, tissue engineering experiments were performed, seeding myoblasts in CDSC patches. 72 In vitro experiments showed that about 85% of the seeded myoblasts were present inside the CDSC matrix and the rest on top of the patch. Mter 4 hours, all cells showed a spherical morphology, sometimes with clear adhesion plaques (Fig. 32.1C). Mter 24 hours, the myoblasts on top of the patch started to form a capsule of spreading cells. Under the capsule, approximately 30% of the cells showed adhesion and spreading between collagen bundles. Between the 3rd and 7th days, the myoblasts showed myotubes (Fig. 32.lD) and deposition of extracellular matrix (collagen and elastin), indicating that myoblasts can survive and differentiate in the CDSC matrix. 72 Myoblast seeded and control CDSC patches were then implanted in small abdominal wall defects in rats. 73 To our regret, after 3 and 6 weeks, the myoblasts had not differentiated into muscle (Fig. 32.3A,B; see color insert). Unfavorable circumstances such as humoral factors, direct cellular interactions (phagocytosis), indirect cellular interactions (cytokines), or absence of vascularization and innervation may have played a role. 73

Conclusion Results of autodermoplasty are encouraging, but further research is needed to improve its efficacy in clinical practice. The clinical results suggest loss of strength in the long term, resulting in bulging of the abdominal wall. Free fascia lata grafts can be used with success for hernia repair, even in a contaminated environment. However, the occurrence of donor site complications in 12 to 18% of the patients is a major drawback. Human dura mater allografts are easy to handle, pliable, and strong, which makes them a good substitute for the myoaponeurotic tissues of the abdominal wall. Because adequate information

about long-term results is lacking, it is impossible to draw conclusions about the ultimate usefulness of dura mater for abdominal wall repair. Cross-linked dermal sheep collagen has been tested only in experimental animals. With tissue engineering, the material seems promising. At present, the application of autologous, homologous, and heterologous collagen-based prosthetic devices in hernia repair is not recommended. In the long term, degradation of the patches may result in reherniation. The feasibility of collagen-based prostheses for induction and stimulation of collagen synthesis and muscle repair to reduce reherniation rate in primary repair depends on further research.

References 1. Simmermacher RKj, Bleichrodt RP, Schakenraad JM. Review: biomaterials for abdominal wall reconstruction. GeUs Mater. 1992;2:281290. 2. Bleichrodt RP, Simmermacher RK, van der Lei B, et al. Expanded polytetrafluoroethylene patch versus polypropylene mesh for the repair of contaminated defects of the abdominal wall. Surg Gynecol Obstet. 1993; 176(1):18-24. 3. Nimni ME, Harkness RD. Molecular structure and functions of collagen. In Nimni ME (ed): Collagen, vol. 1. Boca Raton, fl.: CRC Press Inc.; 1988. 4. Stenzel KH, Miyata T, Rubin AL. Collagen as a biomaterial. Annu Rev Biophys Bioeng. 1974;3:231-253. 5. Loewe O. Uber Hauttransplantation an Stelle der freien Fascienplastik. Munch Med Wochenschr. 1913;60:1320. 6. Rehn E. Das kutane und subkutane Bindegewebe als plastisches Material. Munch Med Wochenschr. 1914;61:118-121. 7. janov VN. Autodermal hernioplasty of big and gigantic incisional and umbilical hernias. 1978, as cited by Korenkov (ref. 14). 8. Kranich H. Behandlung grosser Narben- und Bauchwandhernien mit einer Modifikation der Kutislappenplastik nach E Rehn. Z Chir. 1990; 115:301-309. 9. Gosset J. Bandes de peau totale comme materiel de suture autoplastique en chirurgie. Chirurgie. 1949;75:277-279. 10. Kozuschek W, Farazandeh F. Behandlung monstrossere Bauchwandhernien. Langenbecks Arch Chir. 1983;361:329-323. 11. Wesselhoft R. Cutisplastik nach Rehn und Infektion. Arch Klin Chir. 1959;291:162-170. 12. Rehn E. Uber die funktionelle Anpassung des Bindegewebes im chirurgischen Geschehen. Anat Am. 1931;72:133-152. 13. Reith HB, Dittrich H, Kozuschek W. Morphologie und Einleitung der Kutisplastik bei Bauchwanddefekten. Langenbecks Arch ChiT. 1994;379: 13-19. 14. Korenkov M, Eypasch E, Paul A, et al. Autodermale Hernioplastik-eine seltene und unbekannte technik. Zentralhlatt ChiT. 1997;122:871-878. 15. Rehn E. Das kutane und subkutane Bindegewebe als plastisches Material. Munch Med Wochenschr. 1914;61:118-121. 16. Peacock EE. Subcutaneous extraperitoneal repair of ventral hernias: a biological basis for fascial transplantation. Ann Surg. 1975;181: 722-727. 17. McArthur LL. Autoplastic sutures in hernia and other diseases: preliminary report. JAMA. 1901;37:1162. 18. Gallie WE, Le Mesurier AB. Living sutures in the treatment of hernia. Can Med Assoc) 1923;13:469. 19. Kirschner M. Uber freie Sehne- und Fascientransplantation. Bruns Beitr Klin Chir. 65:472. 20. Pau HW. Revascularization offascia after tympano-plastic grafts: a study by fluorescein angiography. Arch OtorhinolaryngoL 1984;239:7-13.

256 21. Disa jJ, Klein MH, Goldberg NH. Advantages of autologous fascia versus synthetic patch abdominal reconstruction in experimental animal defects. Plast Reconstr Surg. 1996;97:801--806. 22. Guerrerosantos J. Temporoparietal free fascia grafts in rhinoplasty. Plast Reconstr Surg. 1984;74:465-475. 23. Orlando F, Weiss JS, Beyer-Machule CK, et al. Histopathological condition of fascia lata implant 42 years after ptosis repair. Anh Dphthalr mol 1985;103:1518-1519. 24. Das SK, Davidson SF, Walker BL, et al. The fate of free autogenous fascial grafts in the rabbit. Br] Plast Surg. 1990;43:315-317. 25. Madoub HS, Jensen P, Grunert BK, Sanger JR, Yousif NJ. Characteristics of prosthetic mesh and autogenous fascia in abdominal wall reconstruction after prolonged implantation. Ann Plast Surg. 1992;29: 508-511. 26. HamiltonJE. Free mattressed fascia lata patches in the repair oflarge abdominal incisional hernias. Am Surg. 1956;22:217-221. 27. Hamilton JE. The repair of large or difficult hernias with mattressed onlay grafts offuscia lata: a 21-year experience. Ann Surg. 1968;167(1): 85-90. 28. Williams JK, Carlson GW, de Chalain T, et al. Role of tensor fasciae latae in abdominal wall reconstruction. Plast Reconstr Surg. 1998; 101(3):713-718. 29. Sewell WH, Koth DR, Pate jW, et al. The present status of our experiments with freeze---i~.:>'iJJ.. Tissue

~~~~~~=--Tunnel

Muscle/Fascia Peritoneum

Garnjobst and Sullivans advocated the use of Marlex® mesh within a contaminated operative field surrounding a stoma. They reported only minor problems with sepsis in the patients studied. Nevertheless, the use of foreign material in a contaminated operative field should be avoided if possible. We advocate prosthetic mesh for repair of the fascial defect without the problems that bacterial contamination of the operative field presents. The stomal bud is not disturbed, and thus return to normal intestinal function is rapid. In addition, the colon is led out through a mesh flap valve so that further herniation around the colon is unlikely.9,IO

Surgical Procedures The intestine is prepared as for a colonic operation using mechanical and antibiotic preparation. A short course of perioperative systemic antibiotics is begun before surgery. To facilitate location of the colon intraoperatively, a large rubber catheter or colonoscope is passed approximately 20 cm into the colon. The colonic stoma is walled off from the operative field with an adhesive plastic drape. Figure 99.8 shows a large paracolostomy hernia appropriate for this type of repair. Figure 99.9 shows the anatomical situation one may encounter, with small intestine lying alongside the exiting colon and, often omentum caught up in the hernial sac. Fascial edge are attenuated, and the peritoneum and skin are greatly stretched. The surgical approach in this procedure differs from other re-

."1_.

.,"

pairs done for hernias at the site of the colonic stoma in that the old midline or paramedian abdominal incision is reopened. Adair clamps or a self-retaining retractor are used to elevate the fascial edge of the left side of the abdominal incision. As adhesions are dissected away, the contents of the hernial sac are delivered into the abdominal cavity (Fig. 99.10). The portion of the colon exiting through the colonic stomas is easily located because it was earlier intubated with a large catheter or colonoscope. It is important to identifY clearly the fascial ring at the perimeter of the hernia. It is not necessary to dissect the parietal peritoneum out of the hernial sac, but this is usually accomplished without difficulty if the exposure is adequate. A ring of prosthetic mesh is cut so that it will snugly fill the fascial defect. Individual sutures are placed at approximately 1 cm intervals around the fascial ring except directly laterally, where the colon will enter the abdominal cavity from the subcutaneous tissue. Sutures are secured to the mesh so that all sutures are under equal stress, and it is therefore, unlikely that individual sutures will pull through. The colon is led out over the mesh to the left lateral abdominal wall and secured there with sutures (Fig. 99.11). The abdominal incision is closed in a routine manner (Fig. 99.12). One primary and six recurrent paraostomy hernias have been repaired using prosthetic mesh positioned through a peritoneal approach. No recurrences have been observed during a minimum

Abdominal Wall Hernias - Principles and Management. - PDFCOFFEE.COM (2024)

References