Volker Schumpelick

Robert J. Fitzgibbons (Eds.)

Hernia Repair Sequelae

Volker Schumpelick
Robert J. Fitzgibbons (Eds.)

Hernia Repair
Sequelae
In Collaboration with Joachim Conze

With 236 Figures and 97 Tables

1 23
Prof. Dr. Volker Schumpelick Prof. Dr. Robert J. Fitzgibbons
Chirurgische Klinik Department of Surgery
Universitätsklinikum Aachen Creighton University
Pauwelsstraße 30 601 North 30th Street
52074 Aachen Suite 3740
Germany Omaha, NE 68131
e-mail: vschumpelick@ukaachen.de USA
e-mail: fitzjr@creighton.edu

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 V

Preface

At the last Suvretta meeting in 2006 on recurrent hernia prevention and treatment, we dem-
onstrated that with the wide range of available techniques, materials, and meshes at our dis-
posal today, an experienced hernia surgeon will be able to prevent or at least treat a recurrent
hernia.
But whereas recurrences can be treated successfully in most cases, some other hernia
repair sequelae can result in severe, sometimes untreatable problems, e.g. pain, infection, ad-
hesion, or infertility. That was the reason to focus the 5th Suvretta meeting in 2008 on hernia
repair sequelae. We are convinced that such sequelae can be a more serious problem for the
patient than the mostly treatable recurrent hernia. Therefore, it was appropriate to focus the
5th Suvretta meeting on these longterm problems.
During a four-day meeting, we discussed all technical aspects of the various operations
and materials to generate a consensus concerning the best techniques and meshes. We ex-
plored methods to improve surgical techniques to look into the multifactorial causes of post
hernia repair sequelae. In the seclusion of the Swiss plateau valley we had a perfect setting to
discuss these important hernia repair problems in detail with the top hernia specialists in the
world.
With this book, the results of this exceptional 5th Suvretta meeting have been made acces-
sible for every surgeon who is interested in hernia surgery and its sequelae.

V. Schumpelick
 VII

List of First Authors

Alfieri, S. Bachman, S. L. Champault, G. G.

Department of Digestive Surgery University of Missouri Paris University XIII – Medical School
Catholic University of Sacred Heart Department of Surgery »Léonard de Vinci«
Largo Agostino Gemelli 8 Missouri Hernia Institute Department of Digestive Surgery
00168 Rome University of Missouri–Columbia University Hospital Jean Verdier
Italy 414 McHaney Hall Avenue du 14 Juillet
s.alfieri@rm.unicatt.it Columbia, MO 65211 93140 Bondy
USA France
Amid, P. K. gerard.champault@jvr.aphp.fr
Department of Surgery Bellows, C.
David Geffen School of Medicine at Associate Professor of Surgery Chowbey, P. K.
UCLA Chief, General Surgery Minimal Access, Metabolic and
Lichtenstein Hernia Institute at Director of Surgical Research Bariatric Surgery Centre
UCLA General and Laparoscopic Surgery Sir Ganga Ram Hospital
1260 15th Street, Suite 1200 Tulane University Room No. 200 (IInd floor)
Santa Monica, CA 90404 New Orleans, LA New Delhi 110060
USA USA India
pamid@onemain.com chowbey1@vsnl.com
Berger, D.
Arlt, G. D. Department of Surgery Conze, J.
Department of Surgery Stadtklinik Department of Surgery
Park-Klinik Weissensee Balgerstrasse 50 University Hospital RWTH
Schönstrasse 80 76532 Baden-Baden Pauwelsstrasse 30
13086 Berlin Germany 52074 Aachen
Germany d.berger@klinikum-mittelbaden.de Germany
arlt@park-klinik.com jconze@ukaachen.de
Binnebösel, M.
Aufenacker, T. J. Department of Surgery Demirer, S. D.
Department of Surgery (C22) RWTH Aachen University Hospital Ankara University School of
Canisius Wilhelmina Ziekenhuis Pauwelsstrasse 30 Medicine
(CWZ) 52074 Aachen Department of Surgery
Postbus 9015 Germany Ankara
6500 GS Nijmegen mbinneboesel@ukaachen.de Turkey
The Netherlands demirers02@yahoo.com
aufenacker@hetnet.nl Bringman, S.
Clintec, Karolinska Institutet Deysine, M.
Aydede, H. Stockholm, Sweden Professor of Surgery
Associate Professor of Surgery Departments of Surgery, Södertälje Winthrop University Hospital
Celal Bayar University Medical Hospital Mineola, NY
Faculty Södertälje USA
Department of Surgery Sweden maxdey@optonline.net
Manisa sven.bringman@ki.se
Turkey
hasanaydede@hotmail.com
VIII List of First Authors

Diaz, J. J., Jr. Flament, J. B. Hegarty, D.

Division of Trauma and Surgical Department of Surgery Department of Anaesthesia, Inten-
Critical Care Faculty of Medicine sive Care & Pain Medicine
Department of Surgery University of Reims Champagne- Cork University Hospital
Vanderbilt University Medical Ardenne Cork
Center General Surgery Service Ireland
Nashville, TN Hôpital Robert Debré dominichegarty@hotmail.com
USA Rue Serge Kochman
jose.diaz@vanderbilt.edu 51100 Reims Honigsberg, E.
France Mount Sinai Medical Center
Dilek, O. N. jbflament@chu-reims.fr 1010 5th Avenue
Professor of General Surgery New York, NY 10028
School of Medicine Franz, M. G. USA
Kocatepe University Associate Professor of Surgery
PK:70 Chief, Minimally Invasive Surgery Hopf, H. W.
03100 Afyonkarahisar University of Michigan Department of Anesthesiology,
Turkey Department of Surgery University of Utah
ondilek@hotmail.com 2214F Taubman Center Medical Director, Urban Central
1500 East Medical Center Drive Region Wound Care Services
Falagas, M. E. Ann Arbor, MI 48109 LDS Hospital
Department of Medicine, Henry USA 8th Avenue and C Street
Dunant Hospital, Athens, Greece mfranz@umich.edu Salt Lake City, UT 84132
Department of Medicine, Tufts USA
University School of Medicine, Goldenberg, A. harriet.hopf@hsc.utah.edu
Boston, MA, USA Associate Professor
Alfa Institute of Biomedical Sciences Department of Surgery Jansen, M.
(AIBS) Federal University of Sao Paulo Department of Surgery
9 Neapoleos Street, 151 23 Marousi Brazil University Hospital
Athens, Greece goldenb@terra.com.br RWTH Aachen
m.falagas@aibs.gr Pauwelsstrasse 30
Gryska, P. vR. 52074 Aachen
Fawole, A. S. Tufts University School of Medicine Germany
Department of Academic Surgery Boston, MA mjansen@ukaachen.de
St. James’s University Hospital Department of Surgery
Beckett Street Newton-Wellesley Hospital Jansen, P. L.
Leeds LS9 7TF Suite 365, 2000 Washington Street Department of Surgery
UK Newton, MA 0246 University Hospital
adeshina.fawole@midyorks.nhs.uk USA RWTH Aachen
pgryska@partners.org Pauwelsstrasse 30
52074 Aachen
Hansson, B. Germany
Department of Surgery plynen@ukaachen.de
Canisius Wilhelmina Hospital
Nijmegen
The Netherlands
 IX
List of First Authors

Junge, K. Kolbe, T. Montgomery, A.

Department of Surgery Biomodels Austria, University Department of Surgery
Technical University of Aachen of Veterinary Medicine Malmö University Hospital
Pauwelsstrasse 30, Veterinärplatz 1 20502 Malmö
52057 Aachen 1210 Vienna Sweden
Germany Austria agneta.montgomery@skane.se
kjunge@ukaachen.de Thomas.Kolbe@vu-wien.ac.at
Morales-Conde, S.
Kaemmer, D. Kukleta, J. F. University Hospital Virgen del Rocío.
Department of Surgery Klinik Im Park Betis-65, 1º
RWTH Aachen Seestrasse 220 41010 Sevilla
Pauwelsstr. 30 8027 Zurich Spain
52074 Aachen Switzerland smoralesc@gmail.com
Germany jfkukleta@bluewin.ch
dkaemmer@ukaachen.de Muschaweck, U.
Kurzer, M. Hernienzentrum Dr. Muschaweck –
Kavvadias, T. British Hernia Centre München
Department of Obstetrics and 87 Watford Way Arabellastrasse 5
Gynaecology London NW4 4RS 81925 Munich
Lucerne Cantonal Hospital UK Germany
Lucerne m.kurzer@mac.com info@hernien.de
Switzerland
Lammers, B. J. Neumayer, L.
Kehlet, H. Department for Colorectal and Professor of Surgery
Section for Surgical Patho- Hernia Surgery Department of Surgery
physiology 4074 Lukaskrankenhaus Neuss University of Utah
Rigshospitalet Copenhagen Neuss Salt Lake City VA Healthcare System
University Germany 1950 Circle of Hope Room 6540
Blegdamsvej 9 blammers@lukasneuss.de Salt Lake City, UT 84132
2100 Copenhagen USA
Denmark Matthews, B. D. leigh.neumayer@hsc.utah.edu
henrik.kehlet@rh.regionh.dk Chief, Section of Minimally Invasive
Surgery Nordin, P.
Klinge, U. Department of Surgery Head of the Swedish Hernia Register
Institute for Applied Medical Washington University School of Department of Surgery
Engineering Medicine Östersund Hospital
Helmholtz Institute for Applied 660 S. Euclid Ave., Campus Box 8109 831 83 Östersund
Medical Technology St. Louis, MO 63110 Sweden
RWTH Aachen University USA par.nordin@jll.se
Pauwelsstraße 20-30 matthewsbr@wustl.edu
52074 Aachen Otto, J.
Germany Miserez, M. Department of Surgery
Klinge@hia.rwth-aachen.de Department of Abdominal Surgery University Hospital
University Hospitals RWTH Aachen
Herestraat 49 Pauwelsstrasse 30
3000 Leuven 52074 Aachen
Belgium Germany
marc.miserez@uz.kuleuven.ac.be jeotto@ukaachen.de
X List of First Authors

Page, B. P. Schug-Paß, C. Stroh, C.

University Department of Surgery Department of Surgery Department of General, Abdominal
Western Infirmary Center for Minimally Invasive and Paediatric Surgery
Glasgow G11 6NT Surgery Municipal Hospital (Teaching
Scotland Vivantes Hospital Spandau Hospital of the Friedrich-Schiller
blaithin.page@hotmail.com Neue Bergstrasse 6 University at Jena, Germany)
13585 Berlin Strasse des Friedens 122
Pascual, G. Germany 07548 Gera
Department of Medical Specialities christine.schug-pass@vivantes.de Germany
Alcalá University Christine.Stroh@wkg.srh.de
Networking Research Centre on Schumpelick, V.
Bioengineering, Biomaterials and Department of Surgery Stumpf, M.
Nanomedicine (CIBER-BNN) University Hospital RWTH Department of Surgery
Madrid Pauwelsstrasse 30 RWTH Aachen
Spain 52074 Aachen Pauwelsstrasse 30
Germany 52074 Aachen
Peiper, C. vschumpelick@ukaachen.de Germany
Surgical Clinic michale.stumpf@
Evangelisches Krankenhaus Simons, M. P. klinikum-pforzheim.de
Werler Strasse 110 Department of Surgery
58455 Hamm Onze Lieve Vrouwe Gasthuis van der Kolk, B. M.
Germany Postbus 95500 Department of Surgery, Division of
cpeiper@evkhamm.de 1090 HM Amsterdam Abdominal Surgery
The Netherlands Radboud University Nijmegen
Penkert, G. mpsimons@worldonline.nl Medical Center
Friederikenstift Hannover Nijmegen
Department of Neurosurgery Smeds, S. The Netherlands
Humboldtstrasse 5 The Sergel Clinic
30169 Hannover Department of Clinical and Experi- Witkowski, P.
Germany mental Medicine Department of Surgery
goetz@familie-penkert.de Faculty of Health Sciences Division of Abdominal Organ
University Hospital Transplantation
Read, R. C. Linköping University Columbia University
Emeritus Professor of Surgery 58185 Linköping 177 Fort Washington Ave,
304 Potomac Street Sweden 7HS, Room 200C
Rockville, MD 20850 staffan.smeds@carema.se New York, NY 10032
USA USA
read@post.harvard.edu Stanton-Hicks, M. pw2004@columbia.edu
Vice Chairman, Anesthesiology
Schippers, E. Institute
Surgical Clinic Consulting Staff, CCF Shaker
Department of General and Visceral Children’s Pain Rehabilitation
Surgery Cleveland Clinic
Juliusspital Pain Management Department
Juliuspromenade 19 9500 Euclid Avenue – C-25
97070 Würzburg Cleveland, OH 44195
Germany USA
e.schippers@juliusspital.de stantom@ccf.org
 XI

Contents

15 Fate of the Inguinal Hernia Following

I Risk for the Spermatic Cord Removal of Infected Prosthetic Mesh . . . . . . .113
16 Mesh Infection–Therapeutic Options . . . . . . .119
17 Does Antibiotic Prophylaxis Prevent the
1 Are There Adverse Effects of Herniorrhaphy Occurrence of Wound Infection After Groin
Techniques on Testicular Perfusion? . . . . . . . . . . 3 Hernia Surgery? . . . . . . . . . . . . . . . . . . . . . . . . . . . .125
2 The Effects of Mesh Bioprosthesis 18 Infection Control in a Hernia Clinic:
on the Spermatic Cord Structures in a 24-Year Results of Aseptic and Antiseptic
Rat Model . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Measure Implementation in 4,620 »Clean
3 Damage to the Spermatic Cord by the Cases« Based on Up-To-Date Micro-
Lichtenstein Procedure in a Pig Model– biological Research . . . . . . . . . . . . . . . . . . . . . . . .135
Preliminary Results . . . . . . . . . . . . . . . . . . . . . . . . . . 21 19 Components Separation Technique:
4 Influence of Prosthetic Implants on Male Pros and Cons . . . . . . . . . . . . . . . . . . . . . . . . . . . . .143
Fertility in Rabbits and Rats . . . . . . . . . . . . . . . . . 29
5 The Effects of a Mesh Bioprosthesis on
the Spermatic Cord Structures . . . . . . . . . . . . . . 39
6 Influence of Prosthetic Implants on Male III Risk for Pain
Fertility in Rats . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
7 What Can We Do To Decrease the Risk
of Vas Deferens Injury due to Inguinal 20 Self-Assessment of Discomfort and Pain
Hernioplasty? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 after Inguinal Hernia Repair: A Reflection
8 The Long-Term Effect on Testicular of Both Individual Pain Propensity and
Function of a Mesh Bioprosthesis Used for Surgical Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . .155
Inguinal Hernia Repair . . . . . . . . . . . . . . . . . . . . . . 57 21 Chronic Pain After Inguinal Hernia Repair . . .163
9 Reoperation Following Lichtenstein Repair: 22 What Do We Know About the Patho-
What Do Vas and Nerves Look Like? . . . . . . . . . 65 physiology and Pathology of Neuropathic
10 Damage to the Spermatic Cord from Pain? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .169
Groin Herniorrhaphy: A Review . . . . . . . . . . . . . . 71 23 Surgical Trauma of Nerves–Causes of
Neuropathic Pain, Classification, and
Options in Surgical Therapy . . . . . . . . . . . . . . . .177
24 Risks for Pain–Neuropathic Pain:
II Risk for Infection How Should We Handle the Nerves? . . . . . . . .185
25 What To Consider as Clinicians About
Chronic Postoperative Pain and Inguinal
11 Mesh Infection Following Hernia Repair: Herniorrhaphy . . . . . . . . . . . . . . . . . . . . . . . . . . . . .191
A Frequent Problem? . . . . . . . . . . . . . . . . . . . . . . . 79 26 Risk Factors for Chronic Pain After
12 Patient Factors as a Major Determinant Groin Hernia Surgery . . . . . . . . . . . . . . . . . . . . . .199
of Wound Outcome and Infection After 27 Ischemic Inflammatory Response
Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Syndrome as an Alternative Explanation
13 Mesh-Related Infections After Hernia for Postherniorrhaphy Pain . . . . . . . . . . . . . . . . .207
Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 28 Postoperative CRPS in Inguinal Hernia
14 Human Acellular Dermal Matrix for Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .213
Ventral Hernia Repair in the Compromised 29 Chronic Pain After Open Mesh Repair
Surgical Field . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .103 of Incisional Hernia . . . . . . . . . . . . . . . . . . . . . . . .221
XII Contents

30 Clinical Results After Open Mesh Repair . . . .227 47 Effect of Different Mesh Materials on
31 Acute and Chronic Pain After Laparoscopic Adhesion Formation . . . . . . . . . . . . . . . . . . . . . . .353
Incisional Hernia Repair . . . . . . . . . . . . . . . . . . . .233 48 Tissue Ingrowth and Laparoscopic
32 Effect of Nerve Identification on the Rate Ventral Hernia Mesh Materials: An Updated
of Postoperative Chronic Pain Following Review of the Literature . . . . . . . . . . . . . . . . . . . .365
Inguinal Hernia Surgery . . . . . . . . . . . . . . . . . . . .239 49 Porosity and Adhesion in an IPOM
33 Discomfort 5 Years After Laparoscopic Model . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .375
and Shouldice Inguinal Hernia Repair: 50 Benefit of Lightweight and/or Titanium
A Report from the SMIL Study Group . . . . . . .245 Meshes? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .381
34 Recurrence or Complication: The Lesser 51 ePTFE Prostheses and Modifications . . . . . . . .393
of Two Evils? A Review of Patient-Reported 52 The Role of Stem Cells in Abdominal
Outcomes from the VA Hernia Trial . . . . . . . . .251 Wall Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .401
35 Chronic Pain After Inguinal Hernia
Repair: The Choice of Prosthesis
Outweighs That of Technique . . . . . . . . . . . . . .257
36 The Effect of Polypropylene Mesh on V Risk for Migration and
the Ilioinguinal Nerve in Open Mesh Erosion
Repair of Groin Hernia . . . . . . . . . . . . . . . . . . . . .265
37 Lightweight Macroporous Mesh vs.
Standard Polypropylene Mesh in 53 Safety and Durability of Prosthetic Repair
Lichtenstein Hernioplasty . . . . . . . . . . . . . . . . . .275 of the Hiatal Hernia: Lessons Learned from
38 Does the Choice of Prosthetic Mesh Type a 15-Year Experience . . . . . . . . . . . . . . . . . . . . . . .413
Make a Difference in Postherniorrhaphy 54 Mesh Migration into the Esophageal
Groin Pain? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .279 Wall After Mesh Hiatoplasty . . . . . . . . . . . . . . . .421
39 New Understanding of the Causes and 55 Complications After Gastric Banding–
Surgical Treatment of Postherniorrhaphy Results in Germany . . . . . . . . . . . . . . . . . . . . . . . .429
Inguinodynia and Orchialgia . . . . . . . . . . . . . . .287 56 Alloplastic Implants for the Treatment
40 Surgery for Chronic Inguinal Pain: of Stress Urinary Incontinence and Pelvic
Neurectomy, Mesh Explantation, or Both? . . . 293 Organ Prolapse . . . . . . . . . . . . . . . . . . . . . . . . . . . .439
41 Results of Tailored Therapy for Patients 57 Prophylactic IPOM Mesh To Prevent
with Chronic Inguinal Pain . . . . . . . . . . . . . . . . .299 Parastomal Hernias . . . . . . . . . . . . . . . . . . . . . . . .445
58 Laparoscopic Parastomal Hernia Repair:
Pitfalls and Complications . . . . . . . . . . . . . . . . . .451
59 Concept of Visible Mesh and Possibili-
IV Risk for Adhesion ties for Analysis of Mesh Migration and
Shrinkage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .457

42 Adhesion as a Chronic Inflammatory

Problem? Risk for Adhesions, Migration,
and Erosions? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .305 VI Strategy to Improve Results
43 Biological Tissue Graft: Present Status . . . . . .317
44 IPOM Results of 344 Consecutive Patients
with a PVDF-Derived Prosthesis . . . . . . . . . . . . . 323 60 Who Has the Major Role in Hernia Surgery:
45 Pooled Data Analysis of Laparoscopic vs. The Surgeon or the Material? . . . . . . . . . . . . . . .463
Open Ventral Hernia Repair: 14 Years of 61 Two Controversial Concepts: Standard
Patient Data Accrual . . . . . . . . . . . . . . . . . . . . . . .331 Procedure in a Standard Patient Versus
46 Tissue Ingrowth, Adhesion, and Mesh Tailored Surgery with Procedures Adjusted
Contraction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .345 to Individual Patients . . . . . . . . . . . . . . . . . . . . . .467
 XIII
Contents

VII Pro and Contra

62 In Support of a Standard Technique for

Inguinal Hernia Repair . . . . . . . . . . . . . . . . . . . . .475
63 In Support of Individual Selection of
Technique as Related to the Patient–
Improvement by Better Selection of
Patients Who Can Be Offered a Less Risky
Technique: Groin Hernia . . . . . . . . . . . . . . . . . . .479
64 In Support of Standard Procedure in
Abdominal Hernia Repair . . . . . . . . . . . . . . . . . .485
65 In Support of Individualized Procedures
in Abdominal Wall Hernia Repair . . . . . . . . . . .493
66 In Support of Standard Procedure in
Hiatal Hernia Repair . . . . . . . . . . . . . . . . . . . . . . . .503
67 Strategy To Improve the Results?
In Support of Individualized Procedures
in Hiatal Hernia Repair . . . . . . . . . . . . . . . . . . . . .513

68 Questionnaire . . . . . . . . . . . . . . . . . . . . . . . . . . . . .521

Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .525

 I

I Risk for the Spermatic Cord

1 Are There Adverse Effects of Herniorrhaphy Techniques

on Testicular Perfusion? – 3

2 The Effects of Mesh Bioprosthesis on the Spermatic

Cord Structures in a Rat Model – 13

3 Damage to the Spermatic Cord by the Lichtenstein

Procedure in a Pig Model–Preliminary Results – 21

4 Influence of Prosthetic Implants on Male Fertility

in Rabbits and Rats – 29

5 The Effects of a Mesh Bioprosthesis on the Spermatic

Cord Structures – 39

6 Influence of Prosthetic Implants on Male Fertility in Rats – 43

7 What Can We Do To Decrease the Risk of Vas Deferens Injury

due to Inguinal Hernioplasty? – 49

8 The Long-Term Effect on Testicular Function of a Mesh

Bioprosthesis Used for Inguinal Hernia Repair – 57

9 Reoperation Following Lichtenstein Repair:

What Do Vas and Nerves Look Like? – 65

10 Damage to the Spermatic Cord from Groin Herniorrhaphy:

A Review – 71
 1

Are There Adverse Effects

of Herniorrhaphy Techniques
on Testicular Perfusion?
O. N. Dilek
 4 Chapter 1 · Are There Adverse Effects of Herniorrhaphy Techniques on Testicular Perfusion?
Introduction
1 the inguinal canal, the vein joins to form two or
The spermatic cord anatomy has been well studied
because of its important role in testicular physiology
and surgery. The spermatic cord is composed of the
vas deferens; testicular vessels, including the testicu-
lar artery and veins; autonomous nerves; spermatic
muscle; and fascia [1]. Each of these structures can
have various effects on testicular perfusion.
The testicular arteries arise from the abdomi-
nal aorta just below the renal artery and travel in
the intermediate stratum of the retroperitoneum
to reach the internal inguinal ring and become a
component of the spermatic cord [1]. In an intra-
operative dissection study of over 100 spermatic
cords, Beck et al. identified a single internal sper-
matic artery in 50% of cases, with two arteries in
30% of spermatic cords and three arteries in 20%
[1]. At the internal ring, the vessels are joined
by the genital branch of the genitofemoral nerve,
the ilioinguinal nerve, the cremasteric artery, the
vas deferens, and its artery. The testicular artery
branches into an internal artery and an inferior
testicular artery and into a capital artery to the
head of the epididymis [1]. Human testicular pa-
renchyma receives approximately 9 ml of blood
per 100 g of tissue per minute. Silber showed that
an interruption of the testicular blood supply may
result in testicular atrophy [2].
The spermatic veins (testicular veins) collect
the blood from the testis, epididymis, and scrotum.
The testicular veins form several highly anasto-
motic channels that surround the testicular artery
as the pampiniform plexus. This arrangement al-
lows countercurrent heat exchange, which cools
the blood in the testicular artery [1]. The vascular
arrangement in the pampiniform plexus–with the
counterflowing artery and veins separated only by
the thickness of their vascular wall in some areas–
facilitates the exchange of heat and small mol-
ecules. For example, testosterone is transported
from the vein to the artery via a concentration-
limited passive diffusion process. The counter-
current exchange of heat in the spermatic cord
provides blood to the testis, which is a specialized
structure that functions optimally at 2–4°C lower
than the rectal temperatures in normal men [3, 4].
A loss of the temperature differential is associated
[UnitedVRG] - Medical Release Group
with testicular dysfunction [1, 3]. At the level of
three channels and then a single vein that drains
into the inferior vena cava on the right and the
renal vein on the left [1, 5].
The cremasteric muscle is one of the parts of
the spermatic cord. When this muscle contracts,
the cord is shortened, and the testicle is moved
closer up toward the body, a position that pro-
vides slightly more warmth to maintain optimal
testicular temperature. When cooling is required,
the cremasteric muscle relaxes, and the testicle is
lowered away from the warm body and is able to
cool. This phenomenon is known as the cremas-
teric reflex [6]. The dartos muscle is a sympatheti-
cally innervated dermal muscle layer within the
scrotum, distinct from the somatically innervated
cremasteric muscle. Abnormalities of dartos and
cremasteric muscle innervation may impact testis
thermoregulation and spermatogenesis [6].
Autonomous nerves reach the testis accom-
panying the testicular artery and pampiniform
plexus. The vast majority of testicular nerves are
sympathetic axons with vasomotor function. They
innervate the small vessels supplying clusters of
Leydig cells and regulate testicular luteinizing hor-
mone receptors and blood flow [7, 8].
About 10% of people develop some type of her-
nia during their lifetime, and more than 750,000
hernia operations are performed in the United
States each year. Hernias are seven times more
common in males than in females [9]. Abramson
et al. reported that the overall current risk for a
male to have an inguinal hernia is 18%, and the
lifetime risk is 24% [10].
Anatomically, a close relation exists between
the spermatic cord and inguinal hernias. Inguinal
hernias can carry the risk of ischemia of the testis
by intermittent mechanical compression (pressure)
on the testicular vessels [11, 12]. In some reports,
color Doppler ultrasonography showed that, pre-
operatively, the sonographic resistive index (RI)
was significantly elevated in the affected (hernia)
side compared with the normal side [13]. On
the other hand, Muñoz Sánchez et al. concluded
that uncomplicated inguinal hernias cause no sig-
nificant alterations in the arterial circulation of the
testicle [14].
Chapter 1 · Are There Adverse Effects of Herniorrhaphy Techniques on Testicular Perfusion?
The laparoscopic totally extraperitoneal prep-
eritoneal (TEP) hernia repair technique, which is
based on the concept of tension-free high ligation
of the sac, has become widely popular in surgical
practice [15–18]. Lichtenstein hernia repair (LHR)
is one of the most comfortable effective methods of
inguinal hernia repair, and it has similarities with
TEP because of the prosthetic mesh used [19].
Despite the frequency of open and laparoscopic
herniorrhaphy, the effects of a hernia and its sub-
sequent repair on testicular perfusion and function
are unknown. It is presently unclear what the best
method is for reconstructing the deep inguinal
ring in hernia surgery with mesh implantation.
Testicular dysfunction (atrophy) is one of the
most dreaded sequelae of inguinal hernioplasty.
However, literature findings show that testicular
atrophy occurs in 0–2% of patients after hernior-
rhaphy [9, 20]. Yavetz et al. reported that among
8,500 patients attending a fertility clinic because of
infertility, 565 men (6.65%) reported an incidence
of inguinal hernioplasty with or without subse-
quent atrophy of the testis [21].
The preoperative and postoperative use of
color Doppler ultrasound (CDUS) to evaluate the
spermatic cord structure and scrotal structure has
been well documented in testicular pathologies
and hernias [22–24]. CDUS is extremely helpful
in all cases to investigate extratesticular vascular-
ization and testicular perfusion, with parameters
optimized to display low-flow velocities, includ-
ing peak systolic velocity (PSV) and end diastolic
velocity (EDV). Lefort and colleagues showed that
color Doppler examination of the scrotum should
include measurement of intratesticular RI, as an
elevated RI can be suggestive of ischemia [25].
However, most of these conditions have not been
well documented using CDUS after TEP or LHR.
We have discussed the previously unreported use
of testicular CDUS in patients who underwent
TEP or LHR.
Damage to the spermatic cord structures, tes-
ticular atrophy, and dysfunction levels as a conse-
quence of mesh application are not well known in
adults. The purpose of this study was to evaluate
the efficacy of prosthetic meshes on testis perfu-
sion and testis volume with Lichtenstein and TEP
hernia repair techniques.
5 1
Materials and Methods
In our prospective randomized series of 82 pa-
tients, 26 of them (age 24–71 years) fulfilled the
inclusion criteria and underwent elective hernior-
rhaphy for groin hernia [26].
In patients with an American Society of Anes-
thesiologists (ASA) score of more than II, having
a hydrocele and/or a varicocele could alter the tes-
ticular function independent of the hernia repair
[27, 28]. For this reason, patients with the follow-
ing conditions were excluded from the study: her-
nia types Ia, IIb, III, or IV according to the Nyhus
classification [16, 29]; ASA scores of III, IV, or V;
or hydrocele and/or varicocele. Other exclusion
criteria were recurrence, conversion to an open
procedure, or the inability to provide informed
consent. Scrotal hernias or large hernias are pre-
disposing factors for testicular atrophy (type IIb
or larger), and very small hernias (type Ia) are not
suitable for TEP or LHR methods. Thus, giant
scrotal hernias were also excluded in our study
[26]. Each patient was randomly assigned to one
of two groups: TEP (n=13, mean age 46.7±1.6
years) or LHR (n=13, mean age 54.2±2.7 years).
Six of the patients had bilateral hernias (n=3 for
each group).
CDUS of the testes was performed on all pa-
tients the day before operation and 3 months af-
ter operation. The scrotum was examined with
a linear (5 MHz) transducer (ATL Ultramark 9,
USA). Color Doppler settings were optimized to
detect slow flow, with the highest color gain set-
ting allowing an acceptable signal-to-noise ratio,
the lowest wall filter, and the lowest velocity scale.
Ultrasound of the scrotum was performed in the
supine position, and the patient was asked to hold
the penis suprapubically. Blood flow parameters of
the spermatic artery were evaluated and noted as
PSV, EDV, and calculated RI.
The investigation protocol was approved by
the ethics committee of our institution. Patient
groups were compared with each other, and the
nonoperated side was compared with the op-
erated side. Kruskal–Wallis and Mann–Whitney
U–tests were used to evaluate the differences. A
two-sided p-value <0.05 was considered signifi-
cant [26].
 6 Chapter 1 · Are There Adverse Effects of Herniorrhaphy Techniques on Testicular Perfusion?
Results
1 velocity (EDV), and resistive index (RI) measurements
In our series, the mean patient age was 49.6±1.7
(range 24–71) years; in the LHR group, 54.2±2.6
(range 26–71) years; and in the TEP group,
46.7±1.7 (range 32–62) years. We found no sig-
nificant changes in blood flow parameters (PSV,
EDV, RI) when comparing the two groups pre-
operatively and postoperatively (⊡ Tables 1.1 and
1.2). Also, there were no significant changes in the
blood flow parameters when the TEP and LHR
groups were compared with each other [26].
Discussion
All inguinal hernia repair techniques aim to close
the internal ring with a suture or a biomaterial
such as polypropylene mesh. Concern has been
raised about whether the spermatic cord structures
are compromised with these techniques
The spermatic cord structures may be exposed
to invasive surgical intervention during inguinal
hernia reconstruction. Surgical dissection, divi-
sion, or mechanical trauma to the spermatic artery
and veins accounts for serious trophic changes
in the testis. Lee et al. have explained that surgi-
cal manipulation of the spermatic cord imparts
a small but statistically significant morphological
change in testicular size without a deleterious ef-
fect on testicular development, fertility, or fecun-
dity [20].
Many factors can lead to decreased or inter-
rupted testicular perfusion. In some reports, ingui-
nal hernia may impair testicular blood flow, which
may be attributable to the effect of intermittent me-
chanical compression on the funiculus spermaticus
in the inguinal canal [11–13, 25]. Testicular artery
and vein injuries, thrombosis of the spermatic vein
plexus, and testicular torsion are the major factors
influencing testicular perfusion. Furthermore, the
implantation of a nonabsorbable polypropylene
mesh during hernia repair causes a chronic foreign
body reaction involving the surrounding tissue.
In cases of inguinal hernia repair using different
mesh techniques, the spermatic cord structures are
potentially affected by this chronic inflammatory
tissue remodeling [30].
[UnitedVRG] - Medical Release Group
⊡ Table 1.1. Peak systolic velocity (PSV), end diastolic
in the totally extraperitoneal group (NS not significant)
Preoperative Postoperative p
PSV 18.18±1.03 17.84±1.11
NS
EDV 6.68±0.48 6.07±0.37
RI 0.62±0.017 0.63±0.018
⊡ Table 1.2. Peak systolic velocity (PSV), end diastolic
velocity (EDV), and resistive index (RI) measurements
in the Lichtenstein repair group (NS not significant)
Preoperative Postoperative p
PSV 17.30±0.98 17.24±0.78
NS
EDV 5.51±0.29 5.70±0.29
RI 0.65±0.017 0.66±0.014
However, many authors have reported that the
testes have more vessels than expected. Testicular
arterial anatomy has been well studied because of
its important role in testicular physiology and tes-
ticular surgery. Anatomically, the spermatic artery
divides into two branches near the testis. Jarow
et al. showed that the frequent early branching of
the internal spermatic artery prevents inadvertent
interruption of testicular arterial blood flow dur-
ing operations performed on the spermatic cord
within the inguinal canal [31]. The testicular ar-
tery penetrates the tunica albuginea at the lower
pole, proceeding as the capsular artery. Using
CDUS, a transmediastinal artery is visible in the
upper third of the testis in 50%. Branches from the
capsular artery course through the parenchyma in
the testicular septations as afferent arteries and are
directed to the gonadal hilum. The testicular veins
are not consistently visible with CDUS [23].
Many studies suggest an unknown or alter-
native (collateral) connection between vessels of
the cord and other vessels that supply blood to
the testis [14, 32–34]. Zomorrodi and Buhluli
explained that they isolated and ligated the sper-
matic cord at the internal ring of the inguinal
canal for transfixation and placed the allografted
Chapter 1 · Are There Adverse Effects of Herniorrhaphy Techniques on Testicular Perfusion?
Thrombosis
Ligating /Cutting
Testicular
Hematoma
ischemia
Inflammation
Fibrosis
kidney in the retroperitoneal position with anas-
tomoses of the iliac vessels, and that mass ligation
of the spermatic cord did not lead to any ischemic
problems in the follow-up period [33]. Zát’ura et
al. concluded that in the great majority of men,
the blood supply of the testis is ensured by collat-
eral circulation [34].
It is well known that thrombosis, ligation, and/
or cutting of the spermatic vessels may lead to
ischemia, ischemic orchitis, and testicular atrophy
(⊡ Fig. 1.1). Ischemic orchitis typically presents 2–3
days after inguinal hernia surgery and can prog-
ress to infarction. This ischemic injury is likely
due to thrombosis of the venous plexus rather
than to iatrogenic arterial injury or inappropri-
ate closure of the inguinal canal [32]. Venous
outflow obstruction secondary to thrombosis of
the pampiniform plexus can also cause testicular
infarction as a result of overzealous dissection of
the cord or excessive use of diathermy; it may also
be the result of pressure from a large hematoma in
the groin [35].
Testicular torsion significantly reduces testicu-
lar vascular perfusion. Turner et al. reported that
in an experimental study, experimental torsion
significantly reduced testicular vascular perfusion.
Five minutes after torsion repair, the mean flow
values had returned to approximately 70% of the
pretorsion values. Testicular torsion significantly
reduced the venous plasma testosterone concen-
trations at both 3 and 30 days after torsion repair.
These authors suggest that reperfusion/oxidative
stress may play a role in Leydig cell dysfunction, as
well as acting directly in germ cell apoptosis [36].
7 1
Ischemic
orchitis
Testicular
atrophy ⊡ Fig. 1.1. Ischemic conditions and
their relationship to testicular per-
fusion and testicular atrophy
Testis perfusion can be maintained for a prolonged
period in the presence of testicular torsion. Ana-
tomical variability may account for differences in
the duration of viability of the torsed testis [37]. It
is clear that impairment of testicular perfusion can
lead to testicular damage (atrophy). Other causes
also exist, such as obstruction of the vas deferens,
inguinal hematoma, infections, and immunologi-
cal reactions [21, 38].
For about 25 years, the use of prosthetic ma-
terials for repairing inguinal hernias has been
routine in general surgery. An estimated 80%
of inguinal hernia operations involve placement
of a prosthetic mesh to form a »tension-free«
herniorrhaphy. The prosthetic mesh induces a
chronic foreign body fibroblastic response, creat-
ing scar tissue that imparts strength to the floor
and leads to fewer recurrences [38]. The use of
prosthetic materials for inguinal hernia markedly
reduces the recurrence rates, postoperative hospi-
tal stay, pain, and discomfort. But the prosthesis
frequently adheres to the cord structures in most
cases. The disadvantages include local wound
complications, technical difficulties in hernia re-
pair, restriction of mobility by the rigid shell
(⊡ Fig. 1.2), contraction of the mesh, and com-
plications related to the cord structures, such as
varicocele, hydrocele, ischemic orchitis, testicular
atrophy, and, finally, infertility [39].
In our study, we aimed to study the effects of
the TEP and LHR techniques on testicular circu-
lation [26]. We did not find any significant dif-
ferences between the techniques regarding blood
flow in the testes. Our previous report included
 8 Chapter 1 · Are There Adverse Effects of Herniorrhaphy Techniques on Testicular Perfusion?
⊡ Fig. 1.2. Prosthetic mesh induces
a chronic foreign body reaction
involving the surrounding tissue
and the spermatic cord structures,
which could impair testicular perfu-
sion and lead to testicular atrophy
the same population, and neither TEP nor LHR
affected testicular function; TEP did decrease tes-
ticular volume, but by normal limits [40].
The influence of the Lichtenstein and Shoul-
dice operations on the cord structures was inves-
tigated in a canine model. Similar to our results,
no significant differences with regard to testicu-
lar volume and blood flow were found between
the operation groups or between the preoperative
and postoperative results [41, 42]. Many clinical
studies have reported similar results in which the
choice of either the Lichtenstein or TEP hernia
repair technique did not significantly alter tes-
ticular function. Patients with inguinal hernia have
an elevated testicular vascular resistance, which is
reversed after repair. The choice of laparoscopic
or open herniorrhaphy did not affect reversal of
this surrogate of testicular function [13, 42, 43].
Laparoscopic inguinal hernia repair using suture
closure of the internal inguinal ring does not im-
pair testicular perfusion. Advantages of the laparo-
scopic approach also include its technical ease and
the fact that it is an outpatient procedure, the cord
structures remain untouched, the type of hernia is
obvious, and clear visualization of the anatomy can
be achieved [44].
However, some clinical and experimental
studies revealed a dense fibroblastic response en-
compassing the polypropylene mesh that either
[UnitedVRG] - Medical Release Group
trapped or obliterated the testicular vessels and
vas deferens [30, 38]. Peiper et al. [45] reported
that implantation of a nonabsorbable polypropyl-
ene mesh in the inguinal region during hernia
repair causes a chronic foreign body reaction in-
volving the surrounding tissue and the spermatic
cord structures in pigs. They observed that venous
thrombosis of the spermatic veins occurred in
five of 15 cases. The mesh repair may also lead to
decreases in arterial perfusion, testicular tempera-
ture, and the rate of regular spermatogenesis in
seminiferous tubules. Therefore, they recommend
strict indications for implanting a prosthetic mesh
during inguinal hernia repair [45].
Prosthetic meshes can contract by 20–75% of
their original size within a year after implanta-
tion in the inguinal region. Taylor et al. set out to
determine whether this contraction has any effect
on testicular or femoral vessel blood flow follow-
ing open or laparoscopic hernia repair. They found
that mesh contraction following inguinal hernio-
plasty does not adversely affect the testis or femo-
ral vessels and that mesh can be used safely for
both anterior and preperitoneal approaches [46].
With Doppler, the flow in the spermatic ar-
tery and testicular artery and its branches is of
low resistance, with a relatively broad systolic part
and holodiastolic flow. CDUS enables a defini-
tive diagnosis of ischemia and decreased testicular
Chapter 1 · Are There Adverse Effects of Herniorrhaphy Techniques on Testicular Perfusion?
circulation. A pitfall to remember in the diagnosis
is that hypervascularity can occur [47]. Testicu-
lar and epididymal swelling along with a slightly
decreased echogenicity have been reported to de-
velop in the first hours, although in most cases
the hypoechogenicity occurs later, so examining
the testis 3 months after the operation seems to be
more rational, as was done in our study [48, 49].
There are many clinical and experimental
study results concerning whether testicular perfu-
sion is adversely affected. We thought it would be
difficult to impair testicular perfusion after hernia
repair because of the rich arterial supply and col-
lateral capacity. Arterial input and venous drainage
of the testis are assured by many anastomoses that
protect it from ischemic injury [50–52]. Careful
dissection and preservation of the vessels are im-
portant to protect these anastomoses during her-
nia repair. The idea that deep ring repair that is too
tight may cause testicular ischemia is erroneous.
There are also many ways to protect testicular
perfusion. Surgeons should be trained to repair all
inguinal hernias at diagnosis, even if asymptomatic.
This treatment practice will decrease and prevent
complications such as incarceration and strangula-
tion; moreover, herniorrhaphy becomes more dif-
ficult the longer that repair is delayed [9, 11].
Trauma to spermatic cord structures should
be minimized and the incidence of testicular atro-
phy reduced by limiting dissection trauma to the
spermatic cord, by never dissecting beyond the
pubic tubercle, by leaving distal indirect hernia
sacs attached to the cord, and, as in recurrent her-
nias, by avoiding dissection of the spermatic cord
altogether by employing a posterior preperitoneal
approach [35]. Preserving the cremasteric muscle
fibers and reconstructing the fascia can protect the
structures of the spermatic cord from the inflam-
matory reaction [45].
Overzealous dissection of a distal hernia sac,
dislocation of the testis from the scrotum into the
wound, and concomitant scrotal surgery should be
avoided [50].
Patients considering polypropylene mesh
herniorrhaphy need to be carefully advised about
potential obstruction and compromise to future
fertility in men, especially those of young repro-
ductive age or with a solitary testicle [38].
9 1
Preperitoneal repairs should be considered for
repairs of recurrent hernias, not only to reduce
further recurrences but also to avoid testicular
complications [53].
Using an intraperitoneal composite mesh onlay
and assuring safe fixation with fibrin glue could be
an alternative when treating recurrent and compli-
cated inguinal hernias [54].
In conclusion, neither TEP nor LHR affected
testicular circulation in our study [26]. The total
number of patients in our study was a limitation.
It is clear that fine surgical dissection and recon-
struction with respect for anatomy and the use of
proper prosthetic material could lead to the best
results. To be consistent, future animal and clinical
studies must be performed in large groups and fo-
cus on the use of mesh, which may increase the in-
tensity of the mesh reaction to the cord structures.
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46. Taylor SG, Hair A, Baxter GM, O’Dwyer PJ (2001). Does con-
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testicular or femoral vessel blood flow? Hernia 5(1):13–15
47. Leung WYM, Poon M, Fan TW, et al. (1999): Testicular vol-
ume of boys after inguinal herniotomy: combined clinical
and radiological follow-up. Pediatr Surg Int 15: 40–41
48. Oyen RH (2002). Scrotal ultrasound. In: Baert AL (ed) Syl-
labus ultrasound. Springer, Berlin, pp 280–295
49. Hostman WG (1997). Scrotal imaging. Uroradiology
24:653-671
50. Reid I, Devlin HB (1994). Testicular atrophy as a conse-
quence of inguinal hernia repair. Br J Surg 81:91–93
51. Fong Y, Wantz GE (1992). Prevention of ischemic orchi-
tis during inguinal hernioplasty: experience with 6454
hernioplasties in male patients. Surg Gynecol Obstet
174:399–402
52. Koontz AR (1965). Atrophy of the testicle as a surgical risk.
Surg Gynecol Obstet 120:511–513
53. Wantz GE (1993). Testicular atrophy and chronic residual
neuralgia as risks of inguinal hernioplasty. Surg Clin North
Am 73(3):571–581
54. Olmi S, Scaini A, Erba L, Bertolini A, Croce E (2007). Lap-
aroscopic repair of inguinal hernias using an intraperi-
toneal onlay mesh technique and a Parietex composite
mesh fixed with fibrin glue (Tissucol). Personal technique
and preliminary results. Surg Endosc 21(11):1961–1964

Discussion

Fitzgibbons: Your technique with color Doppler

is very good, investigating the circulation of the
testis. How good is it for testing the venous?
Dilek: I don’t have additional information about
that because this part of the study was done by the
radiologist.
Smeds: At first, do you have an idea if there is a
change of the testicular temperature, and second,
do you know if there is a connection between de-
crease of temperature and sperm production?
Dilek: That was not our topic, so I can’t give you
more information about that.
Schumpelick: How can we decide about testicular
function that may be influenced by this method if
we don’t analyze the function? I mean, tempera-
ture is not a function.
[UnitedVRG] - Medical Release Group
 2

The Effects of Mesh Bioprosthesis

on the Spermatic Cord Structures
in a Rat Model
A. Montgomery and F. Berndsen
 14 Chapter 2 · The Effects of Mesh Bioprosthesis on the Spermatic Cord Structures in a Rat Model
Introduction
According to the Swedish Hernia Register [1],
2 an estimated 80% of inguinal hernia operations
involve placement of a polypropylene mesh, with
a majority performed as a Lichtenstein procedure.
The Lichtenstein technique is regarded as the gold
standard in Sweden; this is probably in accordance
with most other countries.
A prosthetic mesh induces a chronic foreign
body reaction with fibroblastic ingrowth into the
mesh and subsequent scar plate formation. This
is believed to reinforce the abdominal wall and
thereby decrease the risk of recurrence by 50–70%
[2]. The foreign body reaction leads to chronic
inflammation, which can cause retraction of the
mesh area and shrinkage of the scar plate. As a
result, tension can be put to the anchoring points
of the mesh, which might cause chronic pain.
Patients might also have individual reactions to
meshes with different properties. These might be
some of the factors causing chronic pain in up to
15–30% of patients operated on for inguinal her-
nias in whom mesh is used [3, 4].
It has been suggested that the foreign body
reaction is proportionate to the weight and struc-
ture of the mesh and that commonly used meshes
contain too much material, producing an exag-
gerated response [5, 6]. To minimize these effects,
composite meshes have been introduced that con-
tain one absorbable and one nonabsorbable part.
By the use of composite meshes, the reinforcement
and manageability properties desired at operation
and in the early phase can thereby be satisfied
together with a reduction in the total amount of
mesh left permanently in the patient.
Problems other than chronic pain that might
be associated with chronic inflammation caused
by mesh include sexual dysfunction and infertility.
These problems are not well understood. Infertil-
ity can be related to the handling of the spermatic
cord during inguinal herniorrhaphy. Injury to the
vas as well as the spermatic vessels can result in in-
fertility. Ischemic injury to the testicle that eventu-
ally leads to atrophy is reported to occur in about
0.5% of patients having primary hernia repair and
5% with recurrent hernia repairs [7, 8]. Another
potential mechanism for infertility is a foreign
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body reaction resulting from the use of mesh that
comes into contact with the spermatic cord.
Bilateral hernia surgery in children is a known
risk factor for infertility [9]. In men investigated
for infertility, 6.4% are reported to have had an iat-
rogenic injury to the vas after hernia surgery [10].
To try to minimize some of the inflammatory
effects, a composite mesh has been introduced that
contains 61% absorbable (polyglactin) and 39%
nonabsorbable material (polypropylene; Vypro II).
The total weight of polypropylene is 32 g/m2. The
aim of this study was to compare a heavyweight
polypropylene mesh with a lightweight composite
mesh to note the effect on spermatic cord struc-
tures and testosterone production in an experi-
mental setting.
Materials and Methods
Thirty male Sprague Dawley rats were randomly
divided into three groups. A 3-cm long incision
was made in the groin, and the spermatic cord was
exposed and dissected free. The cremaster muscle
was split but not divided.
In group I, a suture repair was performed us-
ing 5.0 polypropylene sutures (Prolene, Ethicon,
Somerville, NJ, USA) in the transversalis fascia,
imitating open suture repair.
In group II, a 2×3.5-cm heavyweight polypro-
pylene mesh (Prolene, Ethicon, Somerville, NJ,
USA) was placed, imitating the Lichtenstein repair.
A slit was made in the mesh for the spermatic
cord. The mesh was fixed with 5.0 Prolene sutures,
and the tails were approximated with one suture.
In group III, a large-pore lightweight poly-
propylene/polyglactin composite mesh, Vypro II
(Ethicon, Norderstedt, Germany), was placed as
in group II.
After 90 days, vasography was performed, and
blood samples were taken from the venous plexus
of the spermatic cord on both sides. Analysis of s-
testosterone from the spermatic veins was carried
out using competitive radioimmunoassay. Testicles
from both sides were weighed. The inguinal areas
on both sides were dissected en bloc, including
the spermatic cord, the mesh, and the underlying
abdominal wall. Light microscopy was performed
Chapter 2 · The Effects of Mesh Bioprosthesis on the Spermatic Cord Structures in a Rat Model
for a cross-section of specimen obtained from
the middle of the 3-cm long sample stained with
hematoxylin–eosin and van Gieson’s stain. Inflam-
mation and fibrosis were graded separately using
a scale from 0 to 3. The sections of the spermatic
cord were captured using a camera, and the images
were reduced in pixels to obtain a cross-sectional
area of the vas deferens from both sides.
Continuous and nonparametric data were cal-
culated as the median (interquartile range) and
compared using the Mann–Whitney U-test. For
comparing operated and control sides, the Wil-
coxon signed-rank test was used.
Results
All rats survived the 90-day study period with no
wound complications. Vasography revealed patent
15 2
vas deferens in all animals on both sides (⊡ Fig. 2.1).
There was no significant difference in testicular
weight between the groups or between sides. There
was no difference in s-testosterone values between
the operated and the control sides in group I or II.
However, in group III, s-testosterone values were
significantly lower in the operated compared with
the control side (⊡ Table. 2.1). There was no signifi-
cant difference in vas deferens cross-sectional area
between the operated and the control side in group
I or II, but a difference was seen in group III.
Group I (Suture Repair) vs. Groups II
and III (Mesh Repairs)
There was no difference in s-testosterone from
the spermatic vein between the operated sides
or between the control sides between the groups
(⊡ Table. 2.2). The median grade of inflammation
and fibrosis was significant lower in the suture
repair group compared with the mesh groups. The
inflammation in group I was concentrated around
the sutures; no inflammation was seen in sections
not including sutures. There was no difference
in the cross-sectional area of the vas deferens be-
tween the groups.

Group II (Prolene Mesh) vs. Group III

(Vypro II Mesh)

There was no difference in s-testosterone from the

spermatic vein between the operated and the con-
⊡ Fig. 2.1. Vasography showing patent vas deferens trol side between the groups (⊡ Table. 2.3). There

⊡ Table 2.1. Testicular weight, s-testosterone, and vas deferens diameter: operated vs. control side (medians are presented)

Group I: suture repair Group II: Prolene mesh Group III: Vypro II mesh

Operated Control p Operated Control p Operated Control p

side side side side side side

s-testosterone 127 179 0.176 202 260 0.214 83 127 0.008

(nmol/l)

Vas deferens 157 183 0.753 109 173 0.260 158 187 0.022
cross-sectional
area (pixels)
 16 Chapter 2 · The Effects of Mesh Bioprosthesis on the Spermatic Cord Structures in a Rat Model

⊡ Table 2.2. Group I (suture repair) vs. groups II and III (mesh repairs); medians are presented

Group I: suture repair Groups II and III: mesh repairs p

2 Testosterone (nmol/l):
Operated side 127 176 0.849
Control side 179 174 0.935

Inflammation: grade 0–3 1.0 (0–1.3) 2.0 (2.0–2.0) 0.001

Fibrosis: grade 0–3 1.0 (0.8–2.0) 2.0 (1.0–2.5) 0.046

Vas deferens cross-sectional area:

Operated side 157 152 0.400
Control side 183 176 0.809

⊡ Table 2.3. Group II (Prolene mesh) vs. group III (Vypro II mesh); medians are presented

Group II: Prolene mesh Group III: Vypro II mesh p

Testosterone (nmol/l):
Operated side 202 83 0.052
Control side 260 127 0.123

Inflammation: grade 0–3 2.0 (1.5–2.0) 2.0 (2.0–2.0) 0.481

Fibrosis: grade 0–3 2.0 (1.8–2.0) 2.0 (1.0–3.0) 0.696

Vas deferens cross-sectional area:

Operated side 109 173 0.143
Control side 173 187 0.243

was no difference in the grade of inflammation or groups. No statistical difference in inflammation

fibrosis between the groups. In both groups the in-
flammation was chronic, with histiocytes concen-
trated around the mesh material. Giant cells were,
however, more prominent in group III (Vypro II),
and remaining polyglactin fibres were observed.
There was no difference in the cross-sectional area
of the vas deferens between the groups.
or fibrosis was seen between heavyweight polypro-
pylene mesh and the low-weight composite mesh.
Remaining polyglactin was observed in the low-
weight composite mesh group after 90 days.
Discussion

Polypropylene meshes have been used in hernia

Conclusion
Vasography revealed a patent vas in all animals.
The only effects on the cord structures in a rat
model were impaired s-testosterone production
and a reduced cross-sectional area of the vas after
the use of a low-weight composite mesh compared
with the control side. This was not demonstrated
in the suture repair or heavy polypropylene mesh
surgery for decades, but their use has increased
dramatically the last 10 years. A Cochrane meta-
analysis comparing open mesh repairs and con-
ventional repairs revealed a decreased risk of re-
currence by 50–75% if mesh were used [2]. The
connection between childhood vas injury in in-
guinal hernia repair has been documented [9].
In adult inguinal hernia surgery, this connection
has not been thoroughly studied. This might be of

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Chapter 2 · The Effects of Mesh Bioprosthesis on the Spermatic Cord Structures in a Rat Model
clinical importance because almost 30% of the pa-
tients are operated on for bilateral hernias. There
could be an injury to the duct structures by dis-
section, but theoretically, a foreign body reaction
around the mesh could also affect the spermatic
cord structures because the mesh lies in contact
with the spermatic cord.
Interest in the latter situation has increased
over the last years, and experimental studies
have now been performed on dogs, pigs, rabbits,
and rats. Uzzo et al. were the first to compare
heavyweight polypropylene mesh to conventional
(Shouldice) repair in dogs [11]. In their study,
all vasograms demonstrated patency, and sperm
morphology and motility did not differ between
the groups or between the operated and control
sides. The patency of the vas was also confirmed in
our study. However, Uzzo et al. found morphologic
changes of the testis in three out of six animals in
the mesh group. No evidence of testicular impair-
ment was seen. They also found a decrease in the
cross-sectional diameter of the vas deferens on
the operated side compared with the control side
in both the suture repair and mesh groups. We
reported a cross-sectional reduction only in the
Vypro II group and not in the Prolene or the suture
repair group.
In a later report by Taneli et al., a polypropyl-
ene mesh was compared to a sham-operated group
in rats [12]. It was concluded that mesh implanta-
tion has no effect on testicular hormonal function
and only a limited effect on nitric oxide levels,
which was not sufficient to cause testicular apop-
tosis that could lead to infertility.
Maciel et al. reported on a study in rats in
which bilateral vas deferens dissection was per-
formed and a polypropylene mesh placed on one
side [13]. There were no testicular changes, but
changes in the vas that caused functional obstruc-
tion with dilatation and spermatozoid repression
were seen.
Two experimental studies from the Aachen
group concern findings in pigs and rabbits. The
first study consisted of two series, one on pigs and
one on rabbits [14]. Preperitoneal Shouldice and
Lichtenstein repair were performed, and a poly-
propylene mesh was used preperitoneally and in a
Lichtenstein repair. The mesh repairs resulted in a
17 2
decrease of arterial perfusion, testicular tempera-
ture, and spermatogenesis. The conclusion was
that a strict indication for implantation of a pros-
thetic mesh during hernia repair is recommended.
In the second study, low-weight and heavyweight
polypropylene mesh were compared in rabbits
[15]. Vasography revealed relevant obstructions
located at the mesh margins in 50% of the heavy-
weight and 22% in the lightweight mesh groups
after 6 months. This is in contrast to our results, in
which all vasograms were normal at 3 months.
In another study on rats, Kolbe and Lechner
wrapped heavyweight versus low-weight polypro-
pylene mesh around the vas [16]. Fertility was
tested and was found to be slightly restricted
4 weeks after surgery in both groups. Some rats
in the heavyweight mesh group revealed sperm
granulomas due to lesions to the spermatic cord.
The conclusion was, however, that neither type of
hernioplastic implant indicates a negative influ-
ence on male fertility.
In a prospective study of 73 patients oper-
ated on with the plug-and-patch technique, Zieren
et al. measured testicular perfusion and testicu-
lar volume preoperatively and at 3 and 6 months
postoperatively [17]. No differences between the
contralateral side and operated side were seen at
follow-up.
In the present report, the study period of
90 days was chosen for two reasons. First, the man-
ufacturer claims that the polyglactin part of the
Vypro II mesh is totally absorbed in 56–70 days,
thus not participating in the inflammation/fibrosis
reaction at 90 days. Second, the 90-day period has
previously been used and accepted in studies of
foreign body reactions [6, 18, 19]. Surprisingly,
though, we found remaining polyglactin fibres in
the Vypro II specimens after 90 days. This might
explain the impaired testosterone production and
smaller cross-sectional area of the vas deferens in
the Vypro II group compared with the control side.
There was, however, no difference in inflammation
or fibrosis between the two mesh groups.
It is well known that polypropylene mesh in-
duces a foreign body reaction, with chronic inflam-
mation existing even years after implantation [20],
but despite millions of mesh implants, only a few
reports describe serious adverse effects. Klosterh-
 18 Chapter 2 · The Effects of Mesh Bioprosthesis on the Spermatic Cord Structures in a Rat Model
alfen et al. studied the connection between mesh
weight and foreign body reaction, and according
to their studies, the level of inflammatory response
2 depends on the weight and texture of the mesh
material [20]. The large-pore, lightweight mesh
(Vypro II), which has only 30% polypropylene
compared with standard meshes, has been sug-
gested as leading to less foreign body reaction [21].
Our study did not confirm these findings.
It must be stated that animal studies have their
limitations, and the results cannot be directly trans-
ferred to humans. This type of study, though, is not
possible to do in human patients. The overall effect
of meshes in reducing the frequency of recurrence,
and thereby reducing the frequency of a second,
more complicated hernia operation in which the
spermatic cord could be in danger by dissection,
might well exceed the potential negative effect of
the mesh per se.
References
1. The Swedish Hernia Register (Nationellt kvalitetsregister
för bråckkirurgi). http://www.svensktbrackregister.se/.2
2. The EU Hernia Trialist Collaboration (2002) Open mesh
versus non-mesh repair of groin hernia meta-analysis of
randomized trials based on individual patient data. Her-
nia 6: 130–136
3. Berndsen FH, Petersson U, Arvidsson D, Leijonmarck C-E,
Rudberg C, Smedberg S, Montgomery A (2007) Discom-
fort five years after laparoscopic and Shouldice inguinal
hernia repair: a randomised trial with 867 patients. A
report from the SMIL study group. Hernia 11(4):307–313
4. Fränneby U, Sandblom G, Nordin P, Nyrén O, Gunnarsson
U (2006) Risk factors for long-term pain after hernia sur-
gery. Ann Surg 244(2):212–219
5. Vrijland WW, van der Tol MP, Luijendijk RW, Hop WCJ,
Busschbach JJV, de Lange DCD, van Geldere D, Rottier
AB, Vegt PA, Ijzermans JNM, Jeekel J (2002) Randomized
clinical trial of non-mesh versus mesh repair of primary
inguinal hernia. Br J Surg 89:293–297
6. Klosterhalfen B, Klinge U, Schumpelick V(1998) Functional
and morphological evaluation of different polypropyl-
ene-mesh modifications for abdominal wall repair. Bio-
materials 19:2235–2246
7. Wantz GE (1993) Testicular atrophy and chronic residual
neuraligia as risk of inguinal hernioplasty. Surg Clin North
Am 73:571–581
8. Fitzgibbons RJ (2005) Can we be sure polypropylene
mesh causes infertility? Ann Surg 241(4):559–561
9. Matsuda T, Horii Y, Yoshida O (1992) Unilateral obstruc-
tion of the vas deferens caused by childhood inguinal
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herniorrhaphy in male infertility patients. Fertil Steril
58:609–613
10. Sheynkin YR, Hendin BN, Schlegel PN, Goldstein M (1999)
Microsurgical repair of iatrogenic injury to the vas defer-
ens. J Urol 159:139–141
11. Uzzo RG, Lemack GE, Morrissey KP, Godstein M (1999 )
The effects of mesh bioprosthesis on the spermatic cord
structures: a preliminary report in a canine model. J Urol
161:1344–1349
12. Taneli F, Aydede H, Vatansever S, Ulman C, Ari Z, Uyanik
BS (2005) The long-term effect of mesh bioprosthesis
in inguinal hernia repair on testicular nitric oxide me-
tabolism and apoptosis in rat testis. Cell Biochem Funct
23(3):213–220
13. Maciel LC, Glina S, Palma PC, Nascimento LF, Netto NR Jr
(2007) Histopathological alterations of the vas deferens in
rat exposed to polypropylene mesh. BJU Int 100(1):187–
190
14. Peiper C, Junge K, Klinge U, Strehlau E, Ottinger A,
Schumpelick V (2006) Is there a risk of infertility after
inguinal mesh repair? Experimental studies in the pig and
the rabbit. Hernia 10(1):7–12
15. Junge K, Binnebösel M, Rosch R, Ottinger A, Stumpf M,
Muhlenburch G, Schumpelick V, Klinge U (2008) Influence
of mesh materials on the integrity of the vas deferens fol-
lowing Lichtenstein hernioplasty: an experimental model.
Hernia 12(6):621–626
16. Kolbe T, Lechner W (2007) Influence of hernioplastic im-
plants on male fertility in rats. J Biomed Master Res B
Appl Biomater 81(2):435–440
17. Zieren J, Beyersdorff D, Beier KM, Müller JM (2001) Sexual
function and testicular perfusion after inguinal hernia
repair with mesh. Am J Surg 181:204–206
18. Baykal A, Onat D, Rasa K, Renda N, Sayek I (1997) Ef-
fects of polyglycolic acid and polypropylene meshes on
postoperative adhesion formation in mice. World J Surg
21:579–583
19. Bellón JM, Contreras LA, Buján J, Palomares D, Carrera-
San Martin A (1998) Tissue response to polypropylene
meshes used in the repair of abdominal wall defects.
Biomaterials 19:669–675
20. Klosterhalfen B, Klinge U, Hermanns B, Schumpelick V
(2000) Pathology of traditional surgical nets for hernia
repair after long-term implantation in humans. Chirurg
71:43–51 [German with English abstract]
21. Junge K, Klinge U, Rosch R, Klosterhalfen B, Scumpelick
V (2002) Functional and morphologic properties of a
modified mesh for inguinal hernia repair. World J Surg
26:1472–1480
Discussion
Kukleta: Do you think that Vypro II is a good rep-
resentative for a lightweight mesh? The Vypro II
has a bigger inflammatory impact than any other
lightweight mesh, doesn’t it?
Chapter 2 · The Effects of Mesh Bioprosthesis on the Spermatic Cord Structures in a Rat Model
19 2
Montgomery: Of course. Indeed, this study was
performed in 2003 and published in 2004, and the
available meshes at that time were scientifically the
most interesting ones.
Köckerling: In our various studies with partially
resorbable meshes, we always found after the time
given by the company some remaining resorb-
able material in the animals with a high grade
of inflammatory reaction around it. We should
learn from this to take longer observation periods
because the absorption process obviously takes
longer than given by the company.
Montgomery: That’s why we chose a 90-day inter-
val in our study, but it wasn’t enough.
Conze: I just want to make a remark on the animal
models used in this context. The diameter of the
spermatic cord of small animals differs from hu-
man ones, and therefore, the ratio of the diameter
of mesh fibers and spermatic cord differs. So the
effect of the fibrotic reaction on a very tiny rat vas
is much stronger than it might be on a human vas.
[UnitedVRG] - Medical Release Group
 3

Damage to the Spermatic Cord

by the Lichtenstein Procedure
in a Pig Model–Preliminary Results
K. Junge, M. Binnebösel, C. Kauffmann, R. Rosch, J. Otto, D. Kämmer, F. Schoth,
G. Mühlenbruch, U. Klinge, V. Schumpelick
 22 Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure in a Pig Model–Preliminary Results

Introduction Material and Methods

An estimated 75–80% of inguinal hernia opera- Mesh Materials

tions involve placing a mesh prosthesis, either
laparoscopically or using an open technique, to Two different mesh materials were investigated:
patch the defect in the floor of the inguinal a large porous and elastic mesh made of PVDF
3 canal. Foreign body reactions, with fibroblastic monofilaments and Marlex, a small-pore, stiff
ingrowth and chronic inflammation, are believed mesh made of polypropylene (PP) monofilaments
to reinforce the abdominal wall and decrease (⊡ Fig. 3.1).
the risk of recurrence. It has been proven that
this foreign body reaction is proportionate to
the weight, structure, and polymer of the mesh Animals
and that commonly used meshes contain too
much material, producing an exaggerated for- Six male uncastrated male pigs were housed un-
eign body reaction/tissue response and leading der conditions of constant light and temperature
to clinical complications [1–3]. To minimize the and received a complete diet of feed and water ad
foreign body reaction and clinical complications, libitum throughout the entire study, which was
new types of mesh materials have been intro- performed according to the National Institutes of
duced that have a decreased amount of material
and larger pores, resulting in a nearby physi-
ologic tissue ingrowth [2, 4, 5]. Further improve-
ment of biocompatibility has been achieved using
polyvinylidene fluoride (PVDF) as the polymer
[3]. PVDF is a polymer with improved textile
and biological properties [6]. Compared with
polyester, PVDF is more resistant to hydroly-
sis and degradation. Furthermore, ageing does
not increase the stiffness that is evidently seen
in polypropylene. Although it has been used
in vascular surgery for some years, there have
been limited types of surgical meshes until now.
a
Whereas these so-called lightweight, large-pore,
and elastic mesh materials are known to show
a favourable outcome considering postoperative
pain [7–10] compared with conventional heavy-
weight, small-pore, and stiff mesh materials, just
a few experimental studies have focused on the
influence of different mesh materials on the in-
tegrity of the vas deferens. With the widespread
acceptance and ease of placement, mesh repair
is being increasingly offered to young patients
whose fertility status may well be an issue in
the future.
To further elucidate the impact of different
b
mesh materials following Lichtenstein hernia re-
pair, an animal study in the pig was conducted to ⊡ Fig. 3.1. a A large-pore, elastic mesh made of polyvinylide-
investigate the long-term effect on integrity of the ne fluoride monofilaments. b A small-pore, stiff mesh made of
vas deferens and testicular function. polypropylene monofilaments

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Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure
Health guidelines for the use of laboratory ani-
mals. All animals received bilateral Lichtenstein
hernia repair (n=12).
Surgical Procedure
Operations were carried out under general an-
aesthesia. Following premedication using 4 mg/
kg azaperone, 44 μg/kg atropine, and 15 mg/kg
ketamine intramuscularly, an intravenous catheter
was placed into an ear vein. Anaesthesia was in-
duced by injection of 10–15 mg pentobarbital. An-
aesthesia was continued by isoflurane/oxygen as
well as continuous infusion of fentanyl (45–90 μg/
kg/h). Following anaesthesia, the skin was shaved
and disinfected with a povidone–iodine solution.
An inguinal incision was performed and the
external oblique fascia dissected. Following explo-
ration of the inguinal canal, a Lichtenstein proce-
dure was carried out using a 7×10-cm slitted mesh
sample (PVDF mesh on one side, PP mesh on the
contralateral side). Mesh samples were fixed at the
inguinal ligament and the mesh slit was closed us-
ing 4/0 Prolene sutures. Afterwards, the external
oblique fascia and skin were closed.
No antibiotic treatment was given before or
during the experiments. Throughout the whole
observation period, all animals were objectively
controlled and underwent daily clinical investiga-
tion to assess local and systemic complications. Six
⊡ Fig. 3.2. Explanted inguinal area including testis with injec-
ted x-ray solution
23 3
months after mesh implantation, all animals (n=6)
underwent thermographic investigation of the in-
guinal region and the testes. Thermographic mea-
surements were performed as a parameter of local
perfusion using a VarioCAM basic camera (In-
fraTec, Dresden, Germany). Following measure-
ment of testicular size by ultrasound, the animals
were sacrificed for morphologic observations. The
abdomen was opened for complete exploration.
The intraabdominal part of the vas deferens was
dissected 2 cm before entering the inguinal canal
at both sides, and 10 ml of x-ray solution was
injected for vasography (13.3 g gelatin, 16.6 g
Bleimennige =Pb2PbO4, 100 ml water). Following
ligation of the vas deferens, the whole inguinal
canal–including the mesh sample as well as the
testis–was resected and fixed in 10% formaldehyde
(⊡ Fig. 3.2).
Assessment of Integrity of the
Vas Deferens
Integrity of the vas deferens was assessed semi-
quantitatively using x-ray vasography. Obstruc-
tions of the vas deferens were classified as minor
(0–25% reduction in lumen diameter), medium
(25–75% reduction), or major (>75% reduction)
and were examined at the margins of the mesh
samples as well as within the mesh area.
Histological Analysis
Tissue specimens were embedded in paraffin. His-
tological investigation was performed on 3-μm
sections after haematoxylin and eosin staining. All
sections were processed at the same time to reduce
internal staining variations. Spermatogenesis as
the main testicular function was estimated histo-
logically using the Johnsen score (⊡ Table 3.1) [11].
Immunohistochemistry was done according to the
manufacturer’s instructions. For detection of pro-
liferating cells (Ki67), we used mouse monoclonal
antibody MIB-1, 1:10, from Dako (Glostrup, Den-
mark) and rabbit antimouse antibody 1:300 from
Dako (Glostrup, Denmark) as secondary antibody.
TUNEL histochemistry for the detection of apop-
 24 Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure in a Pig Model–Preliminary Results
⊡ Table 3.1. Johnsen score [11]
10 Complete spermatogenesis with many sperma-
tozoa
9 Many spermatozoa present but germinal epi-
thelium
3 found in testis temperature (PVDF 29.0±1.1°C; PP
8 Only few spermatozoa (<5–10) present in section
7 No spermatozoa but many spermatids present
6 No spermatozoa and only few spermatids
(<5–10) present
5 No spermatozoa, no spermatids but several or
many spermatocytes present
4 Only few spermatocytes (<5) and no spermatids
or spermatozoa present
3 Spermatogonia are the only germ cells present
2 No germ cells but Sertoli cells are present
1 No cells in tubular section
totic cells was performed by an in situ apopto-
sis detection kit (Apoptag, Oncor, cat. no. S7100,
Germany). Sections were examined by standard
light microscopy (Olympus BX51, Hamburg, Ger-
many). For each sample, five regions within the
interface (×400; area 100×100 μm) were captured
by a digital camera (Olympus C-3030, Hamburg,
Germany). The expression of immunohistochemi-
cal parameters was classified by two independent,
blinded observers. The extent of staining was grad-
uated as a percentage of positive-stained cells in
the specimen (0–100%).
Results
Macroscopic Observation
The surgical procedure was well tolerated by all
animals, and the postoperative period was un-
eventful. None of the animals developed signs of
ischaemic orchitis or testicular atrophy. No dif-
ferences were seen in testicular volume between
the PP (18.9±2.2 cm3) and the PVDF mesh groups
(18.1±4.0 cm3).
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Thermography
Investigating the mean inguinal temperature at the
initial incision, no differences were found compar-
ing the PVDF mesh (34.9±0.9°C) with the PP mesh
(34.7±0.9°C). Furthermore, no difference was
29.1±1.1°C; see ⊡ Figs. 3.3 and 3.4).
Integrity of the Vas Deferens
Following explantation, x-ray vasography showed
analysable results for all mesh implantations. Over-
all, relevant obstructions (>75% of lumen diameter;
⊡ Fig. 3.5) were located only at the mesh margins.
Whereas four PVDF explants showed no or minor
obstructions, one out of six PVDF explants had an
obstruction 25–75% of the lumen diameter. The PP
mesh group explants were found to have signifi-
cant obstructions of more than 75% of the lumen
diameter in two specimens, as well as obstructions
of 25–75% of the lumen diameter in another two.
Histologically, no direct infiltration of the mesh fi-
bres into the vas deferens was found. Obstructions
were more or less due to compression of the wall
of the vas deferens, inducing an inflammatory and
fibroblastic reaction in the wall of the vas.
Histological Analysis
Testicular function was estimated histologically.
Each testicular sample of 10 seminiferous tubules
was classified according to the Johnson score. Fol-
lowing PP mesh implantation, a mean Johnson
score of 8.5±0.1 was estimated, which was not sig-
nificantly different from that for the PVDF mesh
samples (8.5±0.3, ⊡ Fig. 3.6).
Analysing three out of six mesh explants, each
group microscopic investigation of the mesh–host-
tissue interface showed typical formation of for-
eign body granulomas. Investigating the percent-
age of apoptotic (TUNEL) and proliferating (Ki67)
cells, no significant differences were found be-
tween the PP (TUNEL 12.7±8.0%; Ki67 7.4±1.8%)
and the PVDF mesh samples (TUNEL 3.4±3.3%;
Ki67 6.0±2.5%; ⊡ Fig. 3.7).
Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure
25 3

⊡ Fig. 3.3. Example of temperature measurement using ther- ⊡ Fig. 3.5. Vasography following mesh implantation; note ob-
mography camera struction of the vas deferens at the margin following polypro-
pylene mesh implantation

⊡ Fig. 3.4. Temperatures

(mean ± standard deviation)
measured using the thermogra-
phy system (PP polypropylene,
PVDF polyvinylidene fluoride)

⊡ Fig. 3.6. Johnsen score, show-

ing mean ± standard deviation
(PP polypropylene, PVDF polyvi-
nylidene fluoride)
 26 Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure in a Pig Model–Preliminary Results
⊡ Fig. 3.7. Percentage
3 (mean ± standard deviation) of
(a) proliferating and (b) apo-
ptotic cells at the interface of
mesh and the host tissue (PVDF
polyvinylidene fluoride, PP po-
lypropylene)
Discussion
Obstructive azoospermia is a rare but serious
complication following inguinal hernia repair. Al-
though an incidence of iatrogenic perioperative
injury to the vas deferens during inguinal hernia
repair of 0.3% in adults and 0.8–2.0% in child-
hood has been described [12], little is known about
the long-term effects of different mesh prosthe-
ses on the integrity of the vas deferens. Because
almost 30% of the patients are operated on for
bilateral hernias, and because mesh repair is be-
ing increasingly offered to young patients whose
fertility status may well be an issue in the future,
this item is of major clinical importance. Aside
from case reports, just one larger clinical series
has been reported. Shin et al. investigated 14 cases
of azoospermia secondary to inguinal vasal ob-
struction related to previous mesh herniorrhaphy
[13]. Following open or laparoscopic hernia mesh
repair, they reported on nine patients with bilateral
obstruction as well as five patients with unilateral
obstruction. Surgical exploration revealed a dense
fibroblastic response encompassing the polypro-
pylene mesh, with either a trapped or obliterated
vas in all patients.
The first experimental study investigating this
matter was performed by Uzzo et al., comparing
six dogs operated with a polypropylene mesh to six
dogs operated with conventional (Shouldice) repair
[14]. They found a decrease in the cross-sectional
diameter of the vas deferens on the operated side
compared with the control side in both the suture
repair and the mesh groups. Furthermore, mor-
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phologic changes of the testis were found in three
of six animals in the mesh group. Goldenberg et
al. investigated 18 dogs with a follow-up of 60 days
and found a chronic inflammatory reaction in
100% on the mesh side, a reduction in spermato-
genesis, and a reduction in lumen diameter of the
vas deferens on the mesh side [15].
However, studies comparing the effect of dif-
ferent mesh prostheses are rather limited. Peiper et
al. investigated spermatic cord perfusion and sper-
matogenesis in rabbits, comparing Lichtenstein
hernia repair using UltraPro (a lightweight, large-
pore, and elastic mesh) and Marlex (a heavyweight,
small-pore, and stiff mesh of polypropylene) with
the Shouldice repair [16]. They found a more ob-
vious decrease in spermatic cord perfusion after
Marlex mesh repair than after Shouldice repair. In
contrast, in our study the analysed temperature (as
a parameter of perfusion) showed no differences
between the mesh samples in the inguinal region
or in the testis. In evaluating spermatogenesis,
Peiper’s group noted a decrease in Johnsen score in
the seminiferous tubules after Lichtenstein repair
independent of the kind of mesh. In our study, a
mean Johnsen score of 8.5±0.1 was estimated fol-
lowing PP mesh implantation, which was not sig-
nificantly different from the group of PVDF mesh
samples (8.5±0.3). No control group had been
analysed until now.
Berndsen et al. compared a low-weight com-
posite mesh (Vypro II) and a heavyweight mesh
(Prolene) used for Lichtenstein repair in rats [17].
Ninety days after implantation, a median cross-
sectional area of the vas deferens was 109 pixels
Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure
for the Prolene and 158 pixels for the Vypro II side,
with no significant difference.
In our study, obstructions were analysed semi-
quantitatively using vasography. Investigations re-
vealed obstructions that were mainly located at the
mesh margins. The stiff PP mesh group showed
an overall higher amount and degree of stenosis
compared with the smooth PVDF mesh. Next to
a significantly reduced inflammatory foreign body
reaction of the PVDF (TUNEL 3.4±3.3%; Ki67
6.0±2.5%) compared with the PP mesh (TUNEL
12.7±8.0%; Ki67 7.4±1.8%), the lower number of
obstructions was probably due to the elastic textile
properties of the PVDF mesh. In contrast to the
study by Shin et al., we could find no direct in-
filtration of the mesh fibres into the vas deferens.
Obstructions were mainly due to compression of
the wall at the mesh side, with an induced inflam-
matory and fibrotic reaction in the wall of the vas
deferens.
To summarize, great effort has been put into
the challenge of creating a mesh material that
optimises patients’ outcomes. The introduction
of improved mesh materials has led to superior
outcomes with regard to postoperative pain and
foreign body sensation. However, the influence of
different mesh materials on spermatic cord struc-
tures has not been studied thoroughly. For the first
time, the construction of a large-pore and elastic
monofilamentous PVDF mesh showed a benefi-
cial effect on the integrity of the vas deferens in
an experimental setting. However, no differences
were observed in testicular function (temperature,
volume, spermatogenesis).
References
1. Klosterhalfen B, Klinge U, Schumpelick V. Functional and
morphological evaluation of different polypropylene-
mesh modifications for abdominal wall repair. Biomateri-
als 1998; 19(24):2235–2246
2. Junge K, Klinge U, Rosch R, Klosterhalfen B, Schumpelick
V. Functional and morphologic properties of a modi-
fied mesh for inguinal hernia repair. World J Surg 2002;
26(12):1472–1480
3. Klinge U, Klosterhalfen B, Ottinger AP, Junge K,
Schumpelick V. PVDF as a new polymer for the con-
struction of surgical meshes. Biomaterials 2002; 23(16):
3487–3493
27 3
4. Junge K, Klinge U, Prescher A, Giboni P, Niewiera M,
Schumpelick V. Elasticity of the anterior abdominal wall
and impact for reparation of incisional hernias using
mesh implants. Hernia 2001; 5(3):113–118
5. Klinge U, Klosterhalfen B, Conze J, Limberg W, Obolenski
B, Ottinger AP et al. Modified mesh for hernia repair that
is adapted to the physiology of the abdominal wall. Eur J
Surg 1998; 164(12):951–960
6. Urban E, King MW, Guidoin R, Laroche G, Marois Y, Martin
L et al. Why make monofilament sutures out of polyvi-
nylidene fluoride? ASAIO J 1994; 40(2):145–156
7. Bringman S, Wollert S, Osterberg J, Smedberg S, Granlund
H, Heikkinen TJ. Three-year results of a randomized clini-
cal trial of lightweight or standard polypropylene mesh in
Lichtenstein repair of primary inguinal hernia. Br J Surg
2006; 93(9):1056–1059
8. O’Dwyer PJ, Kingsnorth AN, Molloy RG, Small PK, Lam-
mers B, Horeyseck G. Randomized clinical trial assess-
ing impact of a lightweight or heavyweight mesh on
chronic pain after inguinal hernia repair. Br J Surg 2005;
92(2):166–170
9. Horstmann R, Hellwig M, Classen C, Rottgermann S,
Palmes D. Impact of polypropylene amount on functional
outcome and quality of life after inguinal hernia repair
by the TAPP procedure using pure, mixed, and titanium-
coated meshes. World J Surg 2006; 30(9):1742–1749
10. Nienhuijs S, Staal E, Strobbe L, Rosman C, Groenewoud
H, Bleichrodt R. Chronic pain after mesh repair of in-
guinal hernia: a systematic review. Am J Surg 2007;
194(3):394–400
11. Johnsen SG. Testicular biopsy score count–a method for
registration of spermatogenesis in human testes: normal
values and results in 335 hypogonadal males. Hormones
1970; 1:2–25
12. Pollak R, Nyhus LM. Complications of groin hernia repair.
Surg Clin North Am 1983; 63(6):1363–1371
13. Shin D, Lipshultz LI, Goldstein M, Barme GA, Fuchs EF,
Nagler HM et al. Herniorrhaphy with polypropylene mesh
causing inguinal vasal obstruction: a preventable cause of
obstructive azoospermia. Ann Surg 2005; 241(4):553–558
14. Uzzo RG, Lemack GE, Morrissey KP, Goldstein M. The ef-
fects of mesh bioprosthesis on the spermatic cord struc-
tures: a preliminary report in a canine model. J Urol 1999;
161(4):1344–1349
15. Goldenberg A, Matone J, Marcondes W, Herbella FA, Farah
JF. Comparative study of inflammatory response and
adhesions formation after fixation of different meshes
for inguinal hernia repair in rabbits. Acta Cir Bras 2005;
20(5):347–352
16. Peiper C, Junge K, Klinge U, Strehlau E, Krones C, Ottinger
A et al. The influence of inguinal mesh repair on the sper-
matic cord: a pilot study in the rabbit. J Invest Surg 2005;
18(5):273–278
17. Berndsen FH, Bjursten LM, Simanaitis M, Montgomery
A. Does mesh implantation affect the spermatic cord
structures after inguinal hernia surgery? An experimental
study in rats. Eur Surg Res 2004; 36(5):318–322
 28 Chapter 3 · Damage to the Spermatic Cord by the Lichtenstein Procedure in a Pig Model–Preliminary Results

Discussion

Kehlet: If we see these very good pictures and

compare them to other studies concerning this
problem, we should have an agreement using only
one model to investigate this problem.
3 Smeds: My question is, you have animals with
damage and without damage in both groups with
both types of meshes. Did you make a deeper anal-
ysis of this damage, and what is the reason for it?
Junge: At this point we didn’t perform deeper
analysis. We have to look on the histological sec-
tions to find out what is the detailed cause for this
damage.

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 4

Influence of Prosthetic Implants

on Male Fertility in Rabbits and Rats
C. Peiper, K. Junge, A. Oettinger, M. Binnebösel
 30 Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
Introduction
Modern concepts for treating inguinal hernias al-
ways include prosthetic mesh repairs. Some sur-
geons use the mesh repair exclusively [1]. Reported
results are promising concerning recurrence rates
[2] and return to physical activity [3]. On the other
hand, there is a certain risk of complications due
4 to the mesh that are difficult to detect. Alterations
of fertility, if observable, may be recorded only in
very large series. We know that prosthetic meshes
implanted into the abdominal wall cause chronic
inflammatory changes of the surrounding tissue [4].
Because of the close contact between mesh and the
structures of the spermatic cord after inguinal mesh
repair, these changes may also alter the reproductive
structures in male patients. Case reports have been
published about spermatic granuloma [5] and sper-
matoceles [6] after Lichtenstein hernia repair. Espe-
cially after mesh implantation in younger patients,
these findings may be of great importance.
In a rabbit experimental model, we investigated
the interaction between mesh and the adjacent
spermatic cord concerning the extent of inflamma-
tory changes and their relationship to the material
used, the integrity of the deferent duct, and the
influence on the testicular function.
Materials and Methods
These experiments were officially approved by
the district president of North Rhine-Westphalia,
Germany (AZ 50.203.2-AC 18, 3/01). All animals
received humane care in accordance with the re-
quirements of the German Animal Protection Act.
All operations were carried out under general an-
esthesia. An intravenous catheter was placed into
an ear vein. After premedication using subcuta-
neous buprenorphine 0.3 ml/kg, anesthesia was
induced by injection of Domitor 0.3 ml/kg and
ketamine 10% 0.2 ml/kg. Anesthesia was contin-
ued by repeated injections of these medications.
Additionally, the animals were ventilated by isoflu-
rane/air after endotracheal intubation. All animals
received pulse oximetry and electrocardiographic
monitoring during the operation. The animals
were fixed in the supine position. After the fur was
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cleaned and shaved, the skin was disinfected using
Braunoderm, and the operating field was covered
by sterile cloths. All operations were carried out
under aseptic and sterile surgical conditions.
Rabbit Study 1
Eight chinchilla rabbits underwent unilateral in-
guinal hernia repair following the Lichtenstein ap-
proach [7]. All rabbits received implantation of a
Marlex mesh (Bard, Cranston, RI, USA). This is
a small-pore, heavyweight polypropylene mesh.
Shouldice repair was carried out on the contral-
ateral side [8]. Another three rabbits served as
controls.
Under aseptic conditions, the inguinal canal
was opened by dividing the external oblique fascia,
and the spermatic cord was secured by a loop. We
preserved the cremasteric muscle. The Lichten-
stein repair was performed with fixation of the
mesh at the inguinal ligament and the internal
oblique muscle using interrupted Miralene sutures
(Miralene 0 HRT 26, Braun-Dexon). The lateral
end of the mesh was slit into two tails and closed
against the lateral aspect of the internal inguinal
ring using Miralene sutures.
Afterwards, the contralateral inguinal region
was prepared. Here, a simple Shouldice repair was
performed following the same extensive prepara-
tion using running Miralene sutures. Thus, every
animal served as its own control.
Animals were kept in standard rabbit cages of
60×60×60 cm at a temperature range of 20–22°C
and a light circle of 12 h. They were fed dry pellets
(Ssniff, 40 g/animal/day).
Three months later, we evaluated testicular
changes. The testicular volume was measured by
ultrasound and calculated using the formula of a
rotating ellipsoid [9]. Testicular temperature was
evaluated using a digital thermometer (Voltcraft
300K) with a needle sensor.
Arterial perfusion of the spermatic cord and
testicles was investigated using the IC-VIEW sys-
tem (Pulsion Medical Systems, Munich, Germany).
Skin and subcutaneous tissue were removed from
the lower abdomen, and the scrotal skin was re-
moved completely (⊡ Fig. 4.1a). A 0.5 mg/kg bolus
Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
a
b tozoa (late spermatids)
c tion was estimated histologically using the Johnsen
⊡ Fig. 4.1. Testicles and spermatic cord of a rabbit after prepa-
ration and before evaluation of arterial perfusion (a), during
flush of indocyanine green and under excitation of near-
infrared light (b), and after transfer of the fluorescence inten-
sity into colors (c)
of indocyanine green (ICG) was injected intra-
venously into the ear vein. Excitation light was
provided by an IC-VIEW system camera-mounted
near a near-infrared (NIR) light source (780 nm).
ICG-derived fluorescence was detected by a
digital camera using the super-night-shot mode
31 4
⊡ Table 4.1. Johnsen score for qualitative evaluation
of spermatogenesis [10]
1 No cells in tubular section
2 No germ cells, but Sertoli cells present
3 Spermatogonia are the only germ cells present
4 Only a few spermatocytes (<5) and no sperma-
tids or spermatozoa present
5 No spermatozoa and no spermatids, but several
or many spermatocytes present
6 No spermatozoa and only a few spermatids
(<5–10) present
7 No spermatozoa, but many spermatids present
8 Only a few spermatozoa (<5–10) present in
section
9 Many spermatozoa present, but germinal epi-
thelium disorganized, with marked sloughing
or obliteration of lumen
10 Complete spermatogenesis with many sperma-
(⊡ Fig. 4.1b) and was transferred to a computer for
further quantification of perfusion-related fluores-
cence intensity (IC-CALC; ⊡ Fig. 4.1c). We calcu-
lated the difference between the intensity before
and the maximum intensity after injection as an
index for maximum perfusion. This parameter was
recorded at the spermatic cord and at the testicles.
Spermatogenesis as the main testicular func-
score [10] (⊡ Table. 4.1).
The spermatic cords were excised, includ-
ing the deep inguinal ring. Representative cross-
sections were obtained at this area and analyzed
histologically using hematoxylin and eosin stains,
focusing on the inflammatory response to the
prosthetic mesh.
Rabbit Study 2
To differentiate among the results of different mesh
materials, we conducted an additional animal
study using the same conditions and techniques
 32 Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
mentioned above. We included 20 male chinchilla
rabbits. All animals underwent bilateral Lichten-
stein repair with a Prolene mesh (Ethicon, Norder-
stedt, Germany) on one side and Ultrapro mesh
(Ethicon, Norderstedt, Germany) on the other
side. Analysis followed after 6 months. After ex-
plantation of the inguinal region of the abdominal
wall, we analyzed the patency of the vas deferens
4 by injecting x-ray solution into the vas (⊡ Fig. 4.2).
Additionally, we used light microscopy to measure
the size of the foreign body granulomas induced
by the meshes.
Global statistical analysis was carried out using
the Kruskal–Wallis test. For statistics among the
groups, we used the Mann–Whitney test.
Injection of x-ray solution
ligation of ductus
ductus
mesh
testicle
⊡ Fig. 4.2. Vasography after resection of the inguinal region of
the abdominal wall
⊡ Fig. 4.3. Testicular volume (ml)
3 months after groin mesh im-
plantation in the rabbit
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Results
Rabbit Study 1
In the postoperative period, we observed an in-
creased testicular volume (⊡ Fig. 4.3), with no dif-
ference between the kinds of repair (p=0.53),
and a decreased testicular temperature com-
pared with the controls (⊡ Fig. 4.4). Here, too,
the differences among the operations were small
(p=0.246).
A cause for these findings may be the re-
duced arterial perfusion that exists after any re-
pair (p<0.05). In comparison to the controls,
this decrease in spermatic cord perfusion was
more obvious after Lichtenstein repair (p=0.03;
⊡ Fig. 4.5) than after the Shouldice operation. The
testicular perfusion was also significantly reduced
after Lichtenstein mesh implantation (p<0.05;
⊡ Fig. 4.6).
Evaluation of spermatogenesis revealed a de-
crease in the Johnsen 10 score in seminiferous
tubules after Lichtenstein repair. Following Shoul-
dice repair, the testicles showed regular spermato-
genesis (p=0.20; ⊡ Fig. 4.7).
During histological evaluation of the surround-
ing tissue, we observed a characteristic foreign
body reaction to the mesh (⊡ Fig. 4.8), which we
did not find after the Shouldice repairs. Destruc-
tion of the vas deferens wall or venous thrombosis
was not detected. The duct was patent in all speci-
mens. Obviously, the preserved cremasteric muscle
protected the structures of the spermatic cord in
this model.
Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
33 4

⊡ Fig. 4.4. Testicular temperature

(°C) 3 months after groin mesh im-
plantation in the rabbit

⊡ Fig. 4.5. Spermatic cord perfusion

(a.u.) 3 months after groin mesh im-
plantation in the rabbit, analyzed by
the IC-VIEW system

⊡ Fig. 4.6. Testicular perfusion (a.u.)

3 months after groin mesh implan-
tation in the rabbit, analyzed by the
IC-VIEW system

⊡ Fig. 4.7. Percentage of mature

spermatogenesis (Johnsen 10)
3 months after groin operation in
the rabbit
 34 Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats

Rabbit Study 2

During vasography, several specimens showed sig-

4 mesh area, we saw no severe obstruction. Mod-
⊡ Fig. 4.8. Inflammatory changes of the spermatic cord 3
months after Marlex mesh implantation in the rabbit (mesh
fiber right upper, deferent duct left lower; hematoxylin and
eosin, 100×)
nificant reduction of the vas deferens diameter
(⊡ Fig. 4.9). Most of the obstructions were observed
at the margin of the mesh. Severe obstruction
(>75%) was found in 50% of the Prolene margins
and 22.2% of the Ultrapro mesh edges. Within the
erate obstruction (25–75%) also occurred more
often in the Prolene group (⊡ Table. 4.2).
Analysis of spermatogenesis revealed the same
postoperative decrease in spermatozoa counted as
Johnsen 10 after mesh implantation as was observed
in the first study. Because of the different mesh
material, the difference in the controls did not reach

⊡ Fig. 4.9. Vasography 6 months

after inguinal Prolene mesh im-
plantation in the rabbit

⊡ Table 4.2. Obstruction of the vas deferens 6 months after mesh implantation in the rat

Obstruction at mesh margin Obstruction within mesh area

0/+ ++ +++ 0/+ ++ +++

(<25%) (25–75%) (>75%) (<25%) (25–75%) (>75%)

Prolene 43.75% (7/16) 6.25% 50% (8/16) 75% (12/16) 25% (4/16) 0%
(1/16) (0/16)

Ultrapro 77.8% (14/18) 0% 22.2% (4/18) 83.3% (15/18) 16.7% (3/18) 0% (0/18)
(0/18)

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Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
statistical difference. The decrease was also not dif-
ferent in the different material types (⊡ Fig. 4.10).
Histological analysis revealed larger foreign
body granulomas after Prolene mesh implantation
than after Ultrapro mesh implantation (p<0.05,
⊡ Fig. 4.11).
Results in Rat Experiments
Berndsen and colleagues conducted groin mesh
implantation in 30 rats and analyzed the animals
after 90 days. They found reduced s-testosterone
35 4
⊡ Fig. 4.10. Percentage of mature
spermatogenesis (Johnsen 10)
6 months after groin mesh im-
plantation in the rabbit
⊡ Fig. 4.11. Size of foreign body
granuloma 6 months after groin
mesh implantation in the rabbit
levels in the spermatic veins compared with the
controls. Furthermore, the cross-sectional area of
the vas deferens was also reduced after mesh im-
plantation [11].
Taneli and colleagues published a study in 2005
that included 40 animals. Analysis was conducted
6 months after groin mesh implantation. An induc-
ible nitric oxide synthase expression was detected
in the ipsilateral testis after mesh implantation.
Apoptotic cells were not detected. The authors
concluded that long-term polypropylene mesh im-
plantation has no effect on testicular hormonal
function and only a limited effect on nitric oxide
 36 Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
levels and that this effect is not sufficient to cause
testis apoptosis that could lead to infertility [12].
Kolbe and Lechner also investigated the effect
of hernioplastic implants on male rat infertility,
comparing the results after Prolene mesh implan-
tation to the effects after Vypro II and with control
animals. They observed some sperm granulomas
in the Prolene group but saw no negative influence
4 on male fertility in juvenile or adult rats [13].
The effect of the mesh on the vas deferens of
the rat was investigated by Maciel and colleagues,
with results published in 2007. They observed a
foreign body reaction of the spermatic cord, in-
cluding histological changes of the vas deferens,
functional obstruction and dilatation of the duct,
spermatozoid repression, and a loss of mucosal
folding proximal to the mesh. In epididymides and
testicles, no changes were found [14].
Discussion
The effect on the surrounding soft tissue of long-
term implantation of a mesh bioprosthesis for her-
nia repair is under current discussion and inves-
tigation. A persisting, inflammatory, proliferative
foreign body reaction with increased cell turnover
in the recipient tissues even years after implanta-
tion has been described [4]. These major inflam-
matory responses to mesh implantation have been
mostly reported after incisional hernia repair, but
also after bioprosthesis implantation in inguinal
hernia operations.
Therefore, we investigated the effect of this
inflammatory reaction on the spermatic cord and
testicular function in a rabbit model. We observed
only minor inflammatory changes. Perhaps this re-
duced reaction was due to the short postoperative
period. Despite this small morphological response,
we found a significant influence on testicular per-
fusion and function. Testicular temperature was
reduced in the postoperative phase after any repair,
while testicular perfusion was lowest following
the Lichtenstein operation. Spermatogenesis also
showed a reaction to the implanted mesh. The
amount of regular spermatogenesis classified as
Johnsen 10 was reduced in comparison to that
after Shouldice repair and in the controls, but this
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difference did not reach statistical significance.
No differences between the mesh materials were
observed. Further experiments with larger groups
seem to be necessary after this study.
At first glance, the observed changes might be
of no major clinical relevance in unilateral repair
and could be important only in bilateral repairs.
However, the literature contains several reports of
serum antisperm antibody production after unilat-
eral ischemic injury to the testis or the spermatic
cord [15]. This has also been reported in patients
after inguinal hernia repair [16, 17]. These antibod-
ies may lead to male infertility even after unilateral
changes and are therefore of major relevance. Fur-
ther research on this topic is mandatory.
The influence on humoral conditions will also
be a topic of further investigations. Akbulut et
al. observed decreased levels of testosterone after
laparoscopic hernia repair (totally extraperitoneal
repair) [18]. This finding is supported by animal
experiments by Uzzo and colleagues in a canine
model [19] and by Berndsen et al. in the rat [11].
One explanation for the morphological and
functional changes observed in our study may be
adhesion formation between the mesh and the
structures of the spermatic cord as a result of the
foreign body reaction. These adhesions were also
described by Fitzgibbons et al. [20] in the pig. They
found adhesions between the mesh and structures
of the spermatic cord even after intraperitoneal
placement of the mesh.
LeBlanc et al. [21] placed a heavyweight poly-
propylene mesh into the preperitoneal space and
also observed severe adhesions to the spermatic
cord 30 days after implantation. Ninety days after
operation, adhesions to the spermatic vessels and
the spermatic cord as well as venous congestion
of the testis were described. This may also serve
as an explanation for the observed deferent duct
obstruction in our experiments.
One additional aspect is the protection of the
structures of the spermatic cord by the cremas-
teric muscle. These structures were protected from
inflammation if the cremasteric muscle was pre-
served, as we did in this rabbit model. Perhaps this
strategy might be advisable instead of complete
resection of the cremasteric muscle during mesh
implantation.
Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats
There are also reports about reactions to ingui-
nal prosthetic mesh in men. The most important
publication on this topic is by Shin and colleagues,
published in 2005. They reported on 14 young
male patients undergoing open or laparoscopic
groin mesh implantation. Nine of them presented
bilateral vas deferens obstruction, and the other
five suffered from unilateral obstruction with con-
tralateral testicular atrophy. The authors suggested
that men–especially those of young reproductive
age or with a solitary testicle–should be care-
fully advised of the potential for obstruction and
compromise to future fertility before undergoing
polypropylene mesh herniorrhaphy [22].
Valenti et al. reported a case of fibrotic vas
deferens obstruction due to direct contact of an
implanted plug with the vas [23].
Wingenbach et al. reported long-lasting pain
during copulation in 3.9% of all cases after laparo-
scopic hernia repair [24].
Langenbach et al. found painful ejaculation
in 10%, 12 weeks after laparoscopic repair [25],
which correlated with the kind of mesh.
Hetzer et al. reported spermatoceles requiring
operation after Lichtenstein repairs in 0.8% [6].
Silich and McSherry reported a case of a sper-
matic granuloma requiring operation 2 years after
mesh repair of an inguinal hernia [5].
Aasvang et al. conducted a questionnaire-based
analysis of 1,015 patients 1 year after mesh-based
inguinal hernia repair. They found relevant pain
during physical activity in 18.4% and pain during
sexual activity in 22.1%. Genital or ejaculatory
pain occurred in 12.3%, and 2.8% of the patients
complained about moderate or severe impairment
of their sexual activity [26]. Out of this popula-
tion, the authors intensified analysis in 10 selected
patients with postherniotomy ejaculatory pain and
pain-related sexual dysfunction. After this analysis,
the authors concluded that postherniotomy genital
and ejaculatory pain that impairs sexual activity is
of neuropathic origin and is anatomically related
to the vas deferens and related structures [27].
Summarizing these publications and our ex-
perimental results, we suggest some negative influ-
ence by the foreign body reaction to the prosthetic
mesh on the structures of the spermatic cord.
Therefore, we caution against implanting poly-
37 4
propylene mesh into the inguinal region without a
good indication.
Conclusion
Until more data are available, we see a limited
indication for mesh implantation during inguinal
hernia repair in young patients, as an effect on
testicular function and spermatogenesis is pos-
sible. Preserving the cremasteric muscle fibers may
protect the spermatic cord.
Acknowledgements
Parts of these experiments were supported by
the Deutsche Forschungsgemeinschaft (AZ KON
709/2002, PE 718/4-1).
References
1. Bittner R, Schmedt CG, Schwarz J, Kraft K, Leibl BJ. Lap-
aroscopic transperitoneal procedure for routine repair of
groin hernia. Br J Surg 2002; 89:1062–1066
2. Wara P, Bay-Nielsen M, Juul P, Bendix J, Kehlet H. Prospec-
tive nationwide analysis of laparoscopic versus Lichtenstein
repair of inguinal hernia. Br J Surg 2005; 92:1277–1281
3. Fenoglio ME, Bermas HR, Haun WE, Moore JT. Inguinal
hernia repair: results using an open preperitoneal ap-
proach. Hernia 2005; 9:160–161
4. Klosterhalfen B, Klinge U, Hermanns B, Schumpelick V.
Pathology of traditional surgical nets for hernia repair
after long-term implantation in humans. Chirurg 2000;
71:43–51
5. Silich RC, McSherry CK. Spermatic granuloma. An uncom-
mon complication of the tension-free repair. Surg Endosc
1996; 10:537–539
6. Hetzer FH, Hotz T, Steinke W, Schlumpf R, Decurtins M,
Largiader F. Gold standard for inguinal hernia repair:
Shouldice or Lichtenstein? Hernia 1999; 3:117–120
7. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM. The
tension-free hernioplasty. Am J Surg 1989; 157:188–193
8. Shouldice EE. Surgical treatment of hernia. Ontar Med
Rev 1945; 4:43
9. Peiper Ch, Ponschek N, Truong S, Schumpelick V. Ultra-
sound-based volumetric evaluation of fluid retention af-
ter inguinal hernia repair. Surg Endosc 2000; 14:666–669
10. Johnsen SG. Testicular biopsy score count–a method for
registration of spermatogenesis in human testes: normal
values and results in 335 hypogonadal males. Hormones
1970; 1:2–25
 38 Chapter 4 · Influence of Prosthetic Implants on Male Fertility in Rabbits and Rats

11. Berndsen FH, Bjursten LM, Simanaitis M, Montgomery with a variant of polypropylene mesh. Urologe A 2003;
A. Does mesh implantation affect the spermatic cord 42:375–381
structures after inguinal hernia surgery? An experimental 26. Aasvang EK, Møhl B, Bay-Nielsen M, Kehlet H. Pain-related
study in rats. Eur Surg Res 2004; 36:318–322 sexual dysfunction after inguinal herniorrhaphy. Pain
12. Taneli F, Aydede H, Vatansever S, Ulman C, Ari Z, Uyanik 2006; 122:258–263
BS. The long-term effect of mesh bioprosthesis in inguinal 27. Aasvang EK, Møhl B, Kehlet: Ejaculatory pain: a specific
hernia repair on testicular nitric oxide metabolism and postherniotomy pain syndrome? Anesthesiology 2007;
apoptosis in rat testis. Cell Biochem Funct 2005;23:213– 107:298–304
220
13. Kolbe T, Lechner W. Influence of hernioplastic implants on
4 male fertility in rats. J Biomed Mater Res B Appl Biomater
2007; 81:435–440
14. Maciel LC, Glina S, Palma PC, Nascimento LF, Netto NR Jr.
Histopathological alterations of the vas deferens in rats
exposed to polypropylene mesh. BJU Int 2007; 100:187–
190
15. Lewis-Jones DI, Moreno de Marval M, Harrison RG. Im-
pairment of rat spermatogenesis following unilateral ex-
perimental ischemia. Fertil Steril 1982; 38:482–490
16. Kapral W, Kollaritsch H, Stemberger H. Correlation of
inguinal hernia and agglutinating sperm antibodies.
Zentralbl Chir 1990; 115:369–377
17. Matsuda T, Muguruma K, Horii Y, Ogura K, Yoshida O.
Serum antisperm antibodies in men with vas deferens
obstruction caused by childhood inguinal herniorrhaphy.
Fertil Steril 1993; 59:1095–1097
18. Akbulut G, Serteser M, Yucel A, Degirmenci B, Yilmaz S,
Polat C, San O, Dilek ON. Can laparoscopic hernia repair al-
ter function and volume of testis? Randomized clinical trial.
Surg Laparosc Endosc Percutan Tech 2003; 13:377–381
19. Uzzo RG, Lemack GE, Morrissey KP, Goldstein M. The ef-
fects of mesh bioprosthesis on the spermatic cord struc-
tures: a preliminary report in a canine model. J Urol 1999;
161:1344–1349
20. Fitzgibbons RJ Jr, Salerno GM, Filipi CJ, Hunter WJ, Watson
P. A laparoscopic intraperitoneal onlay mesh technique
for the repair of an indirect inguinal hernia. Ann Surg
1994; 219:144–156
21. LeBlanc KA, Booth WV, Whitaker JM, Baker D. In vivo study
of meshes implanted over the inguinal ring and exter-
nal iliac vessels in uncastrated pigs. Surg Endosc 1998;
12:247–251
22. Shin D, Lipshultz LI, Goldstein M, Barme GA, Fuchs EF,
Nagler HM, McGallum SW, Niederberger CS, Schoor RA,
Brugh VM 3rd, Honig SC. Herniorrhaphy with polypropyl-
ene mesh causing inguinal vasal obstruction: a prevent-
able cause of obstructive azoospermia. Ann Surg 2005;
241:553–558
23. Valenti G, Baldassarre E, Torino G. Vas deferens obstruc-
tion due to fibrosis after plug hernioplasty. Am Surg
2006; 72:137–138
24. Wingenbach O, Waleczek H, Kozianka J. Laparoscopic
hernioplasty by transabdominal preperitoneal approach.
Analysis and review in 267 cases. Zentralbl Chir 2004;
129:369–373
25. Langenbach M, Schmidt J, Lazika M, Zirngibl H. Urologi-
cal symptoms after laparoscopic hernia repair. Reduction

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 5

The Effects of a Mesh Bioprosthesis

on the Spermatic Cord Structures
A. Goldenberg
 40 Chapter 5 · The Effects of a Mesh Bioprosthesis on the Spermatic Cord Structures
Introduction
We performed two experimental studies in a dog
model [1, 2] and one clinical research study on the
effects of synthetic mesh on fertility.
Experimental Study 1
The first work developed by our group concerned
application of the mesh by video laparoscopy without
5 dissection of the inguinal region. The aim of this
study [1] was to investigate the effects of the synthetic
mesh on the ductus deferens and testicle of dogs.
Methods
Ten adult male dogs were anesthetized, and a
2.5×3.5 cm2 polypropylene mesh was fixed in the
inguinal region in direct contact with the ductus
deferens, using metallic staples without dissection
of the region and, therefore, without manipula-
tion. The right side, with no mesh, was the control.
The operating time was 15 min. The animals were
observed for 30 days, and then they were again
anesthetized and underwent new surgery, during
which the ductus deferens and testicle were re-
moved and sent for histological analysis.
Results
The histological sections of the testicle showed a
focal reduction of spermatogenesis in 20% of the
animals and a degenerative process in 20%. In the
epididymis, chronic inflammation and seminifer-
ous tubule dilatation were observed in 70%. A
chronic inflammatory process was found in 60% of
the vasa deferentia.
Conclusion
The polypropylene mesh in direct contact with the
spermatic funiculus in dogs caused histological
alterations, with minimal reduction of spermato-
genesis.
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Experimental Study 2
In the second investigation we studied the effects
of polypropylene mesh implanted by inguinotomy
in the spermatic cord, epididymis, and testis of
dogs [2].
Methods
Eighteen dogs were included (12–23 kg), separated
into three groups:
-Group A (n=7): left side (with mesh) vs. right side
(without mesh)
-Group B (n=7): left side (without mesh) vs. right
side (with mesh)
-Group C (n=4): no surgical manipulation (control
group)
After being observed for 60 days, the animals were
subjected to bilateral removal of the spermatic
cord, epididymis, and testis, which were submitted
for histological analysis. During the reoperation, a
macroscopic evaluation was performed.
Results
On the mesh side, we noted 100% mesh adherence
to the posterior wall of the inguinal canal, as well
as adherence of the spermatic cord to the mesh.
Congestion of the pampiniform plexus was noted
in three animals.
Chronic inflammation and foreign body reac-
tions in the spermatic cord were observed in 100%
of the animals. On the side that was not implanted
with mesh, a chronic inflammatory reaction was
observed in 71% of the animals. All of the ani-
mals presented a chronic inflammatory reaction
in the deferent duct on the mesh side, and such
a reaction was also present in 11 animals in the
side without the mesh. These alterations were not
found in group C.
There was a considerable statistical reduction
in the average lumen diameter of the deferent duct
on the mesh side. In the epididymis and testis,
macroscopic and microscopic alterations were not
significant, although one animal showed a marked
reduction of spermatogenesis on the mesh side.
Chapter 5 · The Effects of a Mesh Bioprosthesis on the Spermatic Cord Structures
41 5
Conclusion Acknowledgments

When in contact with the spermatic cord of
dogs, the polypropylene mesh caused an intense
chronic inflammatory reaction and a significant
reduction in the diameter of the lumen of the
deferent duct.
I am grateful for the collaboration in my research
to Jaques Matone, Joaquim Ferreira de Paula, and
Edgar Valente Lima Neto.
References

Clinical Study 1. Goldenberg A, Matone J, Marcondes W, Focchi G. Effects

We performed one more study to evaluate testicu-
lar volume and arterial flow in patients undergoing
surgical correction for inguinal hernia with a poly-
propylene prosthesis [3].
Methods
This was an observational prospective clinical
study of 39 male patients with unilateral inguinal
hernia of Nyhus types IIIa and IIIb who under-
went surgical correction with implantation of a
polypropylene prosthesis by means of the Lichten-
stein technique. The patients were evaluated us-
ing Doppler ultrasound before the operation and
selectively 3 and 6 months after the operation. The
variables studied were testicular volume, systolic
and diastolic velocity, resistance index, and pulsa-
tility index.
of the polypropylene mesh in the testicle, epididymis and
ductus deferens of dogs. Acta Cir Bras 2001; 16(4)
2. Goldenberg A, Ferreira de Paula J. Effects of the poly-
propylene mesh implanted through inguinotomy in the
spermatic funiculus, epididium and testis of dogs. Acta
Cir Bras 2005; 20(6):461–467
3. Lima Neto EV, Goldenberg A, Jucá MJ. Prospective study
on the effects of a polypropylene prosthesis on testicular
volume and arterial flow in patients undergoing surgical
correction for inguinal hernia. Acta Cir Bras 2007; 22(4):
266–271
Discussion
Amid: Is there any direct contact between mesh
and the vas deferens during your laparoscopic ap-
proach?
Goldenberg: No, there was no dissection and
therefore no direct contact.

Results

No statistically significant alterations in the stud-

ied variables were observed over the course of
time: testicular volume (p=0.197), systolic ve-
locity (p=0.257), diastolic velocity (p=0.554), re-
sistance index (p=0.998), and pulsatility index
(p=0.582).

Conclusion

No alterations in testicular volume or arterial flow

were observed over a 6-month period in patients
who underwent surgical correction for inguinal
hernia using a polypropylene prosthesis.
[UnitedVRG] - Medical Release Group
 6

Influence of Prosthetic Implants

on Male Fertility in Rats
T. Kolbe and W. Lechner
 44 Chapter 6 · Influence of Prosthetic Implants on Male Fertility in Rats

Introduction

In an effort to find a suitable material for tension-

free repair of inguinal hernias, a variety of natural
and synthetic materials have been used [1]. Cur-
rently, three prosthetic materials are widely used for
repairing inguinal hernias: polyester, polypropylene,
and expanded polytetrafluoroethylene [2]. Despite
their wide acceptance and use in countless surgeries
worldwide, little data exist regarding the effects of
the mesh bioprosthesis on the adjacent spermatic
cord structure and function, particularly the ductus
deferens. Since it was shown that the weight of the
6 implanted material corresponds to the postsurgical
inflammatory reaction [3–5], partially absorbable
meshes have been developed to reduce the amount
of foreign material staying in the patient’s body.
This study explored the vulnerability of the
ductus deferens to mesh-induced inflammation
and shrinkage after hernia repair in a rodent model.
In our study we tested the influence on male fertil-
ity of a widely used mesh of 100% polypropylene
(Prolene) and a mesh containing a mixture of 50%
polypropylene and 50% polyglactin (Vypro II). The
polyglactin component, which should be resorbed
within 56–70 days, makes the mesh more flexible
and reduces the implant’s weight. The bigger pores
are regarded to be advantageous concerning the
inflammatory reaction after implantation [6–8].
Due to the ethical constraints of studies in hu-
mans, we used rats as an animal model to test the
vulnerability of the ductus deferens to the materi-
als mentioned above. Because there are reports of
special sensitivity of the premature male reproduc-
tive organs to surgical manipulations [9, 10], we
tested both mature and premature male rats for
short-term and long-term histological reactions ⊡ Fig. 6.1. Reproductive tract of male rat and implantation
and for subsequent reproductive performance. of meshes

Material and Methods
Two types of implants (Prolene and Vypro II, both
Ethicon, Germany) in the size of 2.25 cm2 were
used in juvenile and adult Hsd:Sprague Dawley SD
rats (8 weeks and 12 weeks, respectively). In two
control groups (juvenile and adult male rats), the
ducti were only bluntly separated from adherent
tissue. Each of the six groups (Prolene juvenile, Pj;
Prolene adult, Pa; Vypro II juvenile, Vj; Vypro II
adult, Va; control juvenile, Cj; control adult, Ca)
consisted of 10 animals.
The meshes were surgically wrapped around
the ductus deferens on each side to ensure direct
contact with the spermatic cord and were fixed
with sutures to remain in position (⊡ Fig. 6.1).

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Chapter 6 · Influence of Prosthetic Implants on Male Fertility in Rats
45 6
4 Weeks After Start:
Histology

The implants and the adjacent part of the ductus

deferens from one side of each male rat were re-
moved surgically for histological examination of
acute inflammatory reaction.
Staining was achieved with mouse antihuman
proliferating cell nuclear antigen (PCNA) for de- a
tection of cell proliferation, rabbit antihuman fac-
tor VIII (Von Willebrand factor) for detection of
angiogenic proliferation, and mouse antihuman
bcl-2 (oncoprotein) for cancerogenic reaction.
Counterstaining was done with Hemalaun.

3–4 Months After Start:

Mating Test

Three months after implantation, each male was b

mated with two or three adult females. Two days
after positive vaginal plug control, the females
were euthanized, and oocytes or embryos were
flushed from the oviducts and uteri. The relation-
ship of unfertilized and degenerated oocytes to
morphologically intact embryos was recorded.

4 Months After Start: Histology

The implant on the opposite side was removed

after euthanasia for histological examination of c
chronic inflammatory reactions using the same
methods as described above.

Results

Histological Examination

Hemalaun Staining
Four weeks after treatment, two animals in the Pj
group showed granulomatous inflammatory reac-
tions with sperm deposits in the connective tissue d
due to injuries of the wall of the ductus deferens.
Other rats in groups Pj and Pa showed incisions ⊡ Fig. 6.2. a The two different implants. b Sperm granuloma.
of the muscularis. There was enhanced production c Minor inflammation around a Prolene fiber (arrow). d Lumen
of collagen fibers at the edges of the Prolene im- of the ductus slightly depressed by Vypro II fibers (arrows)
 46 Chapter 6 · Influence of Prosthetic Implants on Male Fertility in Rats

plants. Areas of inflammation were visible around

the Vypro II implants in groups Vj and Va, with
many multinuclear giant cells (⊡ Fig. 6.2). There
was no visible inflammatory reaction in the mu-
cosa or blockage of the spermatic cord.
In the samples taken after 4 months, we ob-
served no profound differences from the first ex-
amination after 4 weeks. In the Prolene groups,
there were incisions of the muscularis due to im-
plant fibers, but no enhanced cellular reaction or
inflammation-associated changes occurred. Two
rats in the Pj group and three in the Pa group
showed multinuclear giant cells. In the Vypro II
6 groups, only the nonabsorbable component of the
meshes was present. In some cases, the round lu-
men of the ductus deferens was slightly deformed,
comparable to the Prolene groups, but without the
incisions seen in the Pj and Pa groups.

PCNA Reaction
Serosa Cells
The staining for proliferative cells revealed in-
creased inflammatory reactions after 4 months
compared with the values after 4 weeks after treat-
ment (⊡ Fig. 6.3a). While there was only a tendency
in the Vypro and Prolene groups for more PCNA-
positive cells after 4 weeks, this difference was
significant after 4 months (⊡ Fig. 6.3b). There was
no significant difference between the mesh groups.
We did not observe an age effect.

Mucosal Cells
Between the mesh groups and controls, there
was no significant difference in the percentage of
PCNA-positive cells either after 4 weeks or after
4 months. Several groups showed high variation
among individuals and thus a high standard of
group values.
⊡ Fig. 6.3. Proliferating cell nuclear antigen (PCNA)-positive
cells in different cell layers 4 weeks and 4 months after im-
Von Willebrand Factor Staining plantation of meshes around the spermatic cord (mean and
Staining for Von Willebrand factor revealed an SE). a After 4 weeks. b After 4 months
increase in the mean number of blood vessels in
all groups between sampling points (⊡ Fig. 6.4).
This proliferation ranged from 1.6% (Cj group) to
36% (Pj group). However, due to high individual Bcl-2 Staining
variation, there was no statistically significant dif- There was no sign of oncogenic activity by expres-
ference (as shown by analysis of variance) between sion of bcl-2 after either 4 weeks or after 4 months
the experimental groups. compared with positive controls.

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Chapter 6 · Influence of Prosthetic Implants on Male Fertility in Rats
No. of blood vessels per area
25
20
counted
15
10
0
Cj Ca Pj
Experimental Groups
⊡ Fig. 6.4. Number of blood vessels per area counted at 4 weeks and 4 months (mean and range; minimum to maximum)
Mating Test
The flushing of embryos resulted in mean embryo
numbers from 7.7 to 14.7 in the experimental
groups. These were compared to the total number
of unfertilized or fragmented oocytes and embryos
(range 13.0–16.3). All groups exhibited one to
three males with decreased or restricted fertility,
but there were no differences between groups.
There was no indication of a negative influence on
male fertility due to one of the implanted meshes
(analysis of variance).
Discussion
Open and laparoscopic mesh-based techniques
dominate inguinal hernia repairs today. Research is
currently focusing on the search for suitable mesh
materials with regard to inflammatory response,
chemical properties, and applicability [2]. The
more rigid polypropylene mesh is preferred for
laparoscopic hernia repair because it unfolds easily
after introduction into the abdomen through the
endoscope. A disadvantage is the heavy shrinkage
of this material in vivo, which has been reported
both in humans [4] and in animal experiments [5].
In contrast, other authors reported an even greater
shrinkage of the more flexible Vypro II mesh (28%)
compared with a heavyweight polypropylene mesh
(Atrium, 12%) [11].
47 6
after 4 weeks
after 4 months
Pa Vj Va
In our investigation, we used both materials in
both juvenile and adult male rats. A direct mating
test revealed no statistically significant differences
between the two different materials or the different
ages. Histological examination of spermatic cord
explants stained with PCNA showed long-term in-
flammatory reactions in the adjacent serosa but not
in the mucosa. This effect was independent of the
material applied. This effect might be induced by
the smaller pore size of the Prolene mesh, resulting
in enhanced colonization with macrophages after
90 days [12, 13] and resorption of the polyglactin
part in the Vypro II mesh. However, in both cases
the mucosa was not involved.
This result is in contrast to that found by Ro-
sch et al. [14], but it confirms Berndsen et al. [15].
By measuring testicular hormonal function, the
latter authors also confirmed that polypropylene
and polypropylene/polyglactin meshes did not in-
fluence male fertility in the rat model, as had been
concluded in another study [16]. The sharp edges
and the unusual mode of application (wrapping
around the spermatic cord) might be responsible
for the observed sperm granulomas in two male
rats and for the mesh incisions into the muscularis
and granulosa in some rats of the Prolene group.
From this point of view, the 50% absorbable Vy-
pro II mesh with softer material properties seems
to be more difficult to apply, but according to the
results of other investigations [17], it causes less
irritation to the surrounding tissue.
 48 Chapter 6 · Influence of Prosthetic Implants on Male Fertility in Rats

In summary, we did not observe a reduction in 14. Rosch R, Junge K, Quester R, Klinge U, Klosterhalfen B,
fertility of male rats compared with the controls, Schumpelick V (2003) Vypro II mesh in hernia repair: im-
pact of polyglactin on long-term incorporation in rats.
even after direct wrapping of synthetic meshes of
Eur Surg Res 35:445–450
two different types around the ducti deferentia. 15. Berndsen FH, Bjursten LM, Simanaitis M, Montgomery A
Therefore, we conclude that neither mesh has a (2004) Does mesh implantation affect the spermatic cord
negative influence on male fertility. structures after inguinal hernia surgery? An experimental
study in rats. Eur Surg Res 36:318–322
16. Taneli F, Aydede H, Vatansever S, Ulman C, Ari Z, Uyanik
BS (2005) The long-term effect of mesh bioprosthesis
References
in inguinal hernia repair on testicular nitric oxide me-
tabolism and apoptosis in rat testis. Cell Biochem Funct
1. The EU Trialists Collaboration (2002) Repair of groin her- 23:213–220
nia with synthetic mesh: meta analysis of randomized 17. Friis E, Lindahl F (1996) The tension-free hernioplasty in a
controlled trials. Ann Surg 235:322–332 randomized trial. Am J Surg 172:315–319
2. Nathan JD, Pappas TN (2003) Inguinal hernia: an old con-
6 dition with new solutions. Ann Surg 238:148–157
3. Prior MJ, Williams EV, Shukla HS, Phillips S, Vig S, Lewis M
(1998) Prospective randomized controlled trial compar- Discussion
ing Lichtenstein with modified Bassini repair of inguinal
hernia. J R Coll Surg Edinb 43:82–86
Schumpelick: I think this is the first study dealing
4. Schumpelick V, Arlt G, Schlachetzki A, Klosterhalfen B (1997)
Chronic inguinal pain after transperitoneal mesh implanta- with fertility.
tion. Case report of net shrinkage. Chirurg 68:1297–1300 Kolbe: Let me give at first one short comment on
5. Klinge U, Klosterhalfen B, Muller M, Ottinger AP, Schumpe- this animal model. I believe that the rat model is a
lick V (1998) Shrinking of polypropylene mesh in vivo: an very good model to investigate tissue reaction. That
experimental study in dogs. Eur J Surg 164:965–969
seems to be comparable to the human situation. It
6. Klinge, U, Klosterhalfen B, Conze J, Limberg W, Obolenski
B, Ottinger AP, Schumpelick V (1998) A modified mesh seems not to be a good model for investigating tes-
for hernia repair that is adapted to the physiology of the ticular function because there are some differences
abdominal wall. Eur J Surg 164:951 from the human being. The rodent can retract the
7. Klosterhalfen B, Junge K, Klinge U (2005) The lightweight testicles into the body cave with different tempera-
and large porous mesh concept for hernia repair. Expert
tures and conditions for spermatogenesis.
Rev Med Devices 2:103–117
8. Hagerty RD, Salzmann DL, Kleinert LB, Williams SK (2000)
Cellular proliferation and macrophage populations as-
sociated with implanted expanded polytetrafluoro-ethyl-
ene and polyethyleneterephthalate. J Biomed Mater Res
49:489–497
9. Shandling B, Janik JS (1981) The vulnerability of the vas
deferens. J Ped Surg 16:461–464
10. Barrat C, Seriser F, Arnoud R, Trouette P, Champault G
(2004) Inguinal hernia repair with beta glucan-coated
mesh: prospective multicenter study (115 cases)–prelimi-
nary results. Hernia 8:33–38
11. Scheidbach H, Tamme C, Tannapfel A, Lippert H, Kocker-
ling F (2004) In vivo studies comparing the biocompat-
ibility of various polypropylene meshes and their han-
dling properties during endoscopic total extraperitoneal
(TEP) patchplasty: an experimental study in pigs. Surg
Endosc 18:211–220
12. Rosch R, Junge K, Schachtrupp A, Klinge U, Klosterhalfen
B, Schumpelick V (2003) Mesh implants in hernia repair.
Inflammatory cell response in a rat model. Eur Surg Res
35:161–166
13. Schumpelick V, Klinge U (2003) Prosthetic implants for
hernia repair. Br J Surg 90:1457–1458

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 7

What Can We Do To Decrease the Risk

of Vas Deferens Injury due to Inguinal
Hernioplasty?
P. Witkowski
 50 Chapter 7 · What Can We Do To Decrease the Risk of Vas Deferens Injury due to Inguinal Hernioplasty?
Introduction
The implantation of polypropylene mesh in ingui-
nal hernia repair surgery has been a tremendous
breakthrough. It has significantly reduced the her-
nia recurrence rate from 15–20% to 0.5–5% and
therefore has decreased the rate of spermatic cord,
vas deferens, and testicular artery injury due to re-
operation for recurrence [1]. We have only limited
information, however, about the long-term effects
of polypropylene mesh implantation on the vas
deferens, especially with regard to fertility.
Despite new developments, polypropylene
mesh remains the optimal and most commonly
used material for inguinal hernioplasty. This mesh
7 stimulates a pronounced chronic inflammatory
reaction with connective tissue formation that in-
corporates the prosthesis into surrounding tissue.
Although such scar formation fills out the hernia
defect and effectively prevents hernia recurrence,
it may ultimately cause damage to the adherent
organs. This inflammatory process is clinically rel-
evant because it remains active even years after
mesh implantation [2].
Is There a Risk for a Vas Deferens Injury
After Mesh Hernioplasty?
In my opinion, we have enough clinical as well as
experimental data from animal studies to confirm
this risk. Injury may occur in the postoperative
period because of a chronic foreign body reaction
involving tissue surrounding the implanted mesh,
which may also include the spermatic cord and vas
deferens.
Clinical experience indicates that a polypro-
pylene mesh cannot be safely implanted in contact
with any visceral or retroperitoneal organs, espe-
cially if placed under pressure or tension. Extensive
fibrosis around the mesh can trap and damage in-
guinal nerves, the intestine, or the urinary bladder
[3–5]. The mesh can even erode into the wall or
lumen of those organs, leading to pain, infection,
small bowel obstruction, or enterocutaneous fis-
tula formation [3–7]. The same process may even
lead to stenosis or obstruction of the urethra after
polypropylene tape suspension for the treatment
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of stress urinary incontinence [4]. Erosion of the
vagina has also been reported [8, 9]. As a remedy,
a new polypropylene sling with an absorbable cen-
tral suburethral part was developed to separate the
polypropylene part of the sling from the urethra
and vagina [10].
All of the complications described above are
recognizable on obvious clinical presentation and
result from placement of the mesh in close prox-
imity to the organs.
Therefore, it is reasonable to expect that a
structure as delicate as the vas deferens could also
be damaged or occluded if a mesh were placed
close enough to it, especially if left under tension
or pressure.
Animal studies provide more arguments for
an increased risk of vas injury when polypropyl-
ene mesh is used for the repair. In several studies,
mesh was found to be adherent to the spermatic
cord throughout its inguinal course, leading to
significant foreign body reaction in all animals [2,
11–13]. Histology showed fibrosis, extensive skel-
etal muscle degeneration, and histiocytic inflam-
mation along the outer part of the cord [11, 14].
Additionally, the thick muscular layer of the vas
was more prominently attenuated after mesh her-
nia repair than after Shouldice repair in a canine
experiment [11]. This attenuation is important
because the vas is no longer considered a passive
conduit through which the ejaculate travels. The
rich adrenergic innervation, the complexity of the
muscle layers of the vas, and the metabolically ac-
tive vasal epithelium all suggest a very active role
in sperm transport, which may be altered by the
perivasal fibrosis attributable to the mesh [11].
When a mesh was placed in proximity, the lumen
of the vas was narrowed compared with nonsurgi-
cal controls [12].
Other studies also suggest that even if fibrosis
around the vas deferens and within its wall does
not lead to reduction of the lumen of the vas, it
may cause functional obstruction with dilatation
of the proximal segment along with degenerative
changes in mucosa and repression of spermato-
zoa [11, 14]. Foreign body reaction around the
mesh may compromise blood flow within the cord
and eventually compromise fertility [15]. Conges-
tion of the pampiniform plexus was noted in 20%
Chapter 7 · What Can We Do To Decrease the Risk of Vas Deferens Injury
of animals after a Lichtenstein procedure, with
spermatic cord vein thrombosis in up to 33% of
cases after an open preperitoneal approach [2, 14].
Mesh repair led to decreases in arterial perfusion
and testicular temperature and also reduced the
proportion of seminiferous tubules with regular
spermatogenesis [2]. Focal fibrinoid necrosis of
the deferent duct wall was also reported [2].
The above results were observed in animals
shortly after mesh implantation (weeks or months),
whereas in humans, the mesh stays in the body for
years and may cause much more extensive degen-
erative changes.
Finally, several clinical reports conclude that
occlusive injury to the vas deferens resulted from
mesh implantation [7, 16–20]. Because these re-
ports represent only single cases, until recently
they had only anecdotal value. But a recent multi-
center study has drawn attention to the possibility
that vas deferens injury may take place more com-
monly than we think [21]. The authors presented
14 cases of obstructive azoospermia leading to in-
fertility because of bilateral or unilateral vas occlu-
sion, with simultaneous, but different, pathology
of the reproductive organs on the contralateral
side. Mesh-related fibrosis as a cause of vas occlu-
sion was verified during surgical revision of the
inguinal region [21]. Mechanical injury of the vas
by the edge of the mesh has also been blamed as a
possible cause of spermatic granuloma [20]. Fur-
ther reports suggest that vas obstruction may lead
to increased serum levels of antisperm antibody
even without sperm granulomas, which can ad-
ditionally compromise fertility [15, 22].
How Great Is the Risk of Vas Injury
After Mesh Hernioplasty?
Today we cannot estimate the risk because we do
not know how many patients are affected. This
is mainly because of poor clinical presentation of
the injury. Isolated, unilateral occlusion of the vas
is completely asymptomatic. Infertility is the only
potential symptom, and it occurs only with bilat-
eral occlusion or with unilateral injury in a patient
with contralateral sex organ pathology. Diagnosis
of mesh-related vas injury is further complicated
51 7
by that fact that most patients do not test their
fertility before or after surgery, and occlusion can
develop not only shortly after surgery but also
years later, when a patient has finished his procre-
ative activity.
Furthermore, we do not have any noninvasive
methods to detect vas injury or obstruction or to
screen asymptomatic patients.
Because we have animal experimental data in-
dicating that fibrosis around the implanted mesh
compromises vas deferens function, and knowing
that the vas can be occluded when mesh is placed
in proximity, as seen with urethral or small bowel
obstruction, we cannot exclude the possibility that
symptomatic patients from case reports are only
the tip of the iceberg and that there are asymp-
tomatic patients with vas deferens injury and oc-
clusion after inguinal hernioplasty. The majority
of patients may have this complication and may
be completely unaware of it because they either do
not test their fertility or they remain fertile because
of an uncompromised contralateral sex organ.
How Can We Assess the Risk?
Autopsies of patients who received inguinal mesh
repair might give some estimates. Unfortunately,
prospective studies with fertility monitoring be-
fore and after the procedure put a significant
burden on patients and do not seem feasible at the
moment [23].
What Can We Do Now?
Some surgeons may choose not to change anything
and to continue using current surgical techniques
until the actual risk rate is known. For the time
being, I think that for patients whose procreative
ability is of great concern, we should tailor our sur-
gical approach to minimize the risk of vas injury
without compromising repair results. These candi-
dates would include young patients with bilateral
hernia and those with compromised sex organs
and contralateral hernia.
Careful handling of the spermatic cord, in-
cluding the vas deferens, in order to avoid direct
 52 Chapter 7 · What Can We Do To Decrease the Risk of Vas Deferens Injury due to Inguinal Hernioplasty?

intraoperative injury of this structure remains a

constant principle of safe and efficient surgical
technique [15]. To minimize the risk of vas occlu-
sion, the general rule would be to avoid direct con-
tact between the mesh and the vas deferens [24]:
▬ In the preperitoneal space the vas deferens
is bare, so we may choose to avoid implant-
ing mesh there, both in the posterior (lap-
aroscopic, Nyhus, Stoppa, transabdominal
preperitoneal, totally extraperitoneal repair)
and anterior preperitoneal approaches (Rives,
Kugel, Prolene Hernia System repair).
▬ Mesh plug insertion in the deep inguinal ring
for indirect defects causes extensive fibrosis
and may also involve the bare vas deferens;
7 therefore, the plug is not advised in this loca-
tion (Rutkow technique) [24].
▬ In the course of the inguinal canal, the vas
runs in the spermatic cord and is better pro-
tected by the surrounding internal spermatic ⊡ Fig. 7.1. Placement of the mesh on the posterior of the
fascia and cremaster. Therefore, it seems rea- inguinal canal

sonable not to excise the cremaster but instead

to spare it and close it with absorbable suture
after hernia sac dissection and reduction.
▬ Placement of the mesh on the posterior wall
of the inguinal canal is better (Lichtenstein or
Trabucco technique) because the transversalis
fascia can separate the mesh from bare vas
running in the preperitoneal space.
The disadvantage of the Lichtenstein operation,
however, is that the spermatic cord is placed within
the inguinal canal, where it is usually compressed
between the mesh and the aponeurosis of the ex-
ternal oblique abdominal muscle. In such limited
space, fibrosis around the mesh may still involve
the spermatic cord and compromise the vas def-
erens.
Therefore, we may modify our technique; after
placing the mesh on the posterior wall of the ingui-
nal canal, we can reapproximate the aponeurosis of
the external oblique muscle with the sutures below
(instead of above) the spermatic cord, as described
in the Trabucco repair [25] (⊡ Figs. 7.1–7.3).
This modification can be easy applied to the
Lichtenstein operation, as has been previously sug-
gested [26]. In this way, the spermatic cord is sepa-
rated from the mesh with additional fascia and
placed freely in subcutaneous tissue. Therefore,
the risk of damage due to fibrosis surrounding the
prosthesis is eliminated.
Additionally, polypropylene mesh is placed flat
between two fascial layers, the transversalis fascia
and the oblique aponeurosis, which limits fibrotic
tissue ingrowth only to the intrafascial space. Fi-
brosis penetrating the mesh glues the fascial layers
together, creating a uniform, triple-layer (fascia–
mesh–fascia) solid scar, which effectively rein-
forces the abdominal wall around the deep ingui-
nal ring and prevents recurrence. After such repair,
oblique passage of the spermatic cord through the
inguinal canal can thus be avoided; it is not essen-
tial for effectiveness of the repair, as in traditional
suture operations. This approach was developed
by Trabucco in his sutureless technique, in which
a preshaped polypropylene mesh with flat-shape
memory is placed without suture fixation on the
posterior wall of the inguinal canal [25]. Long-
term results of this approach indicate that it is
as effective as any other tension-free technique
[27–30]. This technique is especially popular in
Italy, with thousands of patients and years of expe-
rience. A randomized study could be organized to

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Chapter 7 · What Can We Do To Decrease the Risk of Vas Deferens Injury
⊡ Fig. 7.2. Closure of the aponeurosis of the external oblique
muscle below (instead of above) the spermatic cord
⊡ Fig. 7.3. Closure of the lateral part of the aponeurosis of the
external oblique muscle; the medial part of the aponeurosis is
already closed below the spermatic cord
assess the effectiveness of such modification of the
Lichtenstein technique, but in our opinion, a suf-
ficient amount of indirect confirmatory evidence
exists. Professor Smeds from Sweden started using
this approach after our recent publication [26] a
year ago and found only one (0.3%) recurrence
after 300 repairs (personal communication).
In my opinion, a shutter-valve effect of mesh
tails sutured together and wrapping the cord is
dangerous because it unnecessarily enhances con-
tact between the surface of the mesh with the
cord, creating a cuff that contracts substantially
around the spermatic cord in the postoperative
53 7
period as the mesh contracts. It may compromise
the vas as well as blood vessels within the cord.
Moreover, the sharp edge of the mesh on which
the spermatic cord directly kinks upon entering
the inguinal canal from the deep inguinal ring is
considered a common place for vas injury. A flat,
preshaped onlay mesh with a hole for the sper-
matic cord decreases contact between the mesh
and the cord without compromising the effective-
ness of the Lichtenstein technique. The efficacy of
this approach was clearly proven by the Trabucco
technique and other repairs using a preshaped
onlay mesh with a preformed hole for the sper-
matic cord. In the above proposed approach, direct
kinking of the cord over the mesh is avoided, and
the cord instead folds over the fascia of the exter-
nal aponeurosis while entering the subcutaneous
space. The proposed surgical techniques comply
with the principles of the tension-free operation
and can be easily implemented.
In summary, although the actual rate of vas
deferens injury due to fibroblastic inflammation
around polypropylene mesh is not yet known,
there is strong experimental and clinical evidence
that such processes can and do take place.
Therefore, until the risk is fully investigated, all
patients with any known compromise to their re-
productive health or with concerns about fertility
can be offered a surgical technique that minimizes
the potential risk without diminishing all the ad-
vantages of tension-free hernia repair. Isolating
the spermatic cord from the mesh by placing it
above (not below) the aponeurosis of the oblique
abdominal muscle seems to be an easy, applicable,
and effective solution.
References
1. Fitzgibbons RJ Jr. (2005) Can we be sure polypropylene
mesh causes infertility? Ann Surg 241:55–561
2. Peiper Ch, Klinge U, Junge K, Schumpelick V (2006) Is
there a risk of infertility after inguinal mesh repair? Ex-
perimental study in pig and the rabbit. Hernia 10:7–12
3. Amid PK (2004) Radiologic images of meshoma: a new
phenomenon causing chronic pain after prosthetic repair
of abdominal wall hernias. Arch Surg 139:1297–1298
4. Chuback JA, Singh RS, Sills C, et al. (2000) Small bowel ob-
struction resulting from mesh plug migration after open
inguinal hernia repair. Surgery 127:475–476
 54 Chapter 7 · What Can We Do To Decrease the Risk of Vas Deferens Injury due to Inguinal Hernioplasty?
5. Agrawal A, Avill R (2005) Mesh migration following repair
if inguinal hernia: a case report and review of literature.
Hernia 10:79–82
6. Jeans S, Williams GL, Stephenson BM (2007) Migration
after open mesh plug inguinal hernioplasty: a review of
the literature. Am Surg 73:207–209
7. Weber-Sánchez A, García-Barrionuevo A, Vázquez-Frias
JA, Cueto-Garcia J (1999) Laparoscopic management of
spermatic cord entrapment after laparoscopic inguinal
herniorrhaphy. Surg Laparosc Endosc Percutan Tech
9:296-9
8. Sweat SD, Itano NB, Clemens JQ, et al. (2002) Polypropyl-
ene mesh tape for stress urinary incontinence: complica-
tions of urethral erosion and outlet obstruction. J Urol
168:144–146
9. Dunn JS Jr, Bent AE, Ellerkman RM et al. (2004) Voiding
dysfunction after surgery for stress incontinence: litera-
ture review and survey results. Int Urogynecol J Pelvic
7 Floor Dysfunct 15:25–31
10. Trabucco AF, Blitstein J (2004) T-sling for the treatment of
stress urinary incontinence. Am J Urol Rev 12:583–588
11. Uzzo RG, Lemack GE, Morrissey KP, Goldstein M (1999)
The effects of mesh bioprosthesis on the spermatic cord
structures: a preliminary report in a canine model. J Urol
161(4):1344–1349
12. Goldenberg A, Paula JF (2005) Effects of the polypropyl-
ene mesh implanted through inguinotomy in the sper-
matic funiculus, epididium and testis of dogs. Acta Cir
Bras 20(6):461–467
13. Berndsen FH, Bjursten LM, Simanaitis M, Montgomery A
(2004) Does mesh implantation affect the spermatic cord
structures after inguinal hernia surgery? An experimental
study in rats. Eur Surg Res 36(5):318–322
14. Maciel LC, Glina S, Palma PC, Nascimento LF, Netto NR
Jr. (2007) Histopathological alterations of the vas def-
erens in rats exposed to polypropylene mesh. BJU Int
100:187–190. Erratum in: Costa Nascimento FC [corrected
to Nascimento, Luiz FC] (2007) BJU Int 100:481
15. Ridgway PF, Shah J, Darzi AW (2002) Male genital tract
injuries after contemporary inguinal hernia repair. BJU Int
90:272–276
16. Valenti G, Baldassarre E, Torino G (2006) Vas deferens ob-
struction due to fibrosis after plug hernioplasty. Am Surg
72:137–138
17. Nagler HM, Belletete BA, Gerber E, Dinlenc CZ (2005)
Laparoscopic retrieval of retroperitoneal vas deferens in
vasovasostomy for postinguinal herniorrhaphy obstruc-
tive azoospermia. Fertil Steril 83:1842
18. Meacham RB (2002) From androlog. Potential for vasal
occlusion among men after hernia repair using mesh. J
Androl 23:759-761
19. Aasvang EK, Kehlet H (2008) Postherniotomy dysejacula-
tion: successful treatment with mesh removal and nerve
transection. Hernia 12:645–647
20. Silich RC, McSherry CK (1996) Spermatic granuloma. An
uncommon complication of the tension-free hernia re-
pair. Surg Endosc 10:537–539
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21. Shin D, Lipshultz LI, Goldstein M, Barmé GA, Fuchs EF,
Nagler HM, McCallum SW, Niederberger CS, Schoor RA,
Brugh VM 3rd, Honig SC (2005) Herniorrhaphy with poly-
propylene mesh causing inguinal vassal obstruction: a
preventable cause of obstructive azoospermia. Ann Surg
241:553–558
22. Matsuda T, Muguruma K, Horii Y, Ogura K, Yoshida O
(1993) Serum antisperm antibodies in men with vas def-
erens obstruction caused by childhood inguinal hernior-
rhaphy. Fertil Steril 59:1095–1097
23. Agarwal BB, Sinha BK, Mahajan KC (2008) The risk of com-
municating TEP-related infertility risk is an opportunity
and not a »Cinderella concern« anymore. Surg Endosc
22:1557–1558
24. Valenti G, Baldassarre E (2006) Vasal obstruction after
hernioplasty: the importance of surgical strategy in pre-
venting azoospermia. Ann Surg 244:160; author reply
160
25. Trabucco EE, Trabucco AF (2002) Tension-free, sutureless,
preshaped mesh hernioplasty. In: Nyhus LM, Condon RE
(eds) Hernia, 5th edn. Lippincott Williams & Wilkins, Phila-
delphia, pp 159–164
26. Witkowski P, Trabucco EE (2007) Is there an increased
risk of the vas deferens occlusion after meshes inguinal
hernioplasty and what can we do about it? Ann Surg.
245:153–154
27. Trabucco EE, Trabucco AF (1998) Flat plug and mesh
hernioplasty in the »inguinal box«: description of the
surgical technique. Hernia 2:133–138
28. Adamonis W, Witkowski P, Smietanski M, et al. (2006) Is
there a need for a mesh plug in inguinal hernia repair?
Randomized, prospective study of the use of Herta 1
mesh compared to PerFix Plug. Hernia 10:223–228
29. Cucci M, De Carlo A, Di Luzio P, et al. (2002) The Trabucco
technique in the treatment of inguinal hernias: a six-year
experience. Minerva Chir 57:457– 459
30. Testini M, Miniello S, Piccinni G, et al. (2002) Trabucco ver-
sus Rutkow versus Lichtenstein techniques in the treat-
ment of groin hernia: a controlled randomized clinical
trial. Minerva Chir 57:371–376
Discussion
Deysine: The previous study did not show much
damage caused by the mesh. The differences were
not statistically significant in most cases. So we
don’t have any hard data to prove anything at this
time. I would suggest that until we have more hard
data, human hard data, we should restrain the
kind of language that we use when we express our
impressions.
Köckerling: I have to speak for the endoscopic
procedure. At the moment, we really have no data,
Chapter 7 · What Can We Do To Decrease the Risk of Vas Deferens Injury
55 7
even no clinical data, showing that there is really
a higher problem for vas deferens injury or any
other influence on that system due to endoscopic
inguinal hernia repair. So I wouldn’t go so far as
to exclude this technique in younger patients who
are fertile. Maybe we will have some problems.
We should carefully look at those problems, learn
how to avoid them, and choose the right mesh,
but we shouldn’t go so far as to exclude all mesh
procedures.
Kehlet: I think we are at the state where we can
say that we should not dissect the cremaster from
the cord.
Amid: We have to understand that if we use a mesh
and we don’t remove the cremastic muscle, none of
these potential problems will occur.
[UnitedVRG] - Medical Release Group
 8

The Long-Term Effect on Testicular

Function of a Mesh Bioprosthesis Used
for Inguinal Hernia Repair

H. Aydede
 58 Chapter 8 · The Long-Term Effect on Testicular Function of a Mesh Bioprosthesis Used for Inguinal Hernia Repair
Introduction
Polypropylene mesh currently finds widespread use
throughout the world in hernia repair, as it is well
tolerated by the body and allows tissue ingrowth into
the prosthesis [1]. Experimentally, all meshes cause
an initial inflammatory tissue response in the recipi-
ent after implantation [2]. Interestingly, in most clin-
ical studies in humans, these meshes are described as
inert materials, but systematic morphological exami-
nations of the long-term effects of meshes commonly
used for hernia repair in humans are rare [3].
Nitric oxide (NO), a freely diffusible, water- and
lipid-soluble molecule, is formed from L-arginine
and molecular oxygen by a family of nitric oxide
synthases [4]. In the testis, nitric oxide synthase
(NOS) from endothelial cells (eNOS) is expressed
in the Leydig cell, Sertoli cell, spermatocyte, and
8 spermatid [5]. Expression of inducible NO synthase
(iNOS) requires transcriptional activation, which is
induced by various combinations of cytokines [6].
The upregulation of NOS leads to excessive NO pro-
duction for prolonged periods of time and accounts
for oxyradical-mediated damage [6]. Although little
is known about the mechanism of its toxicity in
germ cell injury from testicular ischemia, NO is
an important mediator of cell death through either
apoptosis or necrosis, depending on the intensity
and duration of injury [7].
The aim of the present study was to investigate
long-term effects of mesh implantation on testicular
hormone function and NO metabolism [8]. Testicu-
lar hormone function was evaluated by assessments
of serum luteinizing hormone (LH) and follicle-
stimulating hormone (FSH) levels. Testicular NO
metabolism was investigated by testicular NO levels,
iNOS, and eNOS expressions. Testicular ischemic
damage impairing spermatogenesis with the pos-
sibility of leading to male infertility was assessed by
germ-cell-specific apoptosis in the rat testis.
Material and Methods
Animals and Surgical Technique
The study comprised 40 male Swiss albino rats,
10–12 weeks old and 200–220 g in weight. The rats
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were housed in a temperature- and light-controlled
environment with ad libitum access to water and rat
food pellets for 3 days before the study. All experi-
mental procedures were approved by the Experi-
mental Animal Research Ethics Committee of the
Faculty of Medicine. All surgical procedures were
performed under general anesthesia administered
by intramuscular injection of ketamine and xylazine
hydrochloride, employing sterile techniques.
Experimental Design
The animals were randomly allocated into two
groups, each containing 20 rats. In group 1, the op-
eration was performed using an infrainguinal inci-
sion above the scrotum, and the inguinal anatomy
was explored. The left spermatic cord was elevated,
and a 0.5×1.0-cm polypropylene mesh (Surgipro,
United States Surgical, Norwalk, CT, USA) was
placed behind the left inguinal spermatic cord.
To avoid displacement, the mesh was sutured to
aponeurotic tissue behind the spermatic cord us-
ing 4/0 polypropylene. In group 2, the sham-op-
erated controls, the left inguinal spermatic cord
was elevated and left in place with no further ma-
nipulations. An intracardiac blood sample (1 ml)
was obtained for biochemical analysis from both
groups during the preoperative period.
All animals were housed in standard condi-
tions in the experimental research laboratory for
6 months. After 6 months, before the rats were
sacrificed, a 2-ml sample of intracardiac blood was
taken, and both testes were removed for examina-
tion. All testes were divided into two halves. One
half of each testicular sample was placed in Bouin’s
fixative solution for histological evaluation, and the
other halves were snap-frozen in liquid nitrogen
and stored at -70ºC for biochemical evaluation.
Assessment of Hormonal Function
of the Testes
Serum samples were frozen at -70ºC for batch
analysis. Serum LH and FSH levels were assessed
by immunoradiometric assay methods with DPC
(Diagnostic Products, Los Angeles, CA, USA) re-
Chapter 8 · The Long-Term Effect on Testicular Function of a Mesh Bioprosthesis
agents. The method sensitivities were 0.15 mIU/
ml-1 and 0.06 mIU/ml-1. Intra-assay precisions
were 1.6 and 7.1%, and interassay precisions were
3.8% and 5.7% for LH and FSH, respectively.
Concentration of NO in Testes
In estimating the tissue NO production, biochemi-
cal assessments of stable NO oxidative metabolite
(nitrite and nitrate) levels were analyzed. Assess-
ments of tissue nitrite and nitrate levels were based
on the Griess method. The absorbance of the re-
action mixture was measured at 545 nm with a
spectrophotometer (Shimadzu, Japan). A standard
curve was obtained with concentrations of 2–10
mmol/l-1 sodium nitrate. Data in this study present
the total nitrite and nitrate, which are NO metabo-
lites and are expressed as mmol/g-1 wet tissue.
Immunohistochemical Evaluation
All specimens were fixed in Bouin’s solution for
24 h. Sections (5 mm thick) from paraffin blocks
were incubated in a solution of 3% H2O2 for 15
min to inhibit endogenous peroxidase activity.
Then sections were washed with phosphate base
solution (PBS) and incubated for 18 h at 4ºC with
primary antibodies: anti-iNOS at a 1/100 dilution
(Zymed 61-7700) and anti-eNOS at a 1/200 dilu-
tion (Biomol SA-258). Afterwards, sections were
washed three times for 5 min each with PBS, fol-
lowed by incubation with biotinylated IgG and
then with streptavidin–peroxidase conjugate
(Dako). They were incubated with DAB (3.3’-di-
aminobenzidine) substrate for detection of im-
munoreactivity. Control samples were processed in
an identical manner, but the primary antibody step
was omitted. Staining intensity was graded as mild
(+), moderate (++), or strong (+++).
Detection of Apoptotic Cell Death
In Situ Using the TUNEL Method
To obtain evidence for induction of programmed
cell death, apoptotic cells were identified using
59 8
a terminal deoxynucleotidyl transferase-mediated
biotin nick end–labeling (TUNEL) method. Frag-
mentation of DNA in the nucleus is one of the first
morphological changes in the apoptotic process
and can be detected in histological sections us-
ing the TUNEL method performed with a com-
mercial kit, such as the DeadEnd Colorimetric
TUNEL system (Promega G7130), according to
the manufacturer’s instructions. The quantification
of apoptosis was carried out in a blind fashion by
two independent observers.
Statistical Evaluation
Statistical analyses were performed with SPSS 10.0
software. Groups were compared using a two-
tailed Student’s t-test, one-way ANOVA test, and
Mann–Whitney U-test. Values of p<0.05 were con-
sidered to indicate statistical significance.
Results
Testicular tissue NO levels in ipsilateral and con-
tralateral testes in the mesh-implanted group
and sham-operated control groups are shown in
⊡ Table 8.1. We found significant increases in the
ipsilateral testicular NO level compared with the
contralateral NO level in the mesh-implanted
group and the control group (p=0.0001, p=0.002,
respectively). Comparison of the mesh-implanted
group and the control group revealed significantly
(p=0.015) higher NO levels in the ipsilateral mesh
group.
The results of hormonal evaluation of testicu-
lar function of the study groups preoperatively and
6 months postoperatively are given as mean ± stan-
dard deviation. Serum LH and FSH levels are sum-
marized in ⊡ Table 8.2 for preoperative serum sam-
ples and 6-month postoperative serum samples in
the mesh-implanted group and the sham-operated
control group. No significant statistical differences
between preoperative and postoperative samples
were seen in serum LH or FSH levels.
We found mild (+) eNOS activity in ipsilat-
eral and contralateral specimens of the mesh-im-
planted and sham-operated groups. However, (+)
 60 Chapter 8 · The Long-Term Effect on Testicular Function of a Mesh Bioprosthesis Used for Inguinal Hernia Repair

⊡ Table 8.1. Testicular tissue nitric oxide (NO) levels in ipsilateral and contralateral testes in the mesh and sham-operated
control groups (values given as mean ± standard deviation)

NO (μmol-1 wet tissue) Ipsilateral testis Contralateral testis P

a
Mesh group 230.3±90.9 180.6±74.8 0.0001

Sham-operated control group 166.56±32.0a 140.88±29.3 0.002

a
P=0.015

⊡ Table 8.2. Serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels in the preoperative and post-
operative periods in the mesh-implanted and sham-operated control groups (values given as mean ± standard deviation)

Mesh-implanted group Sham-operated control group

Preoperative Postoperative Preoperative Postoperative

-1)
LH (mIU/ml 0.582±0.065 0.571±0.084 0.626±0.086 0.636±0.088
-1)
FSH (mIU/ml 0.362±0.050 0.353±0.041 0.385±0.043 0.340±0.050
8

iNOS activity was observed only in the ipsilateral
testis of the mesh-implanted study group, and no
expression was detected in the remaining samples
(⊡ Fig. 8.1). TUNEL (+) apoptotic germ cells were
not detected in any of the samples.
Discussion
The major finding of the present study was that
no apoptotic TUNEL (+) cells were present in
the mesh-implanted study group. Therefore, we
believe that mesh implantation does not cause
secondary ischemic changes in testicular function
over the long term.
It has been shown that acute graded reductions
in testicular blood flow affect the early stages of
spermatogenesis, which may have a major impact
on sperm production [9].
In my study in 2003, we evaluated the long-
term effect of mesh and its localization (i.e., an-
terior or posterior) on testicular perfusion and
function in groin hernia patients. Testicular func-
tion was evaluated with spermiograms and testicu-
lar perfusion with color Doppler ultrasonography.
Group I consisted of 30 posterior preperitoneal
mesh repair patients, and group II consisted of an-
terior tension-free repair patients. There were no
statistically significant differences between the pre-
operative and postoperative spermiogram results
for either group. No statistically significant differ-
ence was found between the two groups in terms
of Doppler flow parameters (peak systolic velocity,
end diastolic velocity, resistive index, pulsatility
index) for preoperative, early, or late postopera-
tive periods. When Doppler flow parameters were
compared for group I, a statistically significant dif-
ference was found between preoperative and early
postoperative values. No statistically significant
difference was found between preoperative and
late postoperative values. This was also true for
early postoperative values versus late postopera-
tive values. When Doppler flow parameters were
compared for group II, a statistically significant
difference was found between preoperative and
early postoperative values. No statistically signifi-
cant difference was found between preoperative
and late postoperative values. This was also true
for early postoperative values versus late postop-
erative values. No statistically significant differ-
ence was observed between preoperative and late
postoperative Doppler flow parameters, nor was a
statistically significant difference seen between the
preoperative and day-75 postoperative spermio-

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Chapter 8 · The Long-Term Effect on Testicular Function of a Mesh Bioprosthesis
Ipsilateral
Mesh
Control
⊡ Fig. 8.1. Mild positive (+) iNOS immunostaining is shown in
the stroma of the ipsilateral testis (a) of the mesh-implanted
study group. Negative (-) iNOS immunostaining is shown in
gram results for either mesh repair group. Bear-
ing in mind the experimentally proven chronic
inflammatory tissue reaction against mesh, these
results indicate that chronic tissue inflammation
has no adverse effect on testicular perfusion or
spermatogenetic function over time [10].
The production of NO as well as its injuri-
ous metabolite peroxynitrite and other reactive
nitrogen species may result in a cascade of events
leading to DNA fragmentation and apoptosis. It is
well known that the early stages of spermatogen-
esis are very sensitive to a moderate, acute reduc-
tion in blood flow, and consistent reductions in
blood flow may interfere with sperm production
and adversely affect fertility [11]. NO is one of
many inflammatory mediators, which include the
adhesion molecules and cytokines that contribute
to the inflammatory cell adherence of testicular
microvascular endothelium and lead to microcir-
culatory failure. Apoptosis is directly linked to the
recruitment of neutrophils to subtunical venules
[11]. NO is important in increasing blood flow and
inhibiting leukocyte accumulation [12]. In addi-
61 8
Contralateral
Mesh
Control
the contralateral (b) testis of the mesh-implanted study group
and ipsilateral (c) and contralateral (d) testes of the sham-
operated control group. ×400 original magnifications
tion, NO has a dual effect. On the one hand, it is
vasodilatory in modest increases and potentially
protective of testicular tissue, but on the other
hand, excessive amounts can exert cytotoxic ef-
fects in combination with other cytokines and may
result in testicular germ-cell-specific apoptosis. In
the present study, we observed a significant in-
crease in NO level and mild (+) iNOS expression
in the ipsilateral side of the mesh-implanted group,
which suggests ischemic/inflammatory injury of
the mesh-implanted testis; however, this injury
was not sufficient to cause germ cell apoptosis in
the testicular tissue.
In a study investigating the eNOS immunos-
taining and apoptosis in testicular ischemia, it
was reported that acute (3 h) testicular ischemia
resulted in germ cell apoptosis, and strong eNOS
immunostaining was detected in the cytoplasm of
degenerating germ cells [13]. The authors suggest
that strong eNOS immunostaining is associated
with germ cell apoptosis. Similarly, in our observa-
tions in the present study, the long-term results
of mesh implantation revealed mild (+) eNOS
 62 Chapter 8 · The Long-Term Effect on Testicular Function of a Mesh Bioprosthesis Used for Inguinal Hernia Repair
expressions in all samples, and no apoptotic germ
cells were observed in testicular tissue.
In the present study we found no statistical
difference in serum hormone levels between the
mesh-implanted study groups and the sham-oper-
ated controls. Thus, long-term mesh implantation
does not cause biochemical alteration of the hor-
monal functions of the testes.
Part of this study was presented at the 13th
European Microscopy Congress in 2004. Our pre-
sented results demonstrated that cells with py-
knotic nuclei, which indicate apoptotic cells, were
observed less in the mesh group than in the con-
trol group when analyzed both by light and elec-
tron microscopy [14].
In conclusion, using prosthetic mesh in hu-
mans did not cause any defects in testicular perfu-
sion or spermatogenetic function. In this experi-
8 mental model, NO level as an oxidative damage
indicator was found to be increased in rat testes,
and iNOS overexpression was detected immuno-
histochemically. The increased level of NO is one
of the apoptotic promoters. However, finding no
difference for apoptosis and no ultrastructural dif-
ference in electron microscopy emphasizes that
this oxidative damage is compensated for by tes-
ticular tissue. Thus, prosthetic mesh repair in pa-
tients undergoing infertility treatment can be me-
ticulously reevaluated.
References
1. DeBorg JR (1998) The historical development of prosthe-
tics in hernia surgery. Surg Clin North Am 78:973–1006
2. Klinge U, Klosterhalfen B, Müller M, Schumpelick V (1999)
Foreign body reaction to meshes used for the repair of
abdominal wall hernias. Eur J Surg 165:665–673
3. Bendavid R (1998) Complications of groin hernia surgery.
Surg Clin North Am 78:1080–1103
4. Moncada S, Palmer RMJ, Higgs EA (1991) Nitric oxide: phy-
siology, pathophysiology and pharmacology. Pharmacol
Rev 43:109–142
5. Zini A, O’Bryan MK, Magid MS, Schlegel PN (1996) Immu-
nohistochemical localisation of endothelial nitric oxide
synthase in human testis, epididymis and vas deferens
suggest a possible role for nitric oxide in spermatogene-
sis, sperm maturation and programmed cell death. Biol
Reprod 55:935–941
6. Nathan C (1997) Inducible nitric oxide synthase: what
differences does it make? J Clin Invest 100:2417–2423
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7. Bonfoco E, Krainc D, Ankarcrona M, Nicotera P, Lipton
SA (1995) Apoptosis and necrosis: two distinct events
induced, respectively, by mild and intense insults with N-
methy-D-aspartate or nitric oxide/superoxide in cortical
cell cultures. Proc Natl Acad Sci USA 92:7162–7166
8. Taneli F, Aydede H, Vatansever S, Ulman C, Arı Z, Uyanık
BS (2005) The long-term effect of mesh bioprosthesis
in inguinal hernia repair on testicular nitric oxide meta-
bolism and apoptosis in rat testis. Cell Biochem Funct
23:213–220
9. Berg A, Collin O, Lissbrant E (2001) Effect of acute graded
reduction in testicular blood flow on testicular morpho-
logy in the adult rat. Biol Reprod 64:13–20
10. Aydede H, Erhan Y, Sakarya A, Kara E, Iklgül O, Can M
(2003) Effect of mesh and its localisation on testicular flow
and spermatogenesis in patients with groin hernia. Acta
Chir Belg 103:607–610
11. Lysiak JJ, Turner SD, Nguyen QAT, Singbarth K, Ley K,
Turner TT (2001) Essential role of neutrophils in germ
cell-specific apoptosis following ischemia/reperfusion of
mouse testis. Biol Reprod 65:718–725
12. Lissbrant E, Lofmark U, Collin O, Berg A (1997) Is nitric
oxide involved in the regulation of rat testicular vascula-
ture? Biol Reprod 56:1221–1227
13. Zini A, Abitbol J, Girardi SK, Schulsinger D, Goldstein M,
Schegel PN (1998) Germ cell apoptosis and endothelial ni-
tric oxide synthase (eNOS) expression following ischemia-
reperfusion injury to testis. Arch Androl 41:57–65
14. Vatansever HS, Taneli F, Kayma F, Köse CF, Müftüoğlu S,
İlgül O (2004) Testicular nitric oxide levels and apoptosis
in rat testes during inguinal hernia repair after using
long-term mesh bioprosthesis. In: Proceedings of the13th
European Microscopy Congress, Antwerp, Belgium, 22–27
August 2004
Discussion
Schumpelick: I looked for your spermiograms.
Did you see any differences in motility or in any
other analysis of testicular function besides the
spermiograms according to the investigation pe-
riod?
Aydede: You are right. In our study we found no
statistical significant difference between the differ-
ent investigation time points.
Klinge: The point I want to address is the method
of statistical analysis. You frequently said that some
differences were statistically significant or not sig-
nificant. I’m not sure whether many of these data
were really normal distributed. If you compare
just the means between two groups, I’m not sure
if some single details, such as a complete constric-
Chapter 8 · The Long-Term Effect on Testicular Function of a Mesh Bioprosthesis
63 8
tion of the vas, will be detected by this test. Did
you use some other statistical tests for subgroups
in your entire cohort?
Aydede: At this time I can’t give you more infor-
mation about statistical analysis than the Mann–
Whitney U-test. We should do a more detailed
analysis.
Gryska: In the very first clinical study, how many
patients did you have in each group?
Aydede: We had about 30 patients in each group.
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 9

Reoperation Following Lichtenstein

Repair: What Do Vas and Nerves Look
Like?
U. Muschaweck
 66 Chapter 9 · Reoperation Following Lichtenstein Repair: What Do Vas and Nerves Look Like?

Introduction

Lichtenstein repair is recommended in national

guidelines as the first choice for uncomplicated
primary inguinal hernia. It is known as easy to
perform, has a short learning curve, and is said
to have the smallest risk for recurrent hernia and
other complications.
However, in the year 2007 we had to reoperate
on 232 patients with recurrent hernia, making up
20% of all our operations. Of these, 31 had had a
previous Lichtenstein repair. In all 31 cases, the
intraoperative findings showed complete incorpo-
ration of at least one nerve, mesh shrinkage and
migration, and excessive scar tissue in the area of ⊡ Fig. 9.1. Case 1: hardened mesh with stiff, sharp edges; vas
adherent to mesh edge
the external oblique fascia, the internal oblique
muscle, and the groin ligament. We always had to
remove the mesh completely because of the tissue
damage in the groin canal. Also, neurectomy of at
least one nerve always had to be done.
9
Case Reports

We have selected six cases of patients with se-

vere chronic groin pain resulting in reoperation
with impressive intraoperative findings. Two of
these had a severed vas that was caused by the
mesh.

⊡ Fig. 9.2. Case 1: ilioinguinal nerve thickened; surface rough,

Case 1: DL, 62-Year-Old Man from not shiny; surrounded by fibrotic tissue. Recurrent hernia
Wales 3×3 cm

History: Lichtenstein repair in Cardiff, Wales, in

October 2006. After 1 year, massive pain in the
groin and radiating, burning pain to the scrotal
area and penis. Unable to walk more than 30 m.

Applied surgical technique: Removal of the

mesh, neurectomy of the ilioinguinal nerve, Lich-
tenstein repair with UltraPro mesh (⊡ Figs. 9.1 and
9.2). Patient immediately free of pain.

Electron microscopy and histological findings:

Heavyweight small-pore polypropylene mesh; in- ⊡ Fig. 9.3. Case 1: heavyweight small-pore polypropylene
growth of nerve with marked perineural fibrosis; mesh; ingrowth of nerve with marked perineural fibrosis;
posttraumatic neuroma (⊡ Fig. 9.3). posttraumatic neuroma

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Chapter 9 · Reoperation Following Lichtenstein Repair: What Do Vas and Nerves Look Like?
67 9
Case 2: HB, 61-Year-Old Man from Electron microscopy and histological findings:
Germany Large-pore polypropylene mesh (⊡ Fig. 9.6), mod-
erate foreign body reaction (epithelioid cell type).
History: Lichtenstein repair in Oldenburg, Ger-
many, in October 2006. After 8 months, new bulge
was present, with pressure and pain in the groin Case 3: MR, 26-Year-Old Man from
and severe pain during ejaculation. Denmark

Intraoperative findings: Excessive scar tissue; mesh History: Lichtenstein repair in September 2007,
surrounding vas at the internal ring (⊡ Figs. 9.4 and with pain starting immediately afterward. Reop-
9.5). eration in December 2007.

Applied surgical technique: Removal of the mesh, Intraoperative findings: Mesh covering the ilio-
neurectomy of the ilioinguinal nerve, minimal repair inguinal nerve completely; nerve partly growing
(suture repair). Patient immediately free of pain. into the mesh (⊡ Fig. 9.7).

⊡ Fig. 9.4. Case 2: excessive scar tissue; mesh surrounds vas at ⊡ Fig. 9.6. Case 2: large-pore polypropylene mesh, moderate
the internal ring foreign body reaction (epithelioid cell type)

⊡ Fig. 9.5. Case 2: ilioinguinal nerve thickened and grown into ⊡ Fig. 9.7. Case 3: mesh covers the ilioinguinal nerve com-
the upper edge of the mesh, surrounded by fibrotic tissue; pletely; nerve partly growing into the mesh; small medial
lateral recurrent hernia 8×2 cm recurrent hernia
 68 Chapter 9 · Reoperation Following Lichtenstein Repair: What Do Vas and Nerves Look Like?

⊡ Fig. 9.8. Case 3: heavyweight small-pore polypropylene ⊡ Fig. 9.9. Case 4: inguinal nerve ingrowth into mesh; lateral
mesh, foreign body granuloma, perineural fibrosis edge of mesh rolled up and penetrating through the fascia and
subcutaneous tissue; palpable through skin. No recurrent hernia

Applied surgical technique: Removal of the mesh

9 with neurectomy and minimal repair.

Electron microscopy and histological findings:

Heavyweight small-pore polypropylene mesh
(⊡ Fig. 9.8), foreign body granuloma, perineural
fibrosis. Low-grade infection with neutrophilic
granulocytes.

Case 4: GM, 40-Year-Old Man from Italy

History: Lichtenstein repair in 2005, with pain

starting immediately afterward. Reoperation in
February 2008.
⊡ Fig. 9.10. Case 4: double-layered, heavyweight, small-pore
Intraoperative findings: Inguinal nerve ingrowth polypropylene mesh
into mesh; lateral edge of mesh rolled up and
penetrating through the fascia and subcutaneous
tissue; palpable through the skin (⊡ Fig. 9.9). No
recurrent hernia. Case 5: JC, 66-Year-Old Man from England

Applied surgical technique: Removal of the mesh History: Lichtenstein repair in 2001, reoperation
with only a neurectomy done. in 2008.

Electron microscopy and histological findings: Intraoperative findings: Mesh corrugated, only
Double-layered, heavyweight, small-pore polypro- partial ingrowth (⊡ Fig. 9.11). Ilioinguinal nerve
pylene mesh, bulky board of scar, beginnings of adherent to mesh over 2 cm. Lateral recurrent her-
calcification (⊡ Fig. 9.10). nia 3×2 cm.

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Chapter 9 · Reoperation Following Lichtenstein Repair: What Do Vas and Nerves Look Like?
69 9

⊡ Fig. 9.11. Case 5: mesh corrugated; only partial ingrowth. ⊡ Fig. 9.12. Case 5: mesh type uncertain, chronic inflamma-
Ilioinguinal nerve adherent to mesh over 2 cm. Lateral recur- tion (giant cells)
rent hernia 3×2 cm

Applied surgical technique: Removal of the

mesh, neurectomy, Lichtenstein repair with Ultra-
Pro mesh.

Electron microscopy and histological findings:

Mesh type uncertain (⊡ Fig. 9.12), chronic inflam-
mation (giant cells).

Case 6: HW, 29-Year-Old Woman from

Germany

History: Lichtenstein repair in March 2006. Pain ⊡ Fig. 9.13. Case 6: Vypro mesh with ingrowth of ilioinguinal
started in August 2007; reoperation in February nerve. Medial recurrent hernia 3×2.5 cm
2008.

Intraoperative findings: Small amount of Vy-

pro mesh with ingrowth of ilioinguinal nerve
(⊡ Fig. 9.13). Medial recurrent hernia 3×2.5 cm.

Applied surgical technique: Removal of the mesh

(⊡ Fig. 9.14), followed by neurectomy and minimal
repair.

Electron microscopy and histological findings:

Vypro mesh with posttraumatic neuroma and
marked perineural fibrosis.

⊡ Fig. 9.14. Case 6: removal of the mesh, followed by neurec-

tomy and minimal repair
 70 Chapter 9 · Reoperation Following Lichtenstein Repair: What Do Vas and Nerves Look Like?

Is the Mesh Type Important?
This sample of six patients whom we looked at
in greater detail is certainly very small. But there
is only a slight tendency that heavyweight mesh
might be more often involved (see ⊡ Table 9.1).
Summary
In these six patients, heavyweight small-pore
meshes were slightly more predominant than
heavyweight large-pore or lightweight meshes. But
more important than the choice of mesh is the
surgical handling of the nerve. (Is a primary resec-
tion better than keeping the nerve?) Therefore, the
indication for mesh repair must be carefully con-
sidered, particularly in young patients.
9 ⊡ Table 9.1. Mesh types encountered in the six cases
and examined by electron microscopy
Polypropylene 4 it is probably not a real problem.
Heavyweight small-pore 3
most cases there is only one nerve left. So I prefer
resecting the mesh and the mesh in this case.
Uzzo: In the literature you find up to a 10%
chronic pain rate after Lichtenstein repair. I think
we should stop saying that Lichtenstein repair is
easy to perform. You said it during your slides.
Obviously, it’s not easy.
Muschawek: You are right. It looks easy, but there
are many details you have to think about.
Heniford: I think we should put all these problem
patients together with a standard study protocol,
and we will get very quickly large numbers of pa-
tients through which we can answer questions.
Klinge: You have a lot of experience with recurrent
hernias. Do you think that it makes a difference in
reoperating after 2 years or after 10 years?
Muschawek: No. You will have the adhesion within
a few weeks after operation.
Kehlet: I just remember the first reports about
pain after Lichtenstein repair. Now we are sitting
here for a full meeting discussing chronic pain. So
I think we have to be careful also with this fertility
problem. We have to look at it, and we cannot say

Heavyweight large-pore 1

Vypro 1

Unknown (could not be analyzed) 1

Discussion

Schumpelick: You mentioned that the nerve has

grown into the mesh, but it may be that the mesh
has grown into the nerve.
Muschawek: You are right; during the explantation
you are not able to see which direction was the
right one.
Miserez: Two questions on the six patients you
operated on for pain and recurrence. First, is it
enough to do a single neurectomy, and second, do
we need to remove the mesh for pain?
Muschawek: I’m sure, because the mesh always
covers the nerve, and if you lift up the mesh you
can see the nerve going into the mesh. And in

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 10

Damage to the Spermatic Cord

from Groin Herniorrhaphy: A Review
R. C. Read
 72 Chapter 10 · Damage to the Spermatic Cord from Groin Herniorrhaphy: A Review
Introduction
Complications following repair of inguinal hernia-
tion have historically been attributed to poor surgi-
cal technique and blamed on inexperience. Those
related to the spermatic cord, testicular atrophy
and occlusion of the vas deferens, are dreaded
because the patient, angry that his manhood has
been threatened, often resorts to litigation. Isch-
emia of the testicle was said to be the result of a
too-tight reconstruction of the internal inguinal
ring [1]. Injury to the vas deferens is presumed to
arise after harsh separation of the hernial sac. The
former may be ligated, divided, or devascularized.
Considered rare, it is underreported because most
men undergoing groin repair tend to be older and
are no longer concerned about their reproduc-
tive capacity. Because most inguinal herniae are
unilateral, younger men rarely face sterility. Nev-
ertheless, a significant minority have bilateral re-
pairs. Further, cryptorchidism or later epididymitis
can eliminate the spermatic contribution from the
contralateral groin.
10
Sutured Repair
During the latter half of the 20th century, the
Shouldice–Bassini procedure became the gold
standard for groin hernioplasty. In the early 1980s,
Wantz and Bendavid, two pioneers in herniology,
separately focused attention on testicular ischemia
and vasal narrowing. In 1982, Wantz [2, 3] re-
ported that 11 of 1,682 patients developed orchitis
within a week. All had had complete removal of
their scrotal sacs. After the same operation was
performed on 311 men for recurrence, seven pro-
gressed to testicular atrophy. Wantz blamed dissec-
tion through scarred tissue. The common feature
was thrombosis affecting the pampiniform plexus
and leading to venous infarction. Wantz pointed
out that constriction at the internal inguinal ring
was not responsible because ligation of testicular
veins at this level, which is standard treatment for
varicocele, does not cause testicular infarction. To
avoid this complication, he recommended that in a
complete indirect inguinal hernia, dissection of the
hernial sac should not proceed beyond the level
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of the pubic tubercle. Division of the peritoneal
sac there allows for reduction and inversion of its
proximal portion into the preperitoneal space. In
cases of recurrent herniation, a posterior prep-
eritoneal approach to repair should be employed,
thereby avoiding dissection of a scarred spermatic
cord. Adopting these ideas for his next group of
4,000 Shouldice hernioplasties resulted in only one
case of ischemic orchitis.
In 1983, Bendavid encountered a patient who
complained of episodes of brief, severe pain in the
groin during ejaculation. He had previously been
operated on using the Shouldice procedure. By
1991, another 16 cases had been identified, two
of whom had not received surgery but suffered
from chronic epididymitis or cancer of the prostate
treated with radiotherapy. The next year, Benda-
vid labeled this new syndrome »dysejaculation«
[4]. Another 13 cases were reported in 1995 [5].
Symptomatology began 1 month to 2 years postop-
eratively. Reoperation showed either separation of
the vas deferens from its blood supply, adherence
to the transversalis fascial floor of the inguinal
canal, kinking, abrasions, stricture, or scarring.
Bendavid considered that the mechanism for pain
was retrograde distension of a blocked vas defer-
ens, since ejaculation begins with peristalsis in the
epididymis, passing down to the seminal vesicles
and prostate. Delay in onset postoperatively in-
dicated scarring secondary to the dissection that
had been required to remove both the cremasteric
musculature and the hernial sac. Because some of
Bendavid’s patients became pain free over time,
conservative treatment was recommended.
Prosthetic Repair [6]
Reinforcement of sutured hernioplasties began in
the last decade of the 19th century, a few years after
Bassini’s cure became well known. In 1894, Phelps
employed silver coils. Later, filigrees of other met-
als were used. However, rigidity, fibrosis, sinuses,
radiopacity, and both patient and surgeon discom-
fort discouraged their use. In 1944, Aquaviva and
Bounet introduced Nylon mesh. Their prosthetic
design remains, but polypropylene, which was first
used by Usher in 1963, is now the most popular
Chapter 10 · Damage to the Spermatic Cord from Groin Herniorrhaphy: A Review
mesh. Nevertheless, it was not until the final de-
cade of the 20th century that a majority of groin
repairs became prosthetic and the Lichtenstein
procedure was the new gold standard. This change
resulted from a significant reduction in the rate of
recurrent herniation.
LeBlanc et al. [7], using endoscopy, placed
mesh preperitoneally overlying the internal ingui-
nal ring of pigs. Examples of venous congestion
in the pampiniform plexus were found, indicat-
ing that the posterior preperitoneal approach to
the groin does not preclude venous infarction of
the testicle. In 1999, Uzzo et al. [8] claimed to be
the first to examine the effects of mesh-induced
fibrosis on components of the spermatic cord. Us-
ing dogs, unilateral inguinal defects were created
and repaired using either polypropylene mesh or
the Shouldice technique. The contralateral groin
served as a control. A year later, autopsies revealed
patent but significantly narrowed vasa deferentia
in both repair groups. Hydroceles and testicular
atrophy were found in half of the dogs treated with
mesh; none followed sutured repair. Taylor et al.
[9] studied patients who had undergone repair of
unilateral inguinal herniation with either the lap-
aroscopic or anterior prosthetic (polypropylene)
technique 3 years previously. There was no signifi-
cant effect on testicular blood flow.
Zieren et al. [10] reported in 2001 that tes-
ticular perfusion remained unchanged 6 months
after patients received plug-and-patch repairs for
inguinal herniation. Aydede et al. [11] obtained
similar results, long term, after randomly assigning
patients to anterior or preperitoneal prosthetic re-
pair. Laparoscopic mesh repair of inguinal herniae
was found to result in dysejaculation that began an
average of 3 months postoperatively in 10% [12]
or 3.9% [13] of patients. Thus, as with damage
to the pampiniform plexus, the preperitoneal ap-
proach does not confer exemption from injury to
the vas deferens. Its incidence appears to increase
with the use of mesh. Silich and McSherry [14]
reported a patient with a sperm granuloma 4 years
after a Lichtenstein repair. They believe it arose
from erosion of the vas deferens by the cut edge
of the mesh at the medial end of the slit made to
recreate the internal inguinal ring. Berndsen et al.
[15] compared the effects of heavy or lightweight
73 10
polypropylene mesh on the spermatic cords of
rats 3 months after Lichtenstein repair, using the
Shouldice procedure as control. Interestingly, they
found impaired testosterone production and nar-
rowing of the vas deferens only with low-weight
composite mesh. There was no difference in the
inflammation or fibrosis evoked by the different
meshes, contrary to results from previous studies
[16, 17].
Dilek et al. [18] measured testicular blood flow
before and 3 months after patients were randomly
assigned to laparoscopic or Lichtenstein repair of
inguinal herniation. Neither technique affected tes-
ticular blood flow. Taneli et al. [19] studied testicu-
lar metabolism in rats whose spermatic cord was
exposed to a layer of polypropylene mesh. Find-
ings were compared to those for sham-operated
controls 6 months later. There was no significant
difference in serum hormone levels or apoptosis
in the testes. Their results support the 2001 results
of Zieren et al. [10] and Taylor et al. [9]. Shin et al.
[20] presented their multi-institutional experience
of 14 younger men previously repaired for inguinal
herniae, mainly using the Lichtenstein procedure,
who reported infertility. Nine had bilateral vasal
obstruction, and five had unilateral obstruction
with contralateral testicular atrophy or epididymi-
tis. The mechanism was dense fibrosis. All had
normal blood hormone levels. The authors point
out that the vasal narrowing described by Uzzo et
al. [8] at 1 year postoperatively could, over time,
become an occlusion. Iatrogenic injury to the vas
deferens such as ligation, cauterization, incision, or
vascular compromise could also be a factor.
Goldenberg and de Paula [21] studied the
2-month effect of simulated polypropylene mesh
repair in the groin of dogs. Observations were
compared with contralateral dissected or unoper-
ated controls. The inflammatory response–100%
with mesh, 71% without–involved the vas deferens
in all subjects in the mesh group, causing statisti-
cally significant narrowing. A third of the animals
that received mesh showed congestion of the pam-
piniform plexus. Peiper et al. [22] experimented
on pigs and rabbits to determine whether a risk
of infertility exists after inguinal mesh repair. In
the former, transinguinal preperitoneal repair with
polypropylene mesh, after resection of the cre-
 74 Chapter 10 · Damage to the Spermatic Cord from Groin Herniorrhaphy: A Review
master, was compared to a contralateral Shouldice
procedure. Within a month, one-third of those
receiving mesh demonstrated venous thrombosis
in the pampiniform plexus even though the sper-
matic cord was exposed to the prosthesis only at
the internal inguinal ring. The rabbits underwent
unilateral Lichtenstein repair with preservation of
the cremaster muscle, and contralateral Shouldice
repair was also undertaken. Testicular parameters
were compared with those of unoperated con-
trols. Each repair reduced perfusion, more so with
Lichtenstein. Kolbe and Lechner [23] wrapped the
vasa deferentia of rats with either heavyweight or
lightweight polypropylene mesh. After 3 months,
their fertility was determined by mating them and
counting the oocytes or embryos. Some sperm
granulomas were observed in the heavyweight
mesh group, but neither prosthesis reduced fer-
tility compared with controls, which had simply
undergone isolation of the vas deferens. Interest-
ingly, both meshes induced a similar inflammatory
reaction, supporting the work of Berndsen et al.
[15] but not that of others [16, 17].
10 Witkowski and Trabucco [24] questioned the
reported increased risk of vas deferens occlusion
after mesh inguinal hernioplasty. They cite Fitzgib-
bons [25], who has argued that »no correlation
between fibrosis and vasal obstruction has been
proven.« Witkowski and Trabucco [24] stated, as
did Shin et al. [20], that it is therefore possible that
intraoperative damage from dissection or fixation
is responsible. Regardless, they suggest separat-
ing the mesh from the spermatic cord by placing
it subcutaneously à la Halsted–Bassini. In 2008
Gventatadze [26] tested the effect of such isola-
tion on sperm morphology in patients undergoing
the modified bilateral Lichtenstein repair. Com-
parison was made with others receiving the classic
procedure. A statistically significant deterioration
(p<0.01) in sperm parameters was found in the
latter.
Conclusions
In summary, venous infarction of the testicle (at-
rophy) and narrowing of the vas deferens (dys-
ejaculation) were rarely reported following su-
[UnitedVRG] - Medical Release Group
tured repair (Shouldice). The risk to the spermatic
cord increases after its isolation by excision of the
cremaster muscle and scrotal sacs. Reoperation
requiring dissection through scar tissue jeopar-
dizes the cord, and tissue reaction to prostheses
augments damage to cord structures. Lightweight
mesh cannot be relied upon to evoke less fibrosis
than heavyweight mesh. Spermatic cord complica-
tions are not avoided by preperitoneal placement
of prostheses. Pathology, secondary to groin dis-
section and the use of mesh, has been shown to af-
fect the vas deferens more often than the pampini-
form plexus. Arterial flow to the testis is affected
little by prosthetic repair unless, in a minority,
venous thrombosis supervenes. Vasal occlusion is
underreported since most inguinal herniorrhapies
are performed on the elderly, who usually are not
concerned about fertility. In younger men, sterility
is generally not a problem because most repairs
are unilateral. However, contralateral diseases or
bilateral hernioplasties can result in sterility. It
has been reported that subcutaneous placement of
the spermatic cord in men after bilateral Lichten-
stein repair, as recommended by Witkowski and
Trabucco, significantly improves fertility compared
with the classic Lichtenstein procedure.
References
1. Koontz AR (1965) Atrophy of the testicle as a surgical risk.
Surg Gynecol Obstet 120:511–513
2. Wantz GE (1982) Testicular atrophy as a risk of inguinal
hernioplasty. Surg Gynecol Obstet 154:570–571
3. Fong Y, Wantz GE (1992) Prevention of ischemic orchi-
tis during inguinal hernioplasty. Surg Gynecol Obstet
174:399–402
4. Bendavid R (1992) »Dysejaculation«: an unusual com-
plication of inguinal herniorrhaphy. Postgrad Gen Surg
4(2):139–141
5. Bendavid R (1995) Dysejaculation. Probl Gen Surg
12(2):237–238
6. Read RC (2004) Milestones in the history of hernia sur-
gery: prosthetic repair. Hernia 8:8–14
7. LeBlanc KA, Booth WV, Whitaker JM et al. (1998) In vivo study
of meshes implanted over the inguinal ring and external
iliac vessels in uncastrated pigs. Surg Endosc 12:247–251
8. Uzzo RG, Lemack GE, Morrissey KP et al. (1999) The effects
of mesh bioprosthesis on the spermatic cord structures: a
preliminary report in a canine model. J Urol 161(4):1344–
1349
Chapter 10 · Damage to the Spermatic Cord from Groin Herniorrhaphy: A Review
75 10
9. Taylor SG, Hair A, Baxter GM et al. (2001) Does contraction 25. Fitzgibbons RJ Jr (2005) Can we be sure polypropylene
of mesh following tension-free hernioplasty affect testi- mesh causes infertility? Ann Surg 241:559–561
cular or femoral vessel blood flow? Hernia 5:13–15 26. Gvenetadze T (2008) Method of spermatic cord isolation
10. Zieren J, Beyersdorff D, Beier KM et al. (2001) Sexual func- from the mesh. In: Proceedings of the American Hernia
tion and testicular perfusion after inguinal hernia repair Society annual meeting, Scottsdale, Arizona, 12–16 March
with mesh. Am J Surg 181:204–206 2008, poster 23
11. Aydede H, Erhan Y, Sakarya A et al. (2003) Effect of mesh
and its localization on testicular flow and spermatoge-
nesis in patients with groin hernia. Acta Chir Belge 103
(6):607–610
12. Langenbach M, Schmidt J, Lazika M et al. (2003) Urological
symptoms after laparoscopic hernia repair. Reduction with
a variant of polypropylene mesh. Urologe 42:375–381
13. Wingenbach O, Waleczek H, Kozianka J (2004) Laparosco-
pic hernioplasty by transabdominal preperitoneal ap-
proach. Analysis and review in 267 cases. Zentralbl Chir
129:369–373
14. Silich RC, McSherry CK (2006) Spermatic granuloma. An
uncommon complication of the tension-free hernia re-
pair. Surg Endosc 10(5):537–539
15. Berndsen FH, Bjursten LM, Simanaitis M et al. (2004) Does
mesh implantation affect the spermatic cord structures
after inguinal hernia surgery? An experimental study in
rats. Eur Surg Res 36:318–322.
16. Klosterhalfen B, Klinge U, Schumpelick V (1998) Functional
and morphological evaluation of different polypropylene
mesh modifications for abdominal wall repair. Biomateri-
als 19:2235–2246
17. Junge K, Klinge U, Rosch R et al. (2002) Functional and
morphological properties of a modified mesh for inguinal
hernia repair. World J Surg 26:1472–1480
18. Dilek ON, Yucel A, Akbulut G et al. (2005) Are there ad-
verse effects of herniorrhaphy techniques on testicular
perfusion? Evaluation by color Doppler ultrasonography.
Urol Int 75:167–169
19. Taneli F, Aydede H, Vatansever S et al. (2005) The long-
term effect of mesh bioprosthesis in inguinal hernia repair
on testicular nitric oxide metabolism and apoptosis in rat
testis. Cell Biochem Funct 23:213–220
20. Shin D, Lipshultz LI, Goldstein M et al. (2005) Herniorrha-
phy with polypropylene mesh causing inguinal vasal obs-
truction. A preventable cause of obstructive azoospermia.
Ann Surg 241(4):553–558
21. Goldenberg A, de Paula JF (2005) Effects of polypropylene
mesh implanted through inguinotomy on the spermatic
funiculus, epididymis and testis of dogs. Acta Cir Bras
20(6):461–467
22. Peiper C, Junge K, Klinge U et al. (2006) Is there a risk of
infertility after inguinal mesh repair? Experimental studies
in the pig and rabbit. Hernia 10(1):7–12
23. Kolbe T, Lechner W (2007) Influence of hernioplastic im-
plants on male fertility in rats. J Biomed Mater Res B Appl
Biomater 81B:435–440
24. Witkowski P, Trabucco EE (2007) Is there an increased
risk of vas deferens occlusion after mesh inguinal her-
nioplasty and what we can do about it? [letter] Ann Surg
245(1):153–154
[UnitedVRG] - Medical Release Group
 II

II Risk for Infection

11 Mesh Infection Following Hernia Repair:

A Frequent Problem? – 79

12 Patient Factors as a Major Determinant of Wound Outcome

and Infection After Surgery – 87

13 Mesh-Related Infections After Hernia Repair – 97

14 Human Acellular Dermal Matrix for Ventral Hernia Repair

in the Compromised Surgical Field – 103

15 Fate of the Inguinal Hernia Following Removal

of Infected Prosthetic Mesh – 113

16 Mesh Infection–Therapeutic Options – 119

17 Does Antibiotic Prophylaxis Prevent the Occurrence

of Wound Infection After Groin Hernia Surgery? – 125

18 Infection Control in a Hernia Clinic: 24-Year Results

of Aseptic and Antiseptic Measure Implementation
in 4,620 »Clean Cases« Based on Up-To-Date
Microbiological Research – 135

19 Components Separation Technique: Pros and Cons – 143

[UnitedVRG] - Medical Release Group
 11

Mesh Infection Following Hernia

Repair: A Frequent Problem?
B. J. Lammers, A. Baer, T. Sauer, P. Pohl, P. E. Goretzki
 80 Chapter 11 · Mesh Infection Following Hernia Repair: A Frequent Problem?
Introduction
Wound and mesh infections after hernia repair are
very severe complications. On the one hand, today
it is well established to repair hernias with meshes
in very different ways, but on the other hand,
knowledge of the incidence of severe infections,
including mesh infection, is quite rare [1, 2].
In this chapter we aim to define which kinds
of infections we can recognise. The rate of infec-
tion after mesh repair differs, of course, between
inguinal hernia repair and incisional hernia repair.
In the United States it is very common to use the
group of ventral hernias of the abdominal wall (in-
cluding incisional, epigastric, Spigelian, and um-
bilical hernias).
According to the infection, we will look at
infections in this group as well as in inguinal her-
nias, including femoral hernias. Therefore, we will
address just two groups: ventral hernias (laparo-
scopic and open) and inguinal hernias (open and
laparoscopic procedures).
Using new techniques and new materials, it is
impossible to define detailed risk factors for wound
and mesh infection that are related to each proce-
11 dure and each material. The literature includes
some references on this; these will be remarked
upon in this chapter regarding some special top-
ics. Further investigations are necessary, and the
authors of other chapters will also comment on
this topic.
Definition of Surgical Site Infection
Using the definition of the Centers for Disease
Control and Prevention, infections are divided into
superficial and deep infections. Superficial infec-
tion occurs in the first 30 days after an interven-
tion, and deep infection occurs within 1 year and
involves the fascia, the muscle layers, and the graft.
We must recognise that there are early infec-
tions within the first 30 days after implantation
and late infections that may occur years after im-
plantation. Furthermore, we may encounter fur-
ther intraabdominal problems, such as abscess for-
mation, bowel injury, peritonitis, and so on, with
both early and late onset.
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Looking through the literature, no definitions
of mesh infection are available. But at the very
least, there is a risk of infection of the mesh with
any kind of wound infection, so we should be alert
for signs of deep infection, including the mesh
(onlay, intraperitoneal onlay, sublay, etc.):
▬ Fever
▬ Signs of infection (swelling, oedema)
▬ C-reactive protein and leucocytosis
▬ Contaminated mesh
Inguinal hernia surgery is primarily sterile sur-
gery with low contamination. In abdominal wall
surgery, the infection rate is higher, so it must be
regarded as contaminated surgery.
Materials and Methods
We did a literature review of papers involving
more than 100 patients with ventral hernia repair
and incisional hernia repair, and we also included
our own data. The main topic of this investigation
was the rate of infections, including mesh-related
infections, if these data were available. However,
many papers lacked information on this problem.
The group of inguinal hernia repairs was cov-
ered by an overview of inguinal hernia repair in
the North Rhine region of Germany for a period of
10 years with almost 200,000 operations [3]. This
period included the development of a reporting
system and the new video-assisted technologies
(transabdominal preperitoneal and totally extra-
peritoneal repair). There are very few papers on
mesh infection in inguinal hernia repair. Fistula
formation is also very rare, so this was not dis-
cussed in this overview. Obviously, the problem in
inguinal hernia repair nowadays is not evident.
Results
Ventral Hernias and Incisional Hernia
Repairs Without Mesh Repair
This operation, which is done in many countries
using direct suture or doubling of the fascia (called
the Mayo repair in Germany), is not standard
Chapter 11 · Mesh Infection Following Hernia Repair: A Frequent Problem?
therapy today because mesh repair is accepted.
However, many patients need a nonmesh repair.
The infection rate with antibiotic prophylaxis is
about 6–10 % [4–6]. Our own experiences with a
long-term run of 20 years show an infection rate
of 12%, including complete wound rupture. These
data show the general problem of incisional hernia
repair: contaminated surgery. The rate of postop-
erative infections is over 10%. The bacteria stay in
the wound for a long time.
Incisional Hernias with Mesh Repair
We analysed the publications involving more than
100 patients. Many of them are multicentre stud-
ies; there is just one randomised multicenter study,
from Conze [7]. Leber et al. showed in a retrospec-
tive study in 1998 that in open mesh repair, many
early and late postoperative problems occur. Par-
ticularly significant was the high rate of infections
and fistulas [1]. They showed that at that time it
was not clear which positions of the meshes related
to the material were possible. The infection rate
reported in the older papers is higher than in the
papers published in the last 3 years [8–12]. Obvi-
ously, surgeons are gaining experience and are able
to manage the problems better. Another possibility
81 11
might be the evolution of new meshes. Ramshaw
et al. [13] and Stoppa [14] have had very high rates
of wound infections, 15–25% (⊡ Table 11.1). In the
last years, open mesh repairs have usually been
associated with a lower rate of wound infections,
0.6–7% [4, 15–17]. But the main topic of these
papers is usually not the infection rate.
Mesh infections and the rate of mesh removal
must be mentioned, although this topic is difficult
to discuss because data on this are not available
in every study. Finan et al. [16] found some risk
factors for infection: immunosuppression, smok-
ing, intraoperative bowel injury, bowel resection
emergency procedures, complicated hernia surgery
(incarcerated, obstructed, or strangulated), and op-
erating time. The variation in rates among different
hospitals reported in this paper is very interesting–
from 1% to 9%. The mesh infection rate was be-
tween 0.3% and 6%. So the rate of mesh infection
differed, and not every infected mesh was removed,
but the data on this problem are very sparse [16].
Tailored Incisional Hernia Surgery –
Our Results
In our experience since 1996 of using a tailored
concept for all operations with mesh (494 of 798),

⊡ Table 11.1. Literature overview of mesh infections in open incisional hernia treatment (minimum 100 cases)

First author Year N Wound infections (%) Mesh infections (%) Mesh removal (%)

Iannitti [15] 2008 455 0.3 0.3 ?

Lammers [17] 2008 774 7 2 0.5

Israelsson [4] 2006 349 9.6

Mahmoud Uslu [18] 2006 291 3.3 0.6

Finan [16] 2005 1505 5 ? ?

Conze [7] 2005 165 17.8 -

Basoglu [32] 2004 264 21.5 2 fistulas

McGreevy [9] 2003 71 8.4 2

Korenkov [30] 2002 160 13

Ramshaw [13] 1999 174 15.5 6 6

Stoppa [14] 1989 368 15 ß

 82 Chapter 11 · Mesh Infection Following Hernia Repair: A Frequent Problem?

we have had a general wound infection rate of
8.9%. For intraperitoneal onlay mesh (IPOM) re-
pair (222 operations), we have had a mesh infec-
tion rate of 4%, and only 2.3% of the meshes were
removed (only expanded polytetrafluoroethylene,
or ePTFE, meshes must be removed). In the onlay
repair group (223 operations), we have had a 2.2%
mesh infection rate, and just one of 223 meshes had
to be removed. We have seen no fistula formation
and no intraperitoneal abscesses (⊡ Table 11.2).
The rate of fistula to the bladder, colon, or
other intestinal organs is very rarely reported in
the literature, usually occurring when meshes were
used that should not be placed intraperitoneally
(heavyweight meshes without a composite struc-
ture, polypropylene and polyester).
The data on mesh removal are also very rare.
We know that infected ePTFE is very difficult to
handle, but in our experience, not every infected
mesh must be removed in open hernia surgery.
Infected polyester meshes are quite difficult to
handle, but lightweight polypropylene meshes are
not especially difficult to treat. In general, they do
not need to be removed.
Mahmoud Uslu et al. described only two cases
11 of 291 patients (modified onlay technique) in which
it was necessary to reoperate and remove the mesh,
whereas the infection rate was 2.7% [18].
The wound infection rate in the study of Conze
et al. [7] was very high, up to 18%, with one-third
of the affected patients needing surgery. The au-
thors did not define mesh infection, but these must
have been deep infections; however, mesh removal
was not necessary. At least, there was no significant
difference between composite and regular meshes.
All patients had sublay repair (⊡ Table 11.1).
Wound and Mesh Infections
in Laparoscopic Hernia Repair
One of the main advantages of laparoscopic IPOM
is the lower mesh infection rate. The wound infec-
tion rate is about 2%, and the mesh infection rate is
between 1% and 5%. But one point is very impor-
tant: Quite often, the data on IPOM are based on a
lot of very easy umbilical and epigastric hernias; the
patients whose procedures were converted are not
included in these data. Also, when a bowel injury is
reported, it is not clear whether this means a mesh
infection. One of the authors, Finan, stated, »This
study had an 8% rate of laparoscopic hernia repairs
with a 3.3% wound infection rate compared to a
4.5% rate in open permanent mesh repairs, demon-
strating no meaningful difference« [16].
Berger, who reports on only incisional hernia
repairs without any selection, has a very low rate
of mesh and wound infections–about 1%. We have
seen no wound infections but saw one mesh infec-
tion caused by an unknown bowel leakage with
peritonitis [9, 19–24] (⊡ Table 11.3).
Infections in Inguinal Hernia Repair
In almost all studies, infection occurring with an
open and laparoscopic inguinal hernia repair is no
problem. Mesh infections are very rare, so they are

⊡ Table 11.2. Our data from 1986 to 2008: infection rates (IPOM intraperitoneal onlay mesh)

N Wound Mesh Mesh Unknown

infections (%) infections (%) removal (%) bowel injury (%)

Incisional hernia total 798 8.9 1.9 0.9 0.1

With mesh 494 6.2 2.8 1.2 0.2

IPOM 222 6.8 4 2.3 0

Onlay 223 7 2.2 0.4 0

Laparoscopic IPOM 49 0 2 2 2

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Chapter 11 · Mesh Infection Following Hernia Repair: A Frequent Problem?
usually not reported; that is why we looked for a
large prospective series.
In the years 1991 to 1999 in the North Rhine
area of Germany, there was a program to col-
lect all the data on inguinal hernia repair. Nearly
200,000 operations were documented. In the data
collection, we discovered that the postoperative
complication rate was much higher in general than
in randomised studies [3, 25–29]: We found a
complication rate of between 5.1% and 9.7%. This
83 11
rate decreased as the laparoscopic management of
hernias increased up to 29%. The seroma rate was
between 3% and 5%, but there were documented
wound infections of 0.79–1.55%, swelling of the
scrotum in about 0.7%, and swelling of the testes
in 0.24–0.52% (as a sign for testicular atrophy in
the future). The reoperation rate was a bit higher
than 1%. These patients are always at risk for
a mesh infection. The mortality rate was 0.1%
(⊡ Table 11.4).

⊡ Table 11.3. Literature overview of mesh infections in laparoscopic ventral hernia therapy

First author Year N Wound infections (%) Mesh infections (%) Mesh removal (%)

Ferrari [20] 2007 99 1 1 1

Heniford [21] 2000 407 1.23 0.98 0.98

McGreevy [9] 2003 65 – 4.6 4.6

Olmi [31] 2007 85 – 1 1

LeBlanc [23] 2000 100 2 1 1

Berger [22] 2002 150 1.3 1 1

Lammers [own 2008 49 0 2 2

data]

⊡ Table 11.4. Results of inguinal hernia surgery in the North Rhine district of Germany [3]

Year 1999 1998 1997 1996 1995 1994 1993 1992 1991 Total

Patients 19,266 18,619 19,732 20,940 19,646 19,907 19,740 18,738 17,605 173,923

Operations 22,015 21,162 22,212 23,245 21,639 21,888 21,354 20,203 19,000 192,718

Postoperative 5.9 5.6 5.5 5.1 6.4 7.6 7.9 8.1 9.7
complications
(%)

Reoperation 1.10 1.16 1.13 1.12 1.17 1.48 1.42 – – –

(%)

Seroma, 3.85 3.27 3.11 2.8 3.54 4.46 4.39 4.27 5.08
haematoma
(%)

Wound 0.89 0.84 0.90 0.79 1.19 1.31 1.51 1.48 1.55
infection (%)

Swelling of 0.55 0.58 0.56 0.44 0.58 0.75 0.77 0.74 0.81
scrotum (%)

Swelling of 0.26 0.28 0.32 0.24 0.34 0.53 0.49 0.42 0.52
testes (%)
 84 Chapter 11 · Mesh Infection Following Hernia Repair: A Frequent Problem?
Discussion
The problem of mesh infection in hernia repair
does not occur very often, but when it does, there
is always the question of whether the mesh has to
be removed. Some studies found that in the case
of an infection with ePTFE, the mesh should be
removed. Most of the meshes that were developed
within the last 7 years (light meshes, composite
meshes) did not have this problem. Fistula forma-
tion is not so rare when the wrong mesh is used
intraperitoneally; the rate could be as high as 3.5%
[1, 19]. Therefore, it is very important to use only
approved meshes intraabdominally and perhaps
even avoid intraperitoneal meshes. Mesh infection
in laparoscopic hernia repair is often associated
with mesh removal, but the data are very sparse.
When studying the literature, it is very difficult
to discover the complication rates because many
studies involved a mixture of ventral and incisional
hernias.
When looking back at older data, it can be seen
that incisional hernia treatment formerly had a
high wound infection rate. When prophylactic an-
tibiotics were used, the rate decreased to 5–7%. The
11 infection rate seems to be higher in large series; the
studies on antibiotics suggest this [25–29].
But the incidence of mesh-associated infec-
tions, including fistula formation, is not clear in
inguinal hernia repair. In general, a higher com-
plication rate is noted when many hospitals are
involved in a study. Deep infection, including in-
fection of the mesh, has a high risk of recurrence
and reoperation.
In the future, more studies are necessary to
look for the advantages related to laparoscopic
incisional hernia repair.
References
1. Leber GE, Gar JL, Aleander AL, et al. Long-term compli-
cations associated with prosthetic repair of incisional
hernias. Arch Surg 1998; 133:378–382
2. Lammers BJ, Voos S, Witt M, Goretzki PE. Results of con-
ventional mesh-augmented incisional hernia repair. Chir
Gastroenterol 2003; suppl 2:24–28
3. Lammers BJ, Meyer HF, Huber HG, et al. Developments in
inguinal hernia surgery based on newly introduced inter-
[UnitedVRG] - Medical Release Group
vention techniques in the North Rhine district. Chirurg
2001; 72:448–452
4. Israelsson LA, Smedberg S, Montomery A, et al. Incisional
hernia repair in Sweden 2002. Hernia 2006; 10:258–261
5. Perez A, Roxas MF, Hilvano SS. A randomized, double-
blind, placebo-controlled trial to determine effectiveness
of antibiotic prophylaxis for tension-free mesh hernior-
rhaphy. J Am Coll Surg 2005; 200:393–398
6. Yerdel MA, Akin EB, Dolalan S, et al. Effect of single-
dose prophylactic ampicillin and sulbactam on wound
infection after tension-free inguinal hernia repair with
polypropylene mesh. The randomized, double-blind, pro-
spective trial. Ann Surg 2001; 233:26–33
7. Conze J, Kingsnorth AN, Flament JB, et al. Randomized
clinical trial comparing lightweight composite mesh with
polyester or polypropylene mesh for incisional hernia
repair. Br J Surg 2005; 92:1488–1493
8. Lammers BJ, Goretzki PE, Witt M, Röher WM. e-PTFE IPOM
versus onlay-repair–results of a prospective randomised
controlled trial. Chir Forum 2001; 30:563–566
9. McGreevy JM, Goodney PP, Birkmeyer CM, et al. A pro-
spective study comparing the complication rates be-
tween laparoscopic and open ventral hernia repairs. Surg
Endosc 2003; 17:1778–1780
10. Arroyo A, Garcia P, Pérez F, et al. Randomized clinical trial
comparing suture and mesh repair of umbilical hernia in
adults. Br J Surg 2001; 88:1321–1323
11. Cassar K, Munro A. Surgical treatment of incisional hernia.
Br J Surg 2002; 89:534–545
12. Langer C, Liersch T, Kley C, et al. 25 Jahre Erfahrung in der
Narbenhernienchirurgie. Chirurg 2003; 74:638–645
13. Ramshaw BJ, Esartia P, Schwab J, et al. Comparison of
laparoscopic and open ventral herniorrhaphy. Am Surg
1999; 65:827–832
14. Stoppa RE. The treatment of complicated groin and inci-
sional hernias. World J Surg 1989; 13:545–554
15. Iannitti DA, Hope WW, Norton HJ, et al. Technique and
outcomes of abdominal incisional hernia repair using a
synthetic composite mesh: a report of 455 cases. J Am
Coll Surg 2008; 206:83–88
16. Finan KR, Vick CC, Kiefe CI, Neumayer L, Hawn MT. Predic-
tors of wound infection in ventral hernia repair. Am J Surg
2005; 190:676–681
17. Lammers BJ, Goretzki PE, Otto T. New aspects in hernia
surgery. Urologe 2005; 44:774–779
18. Mahmoud Uslu HY, Erkek AB, Cakmak A, et al. Incisional
hernia treatment with polypropylene graft: results of 10
years. Hernia 2006; 10:380–384
19. Benhidjeb T, Bärlehner E, Anders S. Laparoscopic incisional
hernia repair. Chir Gastroenterol 2003; 19(suppl):16–22
20. Ferrari GC, Mirando A, Di Lernia S, et al. Laparoscopic
repair of incisional hernia: outcomes of 100 consecutive
cases comprising 25 wall defects larger than 15 cm. Surg
Endosc 2008; 22:1173–1179
21. Heniford BT, Park A, Ramshaw BJ, Voeller G. Laparoscopic
ventral and incisional hernia repair in 407 patients. J Am
Coll Surg 2000; 190:645–650
Chapter 11 · Mesh Infection Following Hernia Repair: A Frequent Problem?
85 11
22. Berger D, Bientzle M, Müller A. Postoperative compli- Lammers: First of all, we know that patients who
cations after laparoscopic incisional hernia repair. Surg have had an infection in former times from the
Endosc 2002; 16:1720–1723
first operation—for example, for bowel with anas-
23. LeBlanc KA, Booth WV, Whitaker JM, Bellanger DE. Lap-
aroscopic incisional and ventral herniorrhaphy in 100 tomosis leakage, they have bacteria even years
patients. Am J Surg 2000; 180:193–197 after the first operation in the wound. That’s the
24. O’Dwyer PJ, Kingsnorth AN, Molloy RG, et al. Randomized advantage of laparoscopic hernia repair because
clinical trial assessing impact of a lightweight or heavy- you don’t open the same wound again. On the
weight mesh on chronic pain after inguinal hernia repair.
other hand, during open hernia repair there is the
Br J Surg 2005; 92:166–170
25. Sanabria A, Dominguez LC, Valdivieso E, Gabriel G. Pro-
possibility to bring bacteria inside the wound, such
phylactic antibiotics for mesh inguinal hernioplasty: a as from the patient’s skin. But there are no studies
meta-analysis. Ann Surg 2007; 245:392–396 available on this problem at the moment.
26. Kuzu M, Hazinedaroglu S, Dolalan S, et al. Prevention of
surgical site infection after open prosthetic inguinal her-
nia repair: efficacy of parenteral versus oral prophylaxis
with amoxicillin-clavulanic acid in a randomized clinical
trial. World J Surg 2005; 29:794–799
27. Perez A, Roxas MF, Hilvano SS. A randomized, double-
blind, placebo-controlled trial to determine effectiveness
of antibiotic prophylaxis for tension-free mesh hernior-
rhaphy. J Am Coll Surg 2005; 200:393–398
28. Yerdel MH, Akin EB, Dolalan S, et al. Effect of single-
dose prophylactic ampicillin and sulbactam on wound
infection after tension-free inguinal hernia repair with
polypropylene mesh. The randomized, double-blind, pro-
spective trial. Ann Surg 2001; 233:26–33
29. Terzi C, Kilic D, Ünek T, et al. Single-dose oral ciprofloxacin
compared with single-dose intravenous cefazolin for pro-
phylaxis in inguinal hernia repair: a controlled random-
ized clinical study. J Hosp Infect 2005; 60:340–347
30. Korenkov M, Sauerland S, Arndt M, et al. Randomized
clinical trial of suture repair, polypropylene mesh or auto-
dermal hernioplasty for incisional hernia. Br J Surg 2002;
89:50–56
31. Olmi S, Scaini A, Cesana GC, et al. Laparoscopic versus
open incisional hernia repair. An open randomized con-
trolled study. Surg Endosc 2007; 21:555–559
32. Basoglu M, Yildirgan MI, Yilmaz I, et al. Late complications
of incisional hernias following prosthetic mesh repair.
Acta Chir Belg 2004; 104:425–428
33. Bingener J, Buck L, Richards M, et al. Long-term outcomes
in laparoscopic vs open ventral hernia repair. Arch Surg
2007; 142:562–567

Discussion

Read: You mentioned bacteria. Are there any viral

infections of mesh?
Lammers: It may be possible, but I have never seen
it, and I have never heard about this.
Schumpelick: Do you know where the bacteria
come from?
 12

Patient Factors as a Major Determinant

of Wound Outcome and Infection After
Surgery
H. W. Hopf
 88 Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection After Surgery
Introduction
Despite major advances in the management of pa-
tients undergoing surgery–including aseptic tech-
nique, prophylactic antibiotics, and advances in
surgical approaches such as laparoscopic surgery–
surgical wound infection remains among the most
common complications of surgery [1]. Wound
complications are associated with prolonged hos-
pitalization and increased resource consumption.
More than 300,000 surgical site infections occur
each year in the United States at an estimated
cost of more than $1 billion [1]. A growing body
of literature supports the concept that patient
factors are a major determinant of wound out-
come following surgery. Comorbidities such as
diabetes and cardiac disease clearly contribute,
but environmental stressors as well as the indi-
vidual’s response to stress are equally important.
In particular, wounds are exquisitely sensitive to
hypoxia, which is both common and preventable.
Perioperative management can be adapted to pro-
mote postoperative wound healing and resistance
to infection. Along with aseptic technique and
prophylactic antibiotics, maintenance of perfu-
sion and oxygenation of the wound is paramount.
There is strong clinical evidence that once perfu-
12 sion is assured, the addition of increased inspired
oxygen substantially reduces surgical site infec-
tions in at-risk patients.
It is becoming clear that the intraoperative
care of patients has repercussions far into the
postoperative period. The impact of anesthetic
technique on postoperative pain, perioperative
myocardial ischemia, and vascular graft patency
is now well established. Similarly, anesthetic tech-
nique can be adapted to promote postoperative
wound healing and resistance to infection. The
most important factors include temperature man-
agement, increased arterial oxygen tension (PaO2),
pain control, fluid management, and, as has been
long recognized, appropriate sterile technique and
administration of prophylactic antibiotics. All but
the last relate particularly to maintaining perfusion
and oxygenation of the wound.
Even when the best care possible is provided,
surgical wounds may become infected or fail to
heal. The progress of wounds healing by secondary
intention can also be optimized. The most impor-
tant factors include attention to perfusion and oxy-
genation, as with acute wounds; moist wound care;
control of bacterial load; nutrition; edema control;
and prevention of ongoing trauma.
Wound Repair
Injury damages the local circulation and causes
platelets to aggregate and release a variety of sub-
stances, including chemoattractants and growth
factors. The initial result is coagulation, which
prevents exsanguination, but also widens the area
that is no longer perfused. Inflammatory cells
(polymorphonuclear leukocytes immediately and
macrophages by 24–48 h) migrate to the wound
and are activated in response to endothelial inte-
grins, fibrin, lactate, hypoxia, foreign bodies, and
growth factors. In turn, macrophages and lym-
phocytes produce more growth factors and lactate
[2]. Activated inflammatory cells consume oxygen
at a high rate, and, coupled with the impaired mi-
crocirculation, this results in hypoxia, especially at
the center of the wound [3]. Lactate is produced
both anaerobically and aerobically, and this results
in concentrations of 5–15 mM even in well-oxy-
genated wounds. Lactate is a strong stimulus for
collagen secretion and angiogenesis [4, 5]. Anti-
inflammatory steroids impair healing by suppress-
ing inflammation at this step.
Angiogenesis is required to replace the injured
microcirculation. Platelets release a number of an-
giogenic factors, including platelet-derived growth
factor, insulin-like growth factor 1, and others. An-
giogenic growth factor levels remain high because
of continued production by macrophages and fi-
broblasts (particularly of fibroblast growth factor
and vascular endothelial growth factor) in response
to hypoxia and lactate, among other things [6]. The
capillary endothelial response to angiogenic agents
(i.e., migration into the wound, tubule formation,
and connecting to sources of blood flow) requires
oxygen, so angiogenesis progresses proportionally
to blood perfusion and arterial PO2 [7].
New blood vessels grow into matrix that is
produced by fibroblasts. Fibroblasts replicate and
migrate mainly in response to growth factors and
Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection
chemoattractants. Lactate and some growth factors
induce collagen mRNA synthesis and procolla-
gen production. Posttranslational modification by
prolyl and lysyl hydroxylases is required to allow
collagen peptides to aggregate into triple helices.
Collagen can be exported from the cell only when
it is in this triple helical structure. The helical con-
figuration is also primarily responsible for tissue
strength. The activity of the hydroxylases is criti-
cally dependent on vitamin C and tissue oxygen
tension [8]. Wound strength, which results from
collagen deposition, is, therefore, highly vulnerable
to wound hypoxia.
Angiogenesis and extracellular matrix (primar-
ily collagen) production are closely linked. Fibro-
blasts cannot produce mature collagen in the ab-
sence of mature blood vessels that deliver oxygen
to the site. On the other hand, new blood vessels
cannot mature without a strong collagen matrix.
Mice kept in a hypoxic environment (13% inspired
oxygen) develop some new blood vessels in a test
wound, but these vessels are immature, with little
surrounding matrix, and demonstrate frequent ar-
eas of hemorrhage [9].
Epithelial cells move and replicate in response
to growth factors and oxygen tension, and epi-
thelization occurs most rapidly in hydrated, well-
oxygenated tissue [10].
Disruption of the normal skin barrier requires
that wounds have the ability to clear foreign mate-
rial and resist infection. Nonspecific phagocytosis
and intracellular killing are the major pathways
activated in wounds [11]. Conversion of oxygen to
superoxide in phagocytic vacuoles is responsible
for the first step in nonspecific intracellular kill-
ing, so resistance to infection is critically impaired
by wound hypoxia and becomes more efficient
as PO2 increases even to very high levels (500–
1,000 mmHg) [12].
Wound Perfusion and Oxygenation
Wound complications include failure to heal, in-
fection, and excessive scarring or contracture.
Rapid repair has the least potential for infection
and excess scarring. Repair proceeds most rapidly
when wound oxygen levels are high, and this is
89 12
achieved only by maintaining perfusion of injured
tissue [13]. Ischemic or hypoxic tissue, on the
other hand, is easily infectable and heals poorly, if
at all. Wound tissue oxygenation depends on the
vascular anatomy, the degree of vasoconstriction,
and arterial PO2. Wound tissue oxygenation is
complex and depends on the interaction of blood
perfusion, arterial oxygen tension, hemoglobin
(Hb) dissociation conditions, carrying capacity,
mass transfer resistances, and local oxygen con-
sumption.
The standard teaching that oxygen delivery
depends more on hemoglobin-bound oxygen (ox-
ygen content) than on arterial PO2 may be true
of working muscle, but it is not true of wound
healing. In muscle, intercapillary distances are
small, and oxygen consumption is high. In sub-
cutaneous tissue, on the other hand, intercapillary
distances are large, and oxygen consumption is
relatively low [14]. In uninjured subcutaneous
tissue, the intercapillary distance is greater than
that in muscle and other highly perfused organs.
In wounds, where the microvasculature is dam-
aged, diffusion distances increase by an order
of magnitude. Peripheral vasoconstriction further
increases diffusion distance [3]. The driving force
of diffusion is partial pressure. Hence, a high PO2
is needed to force oxygen into injured and healing
tissues, particularly in subcutaneous tissue, fascia,
tendon, and bone.
Although oxygen consumption is relatively low
in wounds, it is consumed by processes that require
oxygen at a high concentration. Inflammatory cells
use little oxygen for respiration, producing energy
largely via the hexose-monophosphate shunt [12].
Most of the oxygen consumed in wounds is used
for oxidant production (bacterial killing), colla-
gen synthesis, angiogenesis, and epithelization. The
rate constants for oxygen for these components
of repair all fall within the physiologic range of
25–100 mmHg [10, 12, 15–18]. This means that
the rate at which repair proceeds varies accord-
ing to tissue PO2 from zero to at least 250 mmHg.
In vitro fibroblast replication is optimal at a PO2 of
about 40–60 mmHg. These in vitro observations
are clinically relevant. »Normal« subcutaneous
PO2, measured in test wounds in uninjured, eu-
thermic, euvolemic volunteers breathing room air,
 90 Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection After Surgery
is 65±7 mmHg [19]. Thus, any degree of hypoxia
may impair immunity and repair. In surgical pa-
tients, the rate of wound infections is inversely pro-
portional [20], while collagen deposition is directly
proportional [21] to postoperative subcutaneous
wound tissue oxygen tension.
High oxygen tensions (>100 mmHg) can be
reached in wounds but only if perfusion is rapid
and arterial PO2 is high [13, 22]. This is because
1) subcutaneous tissue serves a reservoir function,
so there is normally flow in excess of nutritional
needs, and 2) wound cells consume relatively little
oxygen, about 0.7 ml/100 ml of blood flow at a
normal perfusion rate [14, 23]. At high levels of
PaO2, this small volume can be carried by plasma
alone. Contrary to popular belief, therefore, oxy-
gen-carrying capacity (i.e., hemoglobin concen-
tration) is not particularly important to wound
healing provided that perfusion is normal [24].
Wound PO2 and collagen synthesis remain normal
in individuals who have hematocrit levels as low as
15–18% provided they can appropriately increase
cardiac output and vasoconstriction is prevented.
Peripheral vasoconstriction, which results
from central sympathetic control of subcutane-
ous vascular tone, is probably the most frequent
and clinically the most important impediment to
12 wound oxygenation. Subcutaneous tissue is both a
reservoir to maintain central volume and a major
site of thermoregulation. There is little local regu-
lation of blood flow, except by local heating [22,
25]. Therefore, subcutaneous tissue is particularly
vulnerable to vasoconstriction. Sympathetically
induced peripheral vasoconstriction is stimulated
by cold, pain, fear, and blood volume deficit [26,
27] and by various medications, including nicotine
(smoking) [19], beta adrenergic antagonists, and
alpha-1 agonists, all commonly present in surgi-
cal situations. Prevention and correction of hypo-
thermia [28] and blood volume deficits [29] have
been shown to decrease wound infections and
increase collagen deposition in patients undergo-
ing major abdominal surgery. Subcutaneous tissue
oxygen tension is significantly higher in patients
with good pain control than in those with poor
pain control after knee surgery [30]. Stress also
causes wound hypoxia and significantly impairs
wound healing and resistance to infection [31, 32].
These effects are clearly mediated, at least in major
part, by raising the partial pressure of oxygen in
the injured tissue.
Greif et al. demonstrated in a randomized,
controlled, double-blind trial that in warm, well-
hydrated patients (n=500) with good pain con-
trol (that is, in well-perfused patients) undergoing
major colon surgery, administration of 80% vs.
30% oxygen intraoperatively and for the first 2 h
postoperatively significantly reduced the wound
infection rate by 50% [33]. Belda et al. [34] rep-
licated these results–noting a significant 40% re-
duction in surgical site infection–in a random-
ized, controlled, double-blind trial in 300 colon
surgery patients randomized to 80% vs. 30% oxy-
gen intraoperatively and for the first 6 h postop-
eratively. Surgical and anesthetic management was
standardized and intended to support optimal
perfusion. Myles et al. demonstrated a significant
reduction in major postoperative complications,
as well as specific wound infections, in 2,050 ma-
jor surgery patients randomized to 80% oxygen in
20% nitrogen vs. 30% oxygen in 70% nitrous oxide
intraoperatively [35].
A smaller (n=165) randomized, controlled
study by Pryor et al. [36] demonstrated a doubling
of surgical site infection in patients randomized
to 80% vs. 35% oxygen intraoperatively. The study
had a number of methodological flaws, but, more
importantly, the two groups of patients were not
equivalent, which likely explained the increase in
infections seen in the 80% oxygen group.
Thus, there is substantial evidence that use
of high inspired oxygen intraoperatively and the
administration of supplemental oxygen postopera-
tively in well-perfused patients undergoing major
abdominal surgery will reduce the risk of wound
infection.
Concerns about the risk of oxygen toxicity,
including pulmonary fibrosis and atelectasis, have
limited adoption of high inspired oxygen. Oxygen
toxicity is not a risk in the short term (less than
days) and therefore is not pertinent in the operat-
ing room. Some degree of atelectasis is inevitable
in all patients undergoing major surgery. Akca et
al. [37] demonstrated similar degrees of atelectasis
in colon surgery patients randomized to 80% vs.
30% oxygen (balance nitrogen) intraoperatively.
Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection
Myles et al. found that high inspired nitrous ox-
ide caused more atelectasis than high inspired
oxygen. Use of positive end expiratory pressure
appears to abrogate the problem of atelectasis [38].
Thus, these issues should not limit the use of
high inspired oxygen. Contraindications to the
use of FiO2 >0.8 include prematurity (retrolental
fibroplasias), recent (possibly lifetime) bleomycin
administration, use of cautery in the airway or
other procedures in which pulmonary or laryngeal
oxygen may leak into the field, and, possibly, acute
pulmonary conditions.
Delivery of antibiotics also depends on perfu-
sion. Parenteral antibiotics given so that high levels
are present in the blood at the time of wounding
clearly diminish, but do not eliminate, wound in-
fections [39]. In one-third of all wound infections,
the bacteria cultured from the wound are sensitive
to the prophylactic antibiotic given to the patient,
even when the antibiotics were given according
to standard procedure. The vulnerable third of
patients appear to be the hypoxic and vasocon-
stricted group.
Intraoperative Management
All anesthetics tend to cause hypothermia 1) by
causing vasodilation, which redistributes heat
from core to periphery in previously vasocon-
stricted patients and increases heat loss, and 2) by
decreasing heat production [40]. Vasoconstriction
is uncommon intraoperatively, as the threshold for
thermoregulatory vasoconstriction is decreased,
but it is often severe in the immediate postopera-
tive period, when anesthesia is discontinued and
the thermoregulatory threshold returns to normal
in the face of core hypothermia. The onset of
pain with emergence from anesthesia adds to this
vasoconstriction. Maintenance of normothermia
intraoperatively has been shown to decrease the
wound infection rate by two-thirds in patients
undergoing colon surgery [28]. Rapid rewarm-
ing of hypothermic patients in the postanesthesia
care unit (PACU) also appears to be effective [41].
Maintenance of a high room temperature or forced
air warming before, during, and after the operation
are significantly more effective than other meth-
91 12
ods of warming such as circulating water blankets
placed under the patient and humidification of
the breathing circuit [42]. Preoperative systemic
(forced air warmers) or local (warming bandages)
warming techniques have also been shown to de-
crease wound infections, even in clean, low-risk
surgeries such as breast surgery and inguinal her-
nia repair [43].
Surgical stress results in increased intravenous
fluid requirements. Inflammatory mediators cause
both vasodilation and an increase in vascular per-
meability [44]. Other known causes of periopera-
tive hypovolemia or fluid loss include preoperative
mechanical bowel preparation, lack of oral intake,
fever, preexisting medical conditions, medications
such as diuretics, and surgical fluid losses, includ-
ing evaporation and blood loss.
Optimizing the perioperative fluid adminis-
tration remains a controversial challenge. Esti-
mates of blood loss, third-space fluid losses, and
maintenance requirements are inaccurate and
may lead to either overreplacement or under-
replacement. Currently, most practitioners rely
on their clinical acumen, vital signs such as heart
rate and blood pressure, and urine output to
manage perioperative fluids. Due to the com-
pensatory action of peripheral vasoconstriction,
surgical patients can be markedly hypovolemic
without a change in any of these variables [13, 21,
45]. Unfortunately, this peripheral vasoconstric-
tion shunts blood away from the skin, increases
wound hypoxemia, and increases the risk of sur-
gical wound infection [20].
Current best recommendations include replac-
ing fluid losses based on standard recommenda-
tions for the type of surgery, replacing blood loss,
and replacing other ongoing fluid losses (e.g., high
urine output due to diuretic or dye administration,
hyperglycemia, or thermoregulatory vasoconstric-
tion).
Pain control should be addressed intraopera-
tively so that patients do not have severe pain
upon emergence from anesthesia. Achieving the
goal is more important than the technique used to
do so. Although regional anesthesia/analgesia may
provide superior pain relief, the effects of specific
analgesic regimens on wound outcome have not
yet been studied.
 92 Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection After Surgery
Postoperative Management
Wounds are most vulnerable in the early hours.
Although antibiotics lose their effectiveness after
the first hours, natural wound immunity (oxygen-
related) lasts longer [46]. Even a short period of
vasoconstriction during the first day is sufficient to
reduce oxygen supply. Correction and prevention
of vasoconstriction in the first 24-48 h after sur-
gery will have significant beneficial effects.
All vasoconstrictive stimuli must be corrected
simultaneously to allow optimal healing. Volume
is the last to be corrected because vasoconstric-
tion for other reasons induces diuresis and ren-
ders the patient hypovolemic (peripherally, not
centrally).
Assessing perfusion, especially in the PACU,
is critical. Unfortunately, urine output is a poor
and often misleading guide to peripheral perfu-
sion [47]. Markedly low output may indicate de-
creased renal perfusion, but normal or even high
urine output has little correlation to wound/tissue
PO2. Many factors commonly present in the pe-
rioperative period, including hyperglycemia, dye
administration, thermoregulatory vasoconstric-
tion, adrenal insufficiency, and various drugs, may
cause inappropriate diuresis in the face of mild
12 hypovolemia.
Physical examination of the patient is a better
guide to dehydration and vasoconstriction. Va-
soconstriction can be determined by a capillary
return time of more than 1.5 s at the forehead and
more than 5 s over the patella. Eye turgor is an-
other good measure of hydration. Finally, patients
can usually distinguish thirst from a dry mouth.
Skin should be warm and dry.
When excessive tissue fluids have accumulated,
diuresis should be undertaken gently so that tran-
scapillary refill can maintain blood volume. This
applies to patients who need renal dialysis as well.
The average dialysis patient vasoconstricts suf-
ficiently to lower tissue PO2 by 30% or more dur-
ing dialysis and needs about 24 h for vasomotor
tone and wound/tissue PO2 to return to normal
[48]. Fluid losses from the vascular system are not
necessarily replaced from the tissues as rapidly as
they are sustained. Tissue edema may be the price
paid for adequate intravascular volume. Edema
increases intracapillary distance, so there may be
a delicate balance between excessive edema and
peripheral vasoconstriction (which worsens the
hypoxia caused by edema).
Care of Wounds Healing by Secondary
Intention
Even with appropriate perioperative management,
some wounds become infected or fail to heal. Fre-
quently this may result from other causes of im-
paired perfusion, such as obesity, prior radiation to
the area, arterial insufficiency, or excessive edema.
It may also result from other problems such as
malnutrition, overwhelming contamination, or
ongoing trauma. If it is a simple case of infection,
the wound will generally heal rapidly by secondary
intention with just attention to basic care. If other
complicating factors are involved, it may take more
effort to achieve healing. In either case, the most
modern and advanced healing devices will not
succeed if proper care is not instituted, so attention
to basic proper wound care is crucial to ensure
success:
1. Reduce the bacterial load. The best way to
achieve this is to wash the wound gently with
mild soap in a warm shower. All open wounds
are contaminated with bacteria. Most bacterial
contamination comes from bacteria normally
resident on the skin. A shower provides the
volume to wash away the bacteria; rinsing
with normal saline does not provide adequate
volume. Moreover, saline is generally kept
refrigerated or at room temperature and thus
will tend to induce local vasoconstriction,
whereas a warm shower will tend to induce lo-
cal vasodilation. Mild soap provides sufficient
detergent effect to assist in dislodging bacteria.
Antibacterial agents, including antibacte-
rial soaps, Betadine, bleach, Dakin’s solution,
hydrogen peroxide, and alcohol, are effective
at reducing bacterial load, but they do so at
the cost of inactivating white cells and harm-
ing granulating tissue. Thus, wounds treated
with these agents are very clean but frequently
demonstrate minimal evidence of healing
(granulation tissue).
Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection
2. Maintain a moist wound environment. Moist
wounds heal about 50% faster than dry ones
[49, 50]. Any number of products may pro-
vide the proper environment, depending on
the wound. Traditional wet-to-damp dress-
ings should be replaced as the standard of
care and essentially never used. They are less
cost-effective than any other dressing on the
market because they have minimal ability to
manage exudates and they induce maceration
of the surrounding skin, thereby potentially
actually enlarging the wound; they pull off
granulation tissue as they debride necrotic
tissue and slough, thus prolonging healing.
They also provide no protection against bacte-
rial contamination (nonocclusive), must be
changed three times a day (TID), and cause
more discomfort. Although a single sheet of
gauze is inexpensive compared with a typical
$10–20 modern dressing, more than one piece
of gauze is used with each dressing change,
and the dressing must be changed TID, thus
raising the supply cost at least as high as more
sophisticated dressings that are only changed
daily or less often. The labor costs of wet-
to-damp dressings are therefore also higher.
Moreover, home care nurses cannot provide
TID dressing changes, which may delay hos-
pital discharge. Finally, given that dressing
changes often cause discomfort, less frequent
changes are clearly a benefit. So use whatever
you want, but don’t use wet to damp! Of note,
gauze impregnated with a nonevaporating
substance such as Aquaphor, silver sulfadiaz-
ine, or a hydrogel does make an excellent filler
for deeper wounds.
3. Pay attention to nutrition. Recent intake
(7 days) is most important [51]. Be aware of a
patient’s NPO status leading to missed meals.
Key elements include protein, which is re-
quired to make the extracellular matrix but is
lost in potentially large quantities from exuda-
tive wounds, and vitamin C, an essential cofac-
tor of prolyl hydroxylase (a central enzyme
in collagen posttranslational modification) as
well as essential for proper neutrophil func-
tion. The type of protein is relatively unim-
portant, although the amino acid arginine im-
93 12
proves wound healing at pharmacologic (more
than nutritional) levels [52]. Arginine-con-
taining protein supplements are available, and
arginine capsules can be obtained at health
food stores. Vitamin A and zinc deficiencies
impair wound healing, and these should be re-
pleted. A 10-day course (25,000 IU vitamin A
and 220 mg zinc daily) is sufficient, as both
may be toxic in excess. Vitamin A specifically
reverses impaired healing resulting from ste-
roids [53, 54]. Topical vitamin A and D oint-
ment (sold for diaper rash over the counter)
applied once daily works well.
4. Pay attention to perfusion. Patients should
be instructed to quit smoking, drink plenty
of fluids, manage their pain aggressively, and
keep their wound covered or insulated for
warmth. Stress reduction is also likely to be
beneficial.
Summary
In patients with moderate to high risk of surgi-
cal site infection, surgeons and anesthesiologists
have the opportunity to enhance wound healing
and prevent wound infections by simple, inex-
pensive, and readily available means [55, 56]. In-
traoperatively, appropriate antibiotic use, preven-
tion of vasoconstriction (volume, warming), and
maintenance of a high PaO2 (300–500 mmHg) are
key. Postoperatively, the focus should remain on
preventing vasoconstriction through pain relief,
warming, and adequate volume administration in
the PACU.
References
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 94 Chapter 12 · Patient Factors as a Major Determinant of Wound Outcome and Infection After Surgery
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95 12
42. Kurz, A., et al., Forced-air warming maintains intraop- of oxygen toxicity, there is no evidence of any in
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Schumpelick: What about anemia and wound
43. Melling, A.C., et al., Effects of preoperative warming on
the incidence of wound infection after clean surgery: a healing?
randomised controlled trial. Lancet, 2001. 358(9285): pp. Hopf: Anemia is good for wound healing as long
876–880 as your heart works because the viscosity goes
44. Holte, K., N.E. Sharrock, and H. Kehlet, Pathophysiology down and you get better blood flow in the wound.
and clinical implications of perioperative fluid excess. Br J
I have measured wound oxygen in a test group of
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45. Gosain, A., et al., Tissue oxygen tension and other indi-
volunteers, and there was no difference in patients
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hemorrhage. Surgery, 1991. 109(4): pp. 523–532 gen, because a better flow combined with a good
46. Knighton, D.R., B. Halliday, and T.K. Hunt, Oxygen as oxygenation leads to good wound oxygen level.
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2006. 117(7 Suppl): pp. 59S–71S

Discussion

Terzi: Is there any risk for patients in giving high

oxygen?
Hopf: Giving patients 100% oxygen is largely risk-
free. If they are newborns, you should probably
avoid 100% oxygen. So for everybody who is afraid
 13

Mesh-Related Infections After Hernia

Repair
M. E. Falagas, G. C. Makris
 98 Chapter 13 · Mesh-Related Infections After Hernia Repair
Introduction
Open or laparoscopic »tension-free« mesh implan-
tation for hernia repair of abdominal wall defects
has been the gold standard treatment because it
appears to reduce the rate of recurrence by an
average of 30–50% in comparison with the simple
nonmesh herniorrhaphy. However, the use of artifi-
cial meshes within the human body is not without
potential clinical problems and might lead to vari-
ous complications such as seromas (fluid accumu-
lation), adhesions, chronic severe pain, migration
or even rejection of the mesh, and, of course,
mesh-related infections [1, 2]. These complications
may even be life-threatening and usually neces-
sitate hospitalization and surgical removal of the
troublesome mesh.
Mesh-related infections, along with seroma
formation, are the most common complications
encountered during ventral or inguinal hernia re-
pair, although infection is definitely the one with
the most devastating consequences for the patient.
Every year almost 30,000 inguinal and just as
many ventral hernia repairs become infected, both
in the United States and Europe. New improved
techniques and stricter aseptic protocols in the
operating room have contributed to a decrease in
wound infection rates after hernia repair, but this
still appears to be center dependent.
13
Risk Factors
The risk factors for surgical site infections (SSIs)
in herniorrhaphy are gender (female > male), age
over 70, comorbidities (diabetes, obesity), operat-
ing time, and the prophylactic use of drainage or
prostheses. Even though artificial implants pose
an independent risk factor for the development of
SSIs, other factors also affect the incidence of pos-
therniorrhaphy mesh-related infection rates [1]:
▬ Type of mesh [polyester, polypropylene (PP),
or polytetrafluoroethylene (PTFE)]
▬ Type of surgical technique used to apply the
mesh (laparoscopic or open)
▬ Relationship of the mesh to the peritoneum
(transabdominal preperitoneal or totally extra-
peritoneal)
▬ Perioperative administration of prophylactic
antibiotics and type of sterile techniques ap-
plied in the operating room
▬ Mesh placement in contaminated tissues
▬ Other factors, such as smoking and immuno-
suppression
Incidence of Mesh-Related Infections
Elective primary abdominal reconstruction with
mesh is considered a clean surgery, with infection
rates of up to 8% being reported [1]. The rate of
infection may vary among centers and appears to
be influenced by underlying comorbidity (diabe-
tes, immunosuppression, obesity) and by specific
factors mentioned earlier, which will be discussed
in following sections.
Operating Technique and Type of Mesh
Laparoscopic hernioplasty compared with open
mesh procedures has been proven to induce a lower
incidence of surgical wound infections, probably
due to the lack or relatively limited physical contact
of the mesh with the surgical wound during the op-
eration. However, the specific type of laparoscopic
technique used (transabdominal preperitoneal ver-
sus totally extraperitoneal mesh implementation) is
not associated with different rates of infections, but
data are still insufficient to support this statement.
The type of implemented mesh is also of vital
importance regarding the development (or not) of
an infection [3]. Monofilament polypropylene (PP)
is the most frequently used biomaterial for repair of
an abdominal wall defect due to the low infection
rates compared with other nonabsorbable types of
meshes. The biocompatibility and the large pore
size of this PP textile permit the relatively uncom-
promised inflammatory response of the immune
system on the surface of this material. Engelsman
et al. [3] reviewed the infection rates of different
kinds of nonabsorbable meshes after open repair
hernioplasty and noted important variations:
▬ Polypropylene meshes: 2.5–5.9%
▬ Expanded polytetrafluoroethylene (ePTFE)
meshes: 0–9.2%
Chapter 13 · Mesh-Related Infections After Hernia Repair
▬ Polyester meshes: most polyester infection ra-
tes are quite similar to those of polypropylene
meshes, but rates of up to 16% have also been
documented
Surgical technique and patient and mesh charac-
teristics are responsible for the above differences.
The pathophysiologic mechanisms and certain
characteristics of the meshes underlying the above
differences will be discussed in a following para-
graph.
Antimicrobial Prophylaxis and
Preoperative Aseptic/Sterilization
Protocols
Preoperative administration of antimicrobial
agents in clean surgical procedures such as pri-
mary hernioplasty has been a matter of consider-
able debate for years, but a recent meta-analysis
by Sanabria et al. [4] of the accumulated evidence
suggests that infection rates were decreased by
almost 50% in the patients who received antimi-
crobial prophylaxis.
Stricter operative aseptic protocols in combi-
nation with proper prophylactic antibiotic cover-
age was also demonstrated to be effective in fur-
ther restricting surgical posthernioplasty wound
infections in a large series of patients who under-
went »clean« surgical repair of abdominal wall
defects.
Mesh Placement in Contaminated
Areas
Hernia repair is considered a clean operation.
Nevertheless, when bowel opening or abdominal
wound infection has previously occurred, this pro-
cedure becomes contaminated; thus, the imple-
mentation of an artificial material was thought
for years to be contraindicated. However, recent
studies suggest that minor morbidity, minimal risk
of infection, and minor wound-related mortality
are observed after mesh placement in contami-
nated tissues. Apparently, more solid evidence is
required.
99 13
Smoking and Other Comorbidities
Smoking, prolonged operating time, and patient
comorbidities such as diabetes, immunosuppres-
sion, and obesity have been incriminated for a
further increase in the incidence of surgical wound
infections after hernioplasty.
Microbiology and Pathophysiology
of Mesh-Related Infections
The isolated microflora in mesh-related infections
are usually associated with Staphylococcus species,
especially S. aureus; Streptococcus spp., including
group B streptococci; and Gram-negative (mainly
Enterobacteriaceae) and anaerobic bacteria [5]. In
addition, microbiological data confirm that strains
of methicillin-resistant S. aureus have been isolated
in mesh-related infections after hernia repair, as
have Candida spp. and Mycobacterium spp., al-
though to a far lesser extent.
Microbes have an extraordinary ability to ad-
here to surfaces to produce colonies and maintain
their functional status. In particular, certain patho-
gens, including S. aureus, may adhere even to arti-
ficial surfaces such as metal and cause implant-re-
lated infections. Bacteria may adhere to inanimate
surfaces, produce slime (which causes stronger and
irreversible adhesion), and form biofilms, which
have the ability to communicate through quorum
sensing and resist internal mechanisms of defense.
In addition, they build tight junctions with the un-
derlying biomaterial, creating complex, large struc-
tures that are not easily ingested by phagocytes.
Highly porous material with a large surface
area and numerous niches–such as the multifila-
ment meshes–provides pathogens with an excel-
lent environment protected from the immune sys-
tem of the host. Niches function as a shelter for
the pathogens’ colonies because of the large size
of phagocytes. Niches are small in diameter, but at
the same time, they substantially increase the total
area of the mesh, raising the possibility for success-
ful bacterial adherence [6]. Porous materials are
connected with higher infection rates because they
downsize the normal inflammatory response of
the infected host organism.
 100 Chapter 13 · Mesh-Related Infections After Hernia Repair
Finally, the hydrophobic or hydrophilic proper-
ties of implanted materials also influence the adher-
ing pattern of bacteria upon them, since they deter-
mine protein absorption from the surface of the
biomaterial. In vitro studies have shown that more
hydrophobic materials, such as PTFE and ePTFE,
may be associated with the development of more
resistant forms of biofilms [6]. The above results
may explain previous clinical findings that infec-
tions related to multifilament, hydrophobic ePTFE
and PTFE meshes are expected to have the worst
prognosis and demand surgical management.
Clinical Manifestation and Diagnosis
The manifestations of mesh-related infections can
be divided into surgical (superficial) wound infec-
tions and deep-seated mesh infections and may
occur 2 weeks to 39 months from the day of mesh
implantation.
Surgical Wound Infections
Surgical wound infections are the most commonly
encountered type of infection, presenting at an
early postoperative stage, usually days or a few
weeks after the mesh placement. The symptoms
and signs are typical of local acute inflammation:
13 pain, erythema, swelling with locally increased
temperature, and confined tenderness.
Inappropriate treatment of surgical wound in-
fections may be complicated by the formation of
a discharging fistula, intraabdominal abscess, or,
rarely, osteomyelitis. The emergence of systemic
symptoms such as fever, chills, or rigor and malaise
should urge prompt investigation and initiation of
therapeutic actions before sepsis occurs.
Deep-Seated Mesh Infections
Deep-seated mesh infections generally manifest
in the early postoperative period, but infrequently
they can also be observed as a late-onset phenom-
enon that is delayed for months or years (up to
4.5 years after the operation) [7]. Deep-seated in-
fections may result from persistent fluid collection
(seromas) leading to chronic groin sepsis. Symp-
toms can be chronic, recurrent, or totally absent
until the progression to sepsis.
Diagnosis
The combination of clinical presentation, physical
examination, laboratory values, and previous medi-
cal history is usually adequate to establish a diagno-
sis. However, when there are doubts regarding dif-
ferential diagnosis, two noninvasive imaging tech-
niques could provide physicians with a solution:
Bedside ultrasound and computerized tomography
may reveal the inflammatory process in the adipose
tissue around the implant because of the different
ultrasonic and density characteristics, respectively.
Complications such as the presence of fistula or
abscess could also be depicted. Diagnostic paracen-
tesis of mesh-associated seromas when there are no
signs of inflammation should be carefully consid-
ered and not performed routinely; there is a high
risk of transforming a potentially aseptic reaction
to an infectious process through the introduction
of bacteria into the previously aseptic seromas.
Treatment and Antimicrobial
Prophylaxis
Therapeutic Options:
Surgical or Conservative
The therapeutic options available following the
development of mesh-related infection can be sep-
arated according to the type and severity of infec-
tion and the type of implanted mesh.
▬ Posthernioplasty superficial wound infections
may have a better prognosis and may be tre-
ated conservatively using proper intravenous
antimicrobial coverage and drainage when
signs of accumulated exudate exist. However,
the use of drainage is still controversial due to
insufficient evidence.
▬ In limited, deep-seated infections of the mesh,
prolonged antibiotic treatment in combina-
tion with percutaneous or open drainage has
Chapter 13 · Mesh-Related Infections After Hernia Repair
been reported to be effective to restrain the
infectious process. However, when extensive
infection is present–due to biofilm formation
and limited penetration of the drug in the
area–mesh removal and surgical cleaning of
the wound pose the best possible treatment
to eradicate the infection. Unfortunately, the
labeling of a mesh-related infection as limited
or extensive remains empirical. Hernia recur-
rence could be a postoperative complication
if adequate fibrous tissue had not developed
earlier (early-onset, deep-seated infections).
▬ The choice between conservative and surgical
treatment could also be influenced by the type
of implanted mesh. Structural (monofilament
or multifilament) and biochemical (hydro-
phobic or hydrophilic) properties influence
the potential response of the infection to the
administered antibiotics. Clinical findings in
combination with recent in vitro experiments
suggest that infected hydrophobic meshes–
such as PTFE and ePTFE–are most likely to be
removed in order to achieve complete cure.
So far, no universal recommendations based on
randomized controlled trials exist for the optimal
treatment of mesh-related infections. Further data
Hospital surgical
site infection rate
High (>1%)
Preoperative
prophylaxis
High-risk patient
Preoperative
prophylaxis
101 13
are warranted to establish evidence-based algo-
rithms for treating infections according to the type
and severity of infection and the type of mesh.
Prophylaxis
Due to the special features of implant devices,
the best way to treat an implant-related infection
without destroying the implant is to take the ap-
propriate measures to avoid initial exposure to
infectious agents. Considerable effort has been
made to develop techniques that will restrain the
fundamental mechanisms for implant-related in-
fections, which are bacterial adhesion and coloni-
zation of artificial surfaces and biofilm formation.
Various strategies such as antimicrobial prophy-
laxis and mesh coatings of antimicrobial biomate-
rials have been developed, but so far, comparative
data are lacking.
Preoperative antimicrobial prophylaxis in elec-
tive, »clean« surgical procedures such as repair of
an abdominal wall defect with a mesh has been
a matter of considerable controversy for years.
Nevertheless, recent meta-analysis of accumulated
data provides evidence of significantly lower SSI
rates after proper prophylaxis. The antimicrobial
Low (<1%)
Assess individual
risk factors
Low-risk patient
⊡ Fig. 13.1. Proposed algorithm
No preoperative for preoperative antimicrobial
prophylaxis prophylaxis
 102 Chapter 13 · Mesh-Related Infections After Hernia Repair

agents most commonly used are cefazolin 1–2 g 5. Falagas ME, Velakoulis S, Iavazzo C, Athanasiou S. Mesh-
(or 1 g erythromycin if the patient is allergic), 1.5 g related infections after pelvic organ prolapse repair sur-
gery. Eur J Obstet Gynecol Reprod Biol 2007; 2:147–156
ampicillin/sulbactam , 2 g amoxicillin/clavulanic
6. Engelsman AF, van der Mei HC, Busscher HJ, Ploeg RJ.
acid, or 1.5 g cefuroxime. Unfortunately, there are Morphological aspects of surgical meshes as a risk factor
still no data regarding the cost-effectiveness of this for bacterial colonization. Br J Surg 2008; 8:1051–1059
approach. Infection rates can be center dependant 7. Delikoukos S, Tzovaras G, Liakou P, Mantzos F, Hatzitheo-
and can be as low as 1% in some cases. Therefore, filou C. Late-onset deep mesh infection after inguinal
hernia repair. Hernia 2007; 1:15–17
researchers have suggested that institutions revise
8. Eriksen JR, Gögenur I, Rosenberg J. Choice of mesh for la-
their SSI rates and decide, according to each pa- paroscopic ventral hernia repair. Hernia 2007; 6:481–492
tient’s special risk factors, whether antimicrobial
prophylaxis is justified. (See ⊡ Fig. 13.1).
Mesh coating with antimicrobial agents or
other biomaterials that decrease the adhesion abil- Discussion
ity of bacteria, increase host tissue ingrowth, or
initiate bacterial destruction have been developed Heniford: When I talk to our patients about lap-
to prevent implant colonization and biofilm for- aroscopic versus open ventral hernia repair, the
mation in the first place. Apart from antibiotic number one reason to recommend laparoscopic
coatings (such as cefoxitin), silver, gold, titanium repair is not pain, and it is not cosmetics—it’s a
carbonitride, polyglactin, gelatin, and other bio- decreased risk of infection, by far. When we look
materials have been used as coatings, with differ- back at our patients and compare the different
ent mechanisms of action. At present, however, risk factors for infection, the number one reason
evidence is based on experimental and animal is smoking.
studies, and the available comparative data are
insufficient to draw safe conclusions
Universal recommendations regarding the
choice of mesh type or the best possible antimi-
crobial prophylaxis cannot be supplied based on
the available evidence from randomized controlled
trials [8]. Until further trials are completed to shed
more light on these controversial issues, the choice
13 of mesh and antibiotic coverage will be center
dependent and, in particular, derived from the sur-
geon’s experience and the financial cost.

References

1. Falagas ME, Kasiakou SK. Mesh-related infections after

hernia repair surgery.
Clin Microbiol Infect 2005; 1:3–8
2. Bliziotis IA, Kasiakou SK, Kapaskelis AM, Falagas ME. Mesh-
related infection after hernia repair: case report of an
emerging type of foreign-body related infection Infection
2006; 1:46–48
3. Engelsman AF, van der Mei HC, Ploeg RJ, Busscher HJ. The
phenomenon of infection with abdominal wall reconst-
ruction. Biomaterials 2007; 14:2314–2327
4. Sanabria A, Domínguez LC, Valdivieso E, Gómez G. Pro-
phylactic antibiotics for mesh inguinal hernioplasty: a
meta-analysis. Ann Surg 2007; 3:392–396
 14

Human Acellular Dermal Matrix

for Ventral Hernia Repair in the
Compromised Surgical Field
J. J. Diaz
 104 Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair in the Compromised Surgical Field
Introduction
Repair of a ventral hernia is one of the most com-
mon surgical procedures performed in the United
States. Yet ventral hernia repair in the setting of
a contaminated surgical field presents a very dif-
ficult surgical dilemma. Prosthetic mesh has been
widely employed since the 1950s for the elective
repair of ventral hernias. Beyond hernia recur-
rence, prosthetic mesh has known complications
such as infection, contracture, and intestinal fistula
formation. In the setting of a clean-contaminated
and/or dirty surgical field, prosthetic mesh is con-
traindicated due to high complication rates [1–4].
The alternative, closing of a ventral hernia with
an absorbable mesh, presents its own set of prob-
lems. Repair with absorbable mesh only serves
to keep the patient from evisceration. It is a tem-
porizing procedure for a planned ventral hernia
repair, and it continues to be associated with a high
rate of wound infection that is unaffected by the
use of an absorbable mesh [5–7].
Patient Population
Patients with complex hernias remain a very dif-
ficult group to repair. Complex hernias are com-
monly described as follows: open abdomen after
trauma/emergency; general surgery resulting in a
planned ventral hernia; presence of an intestinal
fistula, ostomy, or infected mesh. Patients who have
14 a history of multiple hernia repairs, loss of domain,
or loss of abdominal tissue and musculature are
also labeled as having complex hernias. Patients
with a previous history of infected mesh or wound
infection have a high risk of developing another
surgical site infection [8, 9]. In all of these cases,
the use of prosthetic mesh would be considered a
contraindication in hernia repair. To date, no classi-
fication system is universally accepted for defining
ventral hernias. A ventral hernia can range from
a simple periumbilical hernia in a patient with no
comorbidities to an abdominal catastrophe with a
planned ventral hernia, a split-thickness skin graft
over the viscera, and an atmospheric fistula.
Manufacturers have started to develop biologi-
cal mesh with the intent to produce a product that
can become vascularized and resist infection. In
addition, the ideal product must have the tensile
strength of native fascia or be comparable to pros-
thetic mesh, be pliable, and be easy to implant.
To date, only human acellular dermal matrix has
demonstrated its ability to resist infection.
The development of human acellular dermis
(HADM) as a fascial graph replacement presents a
potential alternative to hernia closure in a compro-
mised surgical field. HADM is derived from hu-
man donors (LifeCell, Branchburg, NJ, USA). The
donated human skin is supplied by the American
Association of Tissue Banks and is approved by the
U.S. Food and Drug Administration as banked hu-
man tissue. Under a proprietary process, HADM
is cleansed of any immune reactive cells or cel-
lular components. HADM is being used to reduce
complications seen with prosthetic mesh, such as
infection, adhesions, fistulas, seromas, bleeding,
and skin erosion [10, 11].
Repair Types
The most common ventral hernia repair types
mesh to »bridge« the defect using a tension-free
repair. A prosthetic mesh with 3–4 cm of overlap
of the fascial edge has been used as an onlay or
sublay [12, 13]. Interposition mesh placement is
well known to have the highest recurrence rate
and is not a recommended surgical technique.
Luijendijk et al., in the only randomized controlled
trial of mesh vs. primary suture repair, showed that
the rate of hernia recurrence could be reduced by
using a prosthetic mesh [12].
We hypothesized that a human acellular der-
mal matrix would be a suitable biological tissue
alternative for repairing ventral hernia in the pres-
ence of a contaminated surgical field by better
tolerance to wound infection, thereby reducing the
incidence of prosthesis removal.
Methods
We performed a retrospective study of a single
institution’s experience with HADM (⊡ Fig. 14.1).
Patients were admitted from January 2001 to
Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair
105 14
All study patients
N=75

Clean-contaminated Contaminated or dirty

N=64 N=11

SSI SSI

Yes No Yes No
N=21 N=43 N=4 N=7

Medically Surgically Medically Surgically

managed managed managed managed
N=9 N=12 N=2 N=2

⊡ Fig. 14.1. Study design

Mesh removed =4 Mesh removed =1
(SSI surgical site infection)

December 2004 to Vanderbilt University Medi-
cal Center and included surgical cases from the
trauma, general surgery, and emergency general
surgery services. Before the study began, approval
was granted by the Vanderbilt University Institu-
tional Review Board.
Study Population
Patients were included if they were greater than
15 years of age and had undergone repair of a
ventral hernia or traumatic anterior wall fascial
defect with acellular human dermis (AHD) in a
compromised surgical field. Surgical involvement
of the following organ systems was required for
inclusion: stomach, small bowel, colon, appendix,
hepatobiliary system, urinary bladder, spleen, and
ostomy formation. This also included removal
of infected mesh or repair of an enterocutane-
ous fistula. The medical center’s electronic data
repository (StarPanel) and hospital administrative
database were used to accurately collect patient
data. Demographic data collected (⊡ Table 14.1)
included age, gender, race, hospital length of stay,
and comorbidities, which in turn included dia-
betes mellitus, hypertension, renal insufficiency
(serum creatine <30 mg/h), chronic obstructive
pulmonary disease, heart disease, and hepatic dis-
ease (cirrhosis).
The wound classification was recorded for each
patient. The Centers for Disease Control and Pre-
vention (CDC) wound classification system was
used to define surgical wounds [10] (⊡ Table 14.2).
The operative technique for each hernia repair was
also recorded (⊡ Table 14.3). The type of suture
used for each AHD repair (absorbable vs. perma-
nent) was also recorded in the database. The study
population was divided into two groups: clean-
contaminated (CC) and contaminated/dirty (CD).
 106 Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair in the Compromised Surgical Field

⊡ Table 14.1. Study demographics ⊡ Table 14.2. Wound classification

n 75 Wound Wound criteria

classification
Value % / SD
Clean Elective, not emergency, nontrau-
Age 51.5 14.5
matic; primarily closed; no acute
Gender inflammation; no break in tech-
nique; respiratory, gastrointestinal,
Male 36 48.0
biliary, and genitourinary tracts not
Female 39 52.0 entered

Race (%) Clean-con- Urgent or emergency case that is

taminated otherwise clean; elective opening of
White 60 80.0
respiratory, gastrointestinal, biliary,
Black 11 14.7 or genitourinary tract with minimal
spillage (e.g., appendectomy); no en-
Other 5 6.7
countering of infected urine or bile;
Comorbidity (%) minor technique break

Cardiac 15 20.0 Conta- Nonpurulent inflammation; gross

Hypertension
Diabetes mellitus
Renal
Chronic obstructive
pulmonary disease
minated spillage from gastrointestinal tract;
34 45.3
entry into biliary or genitourinary
23 30.7 tract in the presence of infected bile
or urine; major break in technique;
4 5.3
penetrating trauma <4 h old; chronic
5 6.7 open wounds to be grafted or cov-
ered

Hepatic 3 4.0 Dirty Purulent inflammation (e.g., abscess);

preoperative perforation of respira-
Chronic steroids 4 5.3
tory, gastrointestinal, biliary, or geni-
Hospital tourinary tract; penetrating trauma
>4 h old
Length of stay 16.7 20.8

Charges $158,183 $206,896

Disposition (%)
⊡ Table 14.3. Operative repair type
14 Died (sepsis) 1 1.3

Home 56 74.7 Repair type Repair description

Transfer /rehabilitation 18 24.0 Inlay (sublay) Reinforcing sheet of acellular human

dermis is positioned deep to the an-
terior abdominal wall defect

Outcomes Onlay Reinforcing sheet of acellular human

dermis is positioned superficial to
the defect
The primary outcome measured in this study was
the incidence of surgical site infection (SSI) as per Component Releasing incisions are made in the
separation external oblique muscle with rectus
the CDC definitions for nosocomial infections.
reinforcement with acellular human
Management of the wound infection was divided
dermis
into medical management (intravenous antibiotic
only) and surgical management (operative incision Interposition The edges of the acellular human
dermis graft are sutured directly to
and drainage plus intravenous antibiotics). Also
the edges of the fascial defect
recorded was whether the AHD was removed.
Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair
107 14
Secondary variables included early hernia re- were medically managed (14.1%) and 12 wound
currence (<1 year); septic complications, including infections that were surgically managed (18.8%).
ventilator-associated pneumonia; urinary tract in- The CD group (n=11) had two wound infections
fection; and blood stream infection. that were medically managed (18.2%) and two that
were surgically managed (18.2%). Five of 14 surgi-
cally managed (35.7%) wound infections required
Statistics removal of the mesh.

Statistical analysis was performed using chi-square

tests to evaluate statistical significances between
patient subgroups.
Results
Seventy-five patients met the study criteria. The
overall wound infection rate was 33.3%: 11 medi-
cally managed infections (14.7%) and 14 surgically
managed infections (18.7%). The average length
of hospital stay was 16.7 days (+20.8) with a mean
follow-up of 275 (+209) days.
With respect to the entire patient population,
25 out of 75 patients (33.3%) developed an SSI,
and 12 patients had hernia recurrence (16%). The
CC group (n=64) had nine wound infections that
Subgroup Analysis
The patient population was divided into two sub-
groups based on wound type: clean-contaminated
(CC) and contaminated or dirty (CD). Sixty-four
patients had CC wounds, and 11 patients had CD
wounds (⊡ Table 14.4). Within the CC group, there
were 21 SSI: 9/64 patients (14.1%) were medi-
cally managed, and 12/64 patients (18.8%) were
surgically managed. Of the 12 surgically managed
wound infections, five necessitated removal of the
HADM (33.3%) either because of enterocutaneous
fistula formation (n=4) or HADM infection (n=1;
see ⊡ Table 14.5). Within the follow-up period (av-
erage 269 days), a total of 12 patients (16%) in the
CC group experienced hernia recurrence.

⊡ Table 14.4. Clean-contaminated (CC) and contaminated/dirty (CD) subgroup analysis (HR hernia recurrence;
LOS length of stay; WC wound closure during initial procedure; FUD follow-up days

Groups n HR (%) LOS (SD) WC (%) FD (SD)

Clean-contaminated 64 10 15.6 15.4 19.6 64 100 269 186

Contaminated/dirty 11 2 18.2 24.3 27.7 8 72.7 306 277

Total 75 12 16.0 19.8 23.6 72 96 275 201

⊡ Table 14.5. Inpatient infection rate (MM medical management; SM surgical management)

n (%) Inpatient

Total (%) MM (%) SM (%)

Clean-contaminateda 64 85.3 21 32.8 9 14.1 12 18.8

Contaminated/dirty 11 14.7 4 36.4 2 18.2 2 18.2

Totals 75 100 25 33.3 11 14.7 14 18.7

aMesh
removal in five patients
 108 Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair in the Compromised Surgical Field

Surgical Technique and Suture Analysis
Outcomes were also evaluated with respect to the
type of hernia repair implemented (⊡ Table 14.6).
The ventral hernia repair type with the lowest
occurrence of wound infection was the onlay tech-
nique (n=15), with 6.7% of patients developing
an SSI. This was followed by inlay (n=27; 33.3%),
interposition (n=23; 43.5%), and component sepa-
ration (n=10; 50%). The repair method most suc-
cessful at preventing hernia recurrence was the
inlay method, with only 7.4% of patients devel-
oping a secondary hernia. This was followed by
component separation (10%), onlay (13.3%), and
interposition (30.4%). Although general trends in
differences in wound infection and hernia recur-
rence rates are evident, none of these differences
was statistically significant.
Patients were also stratified by the type of su-
ture used for the procedure, and outcomes were
determined. Thirty-one percent (31.3%) of the pa-
tients who were repaired with absorbable sutures
(n=32) developed a postoperative SSI, and 25%
experienced hernia recurrence. Patients repaired
with permanent sutures (n=38) had a slightly
higher SSI rate at 34.2%, but a lower rate of her-
nia recurrence, at 10.5%. Again, the differences
between infection and recurrence rates were not
statistically significant. It should be noted that the
type of suture used in five patients was unknown,
and two developed a surgical wound infection
(⊡ Table 14.7).
It was concluded that wound infection in the
contaminated surgical field occurred 33.3% of the
time; 18.7% of the cases required surgical manage-
ment, and 35.7% of these required removal of the
HADM.
Discussion
Because of the high rates of infection, hernia re-
currence, and the occasional need for mesh re-
moval with synthetic hernia repair in a contami-
nated surgical field, surgeons continue to search
for other methods and materials to manage this
difficult dilemma [15, 16]. One such material that
has garnered attention is HADM. Studies have
demonstrated that acellular grafts such as HADM
have shown reduced postsurgical inflammation
and rapid cellular infiltration and revasculariza-
tion [17, 18]. This has been attributable to the

⊡ Table 14.6. Surgical repair technique and outcomes (WI wound infection; MM medical management; SM surgical
management; HR hernia recurrence)

Repair type n WI (%) MM (%) SM (%) HR (%)

14 Inlay 27 9 33.3 5 55.6 4 44.4 2 7.4

Onlay 15 1 6.7 1 6.7 0 0.0 2 13.3

Interpositional 23 10 43.5 3 30.0 7 70.0 7 30.4

Component separation 10 5 60.0 2 30 3 30.0 1 20.0

⊡ Table 14.7. Suture type and outcomes (WI wound infection; MM medical management; SM surgical management;
HR hernia recurrence)

Suture typea n WI (%) MM (%) SM (%) HR (%)

Absorbable (PDS) 32 10 31.3 7 70.0 3 30.0 8 25.0

Permanent (Prolene) 38 13 34.2 4 30.8 9 69.2 4 10.5

aSuture
type unknown in five cases
Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair
macroarchitecture of the HADM, which is native
human dermis. The HADM is a three-dimensional
implant of tissue with an intact basement mem-
brane, collagen fibers, elastin filaments, hyaluro-
nan, and proteoglycans, as well as patent capillary
network channels [19]. Once HADM is vascular-
ized, the very nature of its structure allows it to
resist infection when implanted into the anterior
abdominal wall. Animal models have also shown
that HADM offers the same tensile strength as syn-
thetic materials, while achieving superior revascu-
larization [20].
Our study substantiates the increasing amount
of evidence demonstrating the utility of HADM
in ventral hernia repairs, especially in a com-
promised surgical field. It is generally accepted
that synthetic prostheses are contraindicated in a
compromised surgical field because of unaccept-
ably high rates of infection and hernia recurrence.
However, no prospective trials have evaluated out-
comes between HADM and synthetic mesh re-
pairs. Our results and those of others suggest that
ventral hernias repaired with HADM have accept-
ably low rates of infection and hernia recurrence
compared with those repaired with nonbiological
prostheses. Voyles et al. reported nine polypropyl-
ene mesh removals out of 29 (31%) surgically con-
taminated ventral hernia repairs due to infection
or fistula formation [21]. Animal models have
also shown high rates of polypropylene and poly-
tetrafluoroethylene mesh removal due to infection
[22, 23]. Geisler et al. reported hernia recurrence
of 43% with synthetic mesh in compromised sur-
gical fields [24].
The overall rates of wound infection (33.3%)
and hernia recurrence (16%) in this study are con-
sistent with studies reporting complication rates
for synthetic prostheses in compromised surgical
fields. Several previous studies also evaluated out-
comes in hernia repair using HADM and demon-
strated lower complication rates as well. Buinewicz
and Rosen, in a retrospective review of 44 patients
who underwent incisional hernia repair or TRAM
flap surgery using HADM, reported a 7% postop-
erative wound infection rate and 5% hernia recur-
rence in clean surgical fields. No patient required
reoperation or removal of the HADM [10]. Kolker
et al. reported no hernia recurrences and only two
109 14
seromas from a pool of 16 ventral hernia patients
in clean surgical settings [25]. Butler et al. evalu-
ated the effectiveness of HADM in 13 suboptimal
surgical patients in whom polypropylene mesh was
contraindicated (perioperative radiation, place-
ment of mesh directly over the bowel with bacte-
rial contamination) [26]. Only two seromas (15%),
one hematoma (8%), one occurrence of partial flap
necrosis (8%), one case of enterocutaneous fistula
formation (8%), and one case of wound dehiscence
(8%) were noted. This study demonstrates the use-
fulness of HADM in compromised surgical fields.
Scott et al. have also explored the application of
HADM for open abdominal wound closure [27].
HADM was used to definitively close 37 open ab-
domens that would not have otherwise closed pri-
marily. The results were favorable: two SSIs (5.4%),
one intraabdominal abscess (2.7%), and no hernia
recurrences.
A prosthetic mesh infection is a complex sur-
gical problem. In most cases, this progresses to
a chronic septic state, which usually mandates
removal of the mesh. Under these circumstances,
immediate repair requires either autologous tis-
sue material or a staged surgical repair. Yet these
cases have a universally high wound infection rate.
In our study, we had a 33% wound infection rate,
but only five cases required removal of the AHD
during the early experience. The revascularization
of the HADM coupled with early surgical manage-
ment of complex surgical wound infections al-
lowed us to salvage the repair. It became clear that
a surgical wound infection did not always equal a
mesh infection.
The impact of hernia repair type on patient
outcomes demonstrates general agreement with
the existing literature. Several studies have shown
that the interposition technique yields the highest
frequency of complications, whereas the inlay ap-
proach involves complications least frequently [28,
29]. Although no particular method was statisti-
cally superior in our small patient population, the
numbers strongly discourage the use of interpo-
sitional hernia repair. The existing literature also
favors inlay (sublay) repair, but in our study, the
onlay technique proved to be less prone to infec-
tion and just as resistant to hernia recurrence as
the inlay technique. Component separation repairs
 110 Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair in the Compromised Surgical Field
also had a low rate of recurrence (10%) but a much
higher rate of wound infection (50%). Again, the
size of our patient population did not allow for
statistical significance, but the results favor either
inlay or onlay HADM placement.
Repair of these complex ventral defects with
onlay, inlay, or component separation surgical
techniques commonly requires large adjacent skin
flaps. This allows for mobilization of the skin and
primary closure of the surgical wound. This tech-
nique results in large subcutaneous spaces that are
commonly managed with drains to allow egress
of collected fluid, with collapse of the space. In
our study, drains were universally used for this
purpose. White et al. [9] found that abnormal fluid
collections are the most frequent problem in these
types of hernia repairs. However, the use of drains
does not reduce the incidence of complications
such as wound infection or seroma formation.
Strengths and Limitations
This is the largest study to date using AHD in
a compromised surgical field, and it was con-
ducted at a large academic referral center. This is
a retrospective review, with all the limitations and
problems associated with such a study. We did
not have a control arm, and the follow-up period
was extremely limited. This was a heterogeneous
population that included trauma, general surgery,
and emergency general surgery cases. As such, no
14 long-term analysis or conclusions can be gathered
from the data. Future studies are required to di-
rectly compare the use of acellular human dermis
vs. prosthetic mesh regarding the long-term suc-
cess of ventral repair in a prospective fashion.
Conclusion
Our analysis demonstrates the value of AHD for
repairing a ventral hernia in a compromised surgi-
cal field. The relatively low rate of surgical wound
infection and hernia recurrence coupled with the
infrequent necessity for AHD removal favors its
use over synthetic mesh for contaminated ventral
hernia closure [30].
References
1. Trupka AW, Schweiberer L, Hallfeldt K, Waldner H. Ma-
nagement of large abdominal wall hernias with for-
eign implant materials (Gore-tex patch). Zentralbl Chir
1997;122:879–884
2. Bleichrodt RP, Simmermacher RKJ, Van der Lei B, Schaken-
raad JM. Expanded polytetrafluoroethylene patch ver-
sus polypropylene mesh for the repair of contaminated
defects of the abdominal wall. Surg Gyn Obst 1993;176:
18–24
3. Voyles CR,Richardson JD, Bland KI, et al. Emergency ab-
dominal wall reconstruction with polypropylene mesh.
Short term benefits versus long term complications. Ann
Surg 1981; 194:219–223
4. Temudom T, Siadati M, Sarr JG. Repair of complex giant or
recurrent ventral hernias by using tension-free intrapari-
etal prosthetic mesh (Stoppa technique): lessons learned
from our initial experience (fifty patients). Surgery 1996;
120:738–744
5. Finan KR, Vick CC, Kiefe CI, Neumayer L, Hawn MT. Predic-
tors of wound infection in ventral hernia repair. Am J Surg
2005;190(5):676–681
6. Scott BG, Feanny MA, Hirschberg A. Early definitive clo-
sure of the open abdomen: a quiet revolution. Scand J
Surg 2005;94(1):9–14
7. Mayberry JC, Burgess EA, Goldman RK, et al. Enterocuta-
neous fistula and ventral hernia after absorbable mesh
prosthesis closure for trauma: the plain truth. J Trauma
2004;57(1):157–162
8. Houck JP, Rypins EB, Sarfeh IJ, et al. Repair of incisional
hernia. Surg Gynecol Obst 1989; 169:397–399
9. White TJ, Santos MC, Thompson JS. Factors affecting
wound complications in repair of ventral hernias. Am
Surg 1998;64(3):276–280
10. Buinewicz B, Rosen B. Acellular cadaveric dermis (acellular
human dermis): a new alternative for abdominal hernia
repair. Ann Plast Surg 2004; 52:188
11. Bauer JJ, Harris MT, Kreel I, et al. Twelve-year experience
with expanded polytetrafluoroethylene in the repair of
abdominal wall defects. Mt Sinai J Med 1999; 66: 20–25
12. Luijendijk RW, Hop WC, van den Tol MP, et al. A compari-
son of suture repair with mesh repair for incisional hernia.
N Engl J Med 2000; 343(6):392–398
13. Burger JW, Luijendijk RW, Hop WC, et al. Long-term
follow-up of a randomized controlled trial of suture ver-
sus mesh repair of incisional hernia. Ann Surg 2004;
240(4):578–583
14. The Hospital Infection Control Practices Advisory Com-
mittee. Guidelines for prevention of surgical site infection.
Am J Infect Control 1999; 27:109–110
15. Diaz JJ Jr, Gray BW, Dobson JM, et al. Repair of giant ab-
dominal hernias: does the type of prosthesis matter? Am
Surg 2004;70(5):396–401; discussion 401–402
16. Leber GE, Garb JL, Alexander AI, Reed WP. Long-term com-
plications associated with prosthetic repair of incisional
hernias. Arch Surg 1998;133(4):378–382
Chapter 14 · Human Acellular Dermal Matrix for Ventral Hernia Repair
111 14
17. Livesey SA, Herndon DN, Hollyoak MA, et al. Transplanted
acellular allograft dermal matrix. Potential as a template
for the reconstruction of viable dermis. Transplantation
1995;60(1):1–9
18. Eppley BL. Experimental assessment of the revasculariza-
tion of acellular human dermis for soft-tissue augmenta-
tion. Plast Reconstr Surg 2000; 107:757
19. LifeCell. AlloDerm Regenerative Tissue Matrix. http://
www.lifecell.com/products/95/
20. Silverman RP, Singh NK, Li EN, et al. Restoring abdominal
wall integrity in contaminated tissue-deficient wounds
using autologous fascia grafts. Plast Reconstr Surg
2004;113(2):673–675
21. Voyles CR, Richardson JD, Bland KI, et al. Emergency ab-
dominal wall reconstruction with polypropylene mesh:
short-term benefits versus long-term complications. Ann
Surg 1981;194(2):219–223
22. Bleichrodt RP, Simmermacher RKJ, van der Lei B, et al.
Expanded polytetra-fluoroethylene patch versus polypro-
pylene mesh for the repair for contaminated defects of
the abdominal wall. Surg Gynecol Obstet 1993; 176:18
23. Brown GL, Richardson JD, Malangoni MA, et al. Compari-
son of prosthetic materials for abdominal wall reconstruc-
tion in the presence of contamination and infection. Ann
Surg 1985; 201:705
24. Geisler DJ, Reilly JC, Vaughan SG, Glennon EJ, Kondylis PD.
Safety and outcome of use of nonabsorbable mesh for
repair of fascial defect in the presence of open bowel. Dis
Colon Rectum 2003; 46(8):1118–1123
25. Kolker AR, Brown DJ, Redstone JS, Scarpinato VM, Wal-
lack MK. Multilayer reconstruction of abdominal wall
defects with acellular dermal allograft (acellular human
dermis) and component separation. Ann Plast Surg
2005;55(1):36–41; discussion 41–42
26. Butler CE, Langstein HN, Kronowitz SJ. Pelvic, abdominal
and chest wall reconstruction with acellular human der-
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plications. Plast Reconstr Surg. 2005;116(5):1263–1275;
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27. Scott BG, Scott BG, Welsh FJ, et al. Early aggressive clo-
sure of the open abdomen–a new approach. J Trauma
2006;60(1):17–22
28. Ueno T, Pickett LC, de la Fuente SG, et al. Clinical ap-
plication of porcine small intestinal submucosa in the
management of infected or potentially contaminated ab-
dominal defects. J Gastrointest Surg 2004;8:109–112
29. de Vries Reilingh TS, van Geldere D, et al. Repair of
large midline incisional hernias with polypropylene
mesh: comparison of three operative techniques. Hernia
2004;8(1):56–59
30. Langer C, Liersch T, Kley C, Flosman M, et al. Twenty-five
years of experience in incisional hernia surgery. A compa-
rative retrospective study of 432 incisional hernia repairs.
Chirurg 2003;74(7):638–645
 15

Fate of the Inguinal Hernia Following

Removal of Infected Prosthetic Mesh
A. S. Fawole, R. P. C. Chaparala, N. S. Ambrose
 114 Chapter 15 · Fate of the Inguinal Hernia Following Removal of Infected Prosthetic Mesh
Introduction
Over 70,000 groin hernias are repaired each year in
England and Wales. Tension-free mesh hernioplasty
is a commonly performed procedure for repair of
inguinal hernias. It is relatively easy to perform,
with one of the lowest recurrence rates of the avail-
able repairs [1], and studies have shown that this is a
safe procedure with very few complications [2]. But
there are concerns about infection because of the
introduction of a foreign material into the body.
Surgical site infection following inguinal her-
nia repair has been reported to be anything from 0
to 15%. The majority of these are superficial infec-
tions and do not appear to be influenced by the
presence of a mesh [3]. These usually settle sponta-
neously with the use of antibiotics and sometimes
require superficial incision and drainage. However,
deep wound infection is a serious complication
leading to chronic groin sepsis, which requires
removal of the prosthetic mesh material to allow
resolution of the infective process.
Taylor and O’Dwyer [4] identified 12 cases of
chronic groin sepsis following mesh repair of an
inguinal hernia in Scotland over a 4-year period,
all of which required complete or partial removal
of the mesh to resolve the sepsis. Follow-up data
were available for 11 of these 12 patients, two
of whom developed hernia recurrence following
mesh removal, although the duration of follow-up
was not stated for the rest of the patients. One of
these patients, who developed a recurrence about
2 years after initial mesh removal, had a further
mesh repair that, unfortunately, once again led
to groin sepsis requiring removal of the second
15 mesh to control the infection. The other patient
remained asymptomatic on follow-up, and the re-
currence was thus not treated surgically [4].
Case reports have not observed hernia recur-
rence following removal of infected mesh mate-
rial inserted by the open [5] or laparoscopic [6]
techniques. A randomised controlled trial of pro-
phylactic antibiotics in mesh hernioplasties found
four cases of deep infection in the overall popula-
tion of 280 patients studied (1.4%). Three of these
required mesh removal for symptom control, and
all three had no evidence of hernia recurrence at
1 year follow-up [7].
The aim of this study was to determine the
incidence of inguinal hernia recurrence follow-
ing the removal of an infected prosthetic mesh.
In addition, the perioperative complications and
long-term symptoms associated with removal were
reviewed.
Patients and Methods
Over an 8-year period from January 1, 1995, to
December 31, 2002, 2,017 patients [1,892 male,
125 female; median age 60 (range 15–95) years]
had repair of inguinal hernias in our university
teaching hospital. Of these, 122 patients had bilat-
eral hernias repaired, making a total of 2,139 in-
guinal hernias repaired in this study period; 1,955
were primary inguinal hernias, and 184 procedures
were performed for a recurrent inguinal hernia.
A retrospective case note review of patients
who had mesh removal after inguinal hernia repair
was undertaken. These notes were retrieved from
records obtained from the operating theatre data-
base system, which searched for all patients who
had mesh removal. All patients with groin sepsis
requiring mesh removal were included; however,
two patients had removal of mesh for chronic
groin pain and were excluded. Patients were fur-
ther followed up by a telephone interview and were
subsequently reviewed in the surgical outpatient
clinic by one of the authors (NSA) to determine
the outcomes after mesh removal. The main out-
come measures were incidence of hernia recur-
rence and chronic groin pain.
Results
Fourteen patients [11 male, three female; median
age 60 (range 24–77) years] had mesh removal for
chronic groin sepsis during this 8-year period.
Only one of these patients had repair of a re-
current inguinal hernia as the initial procedure; all
the others had repair of primary inguinal hernias.
One patient had repair of bilateral primary ingui-
nal hernias, but there was evidence of infection on
one side, which resulted in removal of the mesh.
An onlay polypropylene mesh was used in all of
Chapter 15 · Fate of the Inguinal Hernia Following Removal of Infected Prosthetic Mesh
the patients except one, who had only a polypro-
pylene mesh plug repair. The mesh was secured
with staples in five patients, and a polypropylene
suture was used in the remaining nine, including
the patient who had a mesh plug repair.
Seven of these 14 patients had their initial
hernioplasty performed as a day-case procedure.
Six patients had a planned overnight stay. One
patient had a delayed discharge (9 days) because
of a scrotal haematoma that was treated conser-
vatively.
Six of the 14 patients received a dose of pro-
phylactic antibiotic at the time of their operation
(Table 15.1). There was no evidence of infection at
the time of discharge in any of these patients.
Two patients developed deep wound infection
at 1 month. Another four were routinely seen at
about 2 months, and none of them had evidence
of infection at that time. The remaining eight pa-
tients did not have a routine postoperative clinic
115 15
appointment and were seen only after developing
deep infection.
Infection was first noticed in the groin at a
mean of 11 (range 1–35) months following hernia
repair (⊡ Table 15.1). There is no statistical differ-
ence between the mean times to first presentation
of those patients who had prophylactic antibiotics
(10 months) and those who did not (12.5 months);
p=0.33.
All patients were initially treated conserva-
tively with repeated courses of antibiotics for a
mean period of 10 (range 1–49) months.
Mesh removals were performed at a mean
of 22 (range 2–62) months following the initial
hernia repair. All mesh removals were performed
under general anaesthetic, and there were no
perioperative complications. Eight patients had
specimens sent for bacteriology at the time of
operation, and six of these grew Staphylococcus
aureus on culture.

⊡ Table 15.1. Use of prophylactic antibiotics, period of conservative management, and timing of operation in patients
who had mesh removal

Patient Prophylactic Duration between initial Period of conservative Duration between

antibiotics operation and first sign management with initial operation and
of infection (months) antibiotics (months) mesh removal (months)

1 Yes 1 4 5

2 None documented 3 3 6

3 None documented 28 1 29

4 Yes 13 49 62

5 None documented 35 9 44

6 None documented 9 25 36

7 None documented 7 1 8

8 None documented 4 26 30

9 Yes 8 3 11

10 None documented 13 4 17

11 Yes 7 10 17

12 Yes 25 4 29

13 Yes 6 6 12

14 None documented 1 1 2
 116 Chapter 15 · Fate of the Inguinal Hernia Following Removal of Infected Prosthetic Mesh
All the patients who had mesh removal were
followed up. After a median period of 44 (range
5–91) months, there were two recurrences, which
were both asymptomatic. One of these patients
noticed a lump in the groin 5 months following
mesh removal, but this was asymptomatic, and
he elected to have this treated conservatively. He
was reviewed 10 months following recurrence and
has remained asymptomatic. The other patient
had a persistent minor groin discharge after mesh
removal, which settled completely after 2 months.
He was reviewed in the clinic 41 months after
mesh removal and had remained asymptomatic,
but clinical examination revealed a cough impulse
suggestive of a small recurrent hernia.
On questioning, none of the patients com-
plained of pain or discomfort that interfered with
their usual level of activity.
Discussion
Chronic groin sepsis is a dreaded complication of
inguinal hernia repair using prosthetic material.
Intuitively, prophylactic antibiotics would appear
to be indicated in hernia repair with mesh, as this
procedure involves introducing a foreign body into
the groin. However, the literature is certainly di-
vided regarding the use of prophylactic antibiotics
in mesh repair of inguinal hernias. A Cochrane
review of the literature [8] was unable to conclude
a benefit for recommending antibiotic prophylaxis
in elective primary inguinal hernia repair. A subse-
quent update in 2007 came to the same conclusion
but suggested that antibiotics could not be argued
15 against when high infection rates are detected.
In this present series, the use of prophylactic
antibiotics was documented in six out of 14 pa-
tients and did not appear to confer a benefit in
preventing mesh infection. Deep infection tends
to present after a delayed period following mesh
repair of inguinal hernias; there was a mean pe-
riod of 10 months’ delay in this group of patients.
Use of prophylactic antibiotics does not appear to
alter the time to presentation with deep infection
(p=0.33).
Available reports suggest that deep wound in-
fection is uncommon following mesh repair of in-
guinal hernias [2, 4, 7], but it does usually require
removal of the mesh to facilitate cessation of the
groin sepsis [4, 5, 9].
We have shown a deep infection rate of about
0.7% (14 out of 2,017 patients). This is higher than
in some reports, 0.03% [2], but is comparable to
other studies that found deep infection rates of
1.4% [7] and even higher rates of superficial infec-
tion [10].
A wide range of surgeons with no particular
interest in hernia repair, including mostly surgical
trainees, performed the operations in this pres-
ent study. This heterogeneous group of operating
surgeons may partly explain the relatively higher
rate of deep infections compared with specialist
hernia repair centres. Inexperienced surgeons may
excessively handle the mesh, which may contrib-
ute to development of deep infection. Although
contamination at the time of operation is the likely
source of infection in superficial infections, this
is unlikely to be the aetiology in deep infections,
which often present after a delayed period. These
may be a result of haematogenous spread from
distant sites [4].
It has been suggested that conservative treat-
ment of groin infections with antibiotics leads to
resolution of infection [11]. This is a reasonable
proposition when there is only superficial infec-
tion of the subcutaneous tissue, but deep infection
persists until there is surgical extirpation of the
infected prosthetic material. In our series, groin
sepsis did not settle even with repeated prolonged
courses of antibiotics in some of the patients.
Removal of infected prosthetic mesh is po-
tentially associated with operative complications
because of the concomitant inflammatory reaction
that may make tissue planes more difficult to find.
Meticulous surgical technique is thus necessary
to ensure careful dissection and prevent intraop-
erative damage to structures, especially within the
spermatic cord. In this study, no complications
were associated with mesh removal. All mesh re-
movals were performed by a consultant surgeon or
a senior surgical trainee under the direct supervi-
sion of the consultant. For most of the patients
(12 out of 14), there were no attempts to reinforce
the transversalis fascia, which was thickened and
fibrosed even after mesh removal. Two patients
Chapter 15 · Fate of the Inguinal Hernia Following Removal of Infected Prosthetic Mesh
had loose plication of the fascia with interrupted
absorbable polydioxanone sutures.
After a median follow-up period of 44
(5–91) months, only two of the 14 patients who
had mesh removal for deep infection had devel-
oped hernia recurrence. These cases remained as-
ymptomatic and were thus treated conservatively.
Deep-seated wound infection has also been
reported following laparoscopic hernia repair and
also requires removal of the mesh, which can be
done laparoscopically or by an open technique.
Even after laparoscopic surgery, mesh removal
does not appear to lead to hernia recurrence [6].
In conclusion, deep-seated wound infection
following inguinal hernia repair is uncommon.
When it does occur, it results in chronic groin sep-
sis, which in the majority of cases requires removal
of the infected material before symptoms resolve.
However, hernia recurrence is not inevitable, sug-
gesting that the strength of a mesh repair lies in the
fibrous reaction evoked within the transversalis
fascia by the prosthetic material rather than in the
physical presence of the mesh itself.
With careful dissection, an infected mesh can
be removed without any associated complications.
Therefore, in established deep infection, physi-
cians should not hesitate to remove an infected
mesh to allow resolution of chronic groin sepsis.
Patients should be warned that they may develop
a recurrence. We would advise repairing this by a
posterior (laparoscopic) approach after removal of
mesh following an anterior (open) mesh hernio-
plasty.
117 15
5. Ismail W, Agrawal A, Zia MI. (2002) Fate of chronically
infected onlay mesh in groin wound. Hernia 6:79–81
6. Avtan L, Avci C, Bulut T, Fourtanier G. (1997) Mesh infec-
tions after laparoscopic inguinal hernia repair. Surg Lap-
arosc Endosc 7:192–195
7. Yerdel MA, Akin EB, Dolalan S, Turkcapar AG, Pehlivan M,
Gecim IE, Kuterdem E. (2001) Effect of single-dose pro-
phylactic ampicillin and sulbactam on wound infection
after tension-free inguinal hernia repair with polypropyl-
ene mesh: the randomized, double-blind, prospective
trial. Ann Surg 233:26–33
8. Sanchez-Manuel FJ, Seco-Gil JL. (2003) Antibiotic pro-
phylaxis for hernia repair. Cochrane Database Syst
Rev:CD003769
9. Hatada T, Ishii H, Ichii S, Ashida H, Yamamura T. (2000)
Late infection after mesh-plug inguinal hernioplasty. Am
J Surg 179:76–77
10. Taylor EW, Duffy K, Lee K, Hill R, Noone A, Macintyre I,
King PM, O’Dwyer PJ. (2004) Surgical site infection after
groin hernia repair. Br J Surg 91:105–111
11. Gilbert AI, Felton LL. (1993) Infection in inguinal her-
nia repair considering biomaterials and antibiotics. Surg
Gynecol Obstet 177:126–130
Discussion
Jacob: Concerning infection after groin hernia
repair, have you looked at those patients who have
a local anesthetic compared to those who have
general anesthesia?
Fawole: We haven’t looked at this special point.
But you are right; there might be a risk for bring-
ing bacteria into the tissue during the local anes-
thesia.

References

1. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM.

(1989) The tension-free hernioplasty. Am J Surg 157:188–
193
2. Shulman AG, Amid PK, Lichtenstein IL. (1992) The safety
of mesh repair for primary inguinal hernias: results of
3,019 operations from five diverse surgical sources. Am
Surg 58:255–257
3. Mann DV, Prout J, Havranek E, Gould S, Darzi A. (1998)
Late-onset deep prosthetic infection following mesh re-
pair of inguinal hernia. Am J Surg 176:12–14
4. Taylor SG, O’Dwyer PJ. (1999) Chronic groin sepsis follow-
ing tension-free inguinal hernioplasty. Br J Surg 86:562–
565
 16

Mesh Infection–Therapeutic Options

E. Schippers
 120 Chapter 16 · Mesh Infection–Therapeutic Options
Introduction
The use of meshes in hernia repair has become
standard procedure throughout the world. Im-
plantation of a mesh has been found to reduce
the rate of recurrence in the repair of incisional
hernias [1–3]. However, mesh-related complica-
tions have become increasingly important. Pos-
therniorrhaphy mesh infection, mesh bowel in-
trusion, fistula formation, and eventual removal
and reinsertion have been induced by mesh con-
tamination during primary surgery. Mesh-related
infections following surgery occur relatively in-
frequently compared with other device-related
infections; an incidence of mesh-related infec-
tions after incisional hernia repair up to 8% has
been reported [4].
The relevance of bacterial contamination is
controversial in the literature, although it is of
considerable clinical importance to the patient
and surgeon. Deysine describes mesh infection
with consecutive migration and fistula formation
as a catastrophe [5]. In vascular surgery, even
more dramatic consequences of infected prosthe-
ses, including a mortality rate of 75%, were re-
ported in earlier times. Patients with an infected
prosthesis would ultimately die from massive
hemorrhage or septicemia unless the prosthesis
was removed [6]. However, in renal transplant
recipients with immunosuppression and comor-
bidities such as obesity, diabetes, and chronic
pulmonary diseases, surgical repair of infected
or contaminated herniation with polypropylene
mesh is safe and effective and yields excellent
results [7].
16 Type of Mesh
Shortly after introducing polyethylene mesh for
replacing tissue defects, Usher [8] underscored the
relevance of mechanical and biological proper-
ties of the mesh that are associated with the type
of tissue structure. In experiments with infected
wounds in dogs, he demonstrated that knitted
material and taffeta weave were equally inert to
infection. He attributed this in part to the use of
a monofilament and to the structure of the knit-
ted fabric, which consists of a series of loops with
no interlocking knots that might harbor serum
and bacteria. With increasing recognition of the
value of biomaterials for the repair of abdomi-
nal wall hernias, knowledge of biomaterial-related
complications required in-depth knowledge and
understanding of the physical properties of the
prostheses. Consequently, Amid [9] proposed a
classification of available biomaterials for hernia
surgery based on their pore size:
Type I: Totally macroporous prostheses con-
taining pores larger than 75 μm, a pore size that
is required for admission of macrophages, fibro-
blasts, blood vessels, and collagen fibers into the
pores
Type II: Totally microporous prostheses; these
prostheses contain pores that are less than 10 μm
in at least one of their three dimensions
Type III: Macroporous prostheses with multi-
filamentous or microporous components, braided
polypropylene mesh, or braided Dacron mesh
Surgical infection promoted by implantation
of biomaterials is caused by infection and pro-
liferation of bacteria into and within the pores
and interstices of these synthetic materials. When
pores are less than 10 μm, bacteria averaging 1 μm
cannot be eliminated by macrophages and neutro-
philic granulocytes, which are too large to enter a
10-μm three- dimensional pore. Type I prostheses
deter housing and growth of bacteria by allowing
macrophages, rapid fibroplasia, and angiogenesis,
which also prevents infiltration and growth of
bacteria. Types II and III prostheses are similar to
braided suture materials, and by harboring bacte-
ria, they can promote their growth, likewise result-
ing in biomaterial-related infection.
With respect to this classification and to the
biomaterial-related complications, Amid con-
cluded that in cases of infection, the totally ma-
croporous prostheses (type I) do not have to be
removed. To manage the infection, drainage and
local wound care are all that is necessary. In cases
of infection with type II or III mesh, total removal
(II) or partial removal of type III is required.
Leber et al. [10] analyzed the long-term com-
plications associated with prosthetic repair of in-
cisional hernia. They found that late infections
appearing months or even years after surgery were
Chapter 16 · Mesh Infection–Therapeutic Options
more challenging. These were often combined with
complex fistulas involving bowel, and the mesh
had to be removed. In their study, multifilamented
polyester mesh was associated with a significantly
greater number of infections.
Based on this clinical observation, the influ-
ence of the presence of either a monofilament
or multifilament mesh material on the bacterial
infection risk was studied in a rat model [11]. The
extent of adherent bacteria corresponded to the
estimated filament surface, thus favoring the use of
monofilament materials.
Robinson et al. reviewed medical device re-
ports from the U.S. Food and Drug Administra-
tion on the use of surgical mesh for hernia repair.
The analysis of 252 reports revealed a percentage
of 42% related to infection. Polytetrafluoroeth-
ylene (PTFE) mesh especially tended to be as-
sociated with more infections. Another conclu-
sion was that cases of polypropylene infections
can be healed without mandatory removal of the
mesh [12].
Role of Bacteria
Deysine [13] categorized meshes into two groups:
those that are hydrophobic, such as expanded
PTFE, and those that are hydrophobic, includ-
ing polyester and polypropylene. Those repelling
water take more time to become integrated by
the fibroblastic response. Likewise, hydrophobic
materials may initially repel the fluids containing
bacteria. The role of bacteria in cases of rejection
was described as follows:
Prostheses are rejected through the process
of suppuration after becoming colonized by bac-
teria [5]. In order to adhere, bacteria undergo
functional changes such as the production of
slime, which enhances an irreversible and strong
adhesion. Slime production is a major pathogenic
property of bacterial strains that form biofilms on
surfaces. Once the microorganisms have adhered
to a biomaterial’s surface, they are protected
against phagocytosis because the microorganisms
and biomaterials together are too large to ingest.
Although a variety of different bacteria can cause
a prosthetic infection, the usual causative organ-
121 16
isms associated with cases of mesh infections
are Staphylococcus spp., especially Staphylococcus
aureus; Streptococcus spp.; gram-negative bacteria
(mainly Enterobacteriaceae); and anaerobic bac-
teria [14]. The reported high rate of 63% of me-
thicillin-resistant Staphylococcus aureus (MRSA)
complicating intraperitoneal mesh implantation
is alarming [4].
Diagnosis
Patients usually present with symptoms and signs
of local acute inflammation: pain, erythema, in-
creased temperature, and tenderness and swelling
in the abdominal wall in the area of the mesh. Sys-
temic manifestations include fever, malaise, and
chills or rigor. Abdominal abscesses and discharg-
ing fistulas can be the first clinical manifestation.
To monitor prosthetic infections, erythrocyte
sedimentation rate (ESR), C-reactive protein, and
white blood cell count are well-established labora-
tory methods. White blood cell counts have a sen-
sitivity of only 20% and a predictive value of 50%.
The combination of ESR and C-reactive protein is
a more powerful diagnostic tool; when both are
negative, the possibility of infection is zero. When
both are positive, the possibility of infection is
83% [15].
Imaging
With the help of ultrasound, a noninvasive pro-
cedure, most mesh-related complications can be
detected or ruled out. An abscess formation is seen
as a hypoechogenic structure caused by cell debris,
with small plump hyperechoic reflections caused
by gas bubbles. The extent of incomplete fistulas
within the abdominal wall can be determined. The
hypoechoic structure of the fistula channel can be
followed through the abdominal wall (⊡ Fig. 16.1).
Computed tomography and magnetic resonance
imaging allow clear identification of abdominal
wall pathologies. Indications for these are sono-
graphically uncertain results; however, the disad-
vantages include higher costs, limited availability,
and the danger of contrast medium allergy. Fistu-
 122 Chapter 16 · Mesh Infection–Therapeutic Options
⊡ Fig. 16.1. Typical sonographic finding of an abscess formati-
on and fistula channel with hypoechoic structures
lography reveals the extent, location, and relation
of fistulas and is therefore a helpful tool in preop-
erative planning.
Treatment
Therapeutic options in cases of mesh infection range
from prevention and intravenous antibiotics to open
wound treatment and mesh removal. The essential
factor in the evolution and persistence of infection
is the formation of a biofilm around the implanted
device [16]. The biofilm is capable of resisting anti-
microbial agents due to the protective mechanism.
Adequate prevention of a biomaterial-centered in-
fection is therefore aimed at the first contact of a
microorganism with a biomaterial. Bacterial adhe-
sions on the biomaterial depend on the material
surface. Mesh coated with different precious metals,
such as titanium, silver, or gold, can successfully re-
duce bacterial attachment [17]. Because ultrasound
16 reduces biofilm formation, several studies on the
effect of ultrasound on bacterial cell growth and
on the treatment of biomaterial-centered infections
have been performed. A positive effect of ultra-
sound in addition to treatment with antibiotics has
been shown. Theoretically, a phenomenon called
the bioacoustic effect enhances the transportation
and penetration of antibiotics within the biofilms.
The contribution of low-frequency and high-inten-
sity ultrasound in the presence of an antibiotic agent
removes and kills microorganisms [18].
Antibiotics
Bacterial susceptibility to pharmacological treat-
ment is significantly reduced when a polymeric
device is present. Possible reasons for the reduced
susceptibility of biofilm-embedded organisms to
antibiotic agents include a slow rate of bacterial
growth within the biofilm, inhibition of antimicro-
bial activity by biofilm substances, and poor pen-
etration of the biofilm by antibiotics [19]. There-
fore, the strategy of monotherapy with intravenous
antibiotics in cases of mesh-related infections has
a poor outcome and consequently has no indica-
tion [14].
Open Wound Treatment
Standard surgical practice supports removing pros-
thetic material when a wound infection involves
the prosthesis. The removal of mesh in this situa-
tion is often technically difficult and may result in
substantial additional complications. Local tissue
incorporation can make removal of mesh danger-
ous because adjacent vascular structures or the
bowel can be injured, which may result in acute
bleeding or subsequent development of an entero-
cutaneous fistula. Because achieving closure of the
fascial defect after mesh removal is usually not
possible, this surgery may result in an incisional
hernia that is larger than the original one.
In early postoperative infections after implan-
tation of porous mesh, it is therefore advised to
introduce an open wound management strategy
combined with a suction-based debridement sys-
tem as an alternative to explantation of the mesh.
The principle of vacuum sealing has been intro-
duced for the treatment of complicated wounds
[20]. The first step is wound opening, followed by
necrosectomy, wound debridement, and irrigation.
A polyvinyl vacuum foam is cut to size and placed
into the wound. A vacuum-assisted closure system
with transparent polyurethane foil is applied to the
open portion of the wound and skin (⊡ Fig. 16.2).
Permanent suction at 60–80 kPa must be estab-
lished. The foam is removed at 2–5-day intervals,
with the transparent foil allowing daily inspection
of the wound. This treatment results in progressive
Chapter 16 · Mesh Infection–Therapeutic Options
b fections are caused by Staphylococcus spp., and
⊡ Fig. 16.2. Steps in vacuum sealing after early mesh infec-
tion. a Cutting the foam to size. b Vacuum-assisted closure
system in place
debridement and granulation of the open wound
and causes a dermatotraction with approximation
of the wound edges. After successful wound condi-
tioning, a secondary closure of skin over the mesh
can be achieved without mesh removal.
However, mesh explantation is recommended
for all type II prostheses (totally microporous) [9].
Furthermore, later infections after months or even
years are more challenging and also require re-
moval of the prosthesis [21]. They are often com-
bined with complex fistulas involving the bowel.
In these cases, preservation of the mesh is likely
to fail, and sooner or later the mesh has to be re-
moved [22] (⊡ Fig. 16.3).
Conclusion
Mesh infection is a serious, but not catastrophic,
complication in hernia surgery. The extent of the
damage correlates with the type of mesh that was
123 16
⊡ Fig. 16.3. Example of a microporous mesh followed by late
infection and fistula that had to be removed
primarily implanted. With respect to prevention
and therapy, the ideal mesh is macroporous, hy-
drophilic, and monofilamented. Two-thirds of in-
methicillin-resistant staphylococci are frequent.
The therapeutic options are both mesh-related and
time-related. Open wound treatment, including
vacuum sealing, is indicated in early postoperative
infection of macroporous meshes. Explantation
should be limited to microporous meshes or late
and chronic infections, which are often compli-
cated by sinus or fistula formation. Monotherapy
with antibiotics should be abandoned. Interesting
aspects for future research in this field include
biofilm formation, bioacoustic effects, and mesh
coatings.
References
1. Luijendijk RW, Hop WC, van den Tol MP, et al. (2000) A
comparison of suture repair with mesh repair for incisio-
nal hernia. N Engl J Med 343:392–398
2. Schumpelick V, Klosterhalfen B, Müller M, et al. (1999)
Minimierte Polypropylen Netze zur präperitonealen Netz-
plastik (PNP): eine prospektive randomisierte klinische
Studie. Chirurg 70:422–430
3. Schippers E, Harsányi A, Thumbs A, Schneider M (2001)
Ergebnisse nach offener Netzplastik der Narbenhernie in
Sublay-Technik. Viszeralchirurgie 36:152–156
4. Copp WS IV, Harris JB, Lokey JS, McGill ES, Klove KL (2003)
Incisional herniorrhaphy with intraperitoneal composite
mesh: a report of 95 cases. In: Proceedings of the Sou-
 124 Chapter 16 · Mesh Infection–Therapeutic Options

theastern Surgical Congress, 7–11 February 2003, Savan- north AN, et al. (eds) Incisional hernia. Springer, Berlin, pp
nah, Georgia. Vol 69, pp. 784–787 217–227
5. Deysine M (2004) The catastrophe: mesh infection and 22. Klinge U, Conze J, Krones CJ, Schumpelick V (2005) Incisio-
migration with fistula formation–life-long risk? In: Schum- nal hernia: open techniques. World J Surg 29:1066–1072
pelick V, Neuhaus LM (eds) Meshes: benefits and risks.
Springer, Berlin, pp 207–227
6. Fry WJ, Lindenauer SM, Arbor A (1967) Infection com-
plicating the use of plastic arterial implants. Arch Surg
94:600–609
7. Antonopoulos IM, Nahas WC, Mazzucchi E, Piovesan AC,
Birolini C, Lucon AM (2005) Is polypropylene mesh safe
and effective for repairing infected incisional hernia in
renal transplant recipients? Urology 66:874–877
8. Usher FC (1961) Knitted Marlex mesh: an improved marlex
prosthesis for repairing hernias and other tissue defects.
Arch Surg 82:153–155
9. Amid PK (1997) Classification of biomaterials and their
related complications in abdominal wall hernia surgery.
Hernia 1:15–21
10. Leber GE, Garb JL, Alexander AI, Reed WP (1998) Long-
term complications associated with prosthetic repar of
incisional hernias. Arch Surg 133:378–382
11. Klinge U, Junge K, Spellerberg B, Piroth C, Klosterhalfen
B, Schumpelick V (2002) Do multifilament alloplastic
meshes increase the infection rate? Analyses of the po-
lymeric surface, the bacteria adherence and the in vivo
consequences in a rat model. J Biomed Materials Res
63:765–771
12. Robinson TN, Clarke JH, Schoen J, Walsh MD (2005) Ma-
jor mesh-related complications following hernia repair:
events reported to the Food and Drug Administration.
Surg Endosc 19:1556–1560
13. Deysine M (1998) Management of prosthetic infections in
hernia surgery. Surg Clin North Am 78:1105–1115
14. Falagas A, Kasiakou SK (2004) Mesh-related infections
after hernia repair surgery. European Society of Clinical
Microbiology and Infectious Diseases, CMI, 11:3–8
15. Salvati EA, Callaghan JJ, Brause BD, et al. (1986) Reimplan-
tation in infection. Elution of gentamicin from cement
and beads. Clin Orthop Rel Res 207:83–93
16. Costerton JW, Stewart PS, Greenberg EP (1999) Bacterial
biofilms: a common cause of persistent infections. Sci-
ence; 284:1318–1322
17. Engelsmann AF, van der Mei HC, Ploeg RJ, Busscher HJ
16 (2007) The phenomenon of infection with abdominal wall
reconstruction. Biomaterials 28:2314–2327
18. Johnson LL, Peterson RV, Pitt WG (1998) Treatment of
bacterial biofilms on polymeric biomaterials using anti-
biotics and ultrasound. J Biomater Sci Polym Ed 9:1177–
1185
19. Darouiche R (2004) Treatment of infections associated
with surgical implants. N Engl J Med 350:1422–1429
20. Fleischmann W, Bacher U, Bischoff M, Hoekstra H (1995)
Vacuum sealing: indication, technique and results. Eur J
Orthop Surg Traumatol 5:37–40
21. Flament JB, Avisse C, Palot JP, Delattre JF (1999) Biomate-
rials–principles of implantation. In: Schumpelick V, Kings-
 17

Does Antibiotic Prophylaxis Prevent

the Occurrence of Wound Infection
After Groin Hernia Surgery?
T. J. Aufenacker
 126 Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection After Groin Hernia Surgery?
Introduction
A mesh-based repair is, in many Western coun-
tries, the most popular technique for repairing
abdominal wall hernia in order to reduce the risk
of recurrence [1–7]. More than 80% of adult ab-
dominal wall hernias occur in the groin, and in
the Western world the majority are being repaired
with the use of a prosthetic mesh. There is a large
variation in techniques used to correct a groin
hernia, with an even larger variety of meshes. Cur-
rently the most popular inguinal hernia technique
is the Lichtenstein hernia repair [8], using a flat
mesh to reinforce the inguinal wall.
The incidence of infection after inguinal her-
nia repair has been reported to vary from 0% to
9% [9]. Especially when a foreign body, such as a
polypropylene mesh, is used, prevention of a deep
infection is of paramount importance because a
deep infection of a mesh may require its removal,
as reported in several cases [10].
A Cochrane Review meta-analysis for inguinal
hernia [11] in 2004 concluded that »antibiotic pro-
phylaxis for elective inguinal hernia repair cannot
be firmly recommended or discarded« because the
number of included patients was limited and that
»further studies are needed, particularly on the use
of mesh repair.«
Although most studies, as discussed later in
this chapter, do not support the use of antibiotic
prophylaxis, its use is still widespread. The reason
for this might be legislative in many cases since
an American attorney, for instance, could ask a
so-called expert during a court of law about a
lack of antibiotic prophylaxis. In some cases, this
expert might well be a psychiatrist without up-
dated knowledge in this area, and his or her advice
would be misleading to those hearing the case.
Many American surgeons admit to continuing to
17 use antibiotic prophylaxis for this reason.
Both in the United States and Europe, over 1.5
million abdominal wall hernia repairs (of which
70% are groin hernia repairs) are performed an-
nually [12]. Therefore, any improvement in their
treatment could have a large medical and eco-
nomic impact. A reduction in the number of
wound infections would especially have a great ef-
fect on patient satisfaction, sick leave, and wound
care. Conversely, discarding the use of antibiotic
prophylaxis in hernia repair could reduce costs,
the risks of toxic and allergic side effects, and the
possible development of bacterial resistance [13]
or superinfections.
To assess whether systemic antibiotic prophy-
laxis prevents wound infection in groin hernia
repair, a systematic review and a meta-analysis of
randomised controlled trials were carried out.
Material and Methods
A search of Medline, EMBASE, CINAHL, DARE,
ACP, LILACS, and the Cochrane Register using
the terms hernia and antibiotic prophylaxis was
done to identify randomised controlled trials on
the subject published between 1966 and May
2008. All languages were considered. The search
was performed independently by two reviewers,
who selected potentially relevant papers based on
title and abstract. References from the selected
papers were used for search completion. Field
experts were contacted for potential data, and
books of the abstracts from leading hernia meet-
ings over the last 8 years were manually checked
for unpublished data. All randomised placebo-
controlled trials using antibiotic prophylaxis in
mesh abdominal wall hernia repair with explicit
defined wound infection criteria and a minimum
follow-up period of 1 month were included. Each
paper was reviewed independently by three re-
viewers, and a quality assessment was performed
according to the scoring system of Jadad et al.
[14]. Discrepancies among the reviewers were
resolved by consensus. Only papers with a Jadad
score ≥3 were considered appropriate for further
analysis.
Data were extracted from the studies and
pooled using the Review Manager software [15]
from the Cochrane Collaboration. A χ2 test for
heterogeneity of study results was performed. If
heterogeneity could not be detected, data were
pooled using a random effects model to correct
for clinical diversity and methodological varia-
tions between studies. The effectiveness of antibi-
otic prophylaxis to prevent wound infection was
expressed as odds ratios (ORs) for dichotomous
Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection
data and their 95% confidence intervals (CIs).
Numbers needed to treat (NNT) and 95% CIs were
calculated from the OR and the background risk
of wound infection for the patients in the placebo
groups. No subgroup analysis was performed. If it
remained unclear from a study whether data were
presented for patients or hernias, a sensitivity anal-
ysis (worst-case scenario) was done by varying the
distribution of bilateral hernia between the treated
and placebo groups.
Results
The search resulted in a large number of poten-
tially relevant studies, identifying nine papers re-
porting prospective randomised data on the use of
antibiotic prophylaxis in groin hernia surgery with
prosthetic reinforcement.
After the Cochrane meta-analysis update in
2007, no additional trials in the area of nonmesh
repairs were published. In this Cochrane analysis,
one study combining three trials with unpublished
data is included. Therefore, the data regarding non-
mesh techniques from the Cochrane meta-analysis
127 17
(⊡ Table 17.1) are used to perform an analysis with
the random-effect model. A nonsignificant effect
of antibiotic prophylaxis in nonmesh techniques
was demonstrated, OR 0.75 (0.53–1.06), NNT 85
(45–359).
Regarding the mesh-based techniques, a sum-
mary of the nine papers that included randomised
trials and the outcome of the assessment is given
in ⊡ Table 17.2. The results of the three assessments
did not differ among the three reviewers. The only
laparoscopic study, by Schwetling and Barlehner
[16], used an incorrect randomisation method and
lacked a definition of wound infection, but in the
absence of more studies on this technique, it was
considered best evidence.
Eight studies were, after the quality assessment,
suited for meta-analysis regarding the use of anti-
biotic prophylaxis in mesh-based repairs. They in-
cluded 2,963 open inguinal and 43 femoral hernia
repairs. The patient and surgical characteristics of
these eight randomised controlled trials are docu-
mented in ⊡ Table 17.3.
The included studies are presented separately
with their main intervention and results in ⊡ Ta-
ble 17.4.

⊡ Table 17.1. Pooled data of six studies on the use of antibiotic prophylaxis for prevention of wound infection after non-
mesh inguinal hernia repair
Review: The effectiveness of antibiotic prophylaxis in inguinal hernia repair
Comparison: 01 Antibiotic prophylaxis vs: placebo
Outcome: 03 Non mesh techniques

Study or Antibiotic Placebo OR (random) Weight OR (random) Year

sub-category n/N n/N 95% Cl % 95% Cl

Evans 1/48 2/49 2.01 0.50 [0.04, 5.70] 1973

Anderson 5/137 6/150 8.14 0.91 [0.27, 3.05] 1980

Platt 4/301 6/311 7.33 0.68 [0.19, 2.45] 1990

Lazorthes 0/155 7/153 1.45 0.06 [0.00, 1.11] 1992

Taylor 25/283 25/280 35.35 0.99 [0.55, 1.77] 1997

Pessaux 68/2008 20/394 45.72 0.66 [0.39, 1.09] 2006

Total (95% Cl) 2932 1337 100.00 0.75 [0.53, 1.06]

Total events: 103 (Antibiotic), 66 (Placebo) 0.1 0.2 0.5 1 2 5 10

Favours treatment Favours control
Test for heterogeneity: Chi2= 4.31, df = 5 (P= 0.51), I2 = 0%
Test of overall effect: Z= 1.63 (P=0.10)
 128 Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection After Groin Hernia Surgery?

⊡ Table 17.2. Results and quality of prospective randomised studies on the use of antibiotic prophylaxis in the prevention
of wound infection after mesh groin hernia repair

Reference Jadad Number Infec- Correct ran- Double- Wound Follow-up Accepted
score of tion domisation? blind? infection period? in meta-
patients % definition? analysis?

Laparoscopic inguinal hernia mesh repair (transabdominal preperitoneal)

Schwetling 0 80 0.0% No, alter- No No Un- No; best

[16] 1998 nately definition known evidence

Open inguinal and femoral hernia mesh repair

Morales [17] 4 524 1.9% Yes Yes Yes 1 year Yes

2000

Yerdel [18] 5 269 4.8% Yes Yes CDC criteria 1 year Yes
2001 [25]

Celdran [19] 4 91 4.4 % Yes Yes CDC criteria 2 years Yes

2004 [25]

Oteiza [20] 3 247 0.4% Yes No CDC criteria 1 month Yes

2004 [25]

Aufenacker 5 1,008 1.7 % Yes Yes CDC criteria 3 months Yes

[21] [25]
2004

Perez [22] 5 360 3.1% Yes Yes CDC criteria 1 month Yes
2005 [25]

Tovaras23 5 379 3,7% Yes Yes Yes 1 month Yes

2007

Jain24 5 120 1.7% Yes Yes CDC crite- 1 month Yes

2008 ria25

The total number of infections after groin
hernia repair with a mesh-based technique was
48/1,526 patients (3.1%) in the placebo group and
24/1,480 patients (1.6%) in the antibiotic group.
The pooled data for the eight studies are presented
in ⊡ Table 17.5. There was no statistical heteroge-
neity (p=0.36). The OR for wound infection after
antibiotic prophylaxis was 0.59 (95% CI 0.34–1.03),
17 resulting in an NNT of 80 (49–1111). A sensitivity
analysis was performed because the Celdran study
[19] did not specify in which group the eight bilat-
eral hernias were included (worst-case scenario: in-
fection rate in Celdran’s placebo group 4/41=9.8%),
resulting in an OR of 0.57 (95% CI 0.32–1.04).
The number of deep infections after inguinal
and femoral hernia repair was 6/1,050 in the pla-
cebo group (0.6%) and 3/1,053 in the antibiotic
prophylaxis group (0.3%), with an OR of 0.50 (95%
CI 0.12–2.09) and an NNT of 352 (199–1961).
The pooled data of six studies (the Morales and
Tzovaras data were not available) are presented in
⊡ Table 17.6.
Discussion
In this systematic review and meta-analysis on
the effectiveness of antibiotic prophylaxis in groin
hernia repair, the six randomised controlled trials
concerning non-mesh-based techniques and the
nine mesh-based trials demonstrate no significant
benefit of antibiotic prophylaxis.
For groin hernias, the wound infection rate re-
ported in randomised controlled trials of 2.4% after
Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection
129 17

⊡ Table 17.3. Patient and study characteristics of eight randomised controlled trials on antibiotic prophylaxis in inguinal and
femoral hernia mesh repair (PHS Prolene Hernia System)

Morales Yerdel [18] Celdran Oteiza [20] Aufenacker Perez Tzovaras Jain [24]
[17] N=269a [19] N=247a [21] [22] [23] N=120a
N=524a N=99b N=1,008a N=360a N=379a

Total 1.9% 4.8% 4.4% 0.4% 1.7% 3.1% 3.7% 1.7%

infections (%)

Deep 0.8% 1.5% 0% 0% 0.3% 0.6% Not docu- 0%

infection (%) mented

Mesh 0.8% 1.1% 0% 0% 0.2% 0.6% 0% 0%

removal (%)

Body mass Not docu- 25.0 26.2 Not docu- Not docu- Not 26.0 Not docu-
index (mean) mented mented mented docu- mented
mented

Diabetes Not docu- Study 18 (18.1%) Not docu- Study Not 13 (3.4%) Study
mented exclusion mented exclusion docu- exclusion
criterion criterion mented criterion

Recurrent 39 (7.4%) Study 13 (13.1%) Study exclu- Study Study Not Study
hernia exclusion sion criterion exclusion exclusion docu- exclusion
criterion criterion criterion mented criterion

Duration of 34 min 63 min 65 min 40 min 40 min 53 min 45 min 58 min

surgery

Surgeons (%) 524 (100%) 0 (0%) 75 (75.8%) 247 (100%) 571 (56.6%) Not Not docu- 120 (100%)
Residents (%) 0 (0%) 269 (100%) 24 (24.2%) 0 (0%) 437 (43.4%) docu- mented 0 (0%)
mented

Bilateral Study exclu- Study Study ex- Study

hernia 0 (0%) 0 (0%) 8 (8.8%) sion criterion 56 (5.6%) exclusion clusion exclusion
criterion criterion criterion

Femoral Study Study ex- Study Study Study ex- Study

hernia 23 (4.4%) exclusion clusion 20 (8.1%) exclusion exclusion clusion exclusion
criterion criterion criterion criterion criterion criterion

Use of drains Study 60 (22.3%) Not docu- Not docu- 15 (1.5%) 0 (0%) 15 (4.0%) 0 (0%)
exclusion mented mented
criterion

Local Not docu- 111 (41.3%) 99 (100%) 226 (91.5%) 17 (1.7%) 0 (0%) 329 Not docu-
anaesthetics mented (86.8%) mented

Day 51 (9.7%) Not docu- 99 (100%) 247 (100%) 463 (45.9%) Not Not docu- 0 (0%)
surgery mented docu- mented
mented

Mesh type Flat, poly- Flat, poly- Flat, poly- Flat, poly- Flat, poly- Flat, Flat, poly- PHS, poly-
propylene propylene propylene propylene propylene polypro- propylene propylene
pylene

Exclusion bias 30/554 11/280 0/91 3/250 (1.2%) 7/1,015 0/360 2/381 0/120 (0%)
[26] (5.4) (3.9%) (0%) (0.7%) (0%) (0.5%)
aN= number of patients
bN= number of hernias (91 patients)
 130 Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection After Groin Hernia Surgery?

⊡ Table 17.4. Results of individual studies accepted in the systematic review on the use of antibiotic prophylaxis for
preventing wound infection after mesh groin hernia repair (NNT number needed to treat)

Reference N Mean Males Type of Infection Infection interven- p-value NNT

age (%) antibiotic placebo group tion group
(years) (patients, %) (patients, %)

Laparoscopic inguinal hernia mesh repair (transabdominal preperitoneal)

Schwetling 80 55 86 Cefuroxime 0/40 0% 0/40 0% 1.0 ∞

[16] 1.5 g

Open inguinal and femoral hernia mesh repair

Morales [17] 524 54 90 Cefazolin 6/287 2.1% 4/237 1.7% 0.737 248
2g

Yerdel [18] 269 56 93 Ampicillin + 12/133 9.0% 1/136 0.7% 0.002 13

sulbactam
1.5 g

Celdran [19] 91 58 90 Cefazolin 4/49a 8.2% 0/50a 0.0% 0.059 13

1g

Oteiza [20] 247 57 85 Amoxicillin 0/123 0.0% 1/124 0.8% 0.318 NNH
+ clavulanic 124
acid 2 g

Aufenacker 1,008 58 96 Cefuroxime 9/505 1.8% 8/503 1.6% 0.813 520

[21] 1.5 g

Perez [22] 360 61 98 Cefazolin 7/180 3.9% 4/180 2.2% 0.540 59

1g

Tzovaras [23] 379 63 94 Amoxicillin 9/189 4.7% 5/190 2.6% 0.4 48

+ clavulanic
acid 1.2 g

Jain [24] 120 41 100 Amoxicillin 1/60 1.7% 1/60 1.7% 0.500 ∞
+ clavulanic
acid 1.2 g
aNumber
of hernias (91 patients)

mesh repair is not higher than the percentage after
conventional sutured repair [11] (4.0%). Because
the use of antibiotics is not likely to increase the
wound infection percentage, the net effect of stud-
17 ies designed as those that were included will almost
always be zero or will be in favour of the patients’
receiving prophylaxis and therefore on the left (an-
tibiotic-favouring) side of the forest plot.
The meta-analysis of six nonmesh studies dem-
onstrated a nonsignificant effect of antibiotic pro-
phylaxis: OR 0.75 (0.53–1.06), NNT 85 (45–359).
The meta-analysis of eight studies on the use of
antibiotic prophylaxis to prevent wound infection
after mesh groin hernia repair did not favour the
use of antibiotic prophylaxis: OR 0.59 (95% CI 0.34–
1.03) and NNT 80 (49–1,111). In the meta-analysis,
only one study of below-average size demonstrated
a large and significant benefit for the prophylaxis
group, but this study can be criticised because of
repeated aspiration of seromas and excessive use of
drains that could cause (secondary) infections; also,
it is likely that the study was underpowered because
it was, unfortunately, prematurely stopped because
of the high rate of wound infection.
However, there can be a debate about the
method used for meta-analysis in this chapter be-
Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection
131 17

⊡ Table 17.5. Pooled data of eight studies on the use of antibiotic prophylaxis for preventing wound infection after mesh
inguinal hernia repair
Review: The effectiveness of antibiotic prophylaxis in inguinal hernia repair
Comparison: 01 Antibiotic prophylaxis vs placebo
Outcome: 01 Total number of wound infections

Study or Antibiotic Placebo OR (random) Weight OR (random) Year

sub-category n/N n/N 95% Cl % 95% Cl

Morales 4/237 6/287 16.78 0.80 [0.22, 2.88] 2000

Yerdel 1/136 12/133 7.02 0.07 [0.01, 0.58] 2001

Aufenacker 8/503 9/505 27.05 0.89 [0.34, 2.33] 2004

Celdran 0/50 4/49 3.51 0.10 [0.01, 1.91] 2004

Oteiza 1/124 0/123 2.97 3.00 [0.12, 74.36] 2004

Perez 4/180 7/180 17.51 0.56 [0.16, 1.95] 2005

Tzovaras 5/190 9/189 21.27 0.54 [0.18, 1.64] 2007

Jain 1/60 1/60 3.89 1.00 [0.06, 16.37] 2008

Total (95% Cl) 1480 1526 100.00 0.59 [0.34, 1.03]

Total events: 24 (Antibiotic), 48 (Placebo) 0.01 0.1 1 10 100

Favours treatment Favours control
Test for heterogeneity: Chi2 = 7.70, df = 7 (P = 0.36), I2 = 9.1%
Test for overall effect: Z = 1.86 (P = 0.06)

⊡ Table 17.6. Pooled data of six studies (Morales and Tsovaras data not available) on the use of antibiotic prophylaxis for
preventing deep wound infection after mesh groin hernia repair
Review: The effectiveness of antibiotic prophylaxis in inguinal hernia repair
Comparison: 01 Antibiotic prophylaxis vs placebo
Outcome: 02 Deep infections

Study or Antibiotic Placebo OR (random) Weight OR (random) Year

sub-category n/N n/N 95% Cl % 95% Cl

Yerdel 1/136 3/133 38.96 0.32 [0.03, 3.13] 2001

Aufenacker 1/503 2/505 34.98 0.50 [0.05, 5.54] 2004

Celdran 0/50 0/49 Not estimable 2004

Oteiza 0/124 0/123 Not estimable 2004

Perez 1/180 1/180 26.12 1.00 [0.06, 16.11] 2005

Jain 0/60 0/60 Not estimable 2008

Total (95% Cl) 1053 1050 100.00 0.50 [0.12, 2.09]

Total events: 3 (Antibiotic), 6 (Placebo) 0.01 0.1 1 10 100

Favours treatment Favours control
Test for heterogeneity: Chi2 = 0.39, df = 2 (P = 0.82), I2 = 0%
Test for overall effect: Z = 0.94 (P = 0.35)
 132 Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection After Groin Hernia Surgery?
cause meta-analysis is a nonperfect technique that
is no substitute for a large and well-designed ran-
domised controlled study. Nonetheless, the tech-
nique is indicated for similar situations in which
the number of patients in the studies is low or
when results are conflicting, as it provides pooled
estimates with narrower CIs and greater statistical
power. But the interpretation of a meta-analysis,
especially which method to use, is essential. The
choice of method should be based on the pres-
ence or absence of statistical heterogeneity within
the data together with the clinical diversity and
methodological diversity of the original studies. In
the presence of statistical heterogeneity, it is better
not to perform a meta-analysis. In the eight stud-
ies used for the current meta-analysis, there is no
statistical heterogeneity (e.g. p=0.36, I2= 9.1). The
studies are, unfortunately, clinically and method-
ologically diverse; for instance, there is large varia-
tion among the included studies regarding recur-
rent hernia, diabetes, bilateral repair, use of local
anaesthetics, and the surgeon’s level of expertise.
To correct for this clinical and methodological di-
versity, the random method should be used rather
than fixed analysis. Especially when the results
of the fixed and random analysis conflict, as in
the current situation, the choice of meta-analysis
method should preferably be conservative, and in
these situations the random method should also be
used [27, 28].
An infection percentage in low-risk patients
should be below 2% [29] when performing clean
inguinal or femoral hernia surgery lasting less than
1 h. Therefore, the question should be, »Should we
administer antibiotics to all patients undergoing
clean surgery to spare a few (sometimes a very
few) superficial wound infections?« [30]. Because
a relatively simple treatment of wound drainage,
frequently combined with antibiotics, is required
17 for superficial infections, and because the rare deep
infections result in a low number of mesh removals
(0.09% [10] –1.1% [18]) with remarkably few her-
nia recurrences, there remains no routine indica-
tion for antibiotic prophylaxis in low-risk patients.
Discarding the use of antibiotic prophylaxis in her-
nia repair could reduce costs, the risks of toxic and
allergic side effects, and the possible development
of bacterial resistance [13] or superinfections.
If a much higher percentage of wound infec-
tions exists because of patient or surgical char-
acteristics [28], as demonstrated by two of the
inguinal hernia studies, the use of antibiotic pro-
phylaxis could be reevaluated. In the trials with
high wound infection percentages, two important
differences can be seen: The duration of surgery
was 1.5 times longer (64 min), and drains were
used more often (22%), both known risk factors
for infection [29, 31].
This review shows the lack of randomised
studies of laparoscopic groin hernia repairs on the
subject of wound infection. The only laparoscopic
inguinal hernia (transabdominal preperitoneal) re-
pair study discussed 80 patients without proper
randomisation (alternately), but it demonstrated
no infections. This study virtually excludes the
presence of a high percentage of wound infections
in laparoscopic repair. There is some logic in this
low infection rate since the minimally invasive ap-
proach consists of small and occluded incisions, al-
though the operating time is an average of 18 min
longer compared with an open repair [32]. Consid-
ering these aspects, and as long as hard evidence is
lacking, it is probably acceptable to conclude that
in laparoscopic inguinal hernia repair, no antibi-
otic prophylaxis is needed.
It is not expected that important publications
were missed in our thorough search of the litera-
ture and our contacts with authorities in the field.
It is, however, difficult to assess the possibility of
publication bias, resulting in studies being left out
that showed no effect of antibiotic prophylaxis for
the procedures included in our analysis. On the
other hand, if publication bias exists, the effect of
antibiotic prophylaxis would be even more mod-
est than we found in our meta-analysis, as failure
to include the grey literature has been reported to
overestimate a treatment effect by 15% [33].
From this meta-analysis it can be concluded
that in clinical settings with low rates of infection,
there will be no significant benefit from using
antibiotic prophylaxis for groin hernia repair in
low-risk patients. Because of an unknown impact
on bacterial resistance [13], the use of routine
antibiotic prophylaxis in primary inguinal her-
nia repair should therefore be discouraged. In the
Netherlands, the cost benefit for one patient is rel-
Chapter 17 · Does Antibiotic Prophylaxis Prevent the Occurrence of Wound Infection
133 17
the use of antibiotic prophylaxis: OR 0.59 (95% CI
⊡ Table 17.7. Patient and operation characteristics that
may influence the risk of wound infections [28] 0.34–1.03) and NNT 80 (49–1,111).
From this meta-analysis it can be concluded
Patient Operation that in clinical settings with low rates of infection,
there will be no significant benefit from using an-
Age Duration of surgical scrub tibiotic prophylaxis for groin hernia repair in low-
Nutritional status Skin antisepsis risk patients. However, if patient or surgical char-
Diabetes Preoperative shaving
acteristics prove the existence of a much higher
Smoking Preoperative skin prep
Obesity Duration of operation percentage of wound infections, as demonstrated
Coexistent infection at Antimicrobial prophylaxis by two of the inguinal hernia studies, the use of
a remote body site Operating room ventilation antibiotic prophylaxis could be reevaluated.
Colonisation with Inadequate sterilisation of
microorganisms instruments
Altered immune Foreign material in the surgi-
response cal site
Acknowledgments
Length of preopera- Surgical drains
tive stay Surgical technique The author wants to thank M. J. Koelemay, M.D.,
Ph.D., and M. P. Simons, M.D., Ph.D., for their
help with this study.

atively limited (€13.20) [34]. Nevertheless, because

of the large number of inguinal hernia repairs
performed in low-risk patients (an estimated 70%
of all hernias) [21], discarding the use of antibiotic
prophylaxis will save at least €10 million in Europe
and the United States. There is, of course, not
enough evidence regarding the high-risk group of
patients (⊡ Table 17.7). To answer this question, an-
other large trial would be needed, or, better yet, the
source data of the separate trials should be analy-
sed. Therefore, an attempt is currently being made
to contact all authors of randomised controlled
trials and ask them to deliver their source data for
final analysis.
Currently it can be stated that surgeons and
hospitals must assess their own surgical site in-
fection rates to define if prophylactic antibiotics
must be widely used in all patients. For clinical
settings with low rates of surgical site infections,
selective use of antibiotics based on patients’ and
surgical risk factors is probably the best therapeu-
tic strategy.
Conclusion
The meta-analysis of eight studies on the use of
antibiotic prophylaxis for preventing wound infec-
tion after mesh groin hernia repair did not favour
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21. Aufenacker TJ, van Geldere D, van Mesdag T, Bossers AN,
Dekker B, Scheijde E, van Nieuwenhuizen R, Hiemstra E,
Maduro JH, Juttmann JW, Hofstede D, van der Linden
CT, Gouma DJ, Simons MP (2004). The role of antibiotic
prophylaxis in prevention of wound infection after Lich-
tenstein open mesh repair of primary inguinal hernia. A
multi-center double-blind randomized controlled trial.
Ann Surg 240:955–961
17 22. Perez AR, Roxas MF, Hilvano SS (2005). A randomized,
double-blind, placebo-controlled trial to determine effec-
tiveness of antibiotic prophylaxis for tension free mesh
herniorrhaphy. J Am Coll Surg 200:393–398
23. Tzovaras G, Delikoukos S, Christodoulides G., Spyridakis
M, Mantzos F, Tepetes K, Athanassiou E, Hatzitheofilou C
(2007). The role of antibiotic prophylaxis in elective ten-
sion-free mesh inguinal hernia repair: results of a single
centre prospective randomised trial. Int J Clin Pract 61
(2):236–239
24. Jain SK, Jayant M, Norbu C (2008). The role of antibiotic
prophylaxis in mesh repair of primary inguinal hernias
using Prolene hernia system: a randomised prospective
double-blind control trial. Trop Doct 38(2):80–82
25. Horan TC, Gaynes RP, Martone WJ, Jaris WR, Emori TG
(1992). CDC definitions of nosocomial surgical site infec-
tions, 1992: a modification of CDC definitions of surgical
wound infections. Am J Infect Control 20:271–274
26. Tierney JF, Stewart LA (2005). Investigating patient exclu-
sion bias in metaanalysis. Int J Epidemiol 34:79–87
27. Alderson P, Green S. Cochrane Collaboration open learn-
ing material for reviewers, version 1.1. Available at http://
www.cc-ims.net
28. Higgins JPT, Green S (eds). Cochrane handbook for sys-
tematic reviews of interventions, version 5.0.2 [updated
September 2009]. The Cochrane Collaboration, 2009.
Available at http://www.cochrane-handbook.org
29. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR
(1999). Guideline for prevention of surgical site infection,
1999. Infect Control Hosp Epidemiol 20:247–280
30. Sitges-Serra A (2002). Ecosurgery. Br J Surg 89:387–388
31. Simchen E, Rozin R, Wax Y (1990). The Israeli study of sur-
gical infection of drains and the risk of wound infection in
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32. Memon MA, Cooper NJ, Memon B, Memon MI, Abrams KR
(2003). Meta-analysis of randomized clinical trials com-
paring open and laparoscopic inguinal hernia repair. Br J
Surg 90:1479–1492
33. McAuley L, Pham B, Tugwell P, Moher D (2000). Does the
inclusion of grey literature influence estimates of inter-
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34. Z-index database of Koninklijke Nederlandse Maatschap-
pij ter bevordering der Pharmacie (KNMP), The Hague,
Netherlands. Available at http://www.knmp.nl [in Dutch].
Accessed December 2003
Discussion
Klinge: Do you think that this problem of mesh
infection and late mesh infection is an issue for
meta-analysis and clinical studies?
Aufenacker: It would be quite difficult to do the
follow-up of such a study. If you want to prove the
short-term effect of this infection, you need a large
population.
Simons: Do you think it would be good to use an-
tibiotics in cases of patients with risk factors, such
as smokers?
Aufenacker: In our study, we do not look at smok-
ing-related factors, so I can’t answer this question
yet.
 18

Infection Control in a Hernia Clinic:

24-Year Results of Aseptic and
Antiseptic Measure Implementation
in 4,620 »Clean Cases« Based on
Up-To-Date Microbiological Research
M. Deysine
 136 Chapter 18 · Infection Control in a Hernia Clinic
Introduction
The wound infection rate for both ventral and
inguinal herniorrhaphy has remained at virtually
the same unacceptable level for the last 60 years:
between 3% and 4% for inguinal hernias and be-
tween 8% and 14% for ventral hernias. Thus, ap-
proximately 30,000 inguinal and 3,000 ventral re-
pairs become infected yearly in the United States
alone, and European figures may be similar [2–3].
During the last 20 years the introduction of
mesh repairs has considerably changed the prog-
nosis of these infections, whose successful treat-
ment requires a sequence of often crippling or
even life-threatening reoperations [4].
This paper reports our 25-year experience
with »clean« postherniorrhaphy wound infection
prevention. During this period, vast advances have
been made by groups studying the biological rela-
tionships among bacteria, prostheses, and hosts
[5–8]. The emerging information solidly supports
the application of seasoned surgical principles that
function by diminishing the number of microbes
entering the wound, decreasing their available
food supply, and killing them with antibiotics
[9, 10]. However, recent discoveries dealing with
bacterial »quorum sensing« and its inhibitors may
favorably apply to the prevention and treatment of
infections related to surgically implanted foreign
bodies.
Our results suggest that with the application of
up-to-date knowledge dealing with the interaction
between biomaterials and bacteria, posthernior-
rhaphy wound infections may become a prevent-
able complication.
Methods and Materials
In 1981 we created a hernia clinic where patients
were treated under a protocol that has been re-
ported elsewhere [11–12]. At the onset, we ad-
18 opted the Shouldice technique for inguinal repairs,
which was progressively replaced by mesh repairs
using expanded polytetrafluoroethylene (ePTFE),
polypropylene, and Dacron polyester meshes. Ven-
tral herniorrhaphy underwent a similar evolution-
ary pattern [10].
Initially, the operating room aseptic and anti-
septic measures used were the standard ones for
so-called clean cases. Wounds were not irrigated,
and we did not use intravenous antibiotics.
In 1982, after the occurrence of five almost
consecutive postinguinal herniorrhaphy wound
infections, we modified our protocol by enhancing
strict aseptic measures created by others. In addi-
tion, patients received a preoperative intravenous
injection of 1 g cefazolin. We also irrigated the
operative sites with a solution of 80 mg gentamicin
sulfate diluted into 250 ml normal saline solution,
starting immediately after opening the external
oblique aponeurosis and continuing intermittently
until the skin was closed. (See ⊡ Table 18.1).
Postoperatively, patients were seen by the au-
thor at 7 days, at 1 month, and at yearly intervals
thereafter. Wound infection was defined as the ap-
pearance of pus or any other exudate anywhere in
a wound, any time after surgery.
Results
Since 1981 we have performed 4,300 »clean« inguinal
herniorrhaphies under a published protocol. We used
the Shouldice technique in 2,500 and mesh or plug
repair for the rest. Five postinguinal herniorrhaphy
wound infections occurred (11%), the last one in
1982. All of them occurred in patients operated
with the Shouldice technique. Four of the wounds
grew coagulase-positive Staphylococcus aureus. All
infections were treated by opening the skin from end
to end and the wound down to the infected layer,
with extensive debridement of all necrotic tissue and
suture material. Wounds were irrigated at daily inter-
vals with normal saline solution, and the patients re-
ceived short-term courses of specific antibiotics. All
wounds healed by secondary intention. Two patients
developed recurrences and were reoperated 6 weeks
after the wounds were completely healed.
Three hundred and thirty »clean« ventral
herniorrhaphies were performed utilizing a variety
of mesh techniques and materials. Three patients
in whom the defects were corrected with ePTFE
meshes developed wound infections (0.9%) re-
quiring mesh removal. All of these wounds grew
coagulase-positive Staphylococcus aureus. These
Chapter 18 · Infection Control in a Hernia Clinic
⊡ Table 18.1. Aseptic and antiseptic measures ad-
opted in 1982 to decrease wound contamination by
operating room environmental bacteria
In the preoperating room:
1. Patient’s abdomen is shaved or clipped just before
surgery
2. Patient receives 1 g intravenous cefazolin
In the operating room:
1. Team emphasis on measures to prevent prosthe-
sis contamination
2. Team awareness of operating room preparations:
face masking, scrubbing, gowning, gloving, in-
strument package handling
3. Double gloving, with changes of the external
glove every 45 min
4. Avoidance of nonessential personnel traffic
through the operating room
5. Team awareness of all moves that may produce
contamination
Surgical measures
1. Ensure that skin preparation vastly exceeds the
wound area; include the scrotum for inguinal
herniorrhaphy
2. Drape the patient carefully
3. Emphasize scissors or scalpel dissection
4. Use electrocautery sparsely
5. Keep dissection circumscribed to relevant areas
6. As soon as the external oblique aponeurosis is
opened (for inguinal or ventral hernias), start
wound irrigations with a solution of 80 mg gen-
tamicin sulfate dissolved in 250 ml normal saline
7. Irrigate as often as possible
8. Approximate tissues to themselves and to the
prosthesis, using the minimum tension necessary
to permit appropriate contact and avoid tissue
strangulation
9. Place the prosthesis into the gentamicin solution
as soon as it leaves the package; consider the op-
erating room air to be contaminated with bacteria
10. Avoid excessive retraction, clamping, or tissue
crushing with any kind of instrument
11. Avoid hand retracting or dissection
12. Excise all devitalized tissue
13. Before closing the external oblique aponeurosis,
debride the wound with a dry gauze to remove
clots, separated fat tissue, etc.
14. Avoid drain placement; if needed, use it for only
24 h, and keep the patient on intravenous antibi-
otics all of that time
patients were reoperated 6–12 months later using
various techniques. No infections were observed
in »clean cases« receiving either polypropylene or
Dacron polyester meshes [10].
137 18
Since the inception of these aseptic and anti-
septic measures in 1982, we have not experienced
wound infections in »clean« inguinal or ventral
hernia repairs
Discussion
After the landmark work of Semmelweis, Pasteur,
and Lister, the wound infection rate for »clean«
general surgical cases fell from virtually 100% to
about 10%. This rate was further reduced around
1950 to approximately 4% by improvements in op-
erating room aseptic and antiseptic measures plus
the introduction of perioperative and postoperative
antibiotics. However, no further improvement in
the »clean« wound infection rate has been recorded
for the last 40 years [4]. This situation may be the
result of less than optimal implementation of time-
tested aseptic measures associated with a false sense
of security emerging from antibiotic availability.
Furthermore, the actual wound status termi-
nology may be deceiving because so-called clean
wounds are far from sterile. Abundant evidence
in the literature demonstrates that such wounds
contain bacteria at the time of closure, coming
from the air, bodies, or surgical instruments. Hub-
ble et al. demonstrated that operating room air
might contain up to 1,000 colony-forming units
per mm3 [13]. Taylor and Bannister showed that a
surgeon leaning over a wound increases the bacte-
rial wound count by 27-fold [14], and Dillon et al.
showed that 23% of »clean wounds« grew bacteria
and that postoperative infections of those wounds
were 10 times more common [15]. This means that
during »clean« surgery, both the wound and the
prosthesis will become contaminated by bacteria
to various degrees.
However, our knowledge of wound infection
has rapidly increased because, during the last 30
years, biochemical engineers, microbiologists, and
general and orthopedic surgeons have clarified
the interactions among bacteria, host tissues, and
prosthetic polymers [5–8, 16–19].
As demonstrated by several investigators
[14–16], bacteria will enter a wound from a variety
of operating theater sources. These microorgan-
isms depend on food substrate for their survival,
 138 Chapter 18 · Infection Control in a Hernia Clinic
and mortified tissue and plasma-coated prosthetic
polymers meet this nutritional demand [20]. Sub-
sequently, by producing high-quality adhesives that
allow their survival and further colonization, bac-
teria rapidly hold fast to those nourishing surfaces.
The forthcoming colonization is then followed by
a host–immune response leading to suppuration
[5, 6, 8].
In 1970, Nealson et al. [21] reported on the
cellular control of the synthesis and activity of a
bacterial luminescent system regulated by a sys-
tem of intercellular communications. This led to
a series of discoveries demonstrating that gram-
positive and gram-negative bacteria communicate
with each other by releasing chemical molecules
called autoinducers, which regulate gene expres-
sion in response to changes in population density.
This process allows bacteria to build community
structures and regulate biofilm and toxin produc-
tion. In essence, the quorum sensum is responsible
for bacterial contamination of tissues and biomate-
rials plus further toxin production.
These landmark discoveries led to the identi-
fication of an autoinducer RAP (33–kDa autoin-
ducer RNAIII-activating protein), which induces
the phosphorylation of the target of RAP (TRAP).
TRAP is a 21–kDa protein that regulates the ex-
pression of toxins. Most importantly, in the absence
of TRAP expression of phosphorylation, bacteria
do not produce toxins, and they fail to cause dis-
ease. Recently, the quorum-sensing inhibitor RIP
[RNAIII-inhibiting peptide (YSPWTNF–NH2)]
showed the capacity to inhibit TRAP phosphory-
lation, thereby preventing infection of implanted
devices in several animal models. Finally, RIP has
been found to have significant activity in treating
methicillin-resistant staphylococcal infections in
a rat model, suggesting its use as a therapeutic
constituent. From these data, it is evident that a
new era of infection control and treatment may be
emerging.
In 1982 we decided to test the effect of ir-
18 rigating inguinal herniorrhaphy wounds with a
concentrated solution of gentamicin sulfate. In ad-
dition, the prosthesis was placed in the gentamicin
solution directly from the package and from there
into the wound. Further to this, a preoperative
intravenous injection of 1 g cefazolin was added to
the protocol. The killing effect of the gentamicin
is concentration dependent and is followed by a
bacteriostatic effect. Although it is most effective
against gram-negative bacteria, gentamicin also
has killing activity against staphylococci, both S.
aureus and S. epidermidis. The empirical choice
of a highly concentrated gentamicin solution may
explain our results because, at the level used, gen-
tamicin would be bactericidal and not bacterio-
static [22]. Most important, because gentamicin
shows antimicrobial synergy when used in combi-
nation with beta-lactams, the cefazolin may have
contributed to successful bacterial killing [23].
Gentamicin is not harmless and can produce
auditory and renal damage at high serum concen-
trations. Concerned about such side effects, we
measured gentamicin serum levels in 10 consecu-
tive postinguinal herniorrhaphy patients 1 h post-
operatively and found undetectable levels. Ven-
tral herniorrhaphies, in contrast, present a larger
surface; for those cases, we recommend avoiding
peritoneal contact with the gentamicin solution
because it will be rapidly absorbed by the sero-
sal surface. Compresses soaked in the gentamicin
solution can be used to protect the wound edges
while or until the peritoneum is closed, at which
time wound irrigations can continue. We have not
encountered any cases of otic or renal toxicity.
Salvati and others have monitored serum gen-
tamicin levels after the treatment of infected or-
thopedic wounds with pellets containing the an-
tibiotic, showing minimal or no detectable levels
[24–27]. Recently, gentamicin irrigations have
been successfully used by neurosurgeons to pre-
vent postcraniotomy infections [28]. Addition-
ally, Junge et al. successfully bonded gentamicin
to polyvinylidene fluoride mesh material, dem-
onstrating that the antibiotic retained its antimi-
crobial activity after implantation. These findings
open the possibility of creating a mesh that could
resist microbial colonization [29].
The use of preoperative intravenous antibiot-
ics is a much debated issue [30–39]. In spite of the
controversy, we choose to use them because we
believe it could balance the infection struggle in
our patients’ favor.
Inguinal herniorrhaphy is one of the few sur-
gical procedures in which the surgeon deals with
Chapter 18 · Infection Control in a Hernia Clinic
initially sterile tissues. Therefore, the amount of
bacteria present at closure should become a con-
trollable factor. Consequently, in addition to the
antibiotic regimen, we strictly emphasized aseptic
measures developed by others because we believed
in their usefulness. Patients were shaved by the
surgeon just before surgery, and the skin prepara-
tion vastly exceeded the operative site. Gowning,
gloving, and draping were strictly supervised to
diminish errors [40–43]. The literature on gloving
is rich in data demonstrating that those devices
routinely perforate [44–46]. Therefore, we used
double gloving.
Electrocautery produces a time- and energy-
dependent coagulation necrosis indistinguishable
from a full-thickness burn [47–50]. To lessen the
amount of necrotic material in the wound, we used
such tools sparingly. Incision and further dissec-
tion were performed with scalpel and delicate scis-
sors. Gentle tissue handling and retracting were
encouraged.
The interpretation of these results is limited by
the logistics of the clinical problem: These patients
could have been randomized; thus, we do not
know whether any of the above measures would,
by themselves, have been sufficient to improve our
patients’ outcomes. Moreover, our success cannot
be attributed to the use of antibiotics only, as other
measures were included to decrease the number of
bacteria entering the wound.
Additionally, the field of ventral herniorrhaphy
poses additional challenges, probably related to the
fact that larger wounds require larger meshes. For
these operations we strongly recommend the in-
corporation of measures that have already yielded
vastly improved results in the field of orthopedic
infections, including dedicated operating rooms
with HEPA-filtered laminar air flow, hooded and
ventilated gowns and masks, and double gloving
[51].
In our hands, the implementation of strict
aseptic measures, atraumatic technique, minimal
electrocautery use, intravenous preoperative anti-
biotics, and early and frequent wound irrigation
with a gentamicin solution have eliminated post-
operative herniorrhaphy infections. The validity of
these results can henceforth be substantiated only
by further studies.
139 18
New discoveries by microbiologists may fur-
ther enhance the field of infection prevention and
treatment.
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we doing all we can? [letter] Hernia 8:90–91 Discussion
Chapter 18 · Infection Control in a Hernia Clinic
141 18
Discussion

Smeds: What are the reasons for your low infec-

tion rate?
Deysine: It’s a combination of things I did. First of
all, I try to get my operating room sterile, and I use
prophylactic antibiotics because it makes sense to
me. It’s only one injection; it works in orthopedic
patients.
Kehlet: We hear about these large personal series
with zero problems in anything. And then we have
these series from randomized studies with infec-
tion rates up to 9%. How can we proceed, because
there is a discrepancy between these difference
experiences?
Deysine: I believe in technique, and I think that
doing this kind of operation properly without ad-
ditional damage of tissue leads to these good re-
sults.
 19

Components Separation Technique:

Pros and Cons
B. M. van der Kolk, T. S. de Vries Reilingh, O. Buyne,
R. P. Bleichrodt
 144 Chapter 19 · Components Separation Technique: Pros and Cons
Introduction
Prosthetic repair is still the most frequently applied
method to repair ventral hernias. However, pros-
thetic materials have several drawbacks. First, the
mechanical properties of the abdominal wall may
be altered, providing less dynamic support and a
less favorable cosmetic result owing to bulging of
the prosthesis. Second, the prosthetic material may
cause damage to the intraabdominal viscera if the
peritoneum or greater omentum cannot be inter-
posed between the prosthesis and the organs [1].
Third, biomaterials increase the risk of infection,
particularly when they are used for reconstruction
in a contaminated environment, such as the ab-
dominal wall in the presence of an enterocutane-
ous fistula [2, 3].
In 1990, Ramirez et al. [4] described a tech-
nique for reconstructing abdominal wall defects
without using prosthetic material. It is based on
enlargement of the abdominal wall surface by
translation of the muscle layers to bridge fascial
defects of up to 28 cm at the waistline without
compromising the innervation and blood supply
⊡ Fig. 19.1. Anatomy of the abdominal wall. The skin and sub-
cutaneous tissue cover the muscles of the ventral abdominal
wall. The muscles of the ventrolateral abdominal wall are the
19 external oblique, internal oblique, and transversus abdominis,
which insert into the anterior and posterior sheaths of the
rectus abdominis muscle. The aponeurosis of the external
oblique muscle forms the anterior rectus sheath. The internal
oblique aponeurosis divides into an anterior and posterior
of the muscles to restore the anatomy of the ventral
abdominal wall. The method and its modifica-
tions have been described in detail by Bleichrodt
and coworkers [5–8]. This chapter describes the
relevant anatomy of the ventral abdominal wall
and the surgical technique, summarizes the results,
and discusses the sequelae and possible solutions
to prevent them.
Anatomy
The anatomy in relation to the components sepa-
ration technique (CST) has been described by Ble-
ichrodt et al. [5] and is summarized here. The skin
and subcutaneous tissue cover the muscles of the
ventral abdominal wall. The muscles of the ventro-
lateral abdominal wall are the external oblique, in-
ternal oblique, and transversus abdominis, which
insert into the anterior and posterior sheaths of the
rectus abdominis muscle (⊡ Fig. 19.1). The arterial
blood supply of the skin comes mainly from the
intercostal arteries and the perforating branches
of the epigastric artery (⊡ Fig. 19.2). The innerva-
part. The anterior part forms the anterior layer of the rectus
sheath, together with the external oblique muscle. The pos-
terior part fuses with the transversus abdominis, forming the
posterior rectus sheath, superior to the linea semilunaris. The
neurovascular bundle runs between the internal oblique and
transversus abdominis muscle and penetrates the posterior
rectus sheath at the posterolateral side. (Reproduced with
permission from Bleichrodt et al. [5])
Chapter 19 · Components Separation Technique: Pros and Cons
⊡ Fig. 19.2. Blood supply of the skin and muscles of the
ventral abdominal wall. The blood supply of the ventral ab-
dominal wall stems mainly from the epigastric and intercostal
arteries. The skin of the ventral abdominal wall is supplied by
the (a) periumbilical musculocutaneous perforators of the
(b) superior and (c) inferior epigastric arteries and the (d)
tion of the anterolateral ventral abdominal wall is
shown in ⊡ Fig. 19.3. The muscles are innervated
by the 7th–12th intercostal nerves and the iliohy-
pogastric and ilioinguinal nerves.
Components Separation Technique
(⊡ Fig. 19.3a–e)
The skin and subcutaneous fat are dissected free
from the anterior rectus sheath and the aponeu-
rosis of the external oblique muscle. By doing this,
the perforating branches of the epigastric artery
are transected. The aponeurosis of the external
oblique muscle is incised 1–2 cm lateral to the
lateral border of the rectus abdominis muscle. The
myoaponeurosis of the external oblique muscle
is transected longitudinally over its full length.
Transection includes the muscular part of the ex-
ternal oblique muscle on the thoracic wall. With
this extension, the rectus abdominis muscle can be
maximally shifted medially in the upper abdomen.
The external oblique muscle is separated from the
internal oblique muscle in the avascular plane be-
tween both muscles. With this technique, the rec-
tus muscle can be advanced 3–5 cm in the upper
145 19
intercostal arteries, but also by branches of the superficial epi-
gastric artery and the superficial circumflex iliac and external
pudendal arteries (c). The blood supply of the muscular layers
of the abdominal wall stems from the (e) superior and (f) infe-
rior epigastric arteries, together with the intercostal arteries
(g). (Reproduced with permission from Bleichrodt et al. [5])
abdomen, 7–10 cm at the waistline, and 1–3 cm in
the lower abdomen. A further gain of 2–4 cm can
be achieved by separating the posterior sheath of
the rectus abdominis muscle. The abdominal wall
is closed in the midline with a running suture of
a nonabsorbable or slowly absorbable suture ma-
terial. Suction drains are placed subcutaneously,
and the subcutis and skin are closed. Defects of
up to 28 cm in the waistline can be bridged in this
way. After closure of the linea alba, the external
oblique muscle and the posterior rectus sheath are
retracted laterally.
Overall Results
The results of CST up to 2007 were reviewed by
de Vries Reilingh et al. [8]. Operative technique,
complications, and recurrence rates were the main
points of interest. As of 2007, 15 series had been
published on the results of abdominal wall repair
using CST: one randomized controlled trial and 14
retrospective series. The technique varied among
the studies. In all studies, transection of the exter-
nal oblique muscle was performed; in six, a release
of the posterior rectus sheath was carried out as
 146 Chapter 19 · Components Separation Technique: Pros and Cons
⊡ Fig. 19.3. The neurovascular bundle in relation to the ab-
dominal wall musculature. The muscles of the anterolateral
ventral abdominal wall are innervated by the 7th–12th inter-
costal nerves and the iliohypogastric and ilioinguinal nerves.
The nerves (a) run forward together with the accompanying
arteries and veins between the internal oblique (b) and the
transversus abdominis (c) muscle. Branches are supplied to
the muscle and the overlying skin (d). The segmental neu-
well. Two studies described an extension of the
original technique [6, 7]: a release of the anterior
rectus sheath in one series and transection of the
transverse abdominal muscle in selected patients.
In three series, incidental prosthetic onlay mesh
support was used.
The overall quality of the studies was moderate
according to the MINORS criteria. One prospec-
tive randomized trial comparing CST and pros-
thetic repair was performed, having a MINORS
index of 12. Fourteen retrospective series includ-
ing 460 patients were published, with a mean MI-
NORS index of 7 (range 3–8). Eleven retrospective
studies with a MINORS index ≥5 were pooled with
the 19 patients in the randomized controlled trial,
giving a total of 479 patients [9–20].
Overall mortality was 1.2% (three out of 248
19 patients in seven series). Wound complications
were observed in 12 series that included 354 pa-
tients. Wound complications were found in 23.8%
[95% confidence interval (CI) 18.3–29.8]. Wound
rovascular bundles penetrate the internal oblique contribu-
tion to the posterior rectus sheath at the posterolateral side
to supply the rectus muscle (g) and the overlying skin. The
neurovascular bundles enter the rectus sheath close to the
axis of the epigastric arteries, about 10–25 mm medially from
the lateral border of the rectus sheath (e). (Reproduced with
permission from Bleichrodt et al. [5])
infection was the most common complication,
found in 18.9% (95% CI 14.9–23.2); seroma in
2.4% (95% CI 1.0–4.2); hematoma in 2.4% (95%
CI 1.0–4.2); and skin necrosis in 1.5% (95% CI
0.5–3.1). A follow-up period of at least 1 year after
operation was reported in five series that included
134 patients; 27 patients (18.2%; 95% CI 5.4–36.2)
had a recurrent hernia.
Sequelae and Prevention
Hematoma, Seroma, and Wound
Infection
When performing CST, a very large subcutaneous
wound surface, approaching 1,000 cm2, is created,
extending from the thorax to the inguinal region
and in the lateral direction to the midaxillary line
on both sides. Hematoma (2.4%), seroma (2.4%),
infection (18.9%), and skin necrosis are the most
Chapter 19 · Components Separation Technique: Pros and Cons
frequent complications and account for 23.8% of
postoperative complications. Hematomas can be
prevented by meticulous hemostasis. Seroma for-
mation is much more difficult to prevent. The in-
flammatory response, which is part of the wound
healing process, creates an exudate between the
fascia and the subcutaneous fat layer. Many tech-
niques such as vacuum drains, subcutaneous su-
tures, fibrin glue, and compression bandages are
insufficient. Most seromas are asymptomatic and
will disappear within 3–6 months. Some seromas
become very large and endanger the wound heal-
ing process in the early phase. If not drained
properly, these seromas will drain spontaneously
through the skin incision, with the risk of second-
ary infection. Chronic seromas can be successfully
punctured, and surgery is seldom required.
Many CST procedures are performed under
contaminated conditions, which may explain the
relatively high wound infection rate. CST is often
performed in the presence of wounds, enterosto-
mies, and even bowel fistulas. Providing adequate
antibiotic prophylaxis, diminishing the dissec-
tion subcutaneously, and sparing the perforating
epigastric arteries may all contribute to a better
result.
Skin Necrosis
The blood supply of the ventral abdominal wall
stems mainly from the epigastric and intercostal
arteries. Transection of the epigastric perforat-
ing arteries endangers the blood supply of the
skin of the ventral abdominal wall. Especially in
patients in whom the intercostal arteries have
been transected–such as in patients with entero-
tomies or laparotomies via transverse incisions–
ischemia or even skin necrosis may occur. Skin
necrosis has been observed in 1.5% of patients
in the literature. Necrosis is mainly located in
the infraumbilical region in the midline. This
complication can be prevented by sparing the
periumbilical epigastric perforators. In our series
of patients, 5% suffered skin necrosis when the
classical technique was performed. Skin necrosis
did not occur in any of the patients in whom the
perforating arteries were spared. In our series,
147 19
skin necrosis occurred in all patients who were
on chronic hemodialysis.
Bulging and Abdominal
Wall Rupture
Bulging of the abdominal wall at the side of the re-
laxing incisions in the external oblique myoaponeu-
rosis may be a cosmetic problem in patients with a
thin subcutaneous fat layer. Because the cosmesis
of the abdominal wall improves considerably after
CST and because most patients have a prominent
subcutaneous fat layer, the vast majority of patients
do not complain about the distinct swelling on the
lateral side of the rectus abdominis muscle.
Rupture of the abdominal wall at the side of
the relaxing incision is, however, a very serious
complication of the technique, causing damage to
the neurovascular bundle, including the intercostal
nerves, which results in paralysis of at least the
rectus abdominis muscle. Since 2000 we have en-
countered three patients (<1%) with an abdominal
wall rupture at the site of incision in the external
oblique muscle. In one of those patients, the rup-
ture occurred during operation and was repaired
with mesh immediately. In the second patient, the
rupture occurred the day after surgery and was
repaired with a mesh as well. In the third patient,
bilateral ruptures occurred 1 h and 1 week after
the initial operation, respectively (⊡ Fig. 19.4). The
hernia was repaired by primary closure and a sub-
lay mesh. In two of the three patients, no hernia-
tion had occurred after 1 and 6 years, respectively.
In the patient with an abdominal wall rupture
on both sides, the reconstruction on the left side,
which was performed 6 days after the index opera-
tion, was complicated by infection and herniation.
Definitive repair was done 1 year later. The cause
of rupture is unknown.
It is essential to properly identify the plane
between the internal and external oblique muscles.
Accidental transection of the internal oblique mus-
cle may result in an abdominal wall rupture because
the transversus abdominis muscle is too weak to
resist the intraabdominal pressure. Some surgeons
advocate an onlay mesh support to prevent recur-
rent hernias or abdominal wall rupture [22].
 148 Chapter 19 · Components Separation Technique: Pros and Cons
⊡ Fig. 19.4. Components separation technique. The patient is
placed in a supine position. The skin is opened via a midline
incision. If a skin defect exists or if the intestine is covered with
a split-thickness skin graft, the abdominal cavity is entered via
an incision just lateral to the defect. The intestine and other
viscera are dissected free from the ventral abdominal wall. By
doing this, the lateral border of the rectus abdominal muscle
can be identified properly from the inside of the abdomen.
a The skin and subcutaneous fat are dissected free from the
anterior rectus sheath and the aponeurosis of the external
oblique muscle to about 5 cm lateral to the lateral border of
the rectus sheath. Mobilization includes transection of the epi-
gastric perforators endangering the blood supply of the skin.
b The aponeurosis of the external oblique muscle is incised
1–2 cm lateral to the lateral border of the rectus abdominis
muscle. The myoaponeurosis of the external oblique muscle
is transected longitudinally over its full length. Transection
includes the muscular part of the external oblique muscle
on the thoracic wall that extends at least 7–10 cm cranially.
Nerve Damage
The muscles of the anterolateral ventral abdomi-
19 nal wall are innervated by the 7th–12th intercos-
tal nerves and the iliohypogastric and ilioinguinal
nerves (⊡ Fig. 19.3). The nerves run forward to-
gether with the accompanying arteries and veins
c The external oblique muscle is separated from the internal
oblique muscle in the avascular plane between both muscles,
superiorly to the midaxillary line. Mobilization is essential
because the fibrous interconnections between both muscles
prevent optimal medial shift of the rectus abdominis muscle.
d A further gain of 2–4 cm can be achieved by separating the
posterior sheath of the rectus abdominis muscle. The poste-
rior sheath is incised posteriorly, near the midline over its full
length. The rectus abdominis muscle can easily be separated
from the posterior rectus sheath. e Attention must be paid to
not damage the neurovascular bundle laterally. Note the en-
trance of the neurovascular bundle that penetrates the fascia
of the internal oblique muscle at a variable distance from the
lateral border of the rectus abdominis muscle, near the axis
of the epigastric artery. Damage to the neurovascular bundle
results in denervation of the rectus abdominis muscle. The
abdominal wall is closed in the midline with a running suture
of a nonabsorbable or slowly absorbable suture material (af-
ter Bleichrodt et al. [5])
between the internal oblique and the transversus
abdominis
muscle, and branches are given to each mus-
cle and the overlying skin. After CST, all patients
have hyposensibility of the ventral abdominal
wall skin as a result of transection of the sensory
nerves. Denervation of the muscles of the ventral
Chapter 19 · Components Separation Technique: Pros and Cons
a Stretching of the nerves may be one explanation.
b complete transection of the external oblique myo-
c positioned between the posterior rectus sheath
⊡ Fig. 19.5. Rupture of the abdominal wall at the site of the re-
laxing incision in the myoaponeurosis of the external oblique
muscle. a Swelling of the abdominal wall that occurred within
1 h of repair using the components separation technique. b At
operation, a complete rupture of the abdominal wall muscu-
lature was found at the lateral border of the rectus abdominis
muscle. c Note that the neurovascular bundle is damaged as
well, resulting in (partial) denervation of the abdominal wall
musculature (adapted from de Vries Reilingh and Bleichrodt
[21] with permission)
149 19
abdominal wall occurs less frequently. Damage
to the nerves that innervate the rectus abdominis
muscle may occur after accidental transection.
This may occur when dissection is performed
in the wrong plane between the internal oblique
muscle and the transverse abdominis muscle, but
also at the entrance of the nerves into the rectus
sheath at the posterolateral side of the rectus
sheath.
After CST, some patients have radiating pain
in the ventral abdominal wall for 6–12 months
postoperatively. The cause of this pain is unknown.
Reherniation
Reherniation after CST is rather frequent. After a
follow-up of at least 1 year, 18.2% had a recurrent
hernia. This percentage is probably actually higher
and approaches the results of suture repair. Most
recurrences are located in the upper abdomen
and are small. Modifying the CST technique may
reduce the incidence of reherniation. Tension-free
repair can be achieved in most patients when
aponeurosis is performed, including mobilizing
the rectus abdominis muscle from the thoracic
wall. Recurrences can be repaired laparoscopically
in most cases.
Recurrence rates in hernia surgery are lower
after mesh repair. This may be the case in CST as
well [21]. Placement of a mesh is simple when the
posterior sheath of the rectus abdominis muscle
can be closed primarily; then the mesh can be
and the rectus abdominis muscle (⊡ Fig. 19.6a).
When the posterior sheath cannot be closed, the
gap in the posterior rectus sheath is bridged with
a mesh, preferably with an antiadhesive layer
against adhesions, such as Proceed mesh or Se-
pramesh (⊡ Fig. 19.6b). The anterior sheath and
rectus abdominis muscles are then closed pri-
marily and cover the mesh. In 2006, a random-
ized controlled trial was initiated to determine
whether a preperitoneal retromuscular mesh in
combination with CST lowers recurrence rates.
Kingsnorth et al. [22] combine CST with onlay
 150 Chapter 19 · Components Separation Technique: Pros and Cons
a reherniation rate is still high but may be decreased
b
⊡ Fig. 19.6. Combined components separation technique
and prosthetic repair following the Stoppa–Reeves technique.
a The mesh is positioned preperitoneally to separate the in-
testine from the mesh and is covered by the rectus abdominis
muscle. b When the posterior rectus sheath cannot be closed
primarily, the gap is bridged by a double-layered mesh that
protects the intestine from contact with the mesh
mesh repair. They report low complication and
recurrence rates.
The Remaining Fascial Gap
In approximately 7% of patients, the fascia can-
not be closed in the midline. Further research is
needed to identify those patients in whom the
abdominal wall cannot be closed primarily. If pri-
mary closure is not possible, the fascial gap is
bridged with a mesh under clean or clean-contam-
inated conditions. Otherwise, repair with the use
of autologous tissue such as free or pedicled fascia
flaps is performed.
Conclusion
CST is an attractive technique for abdominal wall
reconstruction in patients with large midline her-
nias, especially in a contaminated field. The tech-
nique restores the anatomy of the abdominal wall
19 and has good cosmetic results. Postoperative com-
plications are rather frequent. Morbidity may be
decreased by sparing the epigastric perforating
arteries and diminishing the wound surface. The
by combining CST and mesh repair.
References
1. Basoglu M, Yildirgan MI, Yilmaz I, et al. Late complications
of incisional hernias following prosthetic mesh repair.
Acta Chir Belg 2004; 104:425–428
2. Burger JW, Luijendijk RW, Hop WC, et al. Long-term fol-
low-up of a randomized controlled trial of suture versus
mesh repair of incisional hernia. Ann Surg 2004; 240:578–
585
3. Bleichrodt RP, Simmermacher RK, van der Lei B, Schaken-
raad JM. Expanded polytetrafluoroethylene patch versus
polypropylene mesh for the repair of contaminated de-
fects of the abdominal wall. Surg Gynecol Obstet 1993;
176:18–24
4. Ramirez OM, Ruas E, Dellon AL. »Components separa-
tion« method for closure of abdominal-wall defects: an
anatomic and clinical study. Plast Reconstr Surg 1990;
86:519–526
5. Bleichrodt RP, de Vries Reilingh TS, Malyar AW, et al. Com-
ponent separation technique to repair large midline her-
nias. Op Tech Gen Surg 2004; 6:179–188
6. Maas SM, van Engeland M, Leeksma NG, Bleichrodt RP. A
modification of the »components separation« technique
for closure of abdominal wall defects in the presence of
an enterostomy. J Am Coll Surg 1999; 189:138–140
7. Maas SM, de Vries Reilingh S, van Goor H, de Jong D, Ble-
ichrodt RP. Endoscopically assisted »components separa-
tion technique« for the repair of complicated ventral
hernias. J Am Coll Surg 2002; 194:388–390
8. de Vries Reilingh TS, Bodegom ME, van Goor H, et al. Au-
tologous tissue repair of large abdominal wall defects. Br
J Surg 2007; 94:791–803
9. de Vries Reilingh TS, van Goor H, Charbon J, et al. Repair
of large midline abdominal wall hernias: components
separation technique versus prosthetic repair. World J
Surg 2007; 31:756–763
10. de Vries Reilingh TS, van Goor H, Rosman C, et al. »Com-
ponents separation technique« for the repair of large
abdominal wall hernias. J Am Coll Surg 2003; 196:32–37
11. Ewart CJ, Lankford AB, Gamboa MG. Successful closure
of abdominal wall hernias using the components separa-
tion technique. Ann Plast Surg 2003; 50:269–273
12. Cohen M, Morales R Jr, Fildes J, Barrett J. Staged recon-
struction after gunshot wounds to the abdomen. Plast
Reconstr Surg 2001; 108:83–92
13. Jernigan TW, Fabian TC, Croce MA, et al. Staged manage-
ment of giant abdominal wall defects: acute and long-
term results. Ann Surg 2003; 238:349–355
14. Lowe JB III, Lowe JB, Baty JD, Garza JR. Risks associ-
ated with »components separation« for closure of com-
plex abdominal wall defects. Plast Reconstr Surg 2003;
111:1276–1283
Chapter 19 · Components Separation Technique: Pros and Cons
15. Shestak KC, Edington HJ, Johnson RR. The separation
of anatomic components technique for the reconstruc-
tion of massive midline abdominal wall defects: anatomy,
surgical technique, applications, and limitations revisited.
Plast Reconstr Surg 2000;105: 731–738
16. Szczerba SR, Dumanian GA. Definitive surgical treatment
of infected or exposed ventral hernia mesh. Ann Surg
2003; 237:437–441
17. Vargo D. Component separation in the management of
the difficult abdominal wall. Am J Surg 2004; 188:633–
637
18. DiBello JN Jr, Moore JH Jr. Sliding myofascial flap of the
rectus abdominis muscles for the closure of recurrent
ventral hernias. Plast Reconstr Surg 1996; 98:464–469
19. van Geffen HJ, Simmermacher RK, van Vroonhoven TJ,
van derWerken C. Surgical treatment of large contam-
inated abdominal wall defects. J Am Coll Surg 2005;
201:206–212
20. Girotto JA, Chiaramonte M, Menon NG, et al. Recalcitrant
abdominal wall hernias: long-term superiority of autolo-
gous tissue repair. Plast Reconstr Surg 2003; 112:106–114
21. de Vries Reilingh TS, Bleichrodt RP. Reply. World J Surg
2007; 31:2267–2268
22. Kingsnorth AN, Shahid MK, Valliattu AJ, et al. Open onlay
mesh repair for major abdominal wall hernias with selec-
tive use of components separation and fibrin sealant.
World J Surg 2008; 32(1):26–30
151 19
Conclusion of Session II, by J. Kukleta
We had a quite extensive session, which can be di-
vided into three parts: who gets the infection, how
to treat the infection, and how to prevent the in-
fection. To me, we got some take-home massages:
We have to differentiate between wound infections
and mesh infections and between acute mesh in-
fections and late-onset mesh infections.
We have heard interesting stuff about wound
oxygen and its impact on wound healing. We have
heard about biofilms and learned that it’s more
difficult to fight against existing biofilms than to
prevent them. But it still seems to be a complex
part. The impregnation of mesh materials seems
to be a good idea, but we have to learn more about
that, probably with different materials.
I want to close with the following remarks.
Decreasing the infection rates by only 3% means
thousands and thousands of people, so I would not
talk about the price of €15 for antibiotics. This is
our position in Switzerland. For any kind of im-
plants, we use antibiotic prophylaxis.

Discussion

Franz: Can you tell us which mesh you are using in

this randomized study?
Bleichrodt: We are using the Vypro II mesh be-
cause the study was running for a few years and
that was the best mesh at that moment. So we had
to go on with the same mesh; otherwise, we would
have a problem comparing results.
Deysine: Do you use antibiotic irrigation?
Bleichrodt: We use antibiotic prophylaxis in every
patient, and if the operation is longer than 3 hours,
we give it again. Mostly we irrigate the wound with
normal saline to remove, for example, blood clots
and so on, but we don’t add antibacterials. We
don’t have proof that it helps.
 III

III Risk for Pain

20 Self-Assessment of Discomfort and Pain after Inguinal

Hernia Repair: A Reflection of Both Individual Pain Propensity
and Surgical Strategy – 155

21 Chronic Pain After Inguinal Hernia Repair – 163

22 What Do We Know About the Pathophysiology and Pathology

of Neuropathic Pain? – 169

23 Surgical Trauma of Nerves–Causes of Neuropathic Pain,

Classification, and Options in Surgical Therapy – 177

24 Risks for Pain–Neuropathic Pain: How Should We Handle

the Nerves? – 185

25 What To Consider as Clinicians About Chronic Postoperative

Pain and Inguinal Herniorrhaphy – 191

26 Risk Factors for Chronic Pain After Groin Hernia

Surgery – 199

27 Ischemic Inflammatory Response Syndrome as an Alternative

Explanation for Postherniorrhaphy Pain – 207

28 Postoperative CRPS in Inguinal Hernia Patients – 213

29 Chronic Pain After Open Mesh Repair of Incisional

Hernia – 221

30 Clinical Results After Open Mesh Repair – 227

31 Acute and Chronic Pain After Laparoscopic Incisional Hernia
Repair – 233

32 Effect of Nerve Identification on the Rate of Postoperative

Chronic Pain Following Inguinal Hernia Surgery – 239

33 Discomfort 5 Years After Laparoscopic and Shouldice Inguinal

Hernia Repair: A Report from the SMIL Study Group – 245

34 Recurrence or Complication: The Lesser of Two Evils?

A Review of Patient-Reported Outcomes from the
VA Hernia Trial – 251

35 Chronic Pain After Inguinal Hernia Repair: The Choice

of Prosthesis Outweighs That of Technique – 257

36 The Effect of Polypropylene Mesh on the Ilioinguinal

Nerve in Open Mesh Repair of Groin Hernia – 265

37 Lightweight Macroporous Mesh vs. Standard Polypropylene

Mesh in Lichtenstein Hernioplasty – 275

38 Does the Choice of Prosthetic Mesh Type Make a Difference

in Postherniorrhaphy Groin Pain? – 279

39 New Understanding of the Causes and Surgical Treatment

of Postherniorrhaphy Inguinodynia and Orchialgia – 287

40 Surgery for Chronic Inguinal Pain: Neurectomy,

Mesh Explantation, or Both? – 293

41 Results of Tailored Therapy for Patients with Chronic

Inguinal Pain – 299
 20

Self-Assessment of Discomfort
and Pain after Inguinal Hernia Repair:
A Reflection of Both Individual Pain
Propensity and Surgical Strategy

S. Smeds, L. Löfström, O. Eriksson, A. Kald

 156 Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair

Introduction Self-Assessment Instrument:

Sergel Recovery Scale
Discomfort from normal tissue healing after in-
guinal hernia surgery will have largely subsided Self-assessment of preoperative groin problems was
at 3 months. Continued discomfort is referred requested at patients’ first admission to the surgical
to as postherniorrhaphy pain syndromes, which clinic 1–4 weeks before surgery, and SA of postop-
have diverse origins with peripheral neuropathic erative discomfort related to the inguinal hernia
and nonneuropathic sources [1, 2]. In addition to repair was requested 3 months after the operation.
the peripheral surgical trauma, pain perception The preoperative SA questionnaire was given be-
is based on central nervous modulation of pain fore surgery in conjunction with the preoperative
transmission. This may be influenced by age [3,
4] and other biological pain modulators [5, 6].
Expression of pain and discomfort may further be ⊡ Table 20.1. The lower part of column A represents
influenced by socioeconomic factors [7]. Finally, the self-assessment (SA) levels (1–10) in the SA scale.
The »preop« and »postop« columns give the number of
verbal eloquence and the ability to interpret as-
patients in each SA level before and after the operation.
sessment scales may influence final answers on Column B shows the number of patients whose preop-
self-assessment (SA) instruments. erative to postoperative SAs changed by the number
Thus, in addition to the variety of meth- of steps indicated in column A. The maximum number
ods for inguinal herniorrhaphy, each inflicting of steps in the scale that can be registered is 9, i.e. from
level 1 to level 10. This table is automatically updated
a varying degree of peripheral tissue and nerve
when the quality follow-up database program is opened
trauma, the variability of a number of biological
and social factors possibly adds to variability in A Preop Postop B
SA records. It was therefore deemed important -9 0
to closely analyse the SA pattern 3 months after -8 0
hernia repair. The clinic’s register gives further
-7 0
information on the preoperative self-assessed
level of groin discomfort. This gives us an oppor- -6 0
tunity to study the degree of improvement (and -5 1
impairment) following different types of repair at -4 0
a point when a postoperative pain syndrome, by
-3 1
definition, starts.
-2 2
-1 5
Materials and Methods 0 29
1 36 0 49
The Sergel Clinic is responsible for inguinal hernia
2 55 2 65
surgery of all inhabitants in the central part of
the county of Östergötland, Sweden, with a catch 3 112 1 63
area of 228,000 inhabitants. The patient popula- 4 82 2 68
tion covers all primary and recurrent groin hernias 5 69 4 75
among elective patients older than 18 years of both
6 72 9 81
genders and of American Society of Anesthesi-
ologists (ASA) grades I–III. Since February 2004, 7 50 19 74

preoperative and postoperative self-assessed levels 8 53 65 33

of groin discomfort/pain have been recorded by 9 43 134 29
intent by each patient. 10 10 363
20 SUM 582 599 575
Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair
157 20
health report in the reception area, without contact an additional table showing the relative number of
with the surgeon. The postoperative SA question- patients assessing themselves at levels 8–10 (⊡ Ta-
naire was given to the patient at the time of release ble 20.2). Those with postoperative SA at levels 7
from the clinic, with information to send it back and below were offered clinical follow-up.
3 months later. The instrument consists of a visual To analyse the validity of data collected from the
10-box scale in which SA level 10 represents no dis- primary answers, a second request for postoperative
comfort and level 1 represents the worst pain. SA was sent 4–6 months after surgery to 55 patients
A secretary routinely saved patients’ SA registra- who did not answer the first questionnaire. Analysis
tions into a database. When opened, the database of difference by ordinal logistic regression showed
automatically displayed updated information in a no difference between the two groups (⊡ Fig. 20.2).
table, showing the number of patients at each level as
registered before and 3 months after surgery as well
as further numbers of patients who had moved an
Primary and secondary
individually calculated number of steps in positive
self-assessment answers
(improved) and negative (impaired) directions on 2
10-log rel number of answers at each level
the scale (⊡ Table 20.1). Furthermore, the updated
Primary answer
preoperative and postoperative information was 1.6 N=599
presented in two histograms (⊡ Fig. 20.1) and in y = 0.415x - 2.365
1.2 R 2 = 0.9906

0.8
⊡ Table 20.2. Means and medians for preoperative Secondary
and postoperative self-assessment (SA) 3 months after answer
0.4 N=55
open hernia repair (level 10 denotes no discomfort).
y = 0.468x - 2.843
Fractions of patients rating themselves at level 8 and
0 R 2 = 0.9119
higher before and after surgery are indicated. The dif-
ference indicates the mean number of levels that the 1 2 3 4 5 6 7 8 9 10 11
patients changed their rating from their preoperative Assessment levels
to their postoperative SA
⊡ Fig. 20.2. Diagram demonstrating the similarity between the
Preop Postop Difference postoperative ratings from patients without reminders (primary
answers, squares) and the ratings from patients after a reminder
Mean 4.877622 9.292020 4.397163
1 month later (secondary answers, diamonds) at 4 months. The
Median 5 10 5 difference as analysed by logarithmic regression was not sta-
tistically significant. Data are presented as 10-logaritms of the
Fraction>=8 18.2% 93.7%
relative number of patients at self-assessment levels 7–10

400

350

300

250
Preop
200 ⊡ Fig. 20.1. Distribution of patients
Postop
on the 10-level box scale in which 1
150
denotes the worst imaginable pain
100 and 10 denotes no discomfort. White
bars represent preoperative self-as-
50
sessments 1–4 weeks before surgery
0 (n=582), and black bars represent the
1 2 3 4 5 6 7 8 9 10 postoperative rating 3 months after
open hernia repair (n=599)
 158 Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair

Patients Statistical Methods

During the years 2004–2006, 1,439 hernias in 1,369
patients with unilateral and bilateral (8% of case
series) inguinal hernias were operated upon. The
operations were almost exclusively performed as
day surgery under general anaesthesia. Anaesthesia
was induced and maintained with propofol and
remifentanil. Ventilation was controlled with a la-
ryngeal mask. One surgeon performed 92% of the
operations, and 10 consultants performed the ad-
ditional 109 operations. Preoperative SA was ob-
tained from all patients except for a few with mental
disorders. All male, female (8.4%), and recurrent
(6.1%) inguinal hernia patients were included in the
register. The report is based on 562 patients who,
without notice, returned their 3-month SA (41%).
Missing data necessary for comparing preoperative
and postoperative ratings were noted in 21 cases.
Mesh procedures dominated in primary ingui-
nal hernia surgery (77%). Single-plug procedures
(12.8%) were restricted to small medial herniations
with a well-defined hernia neck (low Spigeli hernia-
tion). A combination of plug and mesh was used in
Nyhus IIIb hernias with large defects at the internal
orifice and in large sliding hernias. In total, prosthe-
ses were used in 484 cases (89%). Suture reinforce-
ment of the inner inguinal orifice (annulorraphy)
with additional strengthening of the dorsal wall
(11%) was used in young individuals, including fer-
tile females, in whom sutures towards the inguinal
ligament aligned with the strong internal oblique
muscle. Calculations are based on 484 and 57 cases
with prosthesis and suture repair, respectively.
Data are presented as means with standard de-
viation. For continuous data, Student’s t-test was
used. Two-tailed probability of less than 5% (p-
value <0.05) was considered statistically signifi-
cant. Differences in ordinal data in the 10-box SA
scale were analysed with ordinal logistic regression
(Minitab 15 software).
Results
Self-Assessment in the Register
Information
Distributions of SA levels prior to surgery and
3 months after the operation are shown in ⊡ Fig. 20.1.
At 1–4 weeks before surgery, the distribution of pa-
tients on the scale shows a peak at level 3 with a
mean at level 4.9 (⊡ Table 20.2). Ten patients (1.7%)
had no pain before surgery, and 36 (6.2%) regis-
tered the worst imaginable pain (⊡ Table 20.1). At
3 months after surgery, the mean SA level in the
whole set of information was 9.3, and the mean
number of improvement steps was 4.4 after the per-
formed surgical procedures (⊡ Table 20.2).
The distribution of improvement in the whole
set of information is shown in ⊡ Table 20.1 and
⊡ Fig. 20.3. The majority of cases, 537 out of 575
(93.4%), changed in a positive direction on the
SA scale. Twenty-nine patients (5%) had the same
preoperative and postoperative SA level, mainly at
levels 8–10. Nine cases were impaired (1.6%). The

n
90
80
⊡ Fig. 20.3. This diagram is based 70
on column B in Table 20.1 and 60
demonstrates the number of pa- 50
tients in relation to the number of
40
steps in a positive or negative di-
30
rection corresponding to the level
of self-assessed improvement or 20
impairment (-) between the pre- 10
operative and postoperative rat- 0
20 ings. The y-axis shows the number
of patients
-9 -8 -7 -6 -5 -4 -3 -2 -1 0 1 2 3 4 5 6
Difference between pre- and postoperative SA
7 8 9
Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair
159 20
relative number of patients who rated themselves Only in sutured repair were no postoperative
without discomfort changed from 1.6% (n=10) pre- discomfort registrations below level 7 observed.
operatively to 60.6% (n=363) postoperatively. In other subgroups–i.e. all unilateral and bilateral
cases, all male and female cases, and prosthe-
sis cases–assessments lower than 7 were found
Improvement with Regard to Gender (⊡ Figs. 20.4 and 20.5).
and Type of Repair

There was no significant difference in mean im- Postoperative SA Distribution Slope

provement levels between suture and prosthesis
repair, in male versus female patients, or in uni-
lateral versus bilateral cases (⊡ Table 20.3). Bilateral
suture repair (performed in men only) showed the
lowest improvement, 2.83±2.13 steps on the scale,
whereas the largest step was observed in unilateral
suture repair, 4.76±2.50 (⊡ Table 20.3).
The relationship between the number of pa-
tients and the degree of discomfort as reported
at 3 months appeared to form a slope that might
fit an exponential function (⊡ Fig. 20.6). To test
this, the total number of cases at each SA level in
the 10-box SA scale was transformed to a relative

35 350
30 300
25
Female patients Male patients
250
20 Preop 200 Preop
15 Postop 150 Postop
10 100
5 50
0 0
1 2 3 4 5 6 7 8 9 10 1 2 3 4 5 6 7 8 9 10

⊡ Fig. 20.4. Distribution of preoperative and postoperative self-assessment among female and male patients. There was no dif-
ference as calculated with ordinal logistic regression, p=0.884

40 350

35 300
30
Suture repair Prosthesis repair
250
25
Preop 200 Preop
20
Postop 150 Postop
15
10 100
5 50
0
0
1 2 3 4 5 6 7 8 9 10 1 2 3 4 5 6 7 8 9 10

⊡ Fig. 20.5. Distribution of preoperative and postoperative self-assessment after suture and prosthesis repair, respectively.
There was no significant difference as calculated with ordinal logistic regression, p=0.099. Note the presence of cases in the
lower part of the scale after prosthesis repair compared with suture repair, for which no postoperative registration lower than
level 7 was found
 160 Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair

⊡ Table 20.3. Mean (standard deviation, number) improvement steps in the 10-box self-assessment scale 3 months
after open inguinal hernia surgery following suture or prosthetic repair, respectively. There was no significant difference
between the improvement steps as calculated from the register data, nor between genders, nor between types of repair.
Bilateral suture repair (in males only) showed the lowest mean improvement level, 2.83 steps, but showed no significant
difference compared with unilateral suture repair, p=0.12, or bilateral prosthesis repair, p=0.19

Gender Suture repair Prostheses

Unilateral Female 4.21±2.34 (n=24) 3.95±2.01 (n=23)
Male 4.76±2.50 (n=27) 4.43±2.60 (n=420)
Bilateral Male 2.83±2.13 (n=6) 4.31±2.57 (n=41)

All inguinal hernia operations 2004-2006

390
363
340
290
Number of patients

240
190
140
134
90
65
40
9 19
0 2 1 2 4
⊡ Fig. 20.6. Number of patients at -10
each self-assessment level on the 10- 1 2 3 4 5 6 7 8 9 10
level scale Self-assessment levels

All inguinal hernia operations 2004-2006 number (percent) followed by calculation of the
1.9 10-logarithm of the relative number. The 10-log-
arithms were correlated to corresponding assess-
1.7
ment levels in a diagram, and a straight line was
10-log rel number at each self

1.5 formed, R2=0.9948 (⊡ Fig. 20.7).

1.3
assessment level

1.1 y = 0.406x - 2.284

2
R = 0.9946 Discussion
0.9
0.7
Analyses of the register data create hypotheses
0.5 rather than answering them. In contrast to ran-
0.3 domised studies, however, they reflect the whole
0.1 case mix. In routine clinical quality control on the
basis of postal follow-up, only a fraction of the pa-
-0.1 0 2 4 6 8 10 tients can be expected to return the first question-
Self-assessment level naire. This is a weakness that can be defended only
by a large number of cases and analysis of answers
⊡ Fig. 20.7. Relationship between 10-log of the relative num-
ber of cases in each self-assessment (SA) level and the cor-
after a second request. Results of such analysis in
the present paper indicate a close similarity be-
20 responding SA level. A straight line with R2 =0.9948 indicates
a strong correlation tween first and second answers. It can therefore be
Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair
assumed that the collected register data are repre-
sentative for the register population.
There was a distinct difference in the distribu-
tion of SA levels in the preoperative scale compared
with postoperative ratings. The preoperative as-
sessments were rather evenly distributed along the
scale, with relatively low frequency at the extremes
and with a more pronounced peak at level 3. The
centre of the scale, level 5, divided the preoperative
assessments into two equal parts. Only 10 out of
582 patients, 1.7%, reported no discomfort prior
to surgery. This indicates that pain in addition to
the inguinal herniation is a significant problem for
the patient.
In contrast, the postoperative ratings formed a
linear-curve distribution along the scale. The slope
was strictly fitted to an exponentially defined func-
tion, with approximately 60% of the cases report-
ing no discomfort, i.e. level 10 at 3 months. The re-
maining number of patients with slight discomfort
to severe pain (approximately 40%) is similar to
that observed in a Scottish study in which 43% had
mild and 3% severe pain at 3 months [8].
The contrast between preoperative and post-
operative SA levels (⊡ Fig. 20.8) reflects the wide
variation of self-assessed discomfort/pain in a
nonrandomised register group as compared with
the intention-to-treat situation following a highly
standardised surgical treatment. If one assumes
only minute variations in surgical performance of
the Lichtenstein repair as performed by one sur-
geon in several hundreds of patients, the observed
SA slope in the scale may primarily be explained
by individual variation in reaction patterns to-
10
9.8
Mean of postoperative self-
9.6
assessment
9.4
9.2
9
8.8
8.6
8.4
1 2 3 4
Preoperative self-assessment
161 20
wards the surgical trauma. This variation among
the surgical patients probably includes both vary-
ing inflammatory reaction to the surgical trauma
and prostheses, when present, as well as genetically
determined variation in sensitisation mechanisms
[9]. The gender similarity indicates a common
genetic variation of pain propensity between the
sexes.
There was no significant difference in the
number of improvement steps after prostheses
placement or suture hernia repair. This indicates
that pain reaction to the surgical trauma seems to
be a stronger pain determinant than the additional
presence of a prosthesis. This is in concordance
with previous observations in young males [10].
It was observed, however, that after suture repair,
no patient indicated more discomfort than that
associated with level 7 on the scale, in contrast to a
number of patients receiving prostheses who rated
themselves as having stronger pain. The number of
cases with this important qualitative difference in
their postoperative SA is probably too low to create
a significant difference between the latter groups.
Only a minor number of the 40% of patients
who indicated some discomfort had a stronger
pain reaction. Most of them indicated light dis-
comfort at levels 9 and 8 at 3 months. One hypoth-
esis raised after these observations is that the part
of the scale that covers levels 7–10 may represent
individual variation in sensitivity to the surgical
trauma. The strict exponential distribution in the
patient population of pain assessment in this part
of the scale may support this interpretation. Pa-
tients with SA levels in the lower part of the scale,
⊡ Fig. 20.8. Diagram demons-
trating the gradual reduction
in postoperative assessment
of pain/discomfort (mean) in
relation to preoperative self-
5 6 7 8 9 10
assessment. Level 10 denotes
no discomfort
 162 Chapter 20 · Self-Assessment of Discomfort and Pain after Inguinal Hernia Repair
levels 1– 6, additionally expressed the presence
of a stronger pain component associated with the
use of mesh or plug prostheses, as observed in the
present register. To reach a closer understanding of
these possibly diverse pain mechanisms, the varia-
tion of discomfort/pain must be analysed over a
longer time frame.
References
1. Mikkelsen T, Werner MU, Lassen B, Kehlet H (2004) Pain
and sensory dysfunction 6 to 12 months after inguinal
herniotomy. Anesth Analg 99:146–151
2. Massaron S, Bona S, Fumagalli U, Battafarano F, Elmore U,
Rosati R (2007) Analysis of post-surgical pain after ingui-
nal hernia repair: a prospective study of 1,440 operations.
Hernia 11:517–525
3. Ringkamp M, R Meyer (2006) Does peripheral sensitiza-
tion of primary afferents play a role in neuropathic pain?
In: Campbell JN, et al. (eds) Emerging strategies for the
treatment of neuropathic pain. IASP Press, Seattle, pp
8–102
4. Matthews RD, Anthony T, Kim LT, Wang J, Fitzgibbons RJ
Jr, Giobbie-Hurder A, Reda DJ, Itani KM, Neumayer LA;
Veterans Affairs Cooperative 456 Studies Program Investi-
gators (2007) Factors associated with postoperative com-
plications and hernia recurrence for patients undergoing
inguinal hernia repair: a report from the VA Cooperative
Hernia Study Group. Am J Surg 194:611–617
5. Gordh T, Chu H, Sharma HS (2006) Spinal nerve lesion
alters blood-spinal cord barrier function and activates
astrocytes in the rat. Pain 124:211–221
6. Tegeder I, Costigan M, Griffin RS, et al. (2006) GTP cyclohy-
drolase and tetrahydrobiopterin regulate pain sensitivity
and persistence. Nat Med 12:1269–1277
7. Salcedo-Wasicek MC, Thirlby RC (1995) Postoperative
course after inguinal herniorrhaphy. A case-controlled
comparison of patients receiving workers’ compensa-
tion vs patients with commercial insurance. Arch Surg
130:29–32
8. Courtney CA, Duffy K, Serpell MG, O’Dwyer PJ (2002)
Outcome of patients with severe chronic pain following
repair of groin hernia. Br J Surg 89:1310–1314
9. Tegeder I, Adolph J, Schmidt H, Woolf CJ, Geisslinger G,
Lötsch J (2008) Reduced hyperalgesia in homozygous
carriers of a GTP cyclohydrolase 1 haplotype. Eur J Pain
12:1069–1077
10. Bay-Nielsen M, Nilsson E, Nordin P, Kehlet H; Swedish Her-
nia Data Base; the Danish Hernia Data Base (2004) Chronic
pain after open mesh and sutured repair of indirect ingu-
inal hernia in young males. Br J Surg 91:1372–1376
20
Discussion
Kehlet: You suggested that there was a difference
in pain compliance comparing mesh repair and
suture repair. You may remember that we have col-
laboration between the Danish and Swedish Her-
nia Data base with a very detailed questionnaire
that also compared young male who are at highest
risk with Shouldice repair and Lichtenstein repair.
And in 2000 patients there were no differences
between this two techniques regarding chronic
inguinal pain.
Smeds: I think that there is no difference for the
majority of patients. But in this database there
were only a few patients who have had mesh
repair. I think that in case of suture repair the pa-
tients have had comparable postoperative pain in
general. Only some of them have had more pain,
what may be related to a nerve lesion.
Hopf: Have you investigated whether there is a
difference regarding postoperative pain comparing
local to general anesthesia? Did any of the patients
get ketamin, because there are some data that sug-
gested that patients who get ketamin are of high
risk to develop postoperative pain.
Smeds: All patients were operated using local an-
esthesia. And we never used ketamin in our pa-
tients.
Schumpelick: In my opinion your main message
is, that you have a relation of age and pain. Why is
it so? Is it because of the nerve function? Is it the
tolerance to pain? Is it experience of the patients?
Smeds: We have to listen to those colleagues who
are working on the problem of dorsal ganglion
routes. May be there are mutations in the gene that
processes the enzyme that forms the tetrahydro-
biopterine. This is the first hint that there may be
a genetically determined level of pain. I think that
we will get much more information about the pro-
cess of pain, and I think that it is individually dif-
ferent. However, I think that the preoperative pain
score is very important to identify those patients
who are of high risk of developing postoperative
pain.
 21

Chronic Pain After Inguinal

Hernia Repair
H. Kehlet, E. K. Aasvang
 164 Chapter 21 · Chronic Pain After Inguinal Hernia Repair

Introduction
Preop. pain
21 intensity
There is now general agreement, based on data
from randomised trials comparing different surgical
techniques and larger amounts of epidemiological
Genetics Psyche
data, that chronic pain influencing daily activities
may occur in 5–10% of patients [1–5]. Because little
scientific data exist on evidence-based treatment
of persistent postherniotomy pain, this undesirable
outcome probably represents the most important Acute Surgical
one for improvement in groin hernia repair. postop. pain trauma
The main focus for future research on the
pathogenesis and treatment of chronic post-
herniotomy pain is the role of patient-related ver- Nerve injury
sus surgery-related factors [5] (⊡ Fig. 21.1). This
report gives a short update on recent developments
concerning the pathogenic mechanisms listed in ⊡ Fig. 21.1. Pathogenic mechanisms of persistent pain after
groin hernia repair
⊡ Fig. 21.1. Other factors such as age (decreased
risk of chronic pain), female gender, and surgery
for a recurrent hernia are other well-documented
risk factors [3]; however, these cannot be altered. cation into different risk groups when comparing
different surgical techniques or pharmacological
interventions.
Preoperative Pain

The preoperative intensity of groin pain is a well- Psychological Factors

documented risk factor for developing a persistent
pain state [1, 3, 6] and corresponds to a similar
documented risk following other surgeries [7].
Importantly, remote preoperative pain–i.e., pain
in parts of the body other than the groin–has
also been demonstrated to correlate with persistent
pain, both in groin hernia repair [6, 8, 9] and other
operations [7, 10]. These findings suggest that the
preoperative functional level of the nociceptive
system is an important risk factor, and several
studies have shown a positive correlation between
the pain response to a preoperative nociceptive
stimulus (heat, electrical, cold) [7] and the acute
postoperative pain response, which otherwise has
been demonstrated to correlate with the risk of
developing a persistent pain state [1, 7].
In summary, preoperative pain states and the
level of nociceptive function are well documented
as being important risk factors for developing a
persistent pain state. They should therefore be
included and assessed in all future pain trials,
thereby providing possibilities for patient stratifi-
Preoperative anxiety and depression are well-
known characteristics of patients with chronic
nonmalignant pain and have been demonstrated
to be risk factors for acute pain states [7]. However,
in pain after groin hernia repair, depression and
anxiety were present in few (about 5%) patients
[11] and may therefore not be considered impor-
tant risk factors compared with other postsurgical
persistent pain states in which malignancy, ampu-
tation, etc., may contribute to impaired psychoso-
cial functioning. Nevertheless, preoperative assess-
ment of anxiety and depression should be included
in future high-level scientific studies on chronic
postherniotomy pain.
Acute Postoperative Pain
As mentioned above, in several operations, in-
cluding groin hernia repair, a well-documented
relationship exists between the intensity of the
Chapter 21 · Chronic Pain After Inguinal Hernia Repair
acute postoperative pain response and the risk
of developing persistent pain [7]. For example, a
large consecutive series with well-defined multi-
modal preemptive analgesia (including local an-
aesthesia, nonsteroidal anti-inflammatory drugs,
and paracetamol) showed a threefold higher risk
of chronic pain for patients with moderate to se-
vere early postoperative pain compared to those
with no or low-intensity acute postoperative pain
[12]. Consequently, these and other findings [7]
have led to the hypothesis that improved early
postoperative pain treatment may reduce the risk
of chronic pain (the concept of preemptive an-
algesia). However, so far the data are negative
[7] and instead seem to suggest that the acute
postoperative pain response is determined by the
preoperative function of the nociceptive system,
and thereby also the risk of persistent pain. Nev-
ertheless, there is a need for further randomised
studies, with more effective and prolonged acute
pain treatment, on the risk of developing a persis-
tent pain state.
Nerve Injury
A main pathogenic mechanism for persistent post-
surgical pain states is intraoperative nerve injury
[7]. Obviously, with the three nerves passing the
surgical field in groin hernia repair, there is a sig-
nificant risk of nerve injury. Several studies have
previously reported numbness after groin hernia
repair; unfortunately, these reports did not use
well-described, specific assessments of sensory dis-
turbances as a sign of nerve injury, thereby limit-
ing interpretation. This also includes studies com-
paring laparoscopic versus open repairs. A recent
detailed study using the gold standard quantitative
sensory assessment (QST) [11] in patients with
and without persistent groin hernia pain, includ-
ing patients who had bilateral repair, demonstrated
that persistent postoperative sensory dysfunctions
had a very low specificity for chronic pain, indi-
cating that nerve damage occurs often, even in
patients without chronic pain. However, signs of
neuroplasticity with more frequent and intense
pain after repetitive punctuate and brush stimula-
tion were observed only in chronic pain patients
165 21
[11]. These findings confirm that nerve damage
may be a prerequisite for developing a persistent
pain state after groin hernia repair. However, cor-
responding to findings from other surgical proce-
dures [7], factors other than nerve damage, includ-
ing genetic factors, may contribute to persistent
pain (see below).
All future studies on persistent pain after groin
hernia repair should include preoperative and
postoperative detailed neurophysiological assess-
ment in order to evaluate the relative importance
of different pathogenic mechanisms. This is espe-
cially important for all studies comparing different
surgical techniques such as laparoscopic versus
open repairs, type of mesh, fixation techniques,
and so on.
Surgical Trauma
As mentioned above, surgical injury to one or all
of the three groin nerves may occur frequently,
although all efforts should be made to identify
and preserve these nerves, as discussed in other
chapters in this book. Consequently, the surgical
technique may be important for preventing or
reducing a persistent pain state. However, so far
the literature is not entirely conclusive regard-
ing laparoscopic versus open repair, type of mesh
(composition, lightweight versus heavyweight),
and different fixation techniques. One reason may
be that for each of these topics the other variables
have not been well described, which especially ap-
plies to studies comparing laparoscopic and open
repairs. Ideally, the risk of nerve injury should
be reduced in laparoscopic repair without mesh
fixation–but most reports have insufficiently de-
scribed the fixation technique and its risk in terms
of nerve injury.
Prospective ongoing studies that include all
risk factors (preoperative, intraoperative, and
postoperative) in collaboration with Copenhagen
and Stuttgart and with detailed QST assessments
have completed patient inclusion and 6 months of
follow-up. It is hoped that the data will be able to
clarify the effects of high-expertise laparoscopic
repair without mesh fixation versus high-expertise
open Lichtenstein repair.
 166 Chapter 21 · Chronic Pain After Inguinal Hernia Repair
In summary, there is no doubt that the surgi-
21 cal technique is important for avoiding the risk of
nerve damage, especially when mesh may cause
compression of the nerves [13, 14]. Future trials
are called for, and they need to include high-qual-
ity assessment of the signs of nerve damage when
comparing different techniques.
Genetic Factors
Based on the findings from a variety of surgical
procedures, only a fraction of patients with docu-
mented intraoperative nerve injury develop a per-
sistent pain state [7, 11]. Recent studies with geno-
type characterisation have suggested that COMT
genes are important for pain sensitivity [15] and
that GTP-cyclohydrolase regulates pain sensitivity
in normal subjects and pain-related outcomes after
spinal surgery [16]. Genes controlling the function
of the voltage-gated sodium channel are also im-
portant [15]. Although this is a developing field of
pain research, all future high-level scientific stud-
ies on persistent groin hernia pain should include
characterisation of the genetic architecture of pain
perception to provide further understanding of the
mechanisms and risk factors for persistent groin
hernia pain. Unfortunately, no data are available
so far.
Summary
The pathogenic mechanisms of chronic pain after
groin hernia repair are definitely of multifactorial
origin [5], and previous efforts to classify the syn-
dromes into neuropathic versus nonneuropathic
(inflammatory) pain [17] may not be founded on
clear-cut diagnostic criteria. Thus, nerve injury
after groin hernia repair occurs very frequently
but leads to a chronic pain state in only a fraction
of patients. However, since nerve injury seems to
be a prerequisite for developing persistent pain, all
efforts should be made to develop and character-
ise surgical techniques to avoid peripheral nerve
injury. It is hoped that future studies will include a
complete characterisation of all pathogenic mech-
anisms–something that has not happened before
in the large number of studies with chronic pain
as an outcome [5]. Such characterisation must also
be included in future trials on pharmacological
treatment [7] as well as in studies on surgical treat-
ment with neurectomy and mesh removal [14] and
where preliminary data with detailed neurophysi-
ological characterisation and functional outcomes
suggest such techniques to reduce chronic pain in
some, but not all, patients [18].
References
1. Aasvang E, Kehlet H. Chronic postoperative pain: the case
of inguinal herniorrhaphy. Br J Anaesth 2005; 95:69–76
2. Nienhuijs S, Staal E, Strobbe L, Rosman C, Groenewoud H,
Bleichrodt R. Chronic pain after mesh repair of inguinal
hernia: a systematic review. Am J Surg 2007; 194:394–400
3. Franneby U, Sandblom G, Nordin P, Nyren O, Gunnarsson
U. Risk factors for long-term pain after hernia surgery. Ann
Surg 2006; 244:212–219
4. Ferzli GS, Edwards E, Al-Khoury G, Hardin R. Posthernior-
rhaphy groin pain and how to avoid it. Surg Clin North Am
2008; 88:203–209
5. Kehlet H. Chronic pain after groin hernia repair. Br J Surg
2008; 95:135–136
6. Wright D, Paterson C, Scott N, Hair A, O’Dwyer PJ. Five-
year follow-up of patients undergoing laparoscopic or
open groin hernia repair: a randomized controlled trial.
Ann Surg 2002; 235:333–337
7. Kehlet H, Jensen TS, Woolf CJ. Persistent postsurgical pain:
risk factors and prevention. Lancet 2006; 367:1618–1625
8. Courtney CA, Duffy K, Serpell MG, O’Dwyer PJ. Outcome
of patients with severe chronic pain following repair of
groin hernia. Br J Surg 2002; 89:1310–1314
9. Aasvang EK, Mohl B, Bay-Nielsen M, Kehlet H. Pain rela-
ted sexual dysfunction after inguinal herniorrhaphy. Pain
2006; 122:258–263
10. Brandsborg B, Nikolajsen L, Hansen CT, Kehlet H, Jensen
TS. Risk factors for chronic pain after hysterectomy: a
nationwide questionnaire and database study. Anesthesi-
ology 2007; 106:1003–1012
11. Aasvang EK, Brandsborg B, Christensen B, Jensen TS, Keh-
let H. Neurophysiological characterization of posthernio-
tomy pain. Pain 2008; 137:173–181
12. Callesen T, Bech K, Kehlet H. Prospective study of chronic
pain after groin hernia repair. Br J Surg 1999;86: 1528–
1531
13. Demirer S, Kepenekci I, Evirgen O, Birsen O, Tuzuner A,
Karahuseyinoglu S, Ozban M, Kuterdem E. The effect of
polypropylene mesh on ilioinguinal nerve in open mesh
repair of groin hernia. J Surg Res 2006; 131:175–181
14. Amid PK, Hiatt JR. New understanding of the causes and
surgical treatment of postherniorrhaphy inguinodynia
and orchalgia. J Am Coll Surg 2007; 205:381–385
Chapter 21 · Chronic Pain After Inguinal Hernia Repair
15. Diatchenko L, Nackley AG, Tchivileva IE, Shabalina SA,
Maixner W. Genetic architecture of human pain percep-
tion. Trends Genet 2007; 23:605–613
16. Tegeder I, Costigan M, Griffin RS, Abele A, Belfer I, Schmidt
H, Ehnert C, Nejim J, Marian C, Scholz J, Wu T, Allchorne A,
Diatchenko L, Binshtok AM, Goldman D, Adolph J, Sama S,
Atlas SJ, Carlezon WA, Parsegian A, Lotsch J, Fillingim RB,
Maixner W, Geisslinger G, Max MB, Woolf CJ. GTP cyclohy-
drolase and tetrahydrobiopterin regulate pain sensitivity
and persistence. Nat Med 2006; 12:1269–1277
17. Loos MJ, Roumen RM, Scheltinga MR. Classifying posther-
niorrhaphy pain syndromes following elective inguinal
hernia repair. World J Surg 2007; 31:1760–1765
18. Aasvang EK, Kehlet H. The effect of mesh removal and
selective neurectomy on persistent postherniotomy pain.
Ann Surg 2009; 249:327–334
Discussion
Deysine: Within the population that I operated
there were a lot of young people for instance teenag-
ers. Within this population there was a lot incidence
of drug intake before surgery. In my opinion this
is an important factor in developing postoperative
pain. Did you consider such things in your study?
Kehlet: We know that the management of acute
pain is very difficult in such patients. However, I
have never seen such a problem of drug addiction
in patients operated because of an inguinal hernia.
We don´t have such patients in Denmark, but I
think that this could be a risk factor as well.
Schumpelick: Could you give us some more re-
marks about »pain genes«. This seems to be a very
new story and we want to know a little bit more
about that.
Kehlet: I showed you the references of the two best
candidates that may be important »pain genes«.
In mouse and rat studies there were a lot of more
possible candidate genes. But the two mentioned
genes are the only genes that were also found to be
of interest in humans. One of it was found in fac-
tory workers who were analyzed for chronic man-
dibular pain. And after some years they could pre-
dict those who are of risk to develop this chronic
pain syndrome. But what we have to do in the
future is to combine all the different characteristics
of all »pain genes«. At the moment we were at an
early stage we have not enough information that it
would be relevant for clinical praxis.
167 21
O’Dwyer: Any statements regarding the fact that
every patient with chronic pain has some sort of
sensory deficit? What is your experience with tes-
ticular pain, because 15% of our patients develop
specific testicular pain?
Kehlet: Specific testicular pain is quite rare. But we
have not analyzed it in the current study. However,
we have to do this statistical comparison, because
we included all this data in our data base.
Song-Zhang Ma: Chronic pain is a severe prob-
lem. In China inguinal hernia repair using mesh
materials is performed 150.000 times per year. But
so far I have just a very few reports on postopera-
tive pain. What do you think is the reason? Is this
because of the tolerance of pain?
Kehlet: There could be several explanations. One
could be that patients in China have a different
genetic profile. Another reason could be that you
really have not asked your patients about discom-
fort and postoperative pain. We have had this
hernia meeting several times before, and we have
never talked about chronic postoperative pain. We
didn’t talk about it because we didn´t realized such
problems.
Song-Zhang Ma: I totally agree. Before the opera-
tion we talk about recurrence and infection, but we
didn’t talk about chronic postoperative pain in
detail.
Amid: Few patients following inguinal hernia re-
pair develop specific testicular pain. We did an
investigation that this problem could be related to
the fact that the nerves were involved in the lamina
propria of the vas deference. We have just 12 cases,
therefore it is not enough to make a conclusion,
but it is a very significant finding.
Kehlet: I agree.
Schumpelick: Is there a correlation between in-
come and development of postoperative pain?
Kehlet: There are many factors to consider, how-
ever actually I cannot comment on this. But this is
the reason why we should have a detailed charac-
terization of our patients.
 22

What Do We Know About the

Pathophysiology and Pathology
of Neuropathic Pain?
P. L. Jansen, K. Bas, D. Kämmer
 170 Chapter 22 · What Do We Know About the Pathophysiology and Pathology of Neuropathic Pain?
Introduction
After hernia surgery, severe chronic pain is re-
22 ported in up to 10% of the patients. The treatment
of these patients using neurectomy, mesh explanta-
tion, and symptom control by administration of
analgesics frequently fails and hints at a neuro-
pathic pain syndrome, at least in a subgroup of
patients. Neuropathic pain syndromes are caused
by irreversible changes of the nervous system.
For postoperative neuropathic pain, inflamma-
tion as well as nerve degeneration and pathologi-
cal regeneration are the underlying pathological
mechanisms that precede these central nervous
changes. Advances in understanding the periph-
eral pathophysiological mechanisms are neces-
sary to develop sufficient tools for preventing and
treating neuropathic pain. A pathophysiological
reclassification could provide a new basis for tar-
geted and individualized therapy of patients with
chronic pain after hernia therapy.
Neuropathic Pain
Neuropathic pain is defined as chronic, not self-
limiting pain that can occur after any lesion or
dysfunction of the peripheral or central nervous
system. In contrast to nociceptive and inflam-
matory pain, neuropathic pain has no protective
function and arises by inadequate stimulation of
the peripheral sensory endings [1]. Etiology-based
classifications of painful peripheral neuropathies
include syndromes caused by generalized lesions
of the peripheral nervous system (e.g., polyneu-
ropathies), complex neuropathic disorders (e.g.,
complex regional pain syndromes), and syndromes
caused by focal or multifocal lesions of peripheral
nerves (e.g., postsurgical pain syndromes) [2].
Based on this definition, we can expect neu-
ropathic pain after any surgical intervention, at
least in a subgroup of patients, and even when the
operating field is in close proximity to peripheral
nerves. Indeed, we can observe neuropathic pain
syndromes after Shouldice, Lichtenstein, and even
laparoscopic hernia repair [3]. Neuropathic pain has
to be clearly separated from chronic pain caused by
neuroma formation following nerve injury or affec-
tion of nerves due to mesh-induced foreign body
reaction. For the latter, surgical intervention can be
successful. In contrast, neuropathic pain is associ-
ated with irreversible neuronal changes; therefore,
surgical treatment by neurectomy or mesh explan-
tation may be insufficient [4].
Pathophysiology of Neuropathic Pain
Inflammation, degeneration of nerve fibers, repa-
ratory mechanisms of neural tissue, and the reac-
tion of the connective tissue lead to hyperexcit-
ability in primary afferent nociceptors [2]. The
hyperactivity in nociceptors that is called periph-
eral sensitization induces secondary changes in
processing neurons in the spinal cord and brain
that amplify the state of hyperexcitability and lead
to central sensitization. Normally, these sensitiza-
tion phenomena are limited until the tissue heals
and the inflammation subsides. However, when
primary afferent function is altered permanently,
the state of hyperexcitability persists (⊡ Fig. 22.1).
The resulting clinical signs are the spontaneous
pain, allodynia, and hyperalgesia that are charac-
teristic for patients with neuropathic pain.
A simple focal peripheral nerve injury causes
a variety of changes in the nervous system, which
can all contribute to the persistence of pain and
abnormal sensation. We can observe changes in
the peripheral primary afferent neurons as well
as in the central nervous system. These changes
include upregulation of sodium channels and spe-
cific receptors as well as synthesis and secretion of
cytokines and neurotransmitters, leading to ectopic
impulse generation, reduced activation threshold,
or increased synaptic transmission. At the central
nervous system, the loss of intraspinal inhibition
due to the death of inhibitory interneurons plays a
crucial role [2, 5].
These neuronal changes are independent from
the underlying disease, and the same neuronal
mechanisms are responsible for neuropathic pain
after hernia repair as for other pain syndromes.
Because several mechanisms can cause a specific
pain symptom, a combined therapy is often more
promising than a single one. Peripheral and central
neuronal changes are the common track for neu-
Chapter 22 · What Do We Know About the Pathophysiology and Pathology of Neuropathic Pain?
⊡ Fig. 22.1. Pathophysiology of neuropathic pain (BMI body mass index)
ropathic pain syndromes, but pathophysiological
changes at the site of peripheral nerve injury pre-
cede these neuronal changes.
Inflammation in Neuropathic Pain
Recent publications hint at a pivotal role of the
inflammatory reaction for the development of
neuropathic pain. After tissue injury, mast cells,
macrophages, T-cells, neutrophils, and Schwann
cells are activated and infiltrate from endoneural
blood vessels into the nerve (⊡ Fig. 22.2) [6]. They
secrete huge amounts of cytokines, nerve growth
factors, and proteases. These mediators induce ec-
topic activity via receptor-mediated actions on af-
ferent nerve fibers. Although the impact of nerve
inflammation on neuronal changes has not been
clarified in detail, it is known that the inflamma-
tory reaction after nerve injury initiates and main-
tains sensory abnormalities [2, 6].
Macrophages are key cells after nerve injury.
Barclay et al. found that the depletion of mac-
rophages attenuates the mechanical hyperalgesia
after peripheral nerve lesions in rats [7]. In a
171 22
preliminary study, we investigated a potential role
of macrophages for neuropathic pain in hernia pa-
tients. In contrast to healthy nerves obtained from
pigs, infiltrating macrophages were frequently de-
tected in neurectomy specimens from hernia pa-
tients with chronic pain (⊡ Fig. 22.2). The expres-
sion of matrix metalloproteinase 2 (MMP-2), a
pivotal mediator of macrophages, is also enhanced,
especially in the endoneurium. A role of MMPs in
the development of neuropathic pain after spinal
nerve ligation was demonstrated recently in rats
and mice by Kawasaki et al. [8]. MMP-9 showed
rapid upregulation in injured dorsal route gangli-
ons, whereas MMP-2 was responsible for the late
phase of neuropathic pain and was upregulated in
primary afferent neurons as well as in the dorsal
horn.
This study demonstrated for the first time
that peripheral processes do not occur in isolation
from central neuroinflammation. The separation
between early-phase and late-phase neuropathic
pain mechanisms can lead to important clinical
implications, such as the development of tools
for preventing and treating neuropathic pain. Ka-
wasaki et al. [8] demonstrated that the develop-
 172 Chapter 22 · What Do We Know About the Pathophysiology and Pathology of Neuropathic Pain?
22
⊡ Fig. 22.2. Immunohistochemistry of CD68 (macrophages) and MMP-2 in ilioinguinal nerve specimens from pigs and chronic
pain patients after hernia therapy. Magnification ×200
ment of pain hypersensitivity could be inhibited by
the administration of MMP inhibitors and small
interfering RNA in MMP knockout mice. Inter-
estingly, a role of MMP-2 is also well known to
support mesh-induced chronic foreign body reac-
tion. Mesh implantation in animal models induces
excessive MMP-2 gene transcription and activity
mediated by infiltrating macrophages, and this
pathway may also contribute to the development
of neuropathic pain.
The Role of Fibrosis in Neuropathic
Pain
Next to the inflammatory reaction, nerve injury
activates Schwann cells and fibroblasts. These cells
synthesize fibronectin and, later on, collagens and
are responsible for changes in the extracellular
matrix. The common understanding is that the
fibrotic reaction around the nerve can affect nerve
fibers and lead to the retraction or compression of
nerves by compromising proper function of this
so-called perineurium. Additionally, the fibrotic
reaction can lead to obliteration of Schwann cell
tubes and block axon regeneration or lead to mis-
sprouting of axons, resulting in the formation of
neuromas at the end of injured nerve fibers or
even intraneurally. The extraneural conditions can
be successfully treated by surgical intervention.
In contrast, the composition of the endoneu-
rium can be disturbed after nerve injury. Salonen
et al. analyzed the fibrotic reaction after sciatic
nerve transaction in rats. They found increased
expression of fibronectin and collagens, especially
type III collagen in the endoneurium [9]. Similarly,
we could detect a distinct expression of type I and
type III in nerve specimens from chronic pain pa-
tients (⊡ Fig. 22.3).
Although the impact of a disturbed endoneu-
ronal collagen expression on neuronal changes is
not yet clarified, these changes may be involved in
the induction of ectopic activity of injured primary
afferent nociceptors as well as of spared fibers.
Chapter 22 · What Do We Know About the Pathophysiology and Pathology of Neuropathic Pain?
⊡ Fig. 22.3. Endoneural distribution of type I collagen (red) and type III collagen (green) in neurectomy specimens of chronic
pain patients after hernia therapy. Sirius red staining, magnification ×200
Furthermore, our preliminary data hint at an indi-
vidual reaction to nerve injury.
The Impact of Risk Factors on Neuro-
pathic Pain
In some but not all patients, the nerve lesion trig-
gers molecular changes in nociceptive neurons,
which become abnormally sensitive and develop
pathological spontaneous activity. Several studies
have shown that individual risk factors have an
impact on the development of neuropathic pain.
Major risk factors are age younger than 40 years,
preexisting preoperative pain, severe postopera-
tive pain, and male gender [10–14]. We confirmed
these results in patients who had mesh explanta-
tion either because of chronic pain or reoperation
for hernia recurrence. In our cohort, we found
that age under 50 and body mass index less than 25
were significantly associated with chronic pain. To
determine the tissue reaction in these two groups,
we further analyzed the inflammatory reaction
and found that the young patients who were at
risk for developing chronic pain had significantly
enhanced infiltration of macrophages after mesh
implantation compared with older patients.
173 22
Summary and Outlook
Inflammation, fibrosis, and neuronal regenera-
tion can lead to complex changes in the function,
chemistry, and structure of neurons and glial cells.
These mechanisms are independent from the un-
derlying disease and can occur after any surgical
intervention, even after hernia therapy. Patient-
related risk factors can be additional disturbing
factors in the complex system of pain perception.
Though major progress has been made in the
understanding of cellular and molecular changes af-
ter nerve injury, their relevance for the pathophysi-
ology of pain in neuropathies after hernia therapy
has yet to be determined. A mechanism-based
approach for treating neuropathic pain provides
hope for safer and more specific therapies.
References
1. Treede R-D, Jensen TS, Campbell JN, Cruccu G, Dostrovsky
JO, Griffin JW, Hansson P, Hughes R, Nurmikko T, Serra J:
Neuropathic pain: redefinition and a grading system for
clinical and research purposes. Neurology 2008, 70:1630–
1635
2. Baron R: Mechanisms of disease: neuropathic pain–a clini-
cal perspective. Nat Clin Pract Neurol 2006, 2:95–106
 174 Chapter 22 · What Do We Know About the Pathophysiology and Pathology of Neuropathic Pain?
3. Franneby U, Sandblom G, Nordin P, Nyren O, Gunnarsson
U: Risk factors for long-term pain after hernia surgery. Ann
Surg 2006, 244:212–219
4. Kehlet H: Chronic pain after groin hernia repair. Br J Surg
22 2008, 95:135–136
5. Woolf CJ, Mannion RJ: Neuropathic pain: aetiology, sym-
ptoms, mechanisms, and management. Lancet 1999,
353:1959–1964
6. Thacker MA, Clark AK, Marchand F, McMahon SB: Patho-
physiology of peripheral neuropathic pain: immune cells
and molecules. Anesth Analg 2007, 105:838–847
7. Barclay J, Clark AK, Ganju P, Gentry C, Patel S, Wother-
spoon G, Buxton F, Song C, Ullah J, Winter J, Fox A, Bevan
S, Malcangio M: Role of the cysteine protease cathepsin S
in neuropathic hyperalgesia. Pain 2007, 130:225–234
8. Kawasaki Y, Xu ZZ, Wang X, Park JY, Zhuang ZY, Tan PH,
Gao YJ, Roy K, Corfas G, Lo EH, Ji RR: Distinct roles of mat-
rix metalloproteases in the early- and late-phase develop-
ment of neuropathic pain. Nat Med 2008, 14:331–336
9. Salonen V, Lehto M, Vaheri A, Aro H, Peltonen J: Endoneu-
rial fibrosis following nerve transection. An immunohisto-
logical study of collagen types and fibronectin in the rat.
Acta Neuropathol 1985, 67:315–321
10. Kehlet H, Jensen TS, Woolf CJ: Persistent postsurgical pain:
risk factors and prevention. Lancet 367:1618–1625
11. Aasvang E, Kehlet H: Chronic postoperative pain: the case
of inguinal herniorrhaphy. Br J Anaesth 2005, 95:69–76
12. Matthews RD, Anthony T, Kim LT, Wang J, Fitzgibbons Jr
RJ, Giobbie-Hurder A, Reda DJ, Itani KMF, Neumayer LA:
Factors associated with postoperative complications and
hernia recurrence for patients undergoing inguinal hernia
repair: a report from the VA Cooperative Hernia Study
Group. Am J Surg 2007, 194:611–617
13. Poobalan AS, Bruce J, Smith WC, King PM, Krukowski ZH,
Chambers WA: A review of chronic pain after inguinal
herniorrhaphy. Clin J Pain 2003, 19:48–54
14. Nienhuijs S, Staal E, Strobbe L, Rosman C, Groenewoud H,
Bleichrodt R: Chronic pain after mesh repair of inguinal
hernia: a systematic review. Am J Surg 2007, 194:394–
400
Discussion
Penkert: Do you agree that we have no data that
a certain number of patients develop neuropathic
pain? And please comment on what has been men-
tioned before: Influences the kind of preoperative
drug medication – especially morphium like medi-
caments – the incidence of chronic postoperative
pain following groin hernia repair?
Lynen-Jansen: I totally agree. In the literature con-
cerning the pathophysiology of neuropathic pain,
the authors focus on just one special mechanism.
They focus on fibrosis, they focus on inflammation
or they focus on neuronal changes. Unfortunately
I have no personal experience of preoperative drug
medication and the development of postoperative
pain.
Deysine: You mentioned that there were patho-
logically changes in nerves occurring at this kind
of surgery. But this would mean that the surgeon
physically contacts the nerves. Neurosurgeons par-
ticularly touch nerves just with glass-electrodes.
And we retract nerves while the operation and
touch them with metal instruments. In my opin-
ion the physical contact to the nerves has to be
avoided.
Lynen-Jansen: I totally agree. But I also think it is
a lucky situation if you can avoid contact to a nerve
physically. But injury to the nerves are also pos-
sible by stretching them, especially if you don´t see
them while the operation.
Kehlet: What you mentioned about continuous
development of chronic pain is in contrast to what
we have published. In our studies the pain inci-
dence increases. We have very few prospective data
concerning chronic pain however can you com-
ment on your different findings.
Lynen-Jansen: In my opinion these were only data
in case of mesh implantation. Additionally it was
a retrospective study and therefore it was not so
easy to determine the time point when the pain
occured exactly for the first time.
Köckerling: In case of a patient in later course after
an endoscopic hernia repair, you have to watch
carefully for a recurrence or another morphologi-
cal reason for the pain. I have never seen a patient
with chronic pain without a morphological cause
of chronic pain.
Lynen-Jansen: I totally agree, again this study has
its natural limitations because it was a retrospec-
tive study.
Smeds: Do you have any biological data that would
explain the correlation between pain and age?
Lynen-Jansen: At the moment we just have the
preliminary immunohistochemical investigations
and therefore no satisfying answer for your ques-
tion. But we have some data that the inflammatory
reaction in young patients is different compared
to elder patients. A lot of biological reactions in
younger people are more aggressive, even the in-
Chapter 22 · What Do We Know About the Pathophysiology and Pathology of Neuropathic Pain?
175 22
flammatory reaction. But the main question is,
why do some young patients develop postoperative
chronic pain and why other not. The answer could
be that we have a multifactorial impaired disease.
Stumpf: I want to comment on your immunohis-
tochemical data and on what Dr. Deysine said. It is
not a problem of how to handle the nerve, because
we did this investigation in nerves that we have
never touched before explanation. We explanted
the nerves in case of retroperitoneal neurectomies.
In my opinion it is rather a preexisting disorder
than a consequence of a physical never contact.
Schumpelick: Are there any differences comparing
the two groups in getting a recurrence of develop-
ing postoperative chronic pain?
Lynen-Jansen: In case of the explanted mesh mate-
rial we saw significant differences in the infiltra-
tion of macrophages in patients with chronic pain.
Franz: If you exclude the patients with a recur-
rence, where did you get the nerves from in the
pain free patients?
Lynen-Jansen: The two mentioned studies were
completely different.
 23

Surgical Trauma of Nerves–Causes

of Neuropathic Pain, Classification,
and Options in Surgical Therapy
G. Penkert
 178 Chapter 23 · Surgical Trauma of Nerves–Causes of Neuropathic Pain, Classification, and Options in Surgical Therapy
Introduction
With the introduction of microsurgical methods
applied to peripheral nerve lesions such as entrap-
ment syndromes, pseudoneuroma, and neuroma
formations, as well as lesions with nerve discon-
23 tinuity, the results of nerve surgery have signifi-
cantly improved over the last three to four decades.
But no real mental connection exists between these
successful microsurgical methods for improving or
even restoring nerve function and theories of the
origin of neuropathic pain. This type of hardly
treatable and, until now, not fully explained pain
often causes complete social disintegration of the
patient.
By means and results of microsurgery, we were
encouraged to apply these surgical improvements
to pain related to nerve trauma, but we faced limi-
tations that were difficult to overcome until today.
Experiences in neuromodulation continue to offer
new aspects, and quite recent reports on intraab-
dominal laparoscopic neuromodulation even seem
to offer a solution to painful pelvic nerves.
Microscopic Anatomy of the Peripheral
Nerve System
We regard the nerve axon as the smallest anatomi-
cal unit. The myelin sheath and its Swann cells
are located around the axon membrane. These
structures are enclosed in two or more layers:
one layer with latticed and the other with longi-
tudinal collagen and elastic fiber elements–the
endoneurium. A certain number of such nerve
fibers together with their individual endoneural
sheath are again surrounded by connective tissue–
the perineurium. Again, a certain number of such
bundles (fascicles) are grouped parallel to each
other, and they are again surrounded by connec-
tive tissue–the epineurium.
This group arrangement within peripheral
nerves changes its distribution from central levels
to the periphery. Additionally, individual cross-
connections between these fascicles and groups
of fascicles exist. Nerve roots consist of few but
thicker fascicles divided into sectors by small
membranes, whereas in the periphery, limb nerve
segments have a typical group arrangement with
three to five or more groups of fascicles. Closer
and closer to the periphery, these groups further
subdivide into many small single fascicles. This
special multifascicular structure is the one we also
find within the often painful inguinal nerves, in-
cluding the iliohypogastric, ilioinguinal, and gen-
itofemoral nerves.
Following nerve damage or even transection,
all of the elements constituting the nerve fiber,
axon, and myelin sheath degenerate from the level
of the lesion to the periphery. Our surgical efforts
now normally aim at establishing the best condi-
tions as possible so that these axons can sprout
again into the periphery and achieve their former
targets. Unfortunately, reconstructions of those
multifascicular and small nerves have tended to re-
sult in secondary neuromas at the coaptation sites;
the reason was aberration of all the small fascicles
at the coaptation site because of technical difficul-
ties despite magnification under the microscope.
Types and Degrees of Nerve Lesions
As the result of destructive effects on nerve tissue,
we can distinguish between lesions with and with-
out loss of continuity. In almost all cases, the ques-
tion of continuity of the involved nerve remains
unanswered. Two systems were therefore devel-
oped to describe the potential degrees of nerve
tissue lesion.
In 1943, Seddon established the concepts of
neurapraxia, axonotmesis, and neurotmesis accord-
ing to the degree of destructive forces on the nerve
tissue [18]. Neurapraxia refers to myelin sheath
degeneration within the affected nerve segment.
Axonotmesis is defined as a complete interruption
of the axon’s continuity. Neurotmesis, in contrast to
the other types of lesion, means a complete nerve
interruption. Cases of neurapraxia recover within
a few weeks if the forces that compress the nerve
are removed. Cases of axonotmesis recover within
several months depending on the distance between
lesion and target. Cases of neurotmesis cannot re-
cover, and the targets remain paralyzed.
But the prognosis of axonotmesis cases de-
pends on additional factors. In light of this, in
Chapter 23 · Surgical Trauma of Nerves–Causes of Neuropathic Pain
1951 Sunderland distinguished five degrees of le-
sion [20]. Today we consider his classification to
be more detailed and more suitable than Seddon’s
earlier one:
Grade 1: This grade is identical to Seddon’s
neurapraxia, and it refers to myelin sheath de-
generation restricted on a nerve segment due to a
slight trauma.
Grade 2: As a result of higher compressing
forces, the axons undergo Wallerian degeneration,
but each axon remains enclosed by its basal mem-
brane and endoneurium, and it is able, by axon
sprouting, to regain its former target.
Grade 3: Because of destructive forces on the
endoneurium, the process of axon resprouting is
partially hindered. On the other hand, mis-sprout-
ing leads to more extensive functional deficits:
Without endoneurium, motor axons may sprout
into a sensory pathway, or vice versa, and thus
achieve no function.
Grade 4: Because of disarranged perineurium,
the amount of mis-sprouting increases so exten-
sively that the recovery results after microneuroly-
sis are even more disappointing than with grades
2 and 3 lesions. Especially in cases of small skin
nerves as well as inguinal nerves, the intraneural
destructive effects are easily able to completely
block the axon sprouts, a situation that results in
a neuroma in continuity. This kind of lesion is
comparable to a total nerve interruption, with no
good prognosis as far as spontaneous recovery is
concerned.
Grade 5: This lesion is identical to Seddon’s
neurotmesis, a complete interruption of nerve
trunk continuity. It is associated with a terminal
neuroma at the proximal nerve stump 6–8 weeks
after the nerve trauma.
Secondary Connective Tissue Reactions
Following a nerve injury, not only nerve destruc-
tion but also secondary connective tissue reac-
tions start; histologically, these are well-known
processes referred to as fibrosis. The ensuing scar
tissue develops compressing forces and blocks the
axon-sprouting process. Considering all of these
secondary effects, in 1992 Millesi established a
179 23
classification of different fibrosis types [8]. It was
conceived from a surgical point of view, as Millesi
noted that the fibrosis could originate from quite
different parts of the connective tissue within
nerves. He classified fibrosis into types A–C, re-
garding the fact that only the epineurium, or the
interfascicular connective tissue, or even the in-
trafascicular connective tissue (the endoneurium)
could be involved in the fibrosis. This differentia-
tion became important because, due to this fibro-
sis, surgical limitations arise during microneuroly-
sis. An epineural fibrosis can be easily released by
a longitudinal incision. In contrast, an endoneu-
ral fibrosis limits our surgical efforts completely.
Nerve segments with intrafascicular fibrosis have
to be resected and reconstructed by grafting. Con-
sequently, the surgeon’s task during each operation
is to estimate the type of fibrosis and decide which
microsurgical method is suitable [13].
Microsurgical Options
In general, we distinguish between neurolysis and
nerve reconstruction, with the latter consisting of
either direct nerve suture or nerve grafting.
Both techniques today require a microscope
to guarantee gentle handling of the nerve tis-
sue. With magnification, the epineurium in intact
parts of the nerve proximal and distal to the
injured area can be incised longitudinally. After
that, the external sheath of the epineurium can
be removed. As a next step, individual groups of
fascicles are exposed and slightly separated from
each other. When approaching the injured nerve
segment, the surgeon should try to continue; if
that is not possible, he or she has to switch over to
repair. But at first, at the separated fascicle groups,
the surgeon should try to incise the perineurium
if scarred.
These microneurolysis steps are referred to as
epineurotomy, epineurectomy, and interfascicular
neurolysis. These different surgical steps can be
applied to limb nerves of sufficient caliber; how-
ever, the smaller in diameter the nerve is and the
more multifascicular, the greater the number of
limitations that will arise, particularly in cases of
skin nerves and inguinal nerves.
 180 Chapter 23 · Surgical Trauma of Nerves–Causes of Neuropathic Pain, Classification, and Options in Surgical Therapy
Nerves with loss of continuity or untreatable
intraneural fibrosis should be reconstructed if
possible. The approach to nerve repair that must
be implemented for these lesions changed in the
1960s [9]. The former nerve repair techniques in-
volved the epineural end-to-end suture, but histo-
23 logical studies showed that fibrosis and neuromas
developed on the suture side [3]. The develop-
ment of microsurgical grafting resulted in two
advantages: A more accurate approximation of
corresponding fascicles could be achieved [8, 16],
and restoration of nerve continuity without ten-
sion significantly reduced the amount of fibrosis
at the coaptation sites [10]. Despite the fact that
the axons had to overcome two coaptation sites
after grafting, the end results 40 years ago were so
encouraging that grafting became the method of
choice from then on [9]. In the meantime, all of
the mentioned principles of microsurgery became
well known.
Pain Associated with Nerve Lesions
In former decades, nerve surgeons were convinced
that these microsurgical principles could success-
fully be applied to pain related to nerve injury.
They believed that removal of the neuroma had
to be the solution in pain relief; resprouting of
sensory axons would sufficiently help nociceptive
afferents become stabilized by achieving their for-
mer targets. But this concept did not reliably work.
In 1981, a study on this subject described the high
failure rate of nerve resection and grafting to cure
the associated chronic nerve-related pain [12]. All
of the patients reported in this study underwent
reconstruction of the injured and painful nerve
segment by grafting of the sural nerve. Although
motor or sensory nerve function was successfully
restored in all seven patients, their pain returned
in the precise state and location as experienced
preoperatively. Today, mechanisms proximal to the
nerve lesion are recognized as responsible for the
recurrence of nerve-related pain, and we are even
aware of the risk of duplicating the pain [23].
Entrapment syndromes of limb nerves usually
cause a more or less bearable pain. The pain does
not remain restricted to the autonomous distribu-
tion area of the affected nerve; rather, it is diffuse,
and it disappears after nerve decompression [13].
This type of nerve-trunk-related pain is not a mat-
ter of discussion because a substantial intraneural
nerve lesion usually does not arise in an entrap-
ment situation.
Instead, we have to deal with nerves that (1) are
small in diameter, (2) predominantly contain sen-
sory fibers, (3) easily react with intraneural severe
fibrosis, and (4) additionally limit our microsurgi-
cal efforts while often being unfavorably localized.
In particular, these nerves tend to develop intrac-
table pain, and we need to strictly avoid attach-
ing the label »psychologically peculiar« to persons
with resistant pain of those nerves.
We are thus confronted with three potential
levels of pain:
1. Neuroma pain, a normally nonexistent pain
that occurs when triggered by palpation at
the location where sensory nerve fibers are
blocked from regrowing. Palpation thereby
causes an electric-current-like pain that the
patient localizes in the distribution area of the
injured nerve.
2. Hyperpathic pain, a normally nonexistent pain
of unbearable intensity if the skin in the distri-
bution area of the injured nerve is repeatedly
stimulated
3. Allodynia, a pain that is permanently present
as a burning sensation and that is triggered by
an innocuous stimulus
Both of the last two types of pain are also referred
to as neuropathic pain.
Neuroma pain appears about 6 weeks follow-
ing the nerve lesion because a neuroma needs
this time to develop. Consequently, neuroma pain
starts slowly and achieves a steady state weeks
later. In contrast, neuropathic pain (1) has a sud-
den onset, (2) appears rather early after the nerve
lesion, and (3) immediately achieves a steady
state.
Therefore, it is very important to evaluate all
the details of the patient’s anamnesis to estimate
his or her individual type of pain. It may be of ad-
ditional importance to assess the patient because in
the case of allodynia, you should be able to apply a
quite light stimulus to a small skin area to provoke
Chapter 23 · Surgical Trauma of Nerves–Causes of Neuropathic Pain
a highly painful sensation that spreads away from
the actual stimulus location. This special attribute,
by the way, may be the reason that we sometimes
cannot exactly differentiate which one of the ingui-
nal nerves is really affected. Unfortunately, the dis-
tribution areas of the iliohypogastric, ilioinguinal,
and genitofemoral nerves are located side by side,
and variations also exist [17, 21].
According to animal models and clinical stud-
ies, the following pathophysiological mechanisms
presumably contribute to the occurrence of neu-
ropathic pain:
▬ Continuous abnormal excitation of afferent
fibers due to ongoing compressing forces [1]
▬ Impaired intraneural microcirculation that
might induce ensuing ischemia and nerve
damage [11]
▬ An abnormal excitatory coupling between
sympathetic fibers and afferent nociceptive
fibers, especially within the spinal ganglion [6]
▬ Hindered or interrupted axonal transport in
both directions in the nerve fibers that may
result in loss of control of the biochemical ac-
tivity in the nerve cell body [4]
▬ Central alterations of electrophysiological
activities in an afferent neuron that may
spread transsynaptically to second-order and
higher-order neurons in the spinal cord and
brain [2]
In conclusion, the effects of nerve injury and nerve
damage are not confined to the site of the lesion,
as previously expected. Instead, neuropathic pain
seems to be a result of an earlier unexpected
central nervous plasticity [23], and it is addition-
ally influenced by individually different disposi-
tions. We have no theoretical basis to explain why
some patients, but not all, develop neuropathic
pain. Thus, different individual dispositions seem
to be responsible for the fact that identical nerve
lesions cause varying reactions. Experiments in
1980 on different types of rats revealed different
measurable amounts of autotomy following identi-
cal procedures on nerves. The authors concluded
that different genetic dispositions must exist [5].
The experience in hernia surgery presumably will
be that only some patients will sustain real neuro-
pathic pain following surgery [21].
181 23
Treatment Modalities for Painful
Nerves
Microsurgery
The above-mentioned microsurgical principles of
neurolysis and nerve repair are relevant only if
neuroma pain is present. As far as possible, the
type of pain has to be estimated preoperatively.
Nevertheless, there is a risk of about 30% of induc-
ing an ensuing neuropathic pain. This holds true
if nerves of trunk caliber are affected. But con-
sidering the particular difficulties with the small
abdominal wall nerves encountered in hernia sur-
gery, microsurgery on these nerves is more and
more out of discussion.
If a neuropathic pain is initially presented,
microsurgery even carries the danger of duplicat-
ing the pain level in the patient. Thus, regarding
neuropathic pain, our experience today is that
touching a nerve at the damaged site almost always
induces additional central nervous plasticity. This
experience holds true independent of the nerve
caliber.
Neurotomy
We understand neurotomy as nerve transection
proximal to the primary nerve lesion. Of course,
recurrent neuroma formation will always start
and stop about 6–8 weeks later. If the regrown
neuroma at the proximal nerve end is imbedded
within soft tissue, the risk of ongoing repeated
triggering may be reduced. If, for example, we
operate on Morton’s neuralgia, neurotomy via a
dorsal approach will be the only way to succeed
[13]. But patients with Morton’s neuralgia never
present with a neuropathic pain syndrome. On
the other hand, 27 of 29 laparoscopic »triple neu-
rotomies« of all three inguinal nerves have been
quite successful (N. Kleemann, personal com-
munication). Considering the experience with a
greater number of hyperpathic pain syndromes in
the inguinal area, these results seem to be in con-
trast to the above-mentioned thesis. The actual
impression, therefore, is that neurotomy at least
remains under discussion.
 182 Chapter 23 · Surgical Trauma of Nerves–Causes of Neuropathic Pain, Classification, and Options in Surgical Therapy
Neuromodulation
The idea of achieving pain relief by electrically
stimulating the dorsal columns of the spinal cord
(known as spinal cord stimulation or SCS) was
derived from the gate control theory by Melzack
23 and Wall in 1965 [7]. According to this concept,
stimulation of large afferent A-fibers of periph-
eral nerves should reduce the pain input to the
brain via the small unmyelinated and thinly my-
elinated C-fibers. Because the conduction veloc-
ity of A-fibers is faster than that of the C-fibers,
A-fibers were said to have the capacity to »gate
out« pain stimuli from transmission to the cortex
[7]. Currently, this technique is not only applied
on dorsal columns of the spinal cord but also
on peripheral nerves [19]. If technically pos-
sible, the epineurium of the nerve is pierced, and
a quadripolar electrode is pushed slightly into
the subepineural space a few centimeters distal
or proximal, depending on the affected nerve
and its availability [13]. After a test stimulation
period of a few days, the external screener is
changed to an internal subcutaneously placed
pacemaker.
In cases of painful involvement of very small
nerve branches that are not surgically accessible
for the above-mentioned direct nerve stimulation
(dPNS), and in cases of excessive scarring, the
treatment can consist of subcutaneous peripheral
nerve stimulation (sPNS). Here, the electrode
is percutaneously advanced to the location of
the assumed nerve damage. The intraoperative
test stimulation should induce pleasing paresthe-
sias in the distribution of the affected nerve.
This method often achieves a good response to
painful conditions of injured inguinal nerves
and even has an effect on the frequently associ-
ated localized tenderness in the area of the scar
tissue [22].
But the gold standard in the future may per-
haps be a laparoscopic approach. Possover and
colleagues reported on their recent experiences
applying these techniques to the intrapelvic course
of the inguinal nerves by a laparoscopic approach
[14, 15]. The great advantages of intraabdominal
or pelvic neuromodulation compared with neuro-
tomy are the following:
▬ No additional sensory loss, particularly if int-
raabdominal »triple neurotomies« (neurotomy
of all three inguinal nerves) are used
▬ No risk of inducing a neuropathic pain or du-
plicating the preexisting pain level
Conclusion
The scientific considerations of different types of
nerve lesions, secondary fibrosis, microsurgical
procedures, and the regeneration process after mi-
crosurgery were insufficient for solving the prob-
lem of nerve-related pain until today. A differen-
tiation of whether the patient presents with either
neuroma pain or neuropathic pain is of great im-
portance. Microsurgical methods, with their risks,
can be applied to neuroma pain, and neuromodu-
lation, which carries less risk but is dependent on
technical details, can be used for neuropathic pain.
In cases of affected inguinal nerves, laparoscopic
neuromodulation seems to be a reasonable techni-
cal solution in the future, whereas neurotomy is
under discussion as a high-risk procedure as far as
pain relief is concerned.
References
1. Bennett GJ, Xie Y-K (1988) A peripheral mononeuropathy
in rat that produces disorders of pain sensation like those
seen in man. Pain 33:87–107
2. Devor M (1988) Central changes mediating neuropathic
pain. In: Dubner R, Gebhart GF, Bond MR (Eds) Proceed-
ings of the 5th World Congress on Pain, vol 3. Elsevier,
Amsterdam, pp 114–128
3. Edshage S (1964) Peripheral nerve suture. Acta Chir Scand
(suppl) 331:1–104
4. Herdegen T, Fiallos-Estrada CE, Bravo R, Zimmermann M
(1993) Colocalisation and covariation of c-JUNtranscrip-
tion factor with galanin in primary afferent neurons with
CGRP in spinal motoneurons following transection of rat
sciatic nerve. Mol Brain Res 17:147–154
5. Inbal R, Devor M, Tuchendler O, Lieblick (1980) Autotomy
following nerve injury: genetic factors in the develop-
ment of chronic pain. Pain 9:327-337
6. Jänig W (1991) Sympathetic activity during peripheral
nerve injury. In: Besson JM, Guilbaud G (eds) Lesions of
primary afferent fibers as a tool for the study of clinical
pain. Elsevier, Amsterdam, pp 65–82
7. Melzack R, Wall P (1965) Pain mechanisms: a new theory.
Science 150:971–979
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8. Millesi H (1992) Chirurgie der peripheren Nerven. Urban
& Schwarzenberg, Munich
9. Millesi H, Meissl G, Berger A (1976) Further experiences
with interfascicular grafting of the median, ulnar, and
radial nerves. J Bone Joint Surg 58A:209–218
10. Millesi H, Meissl G (1981) Consequences of tension at
the suture site. In: Gorio A (ed) Posttraumatic peripheral
nerve regeneration; experimental basis and clinical impli-
cation. Raven Press, New York, pp 277–279
11. Myers RR, Yamamoto T, Yaksh TL, Powell HC (1989) The
role of focal ischemia and Wallerian degeneration in pe-
ripheral nerve injury producing hyperesthesia. Anesthesi-
ology 78:308–316
12. Noordenbos W, Wall PD (1981) Implications of the fail-
ure of nerve resection and graft to cure chronic pain
produces by nerve lesion. J Neurol Neurosurg Psychiat
44:1068–1073
13. Penkert G, Fansa H (2004) Peripheral nerve lesions.
Springer, Berlin
14. Possover M, Baekelandt J, Chiantera V (2007) The laparo-
scopic approach to control intractable pelvic neuralgia:
from laparoscopic pelvic neurosurgery to the LION tech-
nique. Clin J Pain 23(9):821–825
15. Possover M, Baekelandt J, Chiantera V (2007) The lap-
aroscopic implantation of neuroprothesis–LION tech-
nique–to control intractable abdomino-pelvic neuralgia.
Neuromodul 10:18–23
16. Samii M, Penkert G (1998) Traumatic disorders of the pe-
ripheral nervous system. In: Cruz J (ed) Neurological and
neurosurgical emergencies. Saunders, Philadelphia, pp
349–362
17. Schumpelik V, Kingsnorth G (1999) Incisional hernia of
the abdominal wall. Springer, Berlin
18. Seddon HJ (1943) Three types of nerve injury. Brain
66:237–288
19. Shetter AG, Racz GB, Lewis R, Heavner JE (1997) Periph-
eral nerve stimulation. In: North RB, Levy RM (eds) Neu-
rosurgical management of pain. Springer, New York, pp
261–270
20. Sunderland S (1951) A classification of peripheral nerve
injuries producing loss of function. Brain 74:491–516
21. Töns CH, Schumpelik V (1990) Das Ramus-genitalis-Syn-
drom nach Hernienoperation. Chir 61:441–443
22. Winkelmüller M (2005) Which nerve is suitable for periph-
eral nerve stimulation? Presentation at the 15th Work-
shop, Pain Section, German Society of Neurosurgery
23. Zimmermann M (1994) Basic neurophysiological mecha-
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Spinal cord stimulation. Springer, Berlin, pp 3–18
Discussion
Amid: We do a lot of triple-neurectomies in pa-
tients with chronic pain. Our neurosurgeons told
us that we should ligate the cut ends in order to
183 23
prevent neuroma formation. I reviewed the lit-
erature and I have not found any data concerning
this question. What do you think is the better to
prevent pain, to ligate the cut ends of the nerve or
to implant them in the muscle? What is your per-
sonal recommendation?
Penkert: There are no conclusive data until now
what to do with a nerve when you have cut it.
However there are some reports which recom-
mend the implantation of a cut nerve in fatty tis-
sue, others recommend the ligation of a cut nerve.
However, we do not have significant data what
to do with a nerve end after transsection. In my
opinion any additional harm to the nerve is not
good. May be after the transsection of a nerve the
implantation in a muscle is the best way. But an-
other important thing is that neuropathic pain oc-
curs within a few days after the harm to the nerve,
whereas chronic pain occurs within weeks after the
damage of a nerve.
Schumpelick: The anesthesiologists told us that
we should give local anesthesia to the nerve before
we cut it, because there is a kind of pain memory.
Can you comment on this? And what is the best
method to dissect a nerve, better to do it with a
scissor or with a scalpel?
Penkert: As a neurosurgeon we try to avoid a dis-
section a nerve. However if necessary you should
try minimize the harm to the nerve. May be local
anesthesia can be beneficial, but only if there is no
additional harm to the nerve. And it doesn’t matter
whether you use a scissor or a scalpel. At least it is
said, that there is a pain memory.
Miserez: You mentioned local neuromodulation.
What is about pharmacological neuromodula-
tion?
Penkert: Mostly those medicaments have notable
side effects. And the most young patients doesn’t
accept those side effects.
Jacob: Are locally applied steroids justified in case
of neuropathic pain?
Penkert: The first step should be the field stimu-
lation in the area of the neuropathic pain. If it
doesn’t work the second step could be the laparo-
scopic approach. These are the only things that
you can do in case of neuropathic pain following
surgery. However it is different in case of chronic
pain.
 24

Risks for Pain–Neuropathic Pain:

How Should We Handle the Nerves?
D. Kaemmer, R. Rosch, M. Stumpf, J. Otto, K. Junge, U. Klinge V. Schumpelick
 186 Chapter 24 · Risks for Pain–Neuropathic Pain: How Should We Handle the Nerves?
Introduction
In hernia surgery, interest has been focused more
and more on pain, a problem that remained un-
derestimated because only relatively few patients
seemed to be affected. Chronic pain evolves in
a high percentage after surgery with the need to
mobilize or even compress nerves [1]; however,
24 after groin hernia repair, symptoms vary to a high
degree [2]. Pain character is mostly neuropathic,
but due to overlapping distribution areas it is not
clearly related to certain nerves [3]. The neuro-
pathic pain character is accompanied by an inflam-
matory pain for some time after operation, which
is understandable, especially when a mesh was
used and foreign material remains in the body.
Nerve damage during and chronic pain after
hernia repair have been poorly evaluated in the
past, but clinical studies illuminate clinical conse-
quences and symptoms [4]. Nevertheless, little ex-
perimental data exist to give clear advice on how
to handle healthy or damaged nerves in the groin.
In groin hernia repair, it is necessary to mobilise
the groin nerves traversing the operating field and
retract them during the procedure. Furthermore,
in recurrent groin hernia repair it is sometimes
necessary to resect nerves incorporated in scar
tissue.
We therefore conducted two pilot studies to
evaluate how to handle nerves during groin hernia
repair and to advocate for further research. Intra-
neural fibrosis as a mechanism for nerve dysfunc-
tion was of obvious interest, as well as the presence
of inflammatory cells revealed by Giemsa staining
and markers for inflammation such as COX-2,
MMP-2, and CD64 as a marker for activated mac-
rophages.
Materials and Methods
In uncastrated male pigs (n=6, control n=1), bi-
lateral Lichtenstein repair was performed using a
common technique. Each animal received repair
with a small-pore polypropylene mesh (mesh M)
on one side and a large-pore polyvinylidene mesh
(mesh P) contralaterally. A nerve specimen from an
untouched nerve served as control. The follow-up
was 6 months. Iliohypogastric, ilioinguinal, and
genitofemoral nerves were explanted bilaterally via
a retroperitoneal approach. Nerves were stored
in paraformaldehyde 4% and were processed for
histology, cross-polarisation microscopy, and im-
munohistochemistry. Antibodies against MMP-2
(1:1000, Biomol, Hamburg, Germany), CD64
(Helmholtz Institute for Applied Medical Engi-
neering, Aachen, Germany), and COX-2 (DCS In-
novative Diagnostic-Systeme, Hamburg, Germany)
were applied for immunohistochemical analyses.
Collagen I/III ratios were analysed as described
previously [5]. Mast cells were detected by Giemsa
staining. Histological findings were evaluated us-
ing a semiquantitative score ranging from 0 to 4
(0: 0% positive cells; 1: 5% positive cells, 2: 5–30%
positive cells; 3: 30–80% positive cells, 4: >80%
positive cells), and scores of nerves were pooled.
In a second series we evaluated pigs (n=3, con-
trol n=1) receiving a neurotomy with cauterisation
of the iliohypogastric, ilioinguinal, and genitofemo-
ral nerves on one side and neurotomy without cau-
terisation contralaterally. The operating procedure
included bilateral exploration of the groin region,
opening of the inguinal canal, and identification
of the nerves. After neurotomy with or without
cauterisation, the inguinal canal was closed without
using a hernia repair technique. A nerve specimen
from an untouched nerve served as control. The
follow-up was 8 weeks. Iliohypogastric, ilioingui-
nal, and genitofemoral nerves were explanted bilat-
erally via a retroperitoneal approach. Nerves were
stored in paraformaldehyde 4% and were processed
for histology, cross-polarisation microscopy, and
immunohistochemistry as described above.
Results
Six months after bilateral Lichtenstein repair, ex-
pression of MMP-2, COX-2, and CD64 was in-
creased compared with controls. Collagen I/III
ratios were also slightly elevated, implying that a
higher relative amount of collagen I was present.
No mast cells were detected in either group (Gi-
emsa staining). Altogether, there were no differ-
ences between the large-pore and the small-pore
meshes (⊡ Fig. 24.1).
Chapter 24 · Risks for Pain–Neuropathic Pain: How Should We Handle the Nerves?
187 24
10
9
8
7
6
score/ratio

5
4
3
2
1 ⊡ Fig. 24.1. Results of first series
6 months after bilateral Lichtenstein
0
MMP-2 COX-2 CD 64 Collagen I/III repair (Mesh M small-pore polypro-
pylene mesh; Mesh P large-pore poly-
Mesh M Mesh P vinylidene mesh)

10
9
8
7
6
score/ratio

5
4
3
2
1
0
MMP-2 COX-2 CD 64 Collagen I/III ⊡ Fig. 24.2. Results of second
series 8 weeks after bilateral groin
cauter scissor exploration

Eight weeks after bilateral groin exploration, Discussion

higher numbers of MMP-2, COX-2, and CD64-
positive cells were observed compared with con-
trol nerves. Expression of MMP-2 was higher than
6 months after Lichtenstein repair. Again, the col-
lagen I/III ratio was increased, and no mast cells
were found.
This effect at 8 weeks after groin exploration
was independent of the method by which neuro-
tomy was performed. The elevations were similar for
neurotomy with cauterisation and neurotomy alone
(⊡ Fig. 24.2). Neither inflammatory markers nor col-
lagen ratios changed in these two groups, but they
were clearly elevated compared with control values.
Patients suffering pain after groin hernia repair have
been an underestimated collective in clinical research
so far. This is mirrored by the confusion about how
to handle intact or damaged nerves during surgery.
It is known that cutaneous afferent neurons
react more sensibly to damage [6]. Although ex-
perimental knowledge exists that little damage is
caused by simply mobilising nerves [7], stretching
[8] or compressing [9] them leads to detectable and
sustaining dysfunction. There has been discussion
about the amount of distension that is tolerable [8];
nevertheless, almost always during hernia repair,
 188 Chapter 24 · Risks for Pain–Neuropathic Pain: How Should We Handle the Nerves?
nerves are at risk for damage because the upper
stretching limit is ~15% of nerve length. It has been
shown that even without clear detectable nerve
damage, pain and measurable dysfunction of the
nerves can persist independent of the use of a mesh
prosthesis [10]. This supports our finding that
no differences exist between different transection
methods or between different large-pore meshes.
24 Even after hernia repair, nerves are at risk
because compression, such as that caused by he-
matoma or seroma, can compromise intraneural
blood flow. Experimental analyses in the rabbit
sciatic nerve revealed a complete interruption
of intraneural blood flow at pressures of about
50–70 mmHg [9]. Whether these pressures are
evoked by seroma or hematoma formation, for
instance, remains to be elucidated, but possible
nerve damage should be taken into account when
deciding whether and to what extent seromas or
hematomas should be treated. It should also be
mentioned that a small impairment of nerve integ-
rity and function could possibly be aggravated by
continuous or rising pressure.
Conclusion
During hernia repair, nerves should be identified
and carefully mobilised if necessary to protect
nerves traversing the operating field from damage.
Stretching of nerves by hooks should be minimised
whenever possible. Compression of nerves after
hernia repair by hematoma or seroma as a possible
source of (further) damage should be avoided.
Although 6 months after Lichtenstein repair
no clear difference existed between large-pore and
small-pore meshes in our model, the impact of al-
loplastic prostheses on chronic pain remains to be
elucidated. This pilot study constitutes a very small
sample and lacked a control group using Shouldice
repair.
Regarding the need for nerve resection during
surgery, we observed no difference between neu-
rotomy with and neurotomy without cauterisation
in our model.
To prevent neuroma formation with the pos-
sibility of neuropathic pain, the proximal nerve
stump must be provided with the most appropriate
surgical method. If a neuroma is already present,
or if resection is necessary for other reasons, the
existing literature seems to favour burying the
proximal nerve end into muscle, with or without
ligation or capping [11, 12]. A general standard
procedure is difficult to suggest because of small
trial sizes. In the case of inguinal nerves, further
research is needed to establish rational treatment.
Acknowledgments
We are grateful to Mrs. Ellen Krott for her excellent
and careful assistance during this investigation.
References
1. H. Kehlet, T.S. Jensen, C.J. Woolf, Persistent postsurgical pain:
risk factors and prevention. Lancet 367 (2006) 1618–1625
2. A.S. Poobalan, J. Bruce, W.C. Smith, et al., A review of chro-
nic pain after inguinal herniorrhaphy. Clin J Pain 19 (2003)
48–54
3. T. Mikkelsen, M.U. Werner, B. Lassen, H. Kehlet, Pain and
sensory dysfunction 6 to 12 months after inguinal hernio-
tomy. Anesth Analg 99 (2004) 146–151
4. E.K. Aasvang, B. Brandsborg, B. Christensen, et al., Neuro-
physiological characterization of postherniotomy pain.
Pain 137 (2008) 173–181
5. R. Rosch, K. Junge, M. Knops, et al., Analysis of collagen-
interacting proteins in patients with incisional hernias.
Langenbecks Arch Surg 387 (2003) 427–432
6. P. Hu, E.M. McLachlan, Selective reactions of cutaneous
and muscle afferent neurons to peripheral nerve transec-
tion in rats. J Neurosci 23 (2003) 10559–10567
7. D.G. Kline, E.R. Hackett, G.D. Davis, M.B. Myers, Effect of
mobilization on the blood supply and regeneration of
injured nerves. J Surg Res 12 (1972) 254–266
8. J. Haftek, Stretch injury of peripheral nerve. Acute effects
of stretching on rabbit nerve. J Bone Joint Surg Br 52
(1970) 354–365
9. K. Ogata, M. Naito, Blood flow of peripheral nerve effects
of dissection, stretching and compression. J Hand Surg
[Br] 11 (1986) 10–14
10. F. Karakayali, M. Karatas, U. Ozcelik, et al., Influence of
synthetic mesh on ilioinguinal nerve motor conduction
and chronic groin pain after inguinal herniorrhaphy: a
prospective randomized clinical study. Int Surg 92 (2007)
344–350
11. J. Lewin-Kowalik, W. Marcol, K. Kotulska, et al., Prevention
and management of painful neuroma. Neurol Med Chir
(Tokyo) 46 (2006) 62–67
12. J. Wu, D.T. Chiu, Painful neuromas: a review of treatment
modalities. Ann Plast Surg 43 (1999) 661–667
Chapter 24 · Risks for Pain–Neuropathic Pain: How Should We Handle the Nerves?
189 24
Discussion

Gryska: How do you exactly handle the nerve in

case of implanting it in a muscle?
Rosch: We just have done a simple dissection of
the nerves. However there are studies showing that
there might be a benefit for the patients if you im-
plant the nerve end in a muscel. And additionally
we didn´t see any differences if we have ligated or
coagulated the nerve in the retroperitoneal space.
However there might be changes in the dorsal
route ganglion.
Peiper: In Lichtenstein hernia repair the ilioin-
guinal nerve runs through the operation field and
following mesh implantation you achieve a distant
contact between the mesh and the nerve. Is there
any place in routine to dissect the nerve in this
situation?
Rosch: If you look to the studies there is no dif-
ference between the patient following Lichtenstein
repair and Shouldice concerning the postoperative
chronic pain. Therefore actually we would recom-
mend any trauma to the nerves in order to avoid
damage to the nerve.
Amid: In some cases an adequate repair of an
inguinal hernia is not possible without dissection
of the ilioinguinal nerve. In those cases we dissect
the nerve. But now it appears that it is important to
implant the nerve in the muscle.
 25

What To Consider as Clinicians

About Chronic Postoperative Pain
and Inguinal Herniorrhaphy
D. Hegarty
 192 Chapter 25 · What To Consider as Clinicians About Chronic Postoperative Pain and Inguinal Herniorrhaphy
Introduction
Inguinal hernias account for 75% of all abdominal
wall hernias, with a lifetime risk of 27% in men and
3% in women [1, 2]. The rate of repair of inguinal
hernia ranges from 10 per 100,000 of the popula-
tion in the United Kingdom to 28 per 100,000 in the
United States [3]. Of these patients, chronic post-
operative inguinal pain occurs in up to 54%. The
persistence of postoperative inguinal herniorrhaphy
pain for longer than 3 months following surgery has
25 gained interest during the last years, becoming the
most important outcome variable besides recur-
rence rates [4–6] because this pain affects and im-
pairs activities of daily life in 12% of patients [7–10].
Indeed, pain-related sexual dysfunction, including
dysejaculation, is now recognised to occur in at least
2% of young men [11]. Therefore, before surgery is
considered for a benign disease, complications such
as severe chronic pain, with its debilitating effects,
must be carefully weighed against the benefits [12].
Many studies have examined the surgical fac-
tors that contribute to development of postoperative
herniorrhaphy pain. For example, the intraoperative
factors shown to be associated with the lower inci-
dence of nondisabling, mild, and moderate chronic
pain include the use of lightweight meshes and the
laparoscopic approach [13]. The traditional assump-
tion that chronic pain after herniorrhaphy pain is
neuropathic in origin, and is secondary to direct
surgical trauma or postoperative inflammation of
the nerves, has therefore been challenged [14].
As clinicians we need to consider the role
of patient-related factors in the development of
chronic postherniorrhaphy pain, not just the sur-
gery-related factors. This overview seeks to exam-
ine these patient factors and to propose an assess-
ment and management model that integrates new
ideas while at the same time maintaining contact
with current therapies and approaches but placing
them in a more open and appropriate context.
The Biopsychosocial Model
The biopsychosocial model proposed by Waddell
et al. [15] draws attention to the interaction of the
patient’s response to his or her situation and the
impact of the work and social environments, as
well as the impact of any tissue abnormality, pain,
and relevant biomedical factors on progression
through the problem and eventual outcome. For
example, psychosocial factors are now acknowl-
edged to predict low back pain outcome far better
than do the available physical and biomedical find-
ings [16]. While the bulk of the recent research is
still in the area of low back pain, it is reasonable to
expect that psychosocial factors also significantly
impact other benign musculoskeletal pain states
and disabilities such as inguinal herniotomy [17].
In order to propose a clinically relevant assess-
ment and management model that integrates new
concepts, compartmentalisation of the important
clinical features is required. Fundamental to this
compartmentalisation strategy is the gathering of
patient-relevant material that can be managed,
adapted, accepted, improved, and resolved using
a balanced combination of patient and clinical
input [18].
Six interrelating compartments need to be as-
sessed, with the potential for management in a
parallel fashion. In this way, treatment of a patient
with chronic herniotomy pain might include the
following:
1. Adequate explanation of the problem, which
is dominated by giving reassuring information
(e.g. causes, likely course, and normal pain
behaviour)
2. An explanation of the treatment and manage-
ment strategy as well as the likely outcome,
using the best available evidence
3. A graded exercise programme to improve
muscle weakness and general fitness
4. A combination of rest and activity using prin-
ciples of pacing and incrementation [19, 20]
5. Encouragement of relaxation, ergonomics, and
the appropriate use of transcutaneous electri-
cal nerve stimulation and analgesics for pain
management
6. Help with preparations for a graded return to
work [21]
The precise integration of these compartments is
not a recipe to be prescribed; rather, it is guided
by the patient’s individual presentation, capacities,
and negotiated goals. This article suggests that each
Chapter 25 · What To Consider as Clinicians About Chronic Postoperative Pain
193 25
case of chronic inguinal herniorrhaphy pain can be Neurological origin
considered using the following six compartments:  Postsurgical neuroma: painful scar
1. Biomedical factors  Neuralgias (i.e. iliohypogastric, ilioinguinal, genito-
2. »Flagging« of psychosocial barriers to recovery femoral)
 Postherpetic neuralgia
3. Reactivation and rehabilitation
 Peripheral neuropathy
4. Identification of physical impairments  Central pain: post stroke or post spinal cord injury
5. Encouragement of physical fitness  Neuralgias (i.e. iliohypogastric, ilioinguinal, genito-
6. Treatment of pain femoral)
 Herniated nucleus pulposus
 Guillain-Barré syndrome
 Neurofibromatosis
Compartment 1: Biomedical Factors
Musculoskeletal origin
 Thoracic, lumbar, or sacral spinal disease
When pain arises from particularly private sites or
 Pelvic floor or abdominal muscular spasm
those associated with basic bodily functions, such  Coccygodynia
as urination or ejaculation, the condition becomes  Fibromyalgia
complicated by psychological as well as unique
Urological
physiological issues. These structures have inner-  Interstitial cystitis
vation that converges within the central nervous  Polycystic kidney
system, making symptoms alone inadequate as di-  Loin pain haematuria
agnostic tools. Even a precise history and meticu-  Stag horn calculus
 Urethral syndrome
lous physical examination may result in diagnostic
 Urethral diverticulum or caruncle
ambiguity. For example, directly asking patients to  Detrusor dyssynergia
localise the epicentre of their inguinal pain on ana-
Male reproductive
tomical charts does not appear to be helpful [14].
 Orchialgia
Patients may contribute further to the ambiguity  Prostatodynia, chronic prostatitis, or chronic pelvic
by omitting observations they find to be too embar- pain syndrome
rassing to describe or discuss (e.g. dysejaculation  Penile pain
[11]). Nevertheless, clinicians have a responsibility Female reproductive (gynaecological) pain
to ensure that another underlying diagnosis is not Cyclical
being overlooked. Consideration should be given to  Mittelschmerz, other ovarian pain
the possibility of a secondary neurological, gastro-  Primary dysmenorrhoea
 Secondary dysmenorrhoea (uterine abnormalities,
intestinal, musculoskeletal, or urological diagnosis
cervical stenosis, uterine leiomyoma, adenomyosis,
to explain the chronic symptoms. ⊡ Table 25.1 high- imperforate hymen)
lights some common differential diagnoses that may
Noncyclical or atypical cyclical
need to be considered in each individual case [22].  Adhesions
 Endometriosis
 Pelvic relaxation, prolapse, retroversion of the uterus
⊡ Table 25.1. Possible differential diagnoses of  Vulvodynia
chronic pain localised to inguinal area structures  Ovarian remnant syndrome
 Dyspareunia without vulvodynia
Gastrointestinal origin  Pelvic congestion syndrome
 Hernia: recurrent bowel obstruction  Adenomyosis
 Colitis: radiation enterocolitis, Crohn’s disease, ulce-  Chronic pelvic pain without obvious pathology
rative colitis
 Diverticular disease of the colon Other pain states
 Irritable bowel syndrome  Chronic pelvic organ ischaemia
 Chronic constipation: faecal impaction  Acute intermittent porphyria
 Proctalgia fugax  Familial Mediterranean fever
 Infectious diarrhoea  Systemic lupus erythematosus
▼  Psychogenic pain
 194 Chapter 25 · What To Consider as Clinicians About Chronic Postoperative Pain and Inguinal Herniorrhaphy
Assessment Tool
Until recently there was no standardised and vali-
dated instrument to assess the severity of postop-
erative pain following inguinal hernia repair. The
Inguinal Pain Questionnaire (IPQ) has evolved
over the past number of years. It is a self-admin-
istrated questionnaire that assesses the intensity of
the pain, its frequency, and the extent to which the
pain interferes with daily activity [6, 22]. Evidence
now supports the use of the IPQ as an instrument
in clinical studies as well as in the clinical routine
25 to assess long-term pain following inguinal hernia
surgery [22].
Contribution of Genetic Factors
The large interindividual variability in the ex-
perience of pain suggests that genetic variability
may play an important role in chronic pain. Ge-
netic variants modulating pain continue to be
discovered, and researchers expect that genetic
information may be exploited to treat pain or
to predict those who are at a greater risk of de-
veloping pain. At present no clinical research is
specifically examining the genetic variants that
may contribute to postoperative herniorrhaphy
pain. Therefore, we must rely on data from gen-
eral pain-related genetic research to assess the
relationship between genotype and phenotype.
For example, functional genetic polymorphisms
of catecholamine-O-methyltransferase (COMT)
are associated with altered sensitivity to pain in-
duced in an experimental environment [23, 24].
High COMT activity correlates with a risk of de-
veloping chronic temporomandibular joint pain
[25]. Results of studies in rodents indicate that
the susceptibility to develop neuropathic pain
has a strong heritable component, but the genes
responsible have yet to be identified [26–28]. The
GTP cyclohydrolase gene has been proposed to
affect pain sensitivity and pain-related outcome
following spinal surgery, although this process is
not completely clear [29, 30].
Given the complexity of neuropathic pain, it is
likely that many genes contribute to the develop-
ment of chronic pain. Studies are underway to cor-
relate single nucleotide polymorphisms in multiple
candidate genes with the risk of developing postin-
jury neuropathic pain [30].
Compartment 2: »Flagging« of
Psychosocial Barriers to Recovery
Clinicians should be encouraged to actively screen
for, identify, and then appropriately manage rele-
vant psychosocial components to identify patients
at risk of developing chronic pain and associated
disability problems from an early stage, perhaps
even as early as the preoperative assessment [31].
This is not an attempt to label a patient’s chronic
postoperative inguinal hernia pain as psychologi-
cally mediated, but rather an attempt to identify
some of the barriers to recovery that might be
present.
The »flagging initiative« used in the manage-
ment of low back pain could be usefully transferred
to the area of chronic herniotomy pain. The pur-
pose of developing flags for chronic herniotomy
would be to do the following [31, 32]:
▬ Provide a method of screening for psychoso-
cial factors
▬ Provide a systematic approach for assessing
psychosocial factors
▬ Suggest strategies for better pain management
for those who appear to be at high risk for
chronicity
The aim of this flagging initiative should be to iden-
tify a number of key psychological factors [32]:
▬ Presence of a belief that the pain is harmful or
severely disabling
▬ Fear-avoidance behaviour patterns with re-
duced activity levels
▬ Tendency to low mood and withdrawal from
social interaction
▬ Expectation that passive treatments rather
than active participation will help
In the management of acute and chronic pain
states, enquiries about psychosocial factors and
their management are highly relevant and need
to be addressed. The results of early preventive
programmes are persuasive and support the de-
velopment of prevention programmes in primary
care for first-time sufferers; such programmes have
been shown to significantly–by eightfold–reduce
disability and the risk of becoming chronic, as
compared to »treatment as usual« [33]. The pro-
Chapter 25 · What To Consider as Clinicians About Chronic Postoperative Pain
gramme includes a thorough examination by a
doctor and a physical therapist; information de-
signed to reduce fear, uncertainty, and anxiety;
self-care recommendations; and the recommen-
dation to remain active and continue everyday
routines [33].
Compartment 3:
Reactivation and Rehabilitation
Reactivation and rehabilitation are strongly linked
to patient beliefs and behaviour, especially those
relating to fear and avoidance (see the section on
Compartment 2). Patients are often wary of mov-
ing or exercising because they lack confidence and
have not been given any clear advice or guidance.
In situations where they feel safe and supported,
patients can find that they are able to start moving
normally and without any particularly bad reper-
cussions [34].
A process using the principles of graded ex-
posure is suggested [35, 36]. Negotiating adequate
and appropriate functional goals with patients is
an important requirement [37]. By commencing
with activities and activity goals in an adequate
rest–activity ratio, the patient’s confidence will
improve, and further activity can be built on
from there. For example, being occupied diverts
attention away from pain, whereas being inactive
leads to deconditioning and is also associated
with withdrawal from work and social activities.
The consequences of this can result in feelings
of hopelessness and helplessness that can lead to
the onset of depression. In addition, improved
circulation, exchange of metabolites, and healing
are promoted by movement. Injured tissues tend
to heal to the strength required by the demands
put on them [38].
The case for (1) the maintenance of function,
activity, or work in the acute management, (2)
the early return of function and activity in acute
and subacute management, and (3) the reestablish-
ment of normal function in chronic pain-disabled
patients is now strong. Patients frequently need
help with pain control and pain management (see
section on Compartment 6: Treatment of Pain), so
this should be ensured as soon as possible.
195 25
Compartment 4: Identification
of Physical Impairments
Physiotherapists are experts at observation, exami-
nation, and correction of physical abnormalities,
such as impairments found in tissue and joint
anatomy, biomechanics, tension, range, mobility,
strength, movement patterns, and functional ac-
tivities. Physiotherapists draw on many impair-
ment-focused skills, techniques, and approaches
that may coincidentally or intentionally also help
relieve pain and improve function [34]. Focused
physiotherapy is important and can assist in en-
suring the best possible outcome for the patient
suffering chronic postoperative inguinal hernior-
rhaphy pain [34].
Compartment 5:
Encouragement of Physical Fitness
Physical activity is perhaps the most powerful
component in pain management programmes. In-
creasing fitness is important not only in reversing
the disuse syndrome but also in giving a power-
ful signal to patients that they are beginning to
regain control over their musculoskeletal system.
It is, therefore, extremely important from both the
physical and the psychological points of view [37].
The detrimental effects of inactivity, immo-
bilisation, disuse, deconditioning, and low physical
fitness, and the beneficial general health effects re-
lated to increased activity and fitness are now well
established and extensively reviewed elsewhere. It
seems essential for clinicians, whether involved
in the management of acute or chronic pain, to
quickly involve the patient in the maintenance or
improvement of his or her general physical health.
Thankfully, a great many of the detrimental effects
are, with effort, reversible.
Compartment 6: Treatment of Pain
Clearly, a major goal of management is to reacti-
vate patients. Pain management and pain control
are important and are often a central feature of
good therapy, ensuring the best possible outcome
 196 Chapter 25 · What To Consider as Clinicians About Chronic Postoperative Pain and Inguinal Herniorrhaphy
for the patient. Targeting the pain source is not al-
ways essential, but understanding the antecedents
for increases and decreases in the pain can often
yield better treatment and management strategies.
Readers are referred elsewhere for details on anal-
gesic options, but basic analgesic management in
combination with advanced interventional strate-
gies should be considered as appropriate on an
individual patient basis. Clearly, a focused and
well-directed analgesic programme is critical for
each case to provide appropriate pain relief while
25 avoiding overreliance on the interventional/anal-
gesic aspect of the treatment.
As with all aspects of pain management, the
emphasis is biased towards patient self-manage-
ment, responsibility, and involvement rather than
overdominance by passive and pain-focused treat-
ments [18].
Summary
Chronic postoperative inguinal herniorrhaphy
pain occurs in up to 54% of patients and sig-
nificantly impairs activities of daily life, including
sexual function [2, 11]. This is particularly disap-
pointing when a complication such as severe pain
and its debilitating effects occurs after surgery for
a benign disease. Unfortunately, we are unable to
predict which individuals are going to develop
chronic postoperative pain, a situation that im-
pedes clinicians who need to consider treatment
options.
This article proposes that we compartmen-
talise our approach to chronic postoperative in-
guinal pain so as to perform clinically relevant
assessments and use a management model that
integrates new ideas, while at the same time main-
taining contact with current therapies. By using
the concept of six compartments that address the
biopsychosocial aspects of the patient’s chronic
pain, it is hoped that clinicians will have a model
for thoroughly examining each case.
In addition, evidence now supports the stan-
dardised use of the IPQ as an instrument in clini-
cal studies and in the clinical routine to assess
long-term pain following inguinal hernia surgery
[22]. We propose that a flagging initiative, similar
to that used for chronic low back pain patients, be
considered in inguinal hernia assessment. In the
future, it is hoped that candidate pain genes can
be identified and exploited to predict those who
are at greater risk of developing pain and to benefit
chronic postoperative inguinal pain management.
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Discussion
Schumpelick: Can you give us a figure of your
success rates?
Hegarty: This strategy is not been completely ap-
plied in a uniformed fashioned way in the mo-
ment. It has not been studied directly therefore I
cannot comment on this.
Stumpf: I want to stress on the things you men-
tioned about the psychological back ground. In
our outpatient clinic we started to work with a
psychiatrist in order to investigate the influence of
psychosomatic reasons for chronic inguinal pain. It
seems to be very important to distinguish patients
with psychosomatic disorders from other patients
with chronic pain.
Hegarty: I totally agree with you. Also it is very
important to get strategies what is going on in case
of female and male patients with chronic pain.
Also pain history is very important.
 26

Risk Factors for Chronic Pain After

Groin Hernia Surgery
P. Nordin
 200 Chapter 26 · Risk Factors for Chronic Pain After Groin Hernia Surgery
Introduction
Assessment of the outcomes of groin hernia surgery
has mainly focused on recurrence. However, with
modern surgical techniques and the introduction
of mesh, the recurrence rate has decreased consid-
erably [1]. More recently there has been increased
attention on other outcomes such as chronic pain,
convalescence, and patient satisfaction [2–8].
It is now well established from many multi-
centre/multinational studies that chronic pain af-
ter inguinal herniorrhaphy represents the most
important and disturbing sequela; it may not only
26 cause discomfort but also limit the individual’s
activities of daily living and have a considerable
impact on the person’s quality of life [7, 9].
Occurrence rates vary extensively in the litera-
ture, which can be explained by the lack of a uni-
form definition of such pain and of a standardised
instrument for its assessment. Also, grading of
pain severity and the social consequences has of-
ten been limited in studies addressing the risk
of long-term pain, and it is often categorised as
a dichotomous (yes/no) variable in the literature
[10]. The reported prevalence rates of residual
pain range between 0% and 53%, but pain impair-
ing daily activities following groin hernia repair is
reported at a level around 10% [7, 9].
Because the development of chronic pain after
groin hernia repair may have major implications
⊡ Table 26.1. Levels of evidence (RCT randomised
controlled trial)
1A Systematic review of RCTs with consistent re-
sults from individual (homogenous) studies
1B RCTs of good quality
2A Systematic review of cohort or case-control
studies with consistent results from individual
(homogenous) studies
2B RCT of poorer quality or cohort or case-
control studies
2C Outcome studies, descriptive studies
3 Cohort or case-control studies of low quality
4 Expert opinion, generally accepted treatments
for costs and quality of life, and because no treat-
ment has been shown to be effective, a detailed
analysis of potential risk factors and the influence
of surgical techniques is important.
This chapter contains a review of risk fac-
tors for chronic pain following herniorrhaphy. The
analysis is based partly on a detailed register-based
questionnaire study from the Swedish Hernia Reg-
ister and partly on the European Guidelines for the
Treatment of Inguinal Hernia [11, 12].
Material and Methods
European Guidelines for the Treatment
of Inguinal Hernia
The guidelines are exclusively evidence-based on
results from scientific research and are divided
into different levels of evidence. The levels vary
from the highest level of evidence (1A), which is
based on results that have been consistently dem-
onstrated in systematic reviews, to the lowest level
(4), which is based only on the opinion of experts
(see ⊡ Tables 26.1 and 26.2). This grading of scien-
tific evidence results in different levels of conclu-
sions and grades of recommendations [12].
As part of the European Hernia Society
Guidelines for the Treatment of Inguinal Hernia,
a review of published findings on risk factors for
⊡ Table 26.2. Grades of recommendation
A Supported by systematic review and/or at
least two randomised controlled trials of
good quality
Level of evidence: 1A, 1B
B Supported by good cohort studies and/or
case-control studies
Level of evidence: 2A, 2B
C Supported by case series, cohort studies of
low quality, and/or »outcomes« research
Level of evidence: 2C, 3
D Expert opinion, consensus committee
Level of evidence: 4
Chapter 26 · Risk Factors for Chronic Pain After Groin Hernia Surgery
chronic pain after groin hernia surgery was car-
ried out. Studies of chronic pain after inguinal
hernia repair were identified using the PubMed,
Cochrane Library, and Ovid search engines. Any
study–randomised, controlled trial, cohort, ques-
tionnaire, or follow-up–of adult (>18 years) pa-
tients with a primary or recurrent inguinal hernia
(asymptomatic or symptomatic; acute or elective)
was included. The search was conducted using
the term pain combined with inguinal hernia,
clinical trial, randomised controlled trial, chronic
pain, hernia repair, and neuropathy. Chronic pain
is defined by the International Association for
the Study of Pain as pain lasting for 3 months or
more [13].
Swedish Hernia Register
The Swedish Hernia Register (SHR) has compiled
detailed information on more than 160,000 groin
hernia repairs since its inception in 1992. Every
inguinal or femoral hernia operation in patients
age 15 or older performed at participating depart-
ments is recorded prospectively according to a
standardised protocol. Annual checks by external
reviewers have found a validity of data of about
98% [4]. For a complete description of the SHR’s
recorded data, validity checks, etc., the reader is
referred to earlier publications [1, 14].
From the population-based SHR, 3,000 pa-
tients age 15–85 years from 59 hospitals were sam-
pled from the 9,280 patients registered as having
undergone a primary groin hernia operation in the
year 2000. Of these, the 2,853 patients still alive in
2003 were requested to fill out a postal question-
naire to investigate the occurrence of residual pain
intensity.
Inguinal Pain Questionnaire
The Inguinal Pain Questionnaire (IPQ) is a self-
recording instrument for chronic pain. It has been
validated and was shown to have high reliability
and validity for assessment of long-term groin
pain [15]. Pain intensity is rated on a seven-step
fixed-point scale with steps operationally linked
201 26
with pain behaviour. The questionnaire consists of
18 items, with pain in the contralateral (not oper-
ated) groin used as a reference.
Results
Results from the SHR-Based
Questionnaire Study
In the Swedish questionnaire study, 2,456 patients
(86%), of whom 2,299 were men and 157 were
women, responded after two reminders. In re-
sponse to a question about the »worst perceived
pain last week,« 758 patients (31%) reported pain
to some extent. In 144 cases (6%), the pain inter-
fered with daily activities.
An age below the median, a high level of
pain before the operation, and occurrence of any
postoperative complications were found to sig-
nificantly and independently predict long-term
pain in multivariate logistic analysis when »worst
pain last week« was used as the outcome variable.
The same variables, along with a repair technique
using an anterior approach, were found to predict
long-term pain with »pain right now« as the out-
come variable.
Swedish Hernia Register
The SHR so far has no mandatory follow-up, but
any reoperation because of chronic pain must be
recorded. ⊡ Figure 26.1 presents reoperation rates
because of chronic pain within 3 years for the dif-
ferent methods of groin hernia surgery used in
Sweden. Plug techniques and open sutured repairs
have the highest risk, and totally extraperitoneal
(TEP), Lichtenstein, and Shouldice repairs have
the lowest risk of reoperation for chronic pain.
Results from the European Guidelines
The guidelines search covered all relevant litera-
ture until April 2007 and literature of all level-1A
and/or level-1B studies until May 2008. The results
were divided into different levels of evidence.
 202 Chapter 26 · Risk Factors for Chronic Pain After Groin Hernia Surgery

0.61%
0.5%

0.46%

0.4% 0.41%

0.3%

0.25%

0.2%
0.19%
0.17%

0.1%
0.10%
26
0.0%
Lichten- Shouldice Open Open Open Plug TAPP TEP
stein nonmesh mesh preperitoneal

⊡ Fig. 26.1. Reoperation rates within 3 years because of chronic pain; n=142 (TAPP transabdominal preperitoneal repair;
TEP totally extraperitoneal repair)

⊡ Table 26.3. Results of multivariate logistic analysis of risk factors predicting any level of pain versus no pain regarding
the perception of »pain right now« (OR odds ratio; CI confidence interval)

Factor Patients perceiving pain, Univariate model Multivariate model

n (%) OR 95% CI OR 95% CI

Age
Median ≤59 years 345/1,026 (34%) 1 Reference 1 Reference
Median >59 years 205/976 (21%) 0.55 0.45–0.68 0.54 0.44–0.66

Gender
Male 517/1,878 (28%) 1 Reference
Female 33/124 (27%) 1.11 0.71–1.73

Preoperative pain level

Low 176/966 (18%) 1 Reference 1 Reference
High 374/1,036 (36%) 2.49 2.02–3.08 2.43 1.97–2.99

Postoperative complications
No 498/1,865 (27%) 1 Reference 1 Reference
Yes 52/137 (38%) 1.76 1.21–2.57 1.77 1.22–2.57

Hernia repair
Anterior approach 532/1,907 (28%) 1 Reference 1 Reference
Posterior approach 18/95 (19%) 0.58 0.34–0.99 0.56 0.33–0.95

Hernia anatomy
Femoral 5/34 (15%) 1 Reference
Medial 171/602 (28%) 2.90 1.02–8.25
Lateral 340/1,228 (28%) 2.44 0.87–6.83
Chapter 26 · Risk Factors for Chronic Pain After Groin Hernia Surgery
Gender
Level 2B: Females were found to have a higher
risk of developing postoperative chronic pain than
males did [9].
Age
Level 2A: In a randomised controlled trial (RCT)
with 319 patients comparing three open mesh
techniques, chronic pain was found to be related to
younger age, and two population-based question-
naire studies found that younger age significantly
increased the risk [11, 16, 17].
Preoperative Pain
Level 2A: Preoperative pain seems to increase the
risk of developing chronic pain, according to some
studies [7, 11, 17].
Preoperative Chronic Pain Conditions
Level 2B: Preoperative chronic pain conditions
such as headache, back pain, and irritable bowel
syndrome were found to correlate significantly
with the development of chronic pain [5].
Strong Postoperative Pain
Level 2B: In an RCT with 319 patients comparing
three open mesh techniques, chronic pain was
found to be related to stronger pain directly after
the operation [16]. In an RCT with 867 patients
and 5-year follow-up comparing transabdominal
preperitoneal (TAPP) and Shouldice repair, no dif-
ferences in late discomfort were found. However,
severe pain during the first postoperative week was
a risk factor for late discomfort in the Shouldice
group [18].
Method of Repair
Level 1A: The incidence of chronic pain is re-
ported to be lower after TAPP and TEP repair
compared to open anterior surgery, with or with-
out mesh [9, 17, 19–22]. Other manifestations of
nerve lesions, numbness, and paraesthesia, are
also fewer following laparoscopic surgery [19, 22].
Meta-analysis of 41 trials of laparoscopic versus
open groin hernia repair with 7,161 participants
(individual patient data were available for 4,165)
revealed less persisting pain and numbness after
laparoscopic repair [23].
203 26
Nonmesh Repair
Level 1B: Most studies comparing mesh with non-
mesh repair report less chronic pain with mesh
repair [7, 9, 20].
Standard Polypropylene Mesh
Level 1B: In three RCTs comparing lightweight
mesh with standard polypropylene mesh, two indi-
cated that the use of lightweight mesh was associ-
ated with significantly less pain on exercise after
6 months [24] and less pain of any severity at 12
months in the lightweight group [25]. In the third
study [26], there was no difference in neuralgic
pain, hypoaesthesia, or hyperaesthesia between the
groups.
Mesh Fixation
Fibrin glue and nonfixation techniques have been
compared with mesh fixation with staples and
tackers in laparoscopic hernia operations. Reduced
early postoperative pain with the nonstapling tech-
niques was found, but there were no differences in
the risk for late chronic pain [27–29].
No Identification of Inguinal Nerves
Level 1A: Based on three randomised studies,
chronic pain after identification and division of the
ilioinguinal nerve was similar to that after identifi-
cation and preservation of the nerve [30].
Level 2B: Two cohort studies suggested that the
incidence of chronic pain was significantly lower
after identification of all inguinal nerves compared
with no identification of any nerves [30].
Intraoperative Nerve Damage
Intraoperative nerve damage in relation to the
development of chronic pain has been discussed.
There is a lack of well-defined studies on intraop-
erative lesions of nerves in the inguinal region in
relation to development of chronic pain [9].
Reoperation for Recurrence
Level 1B: Patients undergoing reoperative surgery
for recurrent hernia were at risk of developing
chronic neuralgia, with a fourfold higher rate of
moderate or severe chronic pain [7, 9, 17].
 204 Chapter 26 · Risk Factors for Chronic Pain After Groin Hernia Surgery
Discussion
The risk of chronic postherniorrhaphy pain may
be the most important outcome or quality vari-
able to consider in groin hernia surgery. Variables
that are most associated with an increased risk of
residual postherniorrhaphy pain include nonmesh
repair, techniques involving an anterior approach,
younger age, preoperative pain and preoperative
chronic pain conditions, strong postoperative pain,
lack of intraoperative identification of inguinal
nerves, and reoperation for recurrence.
Postoperative complications were found to be
26 linked to an increased risk of long-term pain in
the SHR-based questionnaire study. This is in ac-
cordance with two other trials [17–31]. In most
studies, however, chronic pain seems not to have
been evaluated at all among the reported compli-
cations. These findings, correlating chronic pain
with complications, indicate that postoperative
complications may serve as an important vari-
able for improvement of surgical quality regard-
ing risks for long-term postherniorrhaphy pain.
Among the risk factors, only the operative tech-
nique and complications can be controlled by the
surgeon.
Inguinal hernia repair, a relatively small op-
eration, is followed by a substantial risk of chronic
pain. At least three nerves may be damaged during
the procedure. However, quantification of the level
of pain, the exact cause, grading of the severity,
and social consequences of the pain have not been
well described.
Occurrence rates vary extensively in the litera-
ture, which can be explained by the lack of a uni-
form definition of such pain and of a standardised
instrument for its assessment [10].
Assessing chronic pain was not the primary
aim of most of the available studies. In a systematic
review of the literature for the years 1987–2000,
the frequency of chronic pain after hernia repair,
which was reported in 40 studies, ranged from 0%
to 53% [7]. Pain impairing daily activities following
groin hernia repair was reported by about 10% of
patients when asked about it 1–2 years postopera-
tively [3]. These reports are predominantly from
public hospitals and university institutions and are
in contrast to results from dedicated hernia cen-
tres, where the incidence of reported chronic pain
is 0–2% [32–34].
The incidence rates for chronic posthernior-
rhaphy pain derived from large register-based
questionnaire studies have also varied [3, 11, 17,
35]. This may also be explained by the lack of
standardised principles for assessing pain. The
questionnaires used have not been uniform in the
definition of pain, the length of time since surgery,
and the intensity of pain.
Among the strengths of register studies is the
fact that many surgeons with varying backgrounds
and (hernia) surgery experience are involved. The
prevalence of residual pain after hernia surgery
estimated in these studies is considered to mirror
population-based results, and an unselected and
unbiased population is involved. Furthermore, sci-
entific studies with sufficient power to reveal risk
factors for chronic postherniorrhaphy pain would
require considerably large samples.
In the Swedish register-based questionnaire
study, references to the disabling effect of residual
pain with different daily activities were explored by
using the IPQ, which links pain with daily func-
tion. In the IPQ, pain intensity is rated on a seven-
step fixed-point rating scale, with steps operation-
ally linked with pain behaviour. The questionnaire
has been validated and was shown to have high re-
liability and validity for assessing long-term groin
pain [15].
Most of the published studies on laparoscopic
versus open inguinal hernia repair show a ten-
dency towards less chronic pain after laparoscopic
techniques. However, cautious interpretation is
recommended. Many of the studies concerning
laparoscopic treatment of inguinal hernia are of
poor quality regarding pain assessment, as pain
was not the primary outcome variable. But the
data from the better-designed trials may suggest
that the development of chronic pain is less or
similar after laparoscopic hernia repair. The results
from recent randomised clinical trials compar-
ing laparoscopic TEP or TAPP repair with open
tension-free mesh repair are conflicting: Some tri-
als resulted in a lower prevalence of postoperative
pain in the laparoscopic group [36–38], whereas
other trials showed no difference between the
treatment arms [31, 39].
Chapter 26 · Risk Factors for Chronic Pain After Groin Hernia Surgery
Future studies should focus on identifying pre-
operative risk factors; providing a detailed descrip-
tion of the surgical technique (e.g. nerve identi-
fication), the type and intensity of pain, and the
social consequences of the pain; and incorporating
a detailed postoperative follow-up with characteri-
sation of the pain. Most of the existing treatments
for chronic postherniorrhaphy pain have been un-
successful so far and need to be further evaluated.
However, prevention is better than treatment, and
rational prevention and management techniques
can be developed for the future only by careful
studies and assessment of the causes of pain.
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16. Nienhuijs SW, Boelsen OB, Strobbe LJ (2005) Pain after
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Discussion
Smeds: What is strong pain in these types of
recommendations? How should we understand
strong pain?
Nordin: There is no scale in the guidelines.
Miserez: The intraoperative nerve injury is a pre-
dictor for developing postoperative chronic pain?
However I think that we do not have any prospec-
tive studies concerning this special question. Can
you comment on this?
Nordin: It is very difficult to give a comment on
this, because it is not mentioned in every trial. But
the balance if this is the main reason or not is very
difficult to see in the trials.
Köckerling: There are two reasons why TEP gives
the best results regarding the development of
chronic postoperative pain. One is that you never
touch the nerves during that procedure. The sec-
ond and very important point is that you normally
do not fix the mesh.
Nordin: You are right. However we have to wait for
new studies comparing open a laparoscopic hernia
repair.
Kehlet: We cannot interpret the literature as you
have done it. We should select every study were
pain as outcome has been asked as a yes or no
question, because it has no meaning. And ad-
ditionally we should have a close look to those
patients who have severe chronic pain with social
consequences.
Nordin: We will consider this in the next guide-
lines.
Schumpelick: How many people of the Swedish
hernia trial answered to your questionnaire? How
many percent of the patients answered to your
questionnaire? How representative are your data?
Nordin: In a frequency of over 80% answered to
the questionnaire.
Penkert: I would like to give a short remark. Very
often I heard about pain preoperatively as predict-
ing factor to get chronic pain after the operation.
We as neurosurgeons know that some patients feel
inguinal pain which is caused by an alteration of a
nerve in the L4-L5 intervertebral joint. Therefore
ask your patients for such pains before you will
perform an inguinal hernia repair.
 27

Ischemic Inflammatory Response

Syndrome as an Alternative Explanation
for Postherniorrhaphy Pain
M. Stanton-Hicks
 208 Chapter 27 · Ischemic Inflammatory Response Syndrome as an Alternative Explanation for Postherniorrhaphy Pain
Introduction
In general, moderate to severe postherniorrhaphy
pain occurs in 10% of patients. The incidence
is higher after recurrent repair (22%) than after
initial surgery (3%) [1]. Other factors increasing
the risk of postherniorrhaphy pain are poor post-
operative pain control, female gender, young age,
and surgical nerve damage. Although abnormal
inflammatory response is also proposed as a cause
of chronic postherniorrhaphy pain, the specific
signs and symptoms that would satisfy a diagnosis
of complex regional pain syndrome (CRPS; also
known as reflex sympathetic dystrophy or Sudeck’s
atrophy) are lacking. In fact, a strong argument
27 can be made that most postherniorrhaphy pain is
neuropathic in nature and is a direct expression
of neurogenic inflammation in the territory of an
injured nerve or nerves.
This article discusses the supporting literature
and ideas that have been raised at this symposium.
In addition, it presents the new criteria used to de-
fine CRPS, along with recent validation studies.
Literature Review
Preoperative risk factors for the development of
postherniorrhaphy pain include severe preexisting
chronic pain at any site in the body and a surgical
approach that poses a greater risk for nerve dam-
age. In their review, Aasvang and Kehlet identified
a number of hernia repair studies that specified
pain as an adverse outcome [2]. While most stud-
ies of hernia surgery focus on measures to reduce
the rate of recurrence, it is only during the past 10
years that chronic postsurgical pain has received
increasing attention. These have taken the form of
randomized controlled trials and nonrandomized
studies. The role of chronic pain unassociated with
hernia pain in the development of posthernior-
rhaphy pain is well established. Conditions such
as chronic back pain, irritable bowel syndrome,
headache, and peptic ulcer correlate significantly
with the development of chronic pain [3, 4].
The role of surgical technique as it relates to
open versus laparoscopic repair is described else-
where in this text. With respect to neurologic ex-
amination of patients with postherniorrhaphy pain,
only a small number of studies, including Aasvang
and Kehlet’s review, have reported that a physi-
cal examination was done, and only one of these
included a detailed neurological examination and
careful sensory testing at 6 and 12 months [5–9].
Chronic Regional Pain Syndrome
The definition of CRPS includes the following:
1. The presence of an initiating noxious event or
cause of immobilization
2. Continued pain, allodynia, or hyperalgesia,
with the pain being disproportionate to any
inciting event
3. Evidence at some point of edema, changes in
skin blood flow, or abnormal sudomotor activ-
ity in the region of pain
4. The diagnosis is excluded by the existence of
conditions that would otherwise account for
the degree of pain and dysfunction.
In CRPS type I, previously known as reflex sym-
pathetic dystrophy or RSD, there is no evidence of
major nerve damage [10]. CRPS type II describes
the condition in which evidence of major nerve
damage exists [11].
With the introduction of a definition that is
truly descriptive and does not imply any mecha-
nistic overtones, the sensitivity for diagnosis was
increased, but at the expense of specificity. At the
time that the taxonomy underwent its change,
it was recognized that these criteria would be
revised and refined by longitudinal and epidemio-
logical studies. An initial attempt was undertaken
to provide internal validation through a multi-
center study using factor analysis as a statistical
technique [12]. Analysis of the data in 123 patients
revealed that patients clustered in four specifically
perceived groups. The first subgroup had unique
signs and symptoms indicating a disorder of pain
processing. The second subgroup included skin
color and temperature changes, indicating vaso-
motor dysfunction. In the third subgroup, signs
and symptoms showed evidence of edema and
sudomotor dysfunction. The fourth subgroup had
trophic signs and symptoms.
Chapter 27 · Ischemic Inflammatory Response Syndrome as an Alternative Explanation
⊡ Table 27.1. Modified clinical diagnostic criteria
1. Continuing pain disproportionate to any inciting
event
2. Must report at least one symptom in three of the
four categories:
– Sensory: hyperesthesia and/or allodynia
– Vasomotor: temperature asymmetry and/or skin
color changes and/or skin color asymmetry
– Sudomotor/edema: edema and/or sweating and/
or sweating asymmetry
– Motor/trophic: decreased range of motion and/
or motor dysfunction (weakness, tremor, dysto-
nia) and/or trophic changes (hair, nails, skin)
3. Must display at least one sign in two or more of the
following categories:
– Sensory: evidence of hyperalgesia (to pinprick)
and/or allodynia (to light touch) and/or deep
somatic pressure and/or joint movement
– Vasomotor: evidence of temperature asymme-
try and/or skin color changes and/or skin color
asymmetry
– Sudomotor/edema: evidence of edema and/or
sweating and/or sweating asymmetry
– Motor/trophic: evidence of a decreased range
of motion and/or motor dysfunction (weakness,
tremor, dystonia) and/or trophic changes (hair,
nails, skin)
4. There is no other diagnosis to better explain the
signs and symptoms.
⊡ Table 27.3. Summary of sensitivity and specificity for the proposed clinical and research criteria [13]
Criterion Symptoms required Signs required for
type for diagnosis diagnosis
Clinical 3 2
Research 4 2
External validation of the International As-
sociation for the Study of Pain (IASP) criteria
compared the criteria to findings in CRPS patients,
with the application of similar criteria for other
types of neuropathic pain. For example, a CRPS
patient group defined by the IASP criteria can be
compared to patients with non-CRPS neuropathic
pain such as that seen in diabetic neuropathy or
posthepatic neuralgia. To test the proposed criteria
further, the ability to discriminate between CRPS
and non-CRPS neuropathic pain requires the iden-
209 27
⊡ Table 27.2. Modified research diagnostic criteria
1. Continuing pain disproportionate to any inciting
event
2. Must report at least one symptom in each of the
four following categories:
– Sensory: hyperesthesia and/or allodynia
– Vasomotor: temperature asymmetry and/or skin
color changes and/or skin color asymmetry
– Sudomotor/edema: edema and/or sweating and/
or sweating asymmetry
– Motor/trophic: a decreased range of motion and/
or motor dysfunction (weakness, tremor, dysto-
nia) and/or trophic changes (hair, nails, skin)
3. Must display at least one sign at the time of evalua-
tion in two or more of the following categories:
– Sensory: evidence of hyperalgesia (to pinprick)
and/or allodynia (to light touch) and/or deep
somatic pressure and/or joint movement
– Vasomotor: evidence of temperature asymme-
try and/or skin color changes and/or skin color
asymmetry
– Sudomotor/edema: evidence of edema and/or
sweating and/or sweating asymmetry
– Motor/trophic: evidence of a decreased range
of motion and/or motor dysfunction (weakness,
tremor, dystonia) and/or trophic changes (hair,
nails, skin)
4. There is no other diagnosis to better explain the
signs and symptoms.
Sensitivity Specificity
0.85 0.69
0.70 0.96
tification of certain rules, which include meeting
two of four sign categories and three of four symp-
tom categories. The course of this syndrome shows
extreme variability over time. Two versions of the
proposed diagnostic criteria–clinical and research–
have been specified (⊡ Tables 27.1–27.3) [13].
In summary, the IASP diagnostic criteria pro-
vide an objective means to make decisions con-
cerning the identification of those conditions
that represent CRPS in which there is significant
autonomic dysfunction or other painful condi-
 210 Chapter 27 · Ischemic Inflammatory Response Syndrome as an Alternative Explanation for Postherniorrhaphy Pain
tions, such as a type of neuropathic pain. The
current CRPS criteria and now improved validity
are designed to reduce the incidence of medical
overutilization. The data also underscore the fact
that a failure to acknowledge motor/trophic signs
and symptoms in the current criteria may prevent
CRPS from being distinguished from other neuro-
pathic syndromes.
Comparison of Inflammatory
and Neuropathic Pain After
Herniorrhaphy
If one considers the three types of pain–nocicep-
27 tive, inflammatory, and neuropathic–the former
is clearly associated with the acute stimulation
of mechanical, chemical, and thermal nocicep-
tors. The former aspect is normally a perioperative
phenomenon, and a lack of adequate control is a
strong risk factor for the development of chronic
postsurgical pain.
Chronic inflammatory pain, on the other hand,
results from ongoing tissue injury in response to a
chronic stimulus, such as sensitization of nocicep-
tors to mechanical or chemical activity. This pe-
ripheral pain may be associated with synaptic plas-
ticity in the spinal cord, with the development of
central sensitization. Normally this is self-limiting,
and the associated pathophysiological response
will generally run a course of days or weeks, but it
could become chronic if the source of spinal input
remains.
Neuropathic pain occurs after injury to nerves
or their transmission systems within the spinal
cord and brain. The hallmark of neuropathic pain
is loss of sensation in association with hypersen-
sitivity. The partial or complete loss of sensory
input is a source of positive neurological activity
that is expressed by spontaneous pain and hyper-
sensitivity, including allodynia, hyperalgesia, and
disordered sensation (dysesthesia). Furthermore,
light touch or gentle pressure in deeper tissues
of the affected region might give rise to hyper-
algesia.
Neuropathic pain, in contrast to inflamma-
tory or nociceptic pain, is associated with atopic
neurologic activity in the central nervous system
that occurs spontaneously, i.e., without external
evoked stimuli, a so-called ectopic pacemaker.
Biochemical changes in the synaptic transmis-
sion, changes in gene transcription, and upregula-
tion of the A2-δ subunits of voltage-gated calcium
channels all play a part in injury-induced central
sensitization. Tumor necrosis factor δ (TNFδ), a
pain-signaling substance, sensitizes axons, and
microglia in the spinal cord are activated, both of
which increase the overall response at dorsal horn
neurons, sensitization, and central transmission.
Typically, loss of Aδ-fibers and C-fibers from pe-
ripheral nerves is associated with Aß-fiber sprout-
ing with errant synapses to those second-order
neurons vacated by the loss of the Aδ-fibers and
C-fibers.
The role of heritable characteristics clearly in-
fluences the expression of neuropathic pain. Ani-
mal studies have demonstrated these traits [14].
The results of future studies may allow identifica-
tion of those genes responsible for the develop-
ment of injury-induced neuropathic pain.
With the foregoing in mind, nerve injury oc-
curring during herniorrhaphy may in itself not
cause ongoing chronic neuropathic pain. Pain pre-
ceding herniorrhaphy and other predisposing ge-
netic factors may also be important prerequisites
for the development of long-standing posthernior-
rhaphy pain in susceptible individuals. Given our
contemporary uncertainty at predicting many of
these factors, and given the technical variables of
surgery (open versus laparoscopic), it would be
advisable to avoid nerve injury and to certainly not
deliberately resect any of the nerves in the inguinal
region. Continuing improvements in morbidity
with newer laparoscopic techniques should further
reduce the incidence of postherniorrhaphy pain. If
chronic postsurgical pain is associated with signs
and symptoms that fulfill the criteria for CRPS,
then its differential diagnosis should be distinct
from that of neuropathic pain that is secondary
to traumatic nerve injury. Obviously, prevention
of neuropathic pain–which, when chronic, is a
neurodegenerative disease, with maladaptive con-
sequences in the nervous system–should be pre-
vented at all costs. Although CRPS after hernia
surgery is possible, its prevalence in the surgical
hernia population is rare.
Chapter 27 · Ischemic Inflammatory Response Syndrome as an Alternative Explanation
211 27
References Smeds: What is the incidence of CRPS I?
Stanton-Hicks: I have never seen a case of CRPS I
1. Poobalan AS, Bruce J, Smith WC, et al. A review of chro- of the inguinal region. But if you have damage to
nic pain after inguinal herniorrhaphy. Clin J Pain 2003;
the nerve it is CRPS II by definition. But we have
19:48–54
2. Aasvang E, Kehlet H. Chronic postoperative pain: the case
published a case of CRPS I following breast aug-
of inguinal herniorrhaphy. Br J Anaesth 2005; 95:69–76 mentation. Therefore the inguinal region is just the
3. Courtney CA, Duffy K, Serpell MG, et al. Outcome of pa- same problem in another area.
tients with severe chronic pain following repair of groin
hernia. Br J Surg 2002; 89:1310–4
4. Wright D, Paterson C, Scott N, et al. Five year follow-up of
patients undergoing laparoscopic or open groin hernia
repair: a randomized controlled trial. Ann Surg 2002;
235:333–7
5. Heikkinen T, Bringman S, Ohtonen P, et al. Five year out-
come of laparoscopic and Lichtenstein hernioplasties.
Surg Endosc 2004; 18:518–22
6. Liem MS, van Duyn EB, van der GY, et al. Recurrences
after conventional anterior and laparoscopic inguinal
hernia repair; a randomized comparison. Ann Surg 203;
237:136–41
7. Mikkelsen T, Werner MU, Lassen B, et al. Pain and sensory
dysfunction 6 to 12 months after inguinal herniotomy.
Anesth Analg 2004; 99:146–51
8. Picchio M, Palimento D, Attanasio U, et al. Randomized
controlled trial of preservation or elective division of
ilioinguinal nerve on open inguinal hernia repair with
polypropylene mesh I. Arch Surg 2004;139:755–8
9. Verstraete L, Swannet H. Long-term follow-up after Lich-
tenstein hernioplasty in a general surgical unit. Hernia
2003; 7:185–90
10. Stanton-Hicks M, Jänig W, Hassenbusch S, et al. Reflex
sympathetic dystrophy: changing concepts and taxo-
nomy. Pain 1995; 63:127–133
11. Merskey H, Bogduk H (eds) Classification of chronic pain:
descriptions of chronic pain syndromes and definitions of
pain terms. IASP Press, Seattle, 1994
12. Harden RN, Bruehl S, Galer BS, et al. Complex regional
pain syndrome: are the IASP diagnostic criteria valid and
sufficiently comprehensive? Pain 1999; 83:211–219
13. Harden RN, Bruehl S, Stanton-Hicks M, Wilson PR. Pro-
posed new diagnostic criteria for complex regional pain
syndrome. Pain Med 2007; 8(4):326–31
14. Devor M, Raber P. Heritability of symptoms in an experi-
mental model of neuropathic pain. Pain 1990; 42:51–67

Discussion

Amid: What is your definition of neuroma pre-

cisely? And what is the value of mesh material in
developing a neuroma?
Stanton-Hicks: I find it hard to believe that the
mesh acts by pressure. But I also believe that the
fibers of the mesh can cut fibers of the nerves.
 28

Postoperative CRPS in Inguinal Hernia

Patients
U. Klinge, A. Fiebeler, M. K. Tur
 214 Chapter 28 · Postoperative CRPS in Inguinal Hernia Patients
Introduction
Chronic pain is a frequent result after surgical
hernia repair and probably the most difficult com-
plication to treat. Whereas we have several excel-
lent options for handling a recurrence, therapy of
chronic pain may be frustrating, at least in some
patients, and causes a lot of trouble for the surgeon
as well as for the patient. Almost the majority
of patients report some kind of mild complaints
following hernia repair, but some patients suffer
considerably. Feeling that they cannot live with
this pain, they look for any treatment to get rid of
it, and they often undergo one surgical revision
after another.
Usually, one of the first options is a revision
operation, assuming that some of the local nerves
are entrapped in sutures, clips, or scar tissue. In
28 these patients, a neurectomy is usually performed.
Although in some cases it may not be possible to
identify and resect all three nerves (ilioinguinal
nerve, iliohypogastric nerve, and genital branch
of the genitofemoral nerve), or the morphological
analysis of the nerves may reveal no significant pa-
thology, most patients show complete or partial re-
lief of their complaints. However, in some patients
the complaints remain, sometimes even getting
worse, starting a series of many fruitless attempts
to alleviate the discomfort. If these patients had
been treated with adequate neurectomy of all three
nerves, what else might be the reason for such
failures, and how can we identify those patients
beforehand to avoid frustrating operations?
Patients with Neuropathic Pain:
Subgroup with Complex Regional
Pain Syndrome Not Responding
to Surgical Therapy
There is no doubt that pain is related to nerves and
that there are many ways to cause or intensify pain.
But apart from technical reasons, which depend on
the surgical procedure and the surgeon, patient-
related aspects must be considered, too. Several
clinical studies have demonstrated that pain is
mainly a problem of younger patients and that the
risk increases with the number of previous op-
erations and the extent of local scar tissue. Each of
these factors or a combination of them may favour
the development of pain and, correspondingly,
will influence the success of a revision operation.
Whereas pain caused by entrapment through a clip
may be cured causally by neurectomy [1], pain due
to pathology of the wound healing process (involv-
ing age, smoking, local nerve regeneration, etc.) is
more complex and difficult to address.
Generally, pain is classified as either nocicep-
tive, which represents a physiological signal from
injured tissue (= wound pain), or neuropathic, in
which a malfunction of a nerve leads to pain signal-
ling to the brain. Whereas the first is assumed to
disappear after healing of the wound, it is mainly
the latter that is accused of causing chronic pain.
Recently, Aasvang et al. [2] demonstrated that
large- and small-fibre dysfunction can be detected
in all patients following hernia repair but is more
profound in pain patients. Correspondingly, some
sort of nerve dysfunction seems to be common
after surgery in the groin.
However, classification as neuropathic pain
seems to be too nonspecific for selecting therapeu-
tic options. In a 1999 review in Lancet, Woolf and
Mannion [3] stated the following:
▬ Pharmacotherapy for neuropathic pain has
been disappointing.
▬ There is no treatment to prevent the develop-
ment of neuropathic pain.
▬ There is no treatment to adequately, predicta-
bly, and specifically control established neuro-
pathic pain.
▬ There are no predictors to indicate, which pa-
tient will develop neuropathic pain.
▬ As a tool to define treatment strategy, symp-
toms alone are not useful because they are not
equivalent to mechanisms.
Although consideration of neuropathic pain is too
inaccurate, this view neglects to account for two
different mechanisms that may contribute to nerval
function: either direct damage or pathological trig-
gering by perinerval stimuli. In accordance, Aasvang
et al. [2], who investigated postoperative complaints
after mesh repair of groin hernia, concluded that
»whether the underlying pathophysiological mecha-
nisms are related to direct intraoperative nerve in-
Chapter 28 · Postoperative CRPS in Inguinal Hernia Patients
215 28
jury or nerve injury due to an inflammatory (mesh) patient suffered from paraesthesia, possibly caused
response remains to be determined.« by damage of the anterior cutaneous branch of the
In this context, it may be helpful to adopt the femoral nerve, although another neurologist sus-
experiences of other medical fields. Stanton-Hicks pected damage to the genitofemoral nerve. After
published a review on the concept of complex explantation of a heavyweight polypropylene mesh
regional pain syndrome (CRPS) [4]. CRPS is char- that had shrunken from 15×10 cm to 13×4.5 cm,
acterised by the presence of continuing pain, al- the patient showed a complete recovery.
lodynia, or hyperalgesia after nerve injury that is In contrast, a patient with expected CRPS, who
not necessarily limited to the distribution of a spe- received a suture repair of a primary hernia rep-
cific nerve and is often accompanied by oedema, resents a totally different history. In this example,
changes of skin blood flow, or abnormal sudomo- within the first 2 weeks the patient underwent two
tor activity. Two types of CRPS have been recog- revisions, the first for pain and the second for hae-
nised. Type I corresponds to reflex sympathetic
dystrophy and occurs without a definable nerve
lesion. Type II, formerly called causalgia, refers to
cases in which a definable nerve lesion is present,
but this is still controversially discussed [5].
Despite the extreme variability of the patients’
symptoms–which are quite similar to Sudeck’s at-
rophy–there seems to be a subgroup of patients
who suffer in an outstandingly severe manner
from their pain. Often, the pain is not restricted to
a circumscribed area that can be related to a nerve;
instead, it is characterised by intense, burning
sensations and is poorly localised, appearing rather
as neuropathic inflammatory pain, with an inflam-
matory reaction triggered by neural malfunction.
It may be hypothesised that these patients may ⊡ Fig. 28.1. Explanted polypropylene mesh from patient with
not be treatable by operations because any surgical chronic pain, with growth of nerve fibre directed towards the
revision might boost the local disturbance of tissue polypropylene filament
integrity [6].
In cases of nerve injury, the axonal regenera-
tion after Wallerian degeneration fails to reinner-
vate the proper end organs in these patients. In an
analysis of mesh samples that had been explanted
because of chronic pain, some samples revealed
misguided growth of the nerves directed towards
the filament, indicating an inhibition of Schwann
cells by foreign body reaction (⊡ Fig. 28.1). In oth-
ers, the neuropathic inflammation was accompa-
nied by fibrotic degeneration of nerves with fo-
cal axonal degeneration and regeneration of axon
sprouts into the surrounding tissue (⊡ Fig. 28.2).
The following patient history may be a typical
example of a patient with chronic pain that can be
resolved by operation. The pain started with the ⊡ Fig. 28.2. Explanted polypropylene mesh from patient with
implantation of a mesh, with no clip fixation, in the chronic pain, with axon sprouts regenerating into the sur-
right groin for a recurrent hernia. Immediately, the rounding tissue
 216 Chapter 28 · Postoperative CRPS in Inguinal Hernia Patients
matoma. Three months later, a third revision was
done with neurectomy. After transcutaneous elec-
tric stimulation for more than 1 year, retroperitoneal
neurectomy of the iliohypogastric and ilioinguinal
nerves followed, which resulted in temporary im-
provement for only 2 weeks. One year later, laparo-
scopic extraperitoneal revision and reneurectomy
of the genitofemoral nerve did not lead to any im-
provement. A fourth revision 1 year later for recur-
rence was combined with lateral neurectomy and
gave relief only for some weeks. The patient’s final
status is characterised by severe pain in the entire
lower abdomen, both at rest and under strain, and
a demanding consumption of opioids as painkillers,
and has been leading to inability to work any longer.
Because several patients have experienced the
same series of frustrating operations finally lead-
ing to invalidity, a specific »response« of these
28 patients to the tissue injury of a groin hernia repair
may be suspected. In this regard, the concept of
CRPS may offer a valuable tool for selecting pa-
tients at high risk for poor outcomes after surgical
revision–if it is possible to identify patients in this
subgroup preoperatively. These patients may get
a better benefit from nonsurgical therapies, such
as local therapy with anti-inflammatory drugs or
therapeutic injections of glucocorticoids [7].
About 30–40% of patients are considered to
suffer from pain that may be classified as neuro-
pathic [8, 9], but is not clear whether it is a part
of CRPS. Which patients will probably get some
benefit from an operation, and which will not?
Preoperative Assessment of CRPS
To find an answer, we analysed 186 patients who
had been seen in our clinic for chronic pain in
the abdominal wall in the years 2002–2007. In 52
patients (34%), the pain was related to previous
hernia repair in the groin. Therapeutic success
could be verified in 43 of them. Many of these
patients had had multiple previous operations, and
the causal relevance of the specific impact is hard
to identify. However, they reported rather complex
individual histories. The youngest patient was 16
years old. The pain occurred immediately after
hernia repair and was resolved by surgical revision,
so entrapment of a nerve had been assumed but
not proven.
The patients were contacted by phone, and the
success of therapy was coded as follows:
1. Complete relief (CR)
2. Still experiencing intermittent attacks (IA)
3. No improvement despite revision (NI)
4. Conservative therapy (CT).
All of the patients had undergone at least one
surgical revision, and only three had submitted
to a conservative therapy. The remaining 40 were
treated with either neurectomy or explantation
of a heavyweight small-pore polypropylene mesh.
Results provided by telephone revealed complete
relief in 13 patients, intermittent attacks in 13, and
no improvement in 14.
Comparing the various therapeutic outcomes,
patient age did not show any significant differ-
ence among the four groups. Interestingly, the
mean age of all patients was considerably lower
(46.8±12.7 years) than the mean age of patients
with groin hernia disease.
Although males were slightly more likely to
be rid of their pain, this did not reach statistical
significance.
As an attempt to identify patients with CRPS,
we assumed that these patients do not have pain
that occurs immediately after operation and then
remains constant but instead have pain that devel-
ops after a considerable delay and then increases
constantly (⊡ Fig. 28.3). Patients with CRPS are not
Pain
Time
⊡ Fig. 28.3. Time course of pain after hernia repair. Direct
damage to the nerve, such as by entrapment in a clip or su-
ture, is assumed to occur directly postoperatively, remaining
constant afterwards. This is seen in most patients. In contrast,
some patients are pain-free for some time after the operation,
but then after a delay of months or even years they newly
develop pain, which constantly increases
Chapter 28 · Postoperative CRPS in Inguinal Hernia Patients
217 28
expected to respond to a diagnostic pain block
⊡ Table 28.1. Complex regional pain syndrome (CRPS)
with local anaesthesia within 1 h, and they are not scores of 43 patients with chronic pain. Pain: 1= im-
expected to show any significant relief. In patients mediate pain postoperatively; 2= delay/increasing
without CRPS, it should be possible to relate the pain. Block with local anaesthetics: 1= relief; 2= no
relief. Anatomical relationship: 1= related to nerve
pain to the supply area of certain nerves, whereas area; 2= diffuse/not related to nerve area. Success of
in patients with CRPS it is not. therapy: CR complete relief; IA intermittent attacks;
To analyse patients, we created a CRPS scoring NI not improved; CT conservative therapy
system consisting of the following three aspects:
Sum of CRPS 3 4 5 6
1. For pain: 1= immediate postoperative pain; score points
2= delay/increasing pain
n 23 8 9 3
2. For block with local anaesthetics: 1= relief;
2= no relief % 53% 19% 21% 7%
3. For anatomical relationship: 1= related to nerve Therapeutic CRPS
area; 2= diffuse/not related to nerve area. outcome suspected

CR 11 3
To apply this CRPS score, we assigned 2 points to
IA 7 4 2
those signs assumed to indicate CRPS and only
1 point for the others (⊡ Table 28.1). Correspond- NI 5 1 7 1
(= CRPS ?)
ingly, a sum of 6 points indicates the presence of
CRPS, whereas 3 points reflects a low probability CT 3
(= CRPS ?)
for CRPS. Therefore, the success of a surgical

No CRPS CRPS
5

1
r=0.6, p< 0.01

0
2 3 4 5 6 7
CRPS score
⊡ Fig. 28.4. Patients (n=43) treated in the surgical depart- syndrome (CRPS), see Table 28.1. Sums vary between 3 and
ment of the RWTH Aachen 2002–2007 for chronic pain after 6 points; 3 points are assumed to not represent CRPS, whereas
groin hernia repair. Therapy success is coded as 1= complete 6 points are suspected to represent CRPS. The diameter of
relief, 2= intermittent attacks, 3= not improved, 4= conservati- the points is related to the number of patients with a similar
ve therapy. For method of scoring for complex regional pain constellation
 218 Chapter 28 · Postoperative CRPS in Inguinal Hernia Patients
therapy should be highest for patients without
CRPS and lowest for patients with CRPS. Indeed,
the analysis of correlation shows a statistically sig-
nificant relationship between our CRPS scores and
the success of therapy, confirming that patients
scoring 5 and 6 should be treated conservatively
(⊡ Fig. 28.4). The correlation coefficient r between
the therapy index and the CRPS score was 0.6.
However, six of 21 patients, whose treatment suc-
cess was rated as NI or CT scored less than 5 points
on the CRPS score, indicating that this scoring
system needs to be improved, particularly with re-
gard to sensitivity. Fortunately, only two of the pa-
tients with successful therapies (CR, IA) had more
than 4 points in their CRPS scores, confirming the
specificity of the score for excluding patients from
surgical revision.
28
Conclusion
The concept of CRPS has proven to be helpful
for understanding why some patients may fail
to respond to surgical therapy. In many patients,
chronic pain is caused by several different local
reasons that can be influenced technically, either
by neurectomy or mesh explantation. The pres-
ence of CRPS represents a systemic biological
problem of tissue response that will not respond
to any local repair, a concept that is already widely
accepted for the treatment of causalgia or Sudeck’s
atrophy, both diseases with considerable similari-
ties. The assumption that 25% of the patients
with chronic pain possibly have CRPS is well in
accordance with the failure rate of 20–30% after
surgical therapy.
In the future, the validity of the proposed
CRPS scoring system should be confirmed by
comparing it with other methods and measure-
ments. Despite the extremely complex pathogen-
esis of chronic pain, it appears to be possible to
identify patients with CRPS preoperatively. Future
studies will show whether our arbitrary CRPS
score can be improved by integrating further fac-
tors, such as a history of painkillers, detectable
alteration of skin temperature, modified skin re-
action to heat and cold stimulus, signs of atrophy,
or a pathological sweat secretion test.
References
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2. EK Aasvang, B Brandsborg, B Christensen, TS Jensen, H
Kehlet: Neurophysiological characterization of postherni-
otomy pain. Pain 2008, 137:173–81
3. CJ Woolf, RJ Mannion: Neuropathic pain: aetiology, sym-
ptoms, mechanisms, and management. Lancet 1999,
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4. M Stanton-Hicks: Complex regional pain syndrome. Anes-
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5. GD Schott: Complex? Regional? Pain? Syndrome? Pract
Neurol 2007, 7:145–57
6. H Li, W Xie, JA Strong, JM Zhang: Systemic antiinflamm-
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cytokines in a rat model of neuropathic pain. Anesthesio-
logy 2007, 107:469-77
7. S Aroori, RA Spence: Chronic pain after hernia surgery–an
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8. S Massaron, S Bona, U Fumagalli, F Battafarano, U Elmore,
R Rosati: Analysis of post-surgical pain after inguinal her-
nia repair: a prospective study of 1,440 operations. Hernia
2007, 11:517–25
9. MJ Loos, RM Roumen, MR Scheltinga: Classifying post-
herniorrhaphy pain syndromes following elective ingu-
inal hernia repair. World J Surg 2007, 31:1760–1765; dis-
cussion 1766–1767
Discussion
Kehlet: In my opinion you are on the wrong track.
But that is the reason why we are here to discuss
this problem. How can you say that we should
not operate on patients with chronic noziceptor
pain? I find no evidence for that. To say that there
are CRPS I and II is too simple, there are more
subtypes. I ask for mulitcentre collaboration with
detailed neurophysiological, psychological and ge-
netically characterization of the patients to find
out which type of chronic pain we have. We have
to look at the spinal and cortical mechanisms of
pain productions and separate them out to differ-
ent groups. And then we should study the different
types of intervention.
Klinge: First of all is a question of definition. It is
not precisely clear what is noziceptive pain and
what is precisely CRPS. There are still a lot of
Chapter 28 · Postoperative CRPS in Inguinal Hernia Patients
219 28
controversial issues in this matter. Second point Kehlet: There is one thing that we can conclude:
is that there are so many factors that are respon- We don´t understand this problem completely. We
sible. And if you include all these factors which need multicentre trials to collect enough patients,
are responsible for such a pain you have a dif- because the problem is too complicated.
ferent treatment for every patient. And probably Amid: Two third of the patients did not have mesh
this will not be helpful for our young surgeons in repair. How can you correlate mesh repair with the
the outpatient clinics. This is such a proposal to pain if it is not a technical error?
identify subgroups. Thought this cannot reflect the Klinge: Just briefly. In our laboraty we have col-
specific individual situation. But the main question lected about 600 mesh explants. In nearly 94% of
is whether to make a neurectomy or not. the patients in whom the explantation was done
Muschaweck: You recommended a local treatment due to chronic pain it was a heavy-weight mesh
with local anesthesia. What do you think about a small porous polypropylene mesh.
mixture of local anesthesia and cortisone?
Klinge: First of all there is clear evidence that there
is beneficial effect of combination with steroids in
therapeutically injection. The other point is the di-
agnosis. There is difference in those patients who
do not respond to the injection and feel pain even
while the injection comparing to those patients
who respond for instance at least for one hour to
the injection of local anesthesia.
Stanton-Hicks: What diagnostic criteria did you
use to diagnose the CRPS? What clinical signs and
symptoms?
Klinge: In this preliminary study we only looked to
the patients with chronic pain and grouped them
to two groups. I am sure that this is not a good
definition of CRPS. It is probably a sub grouping of
patients with chronic pain. Probably CRPS is not
the right term but it is helpful.
Smeds: I want add a practical thing. As we know
in 80% of the patients with chronic pain the pain
will improve within the first year after the opera-
tion. Therefore we should at least wait one year be-
fore performing another operation.
Klinge: There are may be different ways how to
treat a decision tree to make an immediate opera-
tion or not. I am convinced that the most patients
we will not see within the first 6 month after op-
eration.
Köckerling: Before we name this problem a Sudeck
of the groin we absolutely should be sure that
there are no morphological reasons for the chronic
pain.
Schumpelick: What to do now? Is there some
practical advice for a practical surgeon? What to
do with a patient with pain in the groin?
Klinge: I want to simplify it.
 29

Chronic Pain After Open Mesh Repair

of Incisional Hernia
M. Kurzer, A. Kark, S. T. Hussain
 222 Chapter 29 · Chronic Pain After Open Mesh Repair of Incisional Hernia

Introduction patients still had some symptoms of discomfort,

Chronic or long-term pain following open inci-
sional hernia repair is poorly documented. Tra-
ditionally, studies of incisional hernia repair have
focussed only on short-term complications (infec-
tion, haematoma), major morbidity, hospital stay,
and recurrence. Chronic pain (defined as pain
persisting more than 3 months postoperatively [1])
has not been perceived as a significant issue, a
similar situation to that for inguinal hernia repair
until recently. Indeed, a recent review of surgical
treatment of incisional hernia [2] did not mention
postoperative pain at all. However, with surgeons’
increasing awareness of the importance of patient-
reported outcomes [3], long-term pain following
incisional hernia repair is increasingly recognised
as a significant clinical problem. Although it can
occur following open or laparoscopic repair, this
article will confine itself to the problem of chronic
29 postoperative pain after open mesh repair.
How Common Is Chronic Pain After
Open Incisional Hernia Repair?
McLanahan and colleagues were among the first to
document chronic pain following incisional hernia
repair and discuss its clinical significance [4]. At
12 months following a sublay mesh repair, 45% of
although most were infrequent and mild. However,
11% of patients described the pain as moderate to
severe, and 7% said it limited their activities. In
addition, 34% thought they could feel the mesh.
In this article, McLanahan et al. also stressed the
importance of patient satisfaction and of asking
patients for their assessment of the operation.
Burger et al. [5] and Pajaanen and Hermunen
[6] found the incidence of long-term pain to be
13% and 20%, respectively, after sublay mesh repair.
Kingsnorth, using an onlay technique, reported
similar figures [7]. Two of these studies [6, 7] found
that in 9% or 10% of patients, respectively, this pain
limited their daily activities. The list includes both
onlay and sublay techniques, with an incidence of
chronic pain ranging from 13% to 60%.
Some of this wide variation may relate to how
the pain was assessed. In a study of three differ-
ent techniques reported by Korenkov et al., an
extremely high proportion, 61%, of patients in
the onlay mesh group reported postoperative pain
[8]. Infection complications led to this multicentre
study being halted, and it may be that variations in
technique and other technical factors were respon-
sible for this high incidence of pain and complica-
tions. Other groups have also recognised that pain
following open incisional hernia repair is a real is-
sue that should be addressed [9, 10]. These studies
are listed in ⊡ Table 29.1.

⊡ Table 29.1. Studies addressing pain following open incisional hernia repair (nr not recorded)

First author Year Mesh n Follow-up, Discomfort/ Severe Limitation

position months some pain, % pain, % in activities, %
Sugerman [10] 1996 Prefascial 98 20 6 nr nr
MacLanahan [4] 1997 Sublay 106 >12 55 11 7
Müller [23] 1998 Sublay 41 17 7–30 nr 30
Martin-Duce [11] 2001 Sublay 284 72 28 nr nr
Korenkov [8] 2002 Onlay 54 12 61 nr nr
Paajanen [6] 2004 Sublay 84 36 20 4 10
Burger [5] 2004 Sublay 84 81 20 nr nr
Machairas [9] 2004 Onlay 43 54 7 nr nr
Kurzer [18] 2008 Sublay 106 95 3 0 0
Kingsnorth [7] 2008 Onlay 116 15 18 nr 9
Chapter 29 · Chronic Pain After Open Mesh Repair of Incisional Hernia
Aetiology of the Pain
Martin-Duce et al. reported a 28% incidence of
chronic postoperative pain in 152 incisional hernia
patients [11]. The pain was felt laterally along the
spigelian line and was thought to be related to the
method of mesh attachment, with nonabsorbable
sutures. Its incidence decreased when the surgeons
modified their technique of mesh attachment and
used absorbable sutures. Paajanen and Hermunen,
too, believed that nonabsorbable peripheral su-
tures were the cause of postoperative pain, due to
either tension in the sutures or nerve entrapment
[6]. Costalat et al. [12] and Cubertafond et al. [13]
held similar views. The aetiology of this pain may
be similar to that seen following mesh attachment
at its periphery with transfascial sutures in laparo-
scopic repair.
The long-term follow-up of a Dutch ran-
domised trial found the incidence of scarring or
superficial pain to be similar whether a sutured
or mesh repair was used [5]. However, abdominal
pain was less frequent in the mesh repair patients,
and the researchers concluded that much of the
discomfort was due to midline tension associ-
ated with fascial closure, which is more likely in
sutured-only patients.
Mesh as the Cause of Pain?
Perhaps because our recent recognition of chronic
pain as an important sequela of incisional hernia
repair has coincided with the widespread use of
mesh, the mesh itself has been thought to be a
causative factor.
The Aachen group, who have extensive experi-
ence with the sublay mesh repair technique, have
found that a significant proportion of patients
complain of paraesthesia and discomfort at the
periphery of the mesh, as well as a syndrome of ab-
dominal stiffness after open mesh incisional her-
nia repair. In a number of patients these symptoms
are troublesome enough to require further surgery
and mesh removal. Histological examination of the
explanted mesh has revealed extensive scar tissue,
forming what is termed a scar plate. This sensation
of abdominal restriction, or corsage, had earlier
223 29
been recognised by French surgeons following in-
sertion of large pieces of mesh or sublay repair of
massive incisional hernias [12, 13].
Mechanism of Mesh-Associated
Pain
There is now ample evidence that nonabsorbable
alloplastic meshes made of polypropylene or poly-
ester excite an inflammatory foreign body reaction
that progresses to chronic inflammation and fibro-
sis [14, 15]. This reaction is related to the size and
type of the mesh fibres and is also host dependent.
Most research has focused on polypropylene mesh,
in which the total amount of polypropylene and
the pore size are probably the chief determinants
of the extent and duration of the inflammatory
response [16, 17]. With small-pore (sometimes
called heavyweight) meshes, the areas of scar tis-
sue that form around individual fibres meet and
coalesce, a phenomenon known as bridging. The
consequent formation of a thick, rigid scar plate is
responsible for the discomfort and stiffness felt by
the patient. Histological examination of explanted
mesh in this situation has also demonstrated nerve
entrapment within the scar tissue, another factor
in the aetiology of the pain. With pore sizes greater
than 4 mm, there is a less acute inflammatory reac-
tion, fibrosis is limited to the perifilamentary area,
and the pores between the fibres are filled with fat
rather than fibrotic scar tissue.
Other Complaints with Various
Meshes
A study comparing three different meshes found
that 59% of patients implanted with one type of
standard-weight mesh complained of paraesthesia
in the region of the periphery of the mesh, com-
pared with only 4% of patients implanted with a
lightweight mesh (⊡ Table 29.2) [17]. The tech-
nique of three-dimensional stereography of the
abdominal wall in postrepair patients showed an
increase in stiffness, and this occurred whichever
mesh was used. However, the extent of stiffness
increased with mesh weight and was inversely
 224 Chapter 29 · Chronic Pain After Open Mesh Repair of Incisional Hernia
⊡ Table 29.2. Symptoms following sublay incisional her-
nia repair with different meshes (from Welty et al. [17])
Symptoms % Marlex Atrium
Paraesthesiae 59 16
Complaints, 17 16
heavy work
Complaints, 17 0 4
daily activities
Complaints at rest 9 3
proportional to mesh pore size. Moreover, the
stiffness in the lightweight (or large pore size)
group diminished over time. This study also found
that restricted mobility of the abdominal wall and
an increase in the rate of patient complaints cor-
related with the morphological development of a
29 strong scar plate [17].
The clinical evidence is, however, slightly
equivocal, as a recent randomised multicentre
study of 165 patients failed to show a signifi-
cant difference (clinically or statistically) between
standard-weight and lightweight mesh in terms of
interference with daily activities.
Results from the British Hernia Centre
In January 2008 we wrote to 106 patients who had
undergone open mesh incisional hernia repair at
our institution over the previous 10 years [18].
The technique used was an open sublay repair
with standard-weight polypropylene mesh, and the
overall recurrence rate was 4%. At the time of
writing, 68 patients had replied to the question-
naire (⊡ Table 29.3). Before the operation, 70% of
patients had some degree of pain or discomfort,
and in the vast majority this was improved af-
ter operation (⊡ Table 29.4). Three patients who
had not had preoperative pain had symptoms of
discomfort postoperatively, although this did not
interfere with their daily activities, and they were
pleased to be rid of their hernia. In this retrospec-
tive study, chronic postoperative pain was not seen
as a clinical problem.
⊡ Table 29.3. Postoperative questionnaire to incisional
hernia patients
Vypro 1. Can you remember if you had much pain or dis-
comfort from the hernia before it was repaired or
4 was there just a swelling?
2. If you had pain or discomfort before the operation,
7
is this now better or improved?
3. Do you have abdominal or scar pain now?
4. Did you think about just leaving it?
5. Are you pleased/satisfied with the operation?
6. Is the repair still sound or do you think the hernia
0 might have come back?
⊡ Table 29.4. Questionnaire replies, 68/106
n=68 Yes No
1 Preoperative pain? 47 (70%) 21 (30%)
2 Pain better now? 45 (95%) 2 improved
3 Any pain now? 5 63
4 How disabling? 0 68
5 No operation
option?
6 Satisfied? 68 0a
7 Recurrence 0 68
aNeutral
or no response on questionnaire
Summary and Conclusion
Clinically important pain following open mesh
repair of incisional hernia has an incidence of
approximately 10–20%. It can occur after both
onlay and sublay techniques, although the nature
of the pain may differ. The aetiology of the pain
is probably multifactorial and includes tension in
the repair, nerve entrapment in sutures, and mesh-
associated inflammation and scar plate formation.
Whether it is related to preoperative symptoms (as
in inguinal hernia) is a question that has not yet
been addressed.
At present we also lack data regarding what
patients think about these symptoms and how
much these symptoms affect daily activities. Is
Chapter 29 · Chronic Pain After Open Mesh Repair of Incisional Hernia
mild postoperative discomfort a price that pa-
tients are willing to pay to be rid of an uncom-
fortable, unsightly, enlarging, and potentially life-
threatening abdominal swelling? This information
will be acquired only through accurate preop-
erative assessment, more assiduous follow-up, and
recognition of the importance of patient-reported
outcomes [19–21]. Indeed, the whole subject of
incisional hernia repair is hampered by a »lack of
prospective high-quality studies« [21, 22]. Future
progress and improved results will come not only
from technical factors (including improvements
in mesh technology) but also from better under-
standing of the indications for surgery and the
development of guidelines for appropriate patient
selection.
References
1. International Association for the Study of Pain (1999).
Classification of chronic pain. Description of chronic pain
syndromes and definitions of pain terms. Pain Suppl 3:S1–
226
2. Cassar K, Munro A (2002). Surgical treatment of incisional
hernia. Br J Surg 89:534-545.
3. Holt PJ, Poloniecki JD, Thompson MM (2008). How to im-
prove surgical outcomes. Br Med J 336:900–901
4. McLanahan D, King L, Weems C, et al. (1997). Retrorectus
prosthetic mesh repair of midline abdominal hernia. Am J
Surg 173:445-449
5. Burger JW, Liujendijk RW, Hop WC, et al. (2004). Long-term
follow-up of a randomized controlled trial of suture versus
mesh repair of incisional hernia. Ann Surg 240:578–583;
discussion 83–85
6. Paajanen H, Hermunen H (2004). Long-term pain and re-
currence after repair of ventral incisional hernias by open
mesh: clinical and MRI study. Langenbecks Arch Surg
389:366–370
7. Kingsnorth A (2008). Open onlay mesh repair for major
abdominal wall hernias with selective use of components
separation and fibrin sealant. World J Surg 32:26–30
8. Korenkov M, Sauerland S, Arndt M, et al. (2002). Rando-
mized clinical trial of suture repair, polypropylene mesh
or autodermal hernioplasty for incisional hernia. Br J Surg
89:50–56
9. Machairas A, Misiakos EP, Liakakos T, et al. (2004). Incis-
ional hernioplasty with extraperitoneal onlay polyester
mesh. Am Surg 70:726–729
10. Sugerman HJ, Kellum JMJ, Reinesm HD, et al. (1996).
Greater risk of incisional hernia with morbidly obese than
steroid-dependent patients and low recurrence with pre-
fascial polypropylene mesh. Am J Surg 171:80–84
225 29
11. Martin-Duce A, Noguerales R, Villeta R, et al. (2001). Modi-
fications to Rives technique for midline incisional hernia
repair. Hernia 5:70–72
12. Costalat G, Noel P, Vernhet G (1991). Technique de cure
d’eventration par prothese parietale. Ann Chir 45:882–888
13. Cubertafond P, Sava P, Gainant A, et al. (1989). Cure
chirurgical des eventrations post-operatoires par plaque
prothetique. Chirurgie 115:66–71
14. Klinge U, Klosterhalfen B, Muller M, et al. (1999). Foreign
body reaction to meshes used for the repair of abdominal
wall hernias. Eur J Surg 165:665–673
15. Klosterhalfen B, Klinge U, Hermanns B, et al. (2000). Pa-
thology of traditional surgical nets for hernia repair after
long-term implantation in humans. Chirurg 71:43–51
16. Klosterhalfen B, Junge K, Hermanns B, et al. (2002). Influ-
ence of implantation interval on the long-term biocom-
patibility of surgical mesh. Br J Surg 89:1043–1048
17. Welty G, Klinge U, Klosterhalfen B, et al. (2001). Functio-
nal impairment and complaints following incisional her-
nia repair with different polypropylene meshes. Hernia
5:142–147
18. Kurzer M, Kark A, Selouk S, et al. (2008). Open mesh repair
of incisional hernia using a sublay technique: long-term
follow-up. World J Surg 32:31–36
19. Bitzer EM, Lorenz C, Nickel S, et al. (2008). Patient-reported
outcomes in hernia repair. Hernia 12:407–414
20. Nieuwenhuizen J, Kleinrensink GJ, Hop WC, et al. (2008).
Indications for incisional hernia repair: an international
questionnaire among hernia surgeons. Hernia 12:223–225
21. Nieuwenhuizen JA, Halm J, Jeekel J, et al. (2007). Natural
course of incisional hernia and indications for repair.
Scand J Surg 96:293–296
22. Muller-Riemenschneider F, Roll S, Friedrich M, et al.
(2007). Long-term effectiveness of interventions promo-
ting physical activity: a systematic review. Surg Endosc
21:2127–2136
23. Müller M, Klinge U, Conze J, Schumpelick V. (1998). Abdo-
minal wall compliance after Marlex mesh implantation for
incisional hernia repair. Hernia 2:113–117
Discussion
Conze: Every large hernia was once a small hernia.
Therefore I think that there is a development of
size, but you didn’t mention it in your talk.
Kurzer: In my opinion the size of the hernia stays
stable at one point with a scary border.
Conze: Another thing is that we have to differenti-
ate emergency cases. About 2–3% of emergency
operations were done because of incarcerated her-
nias. Therefore it is important to differentiate who
is of risk for developing an incarceration.
 30

Clinical Results After Open

Mesh Repair
V. Schumpelick, M. Binnebösel, J. Conze
 228 Chapter 30 · Clinical Results After Open Mesh Repair
The incidence of incisional hernia formation re-
mains unchanged between 10% and 20%, depend-
ing on the length of follow-up [1]. It is still one of
the most common complications after abdominal
surgery. Today a large variety of surgical options
for incisional hernia repair are available [2–4]. On
the basis of data from 2006, approximately 40,000
incisional hernia repairs were performed in Ger-
many. Although the results of conventional suture
repair are known to have a recurrence rate of up to
60% depending on the time of follow-up, almost
every second incisional hernia is still repaired with
a suture repair. The other half are performed with
the help of nonresorbable mesh prostheses.
Unfortunately, the operative coding system
does not facilitate differentiation of the surgical
procedures. There is great variability in the place-
ment of the mesh within the abdominal wall: in-
traabdominal as an intraperitoneal onlay mesh,
epifascial onto the anterior fascia (onlay), or be-
hind the muscles onto the posterior rectus sheath
(retromuscular/sublay). Another important techni-
cal aspect is the intended role of the mesh–whether
30 it is used for augmentation (reinforcement) or as a
replacement (bridging of the defect) of the abdom-
inal wall (⊡ Fig. 30.1). This shows the problem and
limitations of a review of open mesh techniques:
We still have no sufficient data available!
AUGMENTATION
DEFECT-BRIDGING
⊡ Fig. 30.1. Role of mesh
First of all, we are confronted with a mix of
terms: incisional or ventral hernia? These are often
used as synonyms, as well as epigastric and um-
bilical hernia. This does not make sense because
the anatomy and pathophysiology of primary and
umbilical hernias differ from that for incisional
hernias.
Second, within the group of incisional her-
nias, no differentiation is made between the differ-
ent hernia locations: median, paramedian, lateral,
transverse, subxiphoid oblique, or flank incisions.
This is due to lack of a classification system for
abdominal wall hernias. There have been several
attempts in the past to develop a classification to
make comparison of different surgical procedures
possible. In 1998 there was a first expert meet-
ing under the guidance of the GREPA/European
Hernia Society (EHS) to create a classification
for incisional hernias. Besides the location of the
previous incision, the experts took defect size and
reducibility into account, but no proposal resulted
from this meeting [5]. Several other attempts fol-
lowed, but to date, none has found its way into the
clinical routine. Too many parameters need to be
considered: location, defect size, width or length
of the defect area, symptomatology, reducibility,
number of recurrences or visibility. One parameter
that all classification attempts include is the size of
onlay
sublay
ipom
onlay
sublay
ipom
Chapter 30 · Clinical Results After Open Mesh Repair
the hernia defect. But there is a vast difference be-
tween a midline hernia defect of 20 cm width and
5 cm length compared to a defect of 5 cm width
and 20 cm length, though the total defect size is
the same. Also, some surgical techniques open
the complete scar of the previous incision, which
results in a much larger defect than preoperatively
described.
Certainly, the total defect size is important, but
the transverse diameter seems to be more relevant
for the intraoperative intention to reach a tension-
free repair.
Just recently, prognostic factors such as age,
gender, consumption of nicotine, obesity, fam-
ily history, wound contamination, and previous
postoperative complications have been taken into
account [6]. Under the aegis of the EHS a new at-
tempt is on its way, but so far, no classification has
reached its goal of international implementation.
Another problem of comparing the existing
data is the design of the follow-up period and
investigation. Knowing that the incidence of in-
cisional hernia formation shows a linear rise, the
length of follow-up is of decisive significance. In
the study of Luijendijk et al., the rate of recurrence
after incisional hernia formation was 44% after
suture repair and 24% after mesh repair [7]. The
follow-up investigation of the same patient popula-
tion by Burger et al. several years later revealed an
increase in recurrence rate with a 10-year cumula-
tive rate of recurrence of 63% after suture repair
and 32% after mesh repair [8]. So even many years
after hernia repair, there was still a steady rise in
recurrence. To evaluate any technique in terms of
recurrence, a follow-up of 2 years does not seem to
be sufficient.
Evaluation of the clinical results of the differ-
ent repairs must consider early postoperative and
late postoperative complications. Early postopera-
tive complications include hematoma, seroma, and
acute postoperative pain. Again, there is no inter-
national consensus on the definition of hematoma
or seroma, detection by ultrasound or clinical in-
vestigation, or size (10 ml or 20 ml)?
Pain is coming more and more into the focus
of clinical research. But there is no standardised
questionnaire being used internationally, so the ex-
isting data cannot really be compared. Infection is
229 30
also one of the major concerns in open incisional
hernia repair, but there is usually no differentia-
tion between superficial wound infection and deep
mesh infection. Must a local erythema be consid-
ered an infection? Again, no definition has found
international implementation.
The same relates to late postoperative compli-
cations such as chronic pain, ileus, and fistula for-
mation. Even the number of recurrences differs ac-
cording to the method of follow-up investigation.
In the Vypro I trial, the recurrences that occurred
in Aachen were asymptomatic and detected only
by ultrasound [9]. If the follow-up investigation
had been done by telephone interview, these recur-
rences would have never been documented.
It remains a comparison of apples with or-
anges, a situation that becomes obvious when one
looks at the only two randomised controlled trials
available on incisional hernia repair. In the study
of Luijendijk et al., the mesh repair was performed
in a retromuscular way, with a Marlex mesh and
an overlap of 2 cm. The anterior fascia in front
of the mesh was closed only when a tension-free
repair could be achieved; in the other cases, a re-
sorbable mesh was interposed, making this study
a mixture of mesh augmentation and mesh bridg-
ing techniques [7]. The other study compared a
large-pore lightweight mesh with three very dif-
ferent conventional meshes. In this international
multicentre trial, the importance of a meticulous
protocol can be observed: Crucial steps in the sur-
gical procedure were left to each centre’s standard
procedure, such as mesh fixation, technique for
closing the anterior fascia, and the kind of suture
material itself [9].
The available studies and their results are sum-
marised in ⊡ Tables 30.1–30.3 [10–32]. A compari-
son of these clinical results of open mesh repair is
possible only with limitations. In open mesh repair,
the retromuscular mesh augmentation seems to
show the best results with the least severe compli-
cations. A worldwide accepted and applicable clas-
sification is needed. Also, a differentiation between
the different surgical procedures with a subdivi-
sion into augmentation and bridging techniques
is urgently necessary. Only then is a comparison
of clinical results in open incisional hernia repair
possible and reasonable.
 230 Chapter 30 · Clinical Results After Open Mesh Repair

⊡ Table 30.1. Results of onlay repair (RCT randomised controlled trial)

Authors Year Study design n Follow-up Compl. Inf. Expl. Rec.

(months) % % %

Vestweber et al. [10] 1997 Retrospective 36 32 ? 27.7 0 6.4

Chevrel [32] 1997 Retrospective 389 1–20 years ? 10.9 0 5.5

Leber et al. [11] 1998 Retrospective 118 80 >20 ? 0 14.8

Rios et al. [12] 2001 Retrospective 246 77 26 17 0 17

Korenkov et al. [ 13] 2002 RCT, stopped 70 14 ? 26 0 8

San Pio et al. [14] 2003 Retrospective 67 68 ? ? ? 15

Machairas et al. [ 15] 2004 Retrospective 43 54 21 ? ? 9

Langer et al. [16] 2005 Retrospective 14 116 32 ? ? 14

Israelsson et al. [17] 2006 Retrospective 281 >12m ? ? ? 19.3

Licheri et al. [18] 2008 Retrospective 64 ? 26.5 ? 0 2/64

Kingsnorth et al. [19] 2008 Prospective 116 15.2 25 8.6 0 3.4

⊡ Table 30.2. Results of retromuscular repair (RCT randomised controlled trial)

Authors Year Study design n follow-up Compl. Inf. Expl. Rec.

30 (months)

Schumpelick et al. [20] 1996 Retrospective 58 54 ? 3.2% 0 7%

McLanahan et al. [21] 1997 Retrospective 106 24 18% 12% 0 3.5%

Ladurner et al. [22] 2001 Retrospective 57 6–33 11% 0 0 2%

Wright et al. [23] 2002 Retrospective 90 32 36% 10% 0 6%

Paajanen and Hermunen [24] 2004 Retrospective 84 36 19% 6% 0 4%

Conze et al. [9] 2005 RCT 165 24 ? 17% 0 12%

Le et al. [25] 2005 Prospective 150 >5 ? 9.3% 2 2%

Israelsson et al. [17] 2006 Retrospective 228 >12 m ? ? ? 7.3%

Kurzer et al. [26] 2008 Retrospective 125 95 ? 1.6% 2 4%

⊡ Table 30.3. Results of open peritoneal onlay mesh repair

Authors Year Study design n Follow-up Compl. Inf. Expl. Rec.

(months)

Marchal et al. [27] 1999 Retrospective 128 48 26% 14% 3 16%

Millikan et al. [28] 2003 Prospective 102 28 6% 0% 0 0%

Heartsill et al. [29] 2005 Retrospective 81 30 >20% 16% 3 15%

Bernard et al. [30] 2007 Prospective 61 35 21% 10% 2 5%

Bingener et al. [31] 2007 Prospective 233 30 15% 6% 6 9%

Chapter 30 · Clinical Results After Open Mesh Repair
231 30
References onal hernia surgery. A comparative retrospective study of
432 incisional hernia repairs. Chirurg 74:638–645
17. Israelsson LA, Smedberg S, Montgomery A, Nordin P,
1. Höer J, Lawong G, Klinge U, Schumpelick V (2002) Factors
Spangen L (2006) Incisional hernia repair in Sweden 2002.
influencing the development of incisional hernia. A retro-
Hernia 10:258–261
spective study of 2,983 laparotomy patients over a period
18. Licheri S, Erdas E, Pisano G, Garau A, Ghinami E, Pomata
of 10 years Chirurg 73:474–480
M (2008) Chevrel technique for midline incisional hernia:
2. Conze J, Junge K, Klinge U, Schumpelick V (2006) Evi-
still an effective procedure. Hernia 12 (2):121-–126
denzbasierte laparoskopische Chirurgie–Narbenhernie.
19. Kingsnorth AN, Shahid MK, Valliattu AJ, Hadden RA, Porter
Viszeralchirurgie 41:246–252
CS (2008) Open onlay mesh repair for major abdominal
3. Conze J, Klinge U, Schumpelick V (2005) Incisional hernia.
wall hernias with selective use of components separation
Chirurg 76:897–909
and fibrin sealant. World J Surg 32:26–30
4. Klinge U, Conze J, Krones CJ, Schumpelick V (2005) Incisio-
20. Schumpelick V, Conze J, Klinge U (1996) Preperitoneal
nal hernia: open techniques. World J Surg 29:1066–1072
mesh-plasty in incisional hernia repair. A comparative
5. Korenkov M, Paul A, Sauerland S, et al. (2001) Classifica-
retrospective study of 272 operated incisional hernias.
tion and surgical treatment of incisional hernia. Results of
Chirurg 67:1028–1035
an experts’ meeting. Langenbecks Arch Surg 386:65-–73
21. McLanahan D, King LT, Weems C, Novotney M, Gibson
6. Dietz UA, Hamelmann W, Winkler MS, Debus ES, Malafaia
K (1997) Retrorectus prosthetic mesh repair of midline
O, Czeczko NG, Thiede A, Kuhfuss I (2007) An alternative
abdominal hernia. Am J Surg 173:445–449
classification of incisional hernias enlisting morphology,
22. Ladurner R, Trupka A, Schmidbauer S, Hallfeldt K (2001)
body type and risk factors in the assessment of prognosis
The use of an underlay polypropylene mesh in compli-
and tailoring of surgical technique. J Plast Reconstr Aes-
cated incisional hernias: successful French surgical tech-
thet Surg 60:383–388
nique. Minerva Chir 56 :1111–1117
7. Luijendijk RW, Hop WC, van den Tol MP, de Lange DC, et
23. Wright BE, Niskanen BD, Peterson DJ, Ney AL, Odland MD,
al. (2000) A comparison of suture repair with mesh repair
VanCamp J, Zera RT, Rodriguez JL (2002) Laparoscopic
for incisional hernia. N Engl J Med 343:392–398
ventral hernia repair: are there comparative advantages
8. Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaasdonk
over traditional methods of repair? Am Surg 68:291–295
EG, Jeekel J (2004) Long-term follow-up of a randomized
24. Paajanen H, Hermunen H (2004) Long-term pain and re-
controlled trial of suture versus mesh repair of incisional
currence after repair of ventral incisional hernias by open
hernia. Ann Surg 240:578–583
mesh: clinical and MRI study. Langenbecks Arch Surg
9. Conze J, Kingsnorth AN, Flament JB, Simmermacher R,
389:366–370
Arlt G, Langer C, Schippers E, Hartley M, Schumpelick V
25. Le H, Bender JS (2005) Retrofascial mesh repair of ventral
(2005) Randomized clinical trial comparing lightweight
incisional hernias. Am J Surg 189:373–375
composite mesh with polyester or polypropylene mesh
26. Kurzer M, Kark A, Selouk S, Belsham P (2008) Open mesh
for incisional hernia repair. Br J Surg 92:1488–1493
repair of incisional hernia using sublay technique: long-
10. Vestweber KH, Lepique F, Haaf F, Horatz M, Rink A (1997)
term follow-up. World J Surg 32:31–36
Mesh-plasty for recurrent abdominal wall hernias–results.
27. Marchal F, Brunaud L, Sebbag H, et al. (1999) Treatment
Zentralbl Chir 122:885–888
of incisional hernias by placement of an intraperitoneal
11. Leber GE, Garb JL, Alexander AI, Reed WP (1998) Long-
prosthesis: a series of 128 patients. Hernia 3:141–147
term complications associated with prosthetic repair of
28. Millikan KW, Baptista M, Amin B, Deziel DJ, Doolas A
incisional hernias. Arch Surg 133:378–382
(2003) Intraperitoneal underlay ventral hernia repair utili-
12. Rios A, Rodriguez JM, Munitiz V, Alcaraz P, Pérez D, Par-
zing bilayer expanded polytetrafluoroethylene and poly-
rilla P (2001) Factors that affect recurrence after incisi-
propylene mesh. Am Surg 69:287–291
onal herniorrhaphy with prosthetic material. Eur J Surg
29. Heartsill L, Richards ML, Arfai N, Lee A, Bingener-Casey J,
167:855–859
Schwesinger WH, Sirinek KR (2005) Open Rives-Stoppa
13. Korenkov M, Sauerland S, Arndt M, Bograd L, Neugebauer
ventral hernia repair made simple and successful but not
EA, Troidl H (2002) Randomized clinical trial of suture re-
for everyone. Hernia 9:162–166
pair, polypropylene mesh or autodermal hernioplasty for
30. Bernard C, Polliand C, Mutelica L, Champault G (2007)
incisional hernia. Br J Surg 89:50–56
Repair of giant incisional abdominal wall hernias using
14. San Pio JR, Damsgaard TE, Momsen O, Villadsen I, Larsen
open intraperitoneal mesh. Hernia 11:315–320
J (2003) Repair of giant incisional hernias with polypropy-
31. Bingener J, Buck L, Richards M, Michalek J, Schwesinger
lene mesh: a retrospective study. Scand J Plast Reconstr
W, Sirinek K (2007) Long-term outcomes in laparoscopic
Surg Hand Surg 37:102–106
vs open ventral hernia repair. Arch Surg 142:562–567
15. Machairas A, Misiakos EP, Liakakos T, Karatzas G (2004) In-
32. Chevrel JP, Rath AM (1997) The use of fibrin glues in the
cisional hernioplasty with extraperitoneal onlay polyester
surgical treatment of incisional hernias. Hernia 1:9–14
mesh. Am Surg 70:726–729
16. Langer C, Liersch T, Kley C, Flosman M, Suss M, Siemer A,
Becker H (2005) Twenty-five years of experience in incisi-
 232 Chapter 30 · Clinical Results After Open Mesh Repair

Discussion

Bellows: Can you comment on the use of allogenic

mesh material for instance alloderm?
Schumpelick: We have never used biological
meshes. Why should I use such meshes?
Deysine: I totally agree that we need a better clas-
sification of incision hernias.

30
 31

Acute and Chronic Pain After

Laparoscopic Incisional Hernia Repair
D. Berger, M. Bientzle
 234 Chapter 31 · Acute and Chronic Pain After Laparoscopic Incisional Hernia Repair
Introduction
Laparoscopic repair of incisional hernias is gain-
ing increasing popularity because it has some ad-
vantages compared to open techniques [1, 2]. The
frequency of infectious complications, for example,
is significantly reduced. Previous studies also dem-
onstrated reduced pain after laparoscopic incisional
hernia repair, a finding that has also been pointed
out in a very recent review [3–7]. In contrast, Pierce
et al. clearly showed that early postoperative pain is
a major issue [1]. The frequency of prolonged pain
was nearly 2% in the laparoscopic group compared
with 0.9% in the open group. A recent study found
dissatisfying pain in 9% in the long run [8].
In our preliminary study, all patients who were
laparoscopically treated for an incisional hernia
were followed up in the early postoperative period
using a visual analogue scale. Long-term follow-up
was performed using a pain score similar to those
used in other studies dealing with chronic pain.
Patients and Methods
31 Since 2002, all patients treated for incisional her-
nias have been prospectively followed up in the
early postoperative period with a visual analogue
scale ranging from 0 to 10. The patients are studied
twice a day in reclining and upright positions until
leaving the hospital.
Our preliminary evaluation comprised 100
patients. Fifty patients had a mesh derived from
expanded polytetrafluoroethylene (e-PTFE), and
starting in May 2004, 50 patients received a mesh
derived from polyvinylidene fluoride (PVDF), Dy-
namesh IPOM. The distribution of age, gender,
and surgical parameters such as hernia size were
not different between the groups. A further clinical
examination was performed after 1, 3, 6, 12 months
and yearly thereafter using a simplified pain score,
which is shown in ⊡ Table 31.1.
Surgical Technique
The surgical technique did not differ over the years.
Routinely, the whole abdominal scar was covered by
⊡ Table 31.1. Classification of long-lasting postopera-
tive pain
0 No pain at all, very satisfied
1 Sometimes minimal pain during work, satisfied
2 Sometimes moderate pain during work, still satisfied
3 Often annoying pain during work, dissatisfied
4 Strong pain at rest, very dissatisfied
the mesh, not just the obvious fascial defect. After
complete adhesiolysis of the whole abdominal wall,
the falciform ligament was dissected in cases with
hernias or incisions reaching the upper abdomen.
In patients with hernias or incisions of the lower ab-
domen, the fatty tissue between the plicae mediales
was dissected to open the Retzius space. The meshes
were fixed with six stay sutures at the corners and
in the midline in the longest extension of the mesh.
Furthermore, spiral tacks were used every 3–4 cm.
For covering the lower abdomen, the mesh was
fixed with spiral tacks at the pubic bone and the
symphysis. In cases of upper abdominal hernias, the
tacks were placed in the rips at the costal arch.
Diclofenac and metamizole were routinely
given in the postoperative period. In some cases,
piritramide was added via a patient-controlled an-
algesia pump.
Statistical analysis was done using analysis of
variance tests for repeated measurements.
Results
As outlined above, the two groups did not differ
concerning demographic or surgical parameters.
As shown in ⊡ Fig. 31.1, the patients suffered from
very strong pain during the first 3 days, espe-
cially when in an upright position. The pain scores
slowly decreased from a median of 7 the morning
of the first postoperative day to 4 and 3 at days 3
and 4, respectively.
However, there is a significant difference be-
tween the groups: Patients treated with DynaMesh
IPOM showed significantly lower pain scores for 5
days than patients who received an ePTFE-derived
mesh, as shown by analysis of variance testing for
repeated measurements. No further correlation of
pain with other parameters–such as age, gender,
Chapter 31 · Acute and Chronic Pain After Laparoscopic Incisional Hernia Repair
2
0 reclining (l) and upright patient
d1ml d1ms d1el d1es d2ml d2ms d2el d2es d3ml d3ms d3el d3es d4ml d4ms d4el d4es d5ml d5ms d5el d5es
body mass index, mesh size, hernia size, duration
of the procedure itself, amount and intensity of ad-
hesions, or number of previous procedures–could
be established.
Chronic pain was observed only during the
first 3 months of the observation period. The me-
dian pain score after 4 weeks was 1.5, which indi-
cates minimal to moderate pain during work. Six
patients were dissatisfied at that time point. Only
one patient was still dissatisfied after 3 months,
but the problems finally resolved without further
treatment. Any correlation of chronic or persisting
pain with clinical parameters could not be estab-
lished because of the low number of patients. For
the same reason, a differentiation between the two
groups did not seem to be appropriate.
Discussion
It is usually believed that a main advantage of lap-
aroscopic procedures is reduced pain in the early
235 31
⊡ Fig. 31.1. Postoperative visual
analogue scale (VAS) scores. Box
plots are demonstrated. The
x-axis shows the time course
between day 1 and day 5, given
as d1m (m morning) to d5e
(e evening). The different time
points differentiate between the
positions (s). The y-axis shows the
VAS level
postoperative period, which has been proven for
inguinal hernia repair [9–11]. Our own clinical ex-
perience, however, showed that after laparoscopic
incisional hernia repair, the patients suffered from
severe pain. The early literature described a re-
duced need for narcotics after laparoscopic repairs
compared with conventional procedures [3–6].
Even today, a review of incisional hernia repair
concluded that laparoscopy is superior compared
with open techniques in terms of postoperative
pain [7].
However, Pierce et al. [1] described in their
analysis that »unlike most other laparoscopic pro-
cedures where incisional pain is typically minimal
and relatively short lived, laparoscopic incisional
hernia repair is associated with substantially more
pain in the postoperative period because of the
methods of mesh fixation.«
Our data clearly show that our patients expe-
rienced annoying pain in the early postoperative
period. The use of an elastic mesh, the properties
of which are comparable to the human abdominal
 236 Chapter 31 · Acute and Chronic Pain After Laparoscopic Incisional Hernia Repair
wall [12], is associated with significantly reduced
pain scores. For inguinal hernias, it is known that
the level of pain in the early postoperative period
strongly correlates with chronic pain problems
[13], thus supporting the recommendation that
elastic meshes should be preferred. A correlation
between acute and chronic pain could not be es-
tablished in our series. The number of patients
studied up to now is probably too small.
Some major prospective studies and reviews
have observed prolonged or chronic pain in up to
9% of patients [1, 2, 8]. Unfortunately, a definition
of prolonged pain is not generally given that would
enable comparison among different publications.
The prolonged pain is usually explained by the
fixation devices, mostly transfascial sutures and
tacks [4]. Local anaesthesia is recommended, fol-
lowed by removal of stay sutures or tacks in other-
wise untreatable cases [4]. In one series with 1.6%
persistent pain, the removal of tacks or stay sutures
did abolish the pain in three of six patients [14].
The success rate is not given in any other series.
In our series, chronic pain resolved spontaneously
after conservative treatment in all cases. However,
one patient was significantly restricted in his daily
31 activities for almost 6 months.
In conclusion, laparoscopic repair of incisional
hernias is a painful treatment needing subsequent
analgesic postoperative therapy. Dynamesh IPOM,
which exhibits a physiological elasticity [12], sig-
nificantly reduces the pain level in the early post-
operative period. The number of patients studied
does not allow any conclusion about the nature of
chronic pain. An association between acute and
chronic pain could not be established for laparo-
scopic incisional hernia repair.
References
1. Pierce RA, Spitler JA, Frisella MM, Matthews BD, Brunt
LM (2007) Pooled data analysis of laparoscopic vs. open
ventral hernia repair: 14 years of patient data accrual. Surg
Endosc 21:378–386
2. Carlson MA, Frantzides CT, Shostrom VK, Laguna LE (2008)
Minimally invasive ventral herniorrhaphy: an analysis of
6,266 published cases. Hernia 12:9–22
3. Carbajo MA, Martin DOJ, Blanco JI, de la Cuesta C, Tole-
dano M, Martin F, Vaquero C, Inglada L (1999) Laparosco-
pic treatment vs open surgery in the solution of major
incisional and abdominal wall hernias with mesh. Surg
Endosc 13:250–252
4. Heniford BT, Park A, Park AF, et al. (2003) Laparoscopic
repair of ventral hernias: nine years’ experience with 850
consecutive hernias. Ann Surg 238:391–400
5. LeBlanc KA, Booth WV, Whitaker JM, Bellanger DE (2001)
Laparoscopic incisional and ventral herniorraphy: our ini-
tial 100 patients. Hernia 5:41–45
6. Park A, Birch DW, Lovrics P (1998) Laparoscopic and open
incisional hernia repair: a comparison study. Surgery
124:816–821
7. Misiakos EP, Machairas A, Patapis P, Liakakos T (2008) La-
paroscopic ventral hernia repair: pros and cons compared
with open hernia repair. JSLS 12:117–125
8. Stickel M, Rentsch M, Clevert DA, Hernandez-Richter T,
Jauch KW, Lohe F, Angele MK (2007) Laparoscopic mesh
repair of incisional hernia: an alternative to the conventi-
onal open repair? Hernia 11:217–222
9. Bringman S, Ramel S, Heikkinen TJ, Englund T, Westman
B, Anderberg B (2003) Tension-free inguinal hernia repair:
TEP versus mesh-plug versus Lichtenstein: a prospective
randomized controlled trial. Ann Surg 237:142–147
10. Collaboration EH (2000) Laparoscopic compared with
open methods of groin hernia repair: systematic review
of randomized controlled trials. Br J Surg 87:860–867
11. Grant AM (2002) Laparoscopic versus open groin hernia
repair: meta-analysis of randomised trials based on indi-
vidual patient data. Hernia 6:2–10
12. Junge K, Klinge U, Prescher A, Giboni P, Niewiera M,
Schumpelick V (2001) Elasticity of the anterior abdominal
wall and impact for reparation of incisional hernias using
mesh implants. Hernia 5:113–118
13. Callesen T, Bech K, Kehlet H (1999) Prospective study of
chronic pain after groin hernia repair. Br J Surg 86:1528–
1531
14. Wassenaar EB, Raymakers JT, Rakic S (2007) Removal of
transabdominal sutures for chronic pain after laparosco-
pic ventral and incisional hernia repair. Surg Laparosc
Endosc Percutan Tech 17:514–516
Discussion
Flament: When you report about the hernia size
you spoke only about the diameter. But there is
still another dimension: The volume of herniated
bowel. Therefore we do a CT-scan before the op-
eration to measure the volume of the bowel in the
abdominal cavity and the volume of the herniated
bowel to exactly estimate the size of the hernia.
Berger: Your approach is very sophisticated and
would be the best of course.
Schippers: You use a minimal invasive approach
and you use a bridging technique and you have a
Chapter 31 · Acute and Chronic Pain After Laparoscopic Incisional Hernia Repair
237 31
long period of postoperative pain. What is your
explanation of this pain?
Berger: I can only speculate. I think that a fixation
trough the peritoneum is the main problem.
Chowbey: A secret of good result in laparoscopic
hernia repair depends on the selection of patients.
In what cases laparoscopic hernia repair can be
done and what cases it cannot be done laparoscop-
ically? Another thing is the number of used tackers
for the mesh fixation. If you use too much tackers
the risk of pain raises.
Berger: I agree concerning your remark about
the number of tackers. However, I never found a
recommendation of the number of tackers used
in study dealing with laparoscopic hernia repair.
Of course there are some hernias that cannot be
repaired laparoscopically. If we cannot reach an
adequate overlap – at least five centimeters on both
sites – we do an open procedure.
 32

Effect of Nerve Identification on the

Rate of Postoperative Chronic Pain
Following Inguinal Hernia Surgery
S. Alfieri, D. Di Miceli, R. Menghi, G. Quero, C. Cina, G. B. Doglietto
 240 Chapter 32 · Effect of Nerve Identification on the Rate of Postoperative Chronic Pain Following Inguinal Hernia Surgery
Introduction
The ilioinguinal nerve, iliohypogastric nerve, and
inguinal segment of the genital branch of the gen-
itofemoral nerve all cross the inguinal channel and
consequently are vulnerable to injury.
But if they are injured, is there any evidence
that they can produce pain syndromes? Should a
suspected injured nerve or a nerve in the way of
repair be cut (divided), resected, or left in place?
Should the cut end of the nerve be left exposed or
buried in the muscle?
Much controversy still exists regarding how
to treat these three inguinal nerves during hernia
repair, with many published studies showing con-
trasting results. Consequently, it is right to wonder
about the following:
▬ Do the inguinal nerves really play a role in the
genesis of postherniorrhaphy inguinodynia
and orchialgia?
▬ Is there any scientific evidence today that
chronic pain is related to the different treat-
ment reserved for the three inguinal nerves
during hernia repair?
In trying to give scientific answers to these ques-
tions, we have evaluated not only the levels of evi-
32 dence (LE) and grades of recommendation (GR) for
every published study in this field, but we also read
each paper in its entirety and evaluated its statistical
validity and the terminology used. It is not surpris-
ing that we discovered some discrepancies between
the data found in the article and the conclusions
extrapolated by systematic reviews (LE, 1a; GR, A).
Definitions and Terminology
An important issue is the need to provide uniform
terminology to be used in this field. In fact, the
terms division, resection, dissection, transection, sec-
tion, and neurectomy were often used and reported
incorrectly in the literature, which influenced and
distorted the real results of the studies, with im-
portant and practical implications involving the
treatment of chronic pain [1].
A clear example of this is demonstrated by the
wrong interpretation of the study by Picchio et al.
[2], which is often cited as demonstrating that pain
is not affected by elective division of the ilioinguinal
nerve. However, when reading the whole paper, it is
possible to learn that the authors actually performed
a neurectomy (dividing the nerve lateral to the in-
ternal ring) instead of a simple division of the nerve
in the operative field. Consequently, the results of
this paper not only have often been distorted but
also may give the erroneous message that the nerves
may be sectioned during operation at any level of
the inguinal canal without any consequence [3].
With the aim of providing uniform terminol-
ogy, the international consensus conference held
in Rome in April 2008 decided to recommend the
following nomenclature:
▬ Cutting or dividing a nerve means interrupt-
ing the continuation of a nerve. It is appro-
priate to mention the way the cut ends were
handled, such as by ligation, cauterisation, or
nothing.
▬ Resection of a nerve or neurectomy means
removing the segment of a nerve along the
inguinal canal. It is recommended to cut the
proximal end up to its intramuscular part. It is
appropriate to mention the handling of the cut
ends and the proximal and distal parts of the
section.
Is There Any Correlation Between
Chronic Pain and Identifying vs. Not
Identifying the Three Inguinal Nerves?
Although it has been demonstrated that preopera-
tive identification of all inguinal nerves is almost
always possible [4], the majority of surgeons con-
tinue to not detect them, as recently emphasised
and confirmed for the iliohypogastric nerve (de-
tected in only 32% of cases) and for the genital
branch of the genitofemoral nerve (detected in
only 36% of cases) [5].
In fact, the vast majority of the studies report
data for only one nerve (generally the ilioinguinal
nerve, probably because is the easiest to recogn-
ise during hernia repair) without giving any data
concerning the other two nerves, neglecting the
fact that all three nerves contribute to the sensory
innervation of the groin.
Chapter 32 · Effect of Nerve Identification on the Rate of Postoperative Chronic Pain
An Italian prospective multicentre study of
973 cases and a French single-centre study of
1,332 cases are the only two published studies
presenting results for all three inguinal nerves
(2,305 cases altogether) with a long follow-up
period (1–5 years) [6, 7]. Both studies concluded
that identification and preservation of all three
inguinal nerves (which occurred in 924 patients
considering the two papers together) during open
inguinal hernia repairs (with or without mesh)
reduces chronic incapacitating groin pain to less
than 1%; the mean incidence of chronic pain was
0.8% (range 0–1.6%). The Italian study also dem-
onstrated that the risk of developing inguinal pain
increased with the number of nerves concomi-
tantly undetected. Likewise, the division of nerves
strongly correlated with the presence of chronic
pain [7]. According to the data in the literature,
we can conclude that identifying and protecting
the three inguinal nerves decreases the risk of
postoperative severe chronic pain.
Should the Identified Nerve Be
Preserved, Divided, or Resected
(Neurectomy)?
All of the published studies report data concern-
ing division versus preservation of only a single
nerve, without giving any data concerning the
other two nerves. In all of these papers, the
results are distorted because the nerves not con-
sidered could have been unintentionally divided
or injured during operation. For these reasons,
chronic pain could be generated [8]. The stud-
ies by Ravichandran et al. [9] (LE, 2b; GR, B)
and Mui et al. [10] (LE, 1b; GR, A) report results
of preservation versus neurectomy of only one
single nerve, and these results are also limited
by very small sample sizes, with only 20 patients
and 50 patients in each arm. Therefore, these
studies do not have substantial statistical power
compared with the study of Dittrik et al. [11] (LE,
2b; GR, B), which also did not have homogeneous
distribution between the two arms (66 patients
versus 24 patients).
In these cases, no conclusions can be evalu-
ated, even if some studies are prospective and ran-
241 32
domised and apparently have the highest recom-
mendation grade [3]. These underpowered studies
are sometimes used in meta-analyses or reviews by
calculating a pooled mean percentage by means of
a randomised model to reach some conclusions.
However, data coming out of such a model that
uses small studies are completely distorted. Pic-
chio et al. [2] (LE, 1b; GR, A) reported that pain is
not affected by elective division of the ilioinguinal
nerve. However, by reading the whole paper (with
400 patients in each arm), one discovers that the
author actually performed more of a neurectomy
(dividing the nerve lateral to the internal ring) than
a simple division of the nerve in the operative field.
The results of this paper have been often distorted;
in fact, some authors wrongly reported that the
nerve was »divided,« and others stated that the
nerve was dissected, without explaining that even if
Picchio et al. did not report where the nerve was di-
vided caudally, they divided the nerve lateral to the
internal ring. Merely concluding that division/dis-
section of the ilioinguinal nerve does not increase
or reduce the risk of chronic pain not only distorts
the researchers’ results, but, more importantly, it
may give the erroneous message that the nerves
may be sectioned during operation at any level of
the inguinal canal without any consequence.
Picchio et al. [2] (LE, 1b; GR, A) report that pain
is not affected by elective neurectomy (according to
the new nomenclature of the consensus conference)
of the ilioinguinal nerve, and Pappalardo et al. [12]
report this for iliohypogastric neurectomy.
According to the literature, we can conclude
that identification and protection of all three
nerves during open inguinal hernia repair (with
or without mesh) reduces the risk of chronic inca-
pacitating pain to less than 1%.
Should the Identified Nerve Be
Isolated or Left in its Natural Bed
Without Manipulation, Taking Care
To Not Remove the Covering Fascia
of the Nerve?
No published data are available regarding ma-
nipulation versus no manipulation of a preserved
nerve. However, considering the anatomical stud-
 242 Chapter 32 · Effect of Nerve Identification on the Rate of Postoperative Chronic Pain Following Inguinal Hernia Surgery
ies [4], we suggest (LE, 5; GR, D) leaving the the
nerves in their natural bed as much as possible and
not removing the covering fascia.
Should a Suspected Injured Nerve or
a Nerve in the Way of Repair Be Saved
by All Means or Resected?
The current literature is inconsistent concerning
this point. Opinions differ considerably, but no
published data are actually available.
Some authors emphasise that when an injury
has occurred, the intramuscular portion of the
nerve must be resected, stating that merely di-
viding the nerve at the point of its emergence is
inadequate [3, 5]. These data are supported by
the increasing success rates of pain relief with
extended versus standard neurectomy procedures,
as obtained by Amid et al. [5] for patients with
chronic postherniorrhaphy pain (LE, 4; GR, C)
and by Alfieri et al. [6], who reported that the
increased risk of developing chronic pain with the
number of nerves divided could be explained by
the fact that resection of the unidentified nerve
has generally been performed distal to its origin;
this leaves the site of the injured nerve intact–and
32 able to continue to generate a pain signal–and ex-
poses it to neuroma formation (LE, 5; GR, D). At
the same time, there is no scientific evidence that
the cut end of the nerve should be left exposed or
buried in the muscle. While we await definitive
results in the literature, it is reasonable to remove
a suspected injured nerve or a nerve in the way of
the repair during any type of repair and to implant
the proximal cut end in the muscle (LE, 5; GR, D).
How Can the Inguinal Segment of the
Genital Branch of the Genitofemoral
Nerve Be Identified and Protected
During the Open Procedure?
Identifying and protecting the inguinal segment
of the genital branch nerve during hernia repair
is not difficult. It can be recognised, identifying
and keeping the external spermatic vein (the so-
called blue line) with the cord. However, the geni-
tal branch nerve can be damaged if inadvertently
sectioned, entrapped, or secured (for example, if a
continuous suture is introduced along the inguinal
ligament), or it can be injured if the external sper-
matic vessels are divided to skeletonise the cord
without its identification.
Should the Cremasteric Layer Be Saved
or Resected?
No published data are available in the literature.
However, it is advisable for hernia mesh repair
to save the cremasteric layer to reduce the risk
of ilioinguinal and genital branch nerve damage
and thus avoid possible incapacitating and chronic
postoperative pain (LE, 5; GR, D).
Should the Cut Ends of the Nerve Be
Left Alone, Ligated, or Cauterised?
No scientific data are reported in the literature
concerning the treatment of the cut ends of the
nerves.
When Glue Is Used, Should We Still
Identify and Protect the Nerves?
No data are present in the literature concerning
whether nerves should be identified and protected
even if glue is used. However, it is reasonable to
consider that nerves should be identified and pro-
tected in any case (LE, 5; GR, D).
Is There Convincing Evidence that
Prophylactic Division or Resection
of Nerves During Hernia Repair Will
Reduce the Rate of Chronic Pain?
Three randomised trials examined the effect of
prophylactic neurectomy on chronic pain [2, 9,
10]. In all of the trials, the ilioinguinal nerve was
either divided or partially resected and the pa-
tients assessed for pain, numbness, and touch and
pain sensation at 1, 6, and 12 months. None of the
Chapter 32 · Effect of Nerve Identification on the Rate of Postoperative Chronic Pain
studies found differences in pain or numbness, al-
though one found significant improvements in ac-
tivities such as cycling and walking in favour of the
nerve division group. In a prospective multicentre
study of 973 patients undergoing inguinal hernia
repair in which all nerves were identified [6],
nerve division was associated with an increased
risk of moderate to severe pain.
According to the published results in the lit-
erature, we can conclude that there is no evidence
that prophylactic neurectomy reduces chronic pain
after inguinal hernia repair. On the contrary, indi-
rect evidence suggests that identification and pres-
ervation of all nerves may be beneficial. However,
further studies addressing this issue are required.
Conclusions
The data would suggest that if one or more nerves
is not detected during surgery, it is possible that
they could be inadvertently sectioned, entrapped,
or secured (for example, if a continuous suture is
introduced along the inguinal ligament), or they
could be injured (such as if the external spermatic
vessels are divided to skeletonise the cord).
It should not be forgotten that nerves are most
often injured when the surgeon is unaware of their
location and course, or when he or she fails to
recognise them during surgery. Caution is stressed
when teaching this common procedure to resident
physicians.
Finally, it is very important to develop a uni-
form terminology for this field in order to better
analyse and compare the studies and thereby avoid
giving wrong messages to the community.
References
1. Alfieri S., Di Miceli D., Doglietto G.B. Re: nerve manage-
ment during open hernia repair Br J Surg 2007; 94(7):914
2. Picchio M., Palimento D., Attanasio U., Matarazzo P.F.,
Bambini C., Caliendo A. Randomized controlled trial of
preservation or elective division of ilioinguinal nerve on
open inguinal hernia repair with polypropylene mesh.
Arch Surg 2004; 139(7):755–758
3. Alfieri S. Is there a consensus concerning the relationship
between post-operative chronic pain and treatment to
243 32
preserve the 3 inguinal nerves during hernia repair? Ann
Surg 2008; 247(6)
4. Wijsmuller, A.R., et al. Nerve-identifying inguinal hernia
repair: a surgical anatomical study. World J Surg 2007;
31(2):414–420; discussion 421–422
5. Amid P.K., Hiatt J.R. New understanding of the causes and
surgical treatment of postherniorrhaphy inguinodynia
and orchialgia. J Am Coll Surg 2007; 205(2):381–385
6. Alfieri S., Rotondi F., Di GiorgioA., Fumagalli U., Salzano A.,
Di Miceli D., Ridolfini M.P., Sgagari A., Doglietto G.B., Groin
Pain Trial Group. Influence of preservation versus division
of ilioinguinal, iliohypogastric, and genital nerves du-
ring open mesh herniorrhaphy: prospective multicentric
study of chronic pain. Ann Surg 2006; 243(4):553–558
7. Izard G., Gailleton R., Randrianasolo S., Houry R. Treatment
of inguinal hernias by McVay’s technique in a series of
1332 cases. Ann Chir 1996; 50(9):755–756
8. Alfieri S., Di Miceli D., Doglietto G.B. Prophylactic ilioingu-
inal neurectomy in open inguinal hernia repair. Ann Surg
2007; 245(4):663
9. Ravichandran D., Kalambe B.G., Pain J.A. Pilot randomized
controlled study of preservation or division of ilioinguinal
nerve in open mesh repair of inguinal hernia. Br J Surg
2000; 87(9):1166–1167
10. Mui W.L., Ng C.S., Fung T.M., Cheung F.K., Wong C.M., Ma
T.H., Bn M.Y., Ng E.K. Prophylactic ilioinguinal neurectomy
in open ilioinguinal repair: a double-blind randomized
controlled trial. Ann Surg 2006; 244(1):27–33
11. Dittrick G.W., Ridl K., Kuhn J.A., McCarty T.M. Routine ilioin-
guinal nerve excision in inguinal hernia repairs. Am J Surg
2004; 188(6):736–740
12. Pappalardo G., Frattaroli F.M., Mongardini M., Salvi P.F.,
Lombradi A., Conte A.M., Arezzo M.F. Neurectomy to
prevent persistent pain after inguinal herniorrhaphy: a
prospective study using objective criteria to assess pain.
World J Surg 2007; 31(5):1081–1086
Discussion
Amid: To present the results of the consensus con-
ference in ten minutes is not enough time.
Schippers: One of your recommendations was to
leave the nerve where it was. You recommend not
touching the nerve anyway. But with this recom-
mendation you have problems to do the Shouldice
repair properly.
Alfieri: But this is just a personal comment and the
evidence level is very low.
 33

Discomfort 5 Years After Laparoscopic

and Shouldice Inguinal Hernia Repair:
A Report from the SMIL Study Group
A. Montgomery
 246 Chapter 33 · Discomfort 5 Years After Laparoscopic and Shouldice Inguinal Hernia Repair
Introduction
Hernia recurrence used to be the main outcome
measurement when reporting on the results of
inguinal hernia surgery. Today the problem of re-
currence is limited as a result of standardised mesh
techniques. A recurrence does not always result in
a problem for the patient, and if it does, it can usu-
ally be resolved after a new repair.
Chronic pain and discomfort is considered to
be the most important outcome measure of inguinal
hernia repair. Chronic pain and discomfort are often
difficult to handle, and even small constant prob-
lems can be an annoying reminder to the patient of
the former hernia. This is why the indications for
surgery must be very strict. The study on »watch-
ful waiting« in patients with very mild symptoms is
therefore of great importance in this respect [1].
Chronic pain is commonly defined as pain or
discomfort that lasts for more than 3 months post-
operatively. The incidence of chronic pain varies
widely in different publications: between 0% and
75% in open mesh repair and between 0% and 29%
after laparoscopic hernia repair [2–4]. Most of the
problems are described as mild discomfort. Pain
affecting daily activities has been reported to be as
high as 5–6% [5, 6]. Some authors claim that mesh
repair results in less chronic pain than nonmesh
repair and that laparoscopic repair is more favour-
able than open mesh repair in this regard [7–9].
33 The lack of description and definition of pos-
therniorrhaphy pain and discomfort is a problem,
making it impossible to compare the results from
different studies. Professor Kehlet from Denmark
and his colleagues have called for »uniform as-
sessment on postherniorrhaphy pain« to facilitate
interpretation of further studies [10]. Such as-
sessment is complicated, though, and must take
many aspects into account. Fränneby et al. have at-
tempted this by constructing an 18-question form,
a specific inguinal pain questionnaire called the
IPQ, which has been validated [11].
Another problem is that the patients who are
included in different studies often show a mixture of
different techniques for both open and laparoscopic
repair and for primary and recurrent hernias, and
there are variations in the length of follow-up. An
additional complication is the number of patient
drop-outs for the long-term follow-up. The method
of follow-up is also important. A clinical examina-
tion and a standardised protocol are seldom used.
Several large randomised studies comparing
laparoscopic to open repair for primary unilateral
inguinal hernias with a long follow-up have been
performed, with a primary end point of recurrence
rate. Most of these studies were initiated during the
1990s. Chronic pain is reported as a secondary end
point [12–15]. The SMIL study group described
below has reported on some large randomised
studies. This chapter mainly concentrates on the
discussion of chronic pain and discomfort from
the first study–SMIL I.
SMIL Study Group
The Swedish Multicentre Trial of Inguinal Hernia
Repair by Laparoscopy study group (SMIL for
short) was formed in 1993 to evaluate the possible
benefit of laparoscopic repair compared with open
techniques. The aim was to conduct well-designed
large multicentre randomised controlled trials
within general surgeon practices in the normal
clinical setting. The group has conducted two large
studies comparing laparoscopic and open repair.
SMIL I started in 1993 and compares transabdom-
inal preperitoneal (TAPP) repair with Shouldice
repair for primary inguinal hernias. This study has
resulted in three publications [16–18].
SMIL II was the second large study, initiated
in 1996 as a result of the development of both the
laparoscopic and the open inguinal hernia repair
techniques. At that time, the totally extraperitoneal
(TEP) technique had been introduced, avoiding
the transabdominal approach. At the same time,
larger meshes were recommended for a larger
overlap of the hernial orifices, with the aim of re-
ducing the risk of a recurrence. In this study, TEP
was compared with the open mesh technique of
Lichtenstein, which was the gold standard at that
time. This study has resulted in two publications,
and another two have been submitted [19, 20].
The third study is an early study of the use of
small meshes in the laparoscopic group, compar-
ing TAPP with Lichtenstein for recurrent hernias.
This has resulted in one publication [21].
Chapter 33 · Discomfort 5 Years After Laparoscopic and Shouldice Inguinal Hernia Repair
All three studies were designed with a primary
end point of recurrence after 5 years.
TAPP vs. Shouldice–SMIL I
The TAPP technique was compared to the open
Shouldice operation in primary inguinal hernias in
male patients between 30 and 70 years of age. A to-
tal of 25 board-certified surgeons using either tech-
Have you noticed signs of recurrence of your hernia
(a bulge in the operated groin)?
Yes No
Do you have any other complaints?
Yes No
247 33
nique from seven different hospitals participated
in the study. Both preoperative and perioperative
variables were recorded, and short-term outcomes
regarding pain were recorded on a visual analogue
scale (VAS) daily during the first week. The patient’s
functional status was also recorded. A clinical exam
was performed at 1 and 5 years postoperatively, look-
ing for recurrences and complaints, and a written
questionnaire was answered at 1, 2, 3, and 5 years.
The patient was asked to describe his experience of
any discomfort after the operation according to the
form depicted in ⊡ Fig. 33.1. In cases of suspected
recurrence or severe complaints, the patient was ex-
amined clinically. Complaints were graded accord-
ing to the definitions of discomfort described in
⊡ Fig. 33.2. Two independent and blinded observers
performed the grading. A consensus discussion was
held when opinions differed.

If yes, describe them here.

Results

A total of 1,068 patients were operated on within

⊡ Fig. 33.1. Form used by the patient to describe complaints
after inguinal hernia surgery
Mild: Occasional discomfort or pain that
does not interfere with daily life
Moderate: Occasional discomfort or pain that
interferes with daily life
Severe: Daily discomfort and pain that
interferes with daily life
⊡ Fig. 33.2. Definitions of discomfort
the study. Patient characteristics were similar in
the two groups. A total of 867 patients (81.2%)
were eligible for analysis after 5 years. Levels of
discomfort and pain in the two groups at the dif-
ferent time points are reported in ⊡ Table 33.1. The
total percentage of patients who experienced dis-
comfort of any kind was 8.5% in the TAPP group
and 11.4% in the Shouldice group, with no sig-
nificant difference between the groups. Although
discomfort was usually mild, it was severe in 0.2%
of the laparoscopic group and 0.7% of the open re-
pair group. Severe pain the first postoperative week
was the only risk factor for late discomfort in the
Shouldice group [odds ratio (OR) 2.25, P=0.022].

⊡ Table 33.1. Grade of discomfort at different time points in the SMIL I study (TAPP transabdominal preperitoneal)

1 Year 2 years 3 years 5 years

Tapp Open Tapp Open Tapp Open Tapp Open
Mild 9.4 10.5 8.9 13.4 9.2 10.6 5.5 7.9
Moderate 3.1 3.4 2.2 2.8 2.3 3.8 2.8 2.8
Severe 0.2 0 0 0.2 0 0 0.2 0.7
Total 12.7 13.9 11.2 16.4 11.5 14.4 8.5 11.4
 248 Chapter 33 · Discomfort 5 Years After Laparoscopic and Shouldice Inguinal Hernia Repair
No other risk factor for late discomfort was found
in either group.
Discomfort in SMIL I Compared with
SMIL II
The SMIL II study had the same protocol as SMIL
I, but the operating techniques were different, as
described above. A total of 1,370 patients were op-
erated on, and 1,275 had a 5-year follow-up. Having
the same protocol enables more appropriate com-
parison of all four techniques regarding postopera-
tive pain. Discomfort at 1, 2, 3, and 5 years is shown
in ⊡ Fig. 33.3. There was a statistically difference
between Shouldice and TAPP only at the 2-year
point. There was a statistically significant difference
between Lichtenstein and TEP at all time points
in favour of the TEP technique. The risk of having
chronic pain was approximately twice as high in
the Lichtenstein group as in the other groups at all
time points; almost 20% in the Lichtenstein group
reported discomfort at all time points.
%
* *
20
33 18 *
16
14
12
10
8 Lichtenstein
6
4
2
0
1 2
⊡ Fig. 33.3. Total amount of discomfort for different techniques at different time points in the SMIL I and II studies. Significant
differences between groups are indicated by an asterisk (*)
The number of patients classified as having
severe pain was low in both groups. Patients with
severe or moderate pain were therefore merged,
creating the moderate/severe pain group. The re-
sults are demonstrated in ⊡ Fig. 33.4. There was
a statistically significant trend over time for a
decrease in frequency of moderate/severe chronic
pain for Lichtenstein repair but not for the other
techniques.
In a multivariable analysis, risk factors for
chronic pain in the TEP group were impairment
in the physical test after 1 week, longer recovery
time than the median, and weight below the 3rd
quartile. For the Lichtenstein group, the risk factor
was pronounced postoperative pain.
Discussion
Discomfort and chronic pain was not the primary
end point in any of the large randomised studies
comparing laparoscopic and open hernia inguinal
hernia repair. Altogether, there are four studies on
*
*
TAPP
Shouldice
TEP
3 5 years
Chapter 33 · Discomfort 5 Years After Laparoscopic and Shouldice Inguinal Hernia Repair
chronic pain besides the SMIL studies, including
more than 400 patients [12–15]. There are huge dif-
ferences in these studies in follow-up time, which
varies between 1 and 5 years. There are also huge
differences in the percentage of attendees at the last
follow-up, varying between 61% and 96%. The defi-
nition of chronic pain is also difficult to compare
among the studies, but all studies report less pain
with the laparoscopic technique. However, this var-
ies in the studies, too, being between 0% and 18%
for the laparoscopic technique and between 1% and
20% for the open techniques. The overall percentage
of chronic pain at 5 years in the SMIL I study was
8.5% for TAPP and 11.4% for Shouldice. This dif-
ference is, however, not significant. In SMIL II there
was a bigger difference between chronic pain in
the TEP-operated and Lichtenstein groups–9% and
19%, respectively. However, the high attendance,
with clinical examination and a standardised ques-
tionnaire, at 5-year follow-up in both SMIL studies
is one of the SMIL studies’ strengths.
A heavy polypropylene mesh was fixated us-
ing a stapling device in both the TAPP and TEP
249 33
procedures. The same mesh was used for the Lich-
tenstein operation. In recent research, anchoring
of the mesh has been discussed as one cause of
chronic pain. Several randomised studies have
been performed on different fixation techniques,
showing advantages for the nonfixated or glued
mesh in endoscopic methods [22–25]. The advan-
tage of less pain by using a low-weight mesh with
large pores has also been discussed [26, 26].
All in all, the endoscopic preperitoneal tech-
nique seems to be more favourable for patients from
the aspect of preventing chronic pain and discom-
fort. Development of new meshes and avoidance of
fixation might favour the patients even further.
References
1. Fitzgibbons RJ, Giobbie-Hurder A et al. (2006) Watchful
waiting vs repair of inguinal hernia in minimally symp-
tomatic men. A randomized clinical trial. JAMA 295:285–
292
2. Nienhuijs SW, van Oort I, Keemers-Gels ME, Strobbe LJA,
Rosman C. (2005) Randomized clinical trial comparing

%
20
18
16
14
12 TAPP
Shouldice
10
* TEP
8 Lichtenstein
6 *
4
2
0
1 2 3 5 years

⊡ Fig. 33.4. Moderate or severe discomfort for different techniques at different time points in the SMIL I and II studies. Signifi-
cant differences between groups are indicated by an asterisk (*)
 250 Chapter 33 · Discomfort 5 Years After Laparoscopic and Shouldice Inguinal Hernia Repair
the Prolene Hernia System, mesh plug repair and Lich-
tenstein method for open inguinal hernia repair. Br J Surg
92:33–38
3. Poolban AS, Bruce J, Smith WC, King PM, Krukowski ZH,
Chambers WA. (2003) A review of chronic pain after ingui-
nal herniorrhaphy. Clin J Pain 19(1):48–54
4. PageB, Paterson C, Young D, O´Dwyer PJ. (2002) Pain from
primary inguinal hernia and the effect of repair on pain.
Br J Surg 89(10):1315–1318
5. Kalliomäki ML, Sandblom G, Gunnarsson U, Gordh T.
(2009) Persistent pain after groin hernia surgery: a quali-
tative analysis of pain and its consequences for quality of
life. Acta Anaesthesiol Scand 53(2):236-246
6. Fränneby U, Sandblom G, Nordin P, Nyrén O, Gunnarsson
U. (2006) Risk factors for long-term pain after hernia sur-
gery. Ann Surg 244(2):212–219
7. Schmedt C-G, Sauerland S, Bittner R. (2005) Compari-
son of endoscopic procedures vs Lichtenstein and other
open mesh techniques for inguinal hernia repair. A me-
ta-analysis of randomized controlled trials. Surg Endosc
19:188–199
8. Bittner R, Sauerland S, Schmedt C-G. (2005) Comparison
of endoscopic techniques vs Shouldice and other open
nonmesh techniques for inguinal hernia repair. A meta-
analysis of randomized controlled trials. Surg Endosc
19:605–615
9. McCormack K, Scott NW, Go PM, Ross S, Grant AM and
the EU Hernia Trialists Collaboration. (2003) Laparoscopic
techniques versus open techniques for inguinal hernia
repair. Cochrane Database Syst Rev (1)CD001785
10. Kehlet H, Bay-Nielsen M, Kingsnorth A. (2002) Chronic
postherniorrhaphy pain–a call for uniform assessment.
Hernia 6:178–181
11. Fränneby U, Gunnarsson U, Andersson U, Heuman R,
Nordin P, Nyrén O, Sandblom G. (2008) Validation of an
inguinal pain questionnaire for assessment of chronic
33 pain after groin hernia repair. Br J Surg 95(4):488–493
12. Grant AM, Scott NW, O´Dwyer PJ, on behalf of the MRC
Laparoscopic Groin Hernia Trial Group. (2004) Five-
year follow-up of a randomized trial to assess pain and
numbness after laparoscopic or open repair of groin her-
nia. Br J Surg 91:1570–1574
13. Liem MSL, Van Der Graaf Y, Van Steensel CJ, Boelhouwer
RU, Clevers GJ, Meijer WS, Stassen LP, Vente JP, Weidema
WF, Schrijvers AJ, van Vroonhoven TJ. (1997) Comparison
of conventional anterior surgery and laparoscopic sur-
gery for inguinal hernia repair. N Engl J Med 336:1541–
1547
14. Johansson B, Hallerbäck B, Glise H, Anesten B, Smedberg
S, Román J. (1999) Laparoscopic mesh versus open prepe-
ritoneal mesh versus conventional technique for inguinal
hernia repair: a randomized multicenter trial (SCUR Her-
nia Repair Study). Ann Surg 230(2):225–231
15. Neumayer L, Giobbe-Hurder A, Jonasson O, Fitzgibbons R
Jr, Dunlop D et al. (2004) Open mesh versus laparoscopic
mesh repair of inguinal hernia. N Engl J Med 350:1819–
1827
16. Berndsen F, Arvidsson D, Enander L-K, Leijonmarck CE,
Wingren U, Rudberg C, Smedberg S, Wickbom G, Montgo-
mery A. (2002) Postoperative convalescence after ingui-
nal hernia surgery: prospective randomised multicenter
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repair in 1042 patients. Hernia 6:56–61
17. Arvidsson D, Berndsen FH, Larsson LG, Leijonmarck CE,
Rimback G, Rudberg C, Smedberg S, Spangen L, Montgo-
mery A. (2005) Randomized clinical trial comparing 5-year
recurrence rate after laparoscopic versus Shouldice repair
of primary inguinal hernia. Br J Surg 92:1085–1091
18. Berndsen F, Petersson U, Arvidsson D, Leijonmarck C, Rud-
berg C, Smedberg S, Montgomery A. (2007) Discomfort
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from the SMIL study group. Hernia 11(4):307–313
19. Ekelund A, Rudberg C, Smedberg S, Enander LK, Leijon-
marck CE, Österberg J and Montgomery A. (2006) Short-
term results of a randomized clinical trial comparing
Lichtenstein open repair with totally extraperitoneal lapa-
roscopic inguinal hernia repair. Br J Surg 93:1060–1068
20. Eklund A, Montgomery A, Rasmussen I, Sandbue R, Bergk-
vist L, Rudberg C. (2009) Low recurrence rate after lapa-
roscopic (TEP) and open (Lichtenstein) inguinal hernia
repair. Ann Surg 249(1):33–38
21. Eklund A, Rudberg C, Leijonmarck CE, Rasmussen I, Span-
gen L, Wickbom G, Wingren U, Montgomery A. (2007)
Recurrent inguinal hernia: randomized multicenter trial
comparing laparoscopic and Lichtenstein repair. Surg En-
dosc 21:634–640
22. Taylor C, Layani L, Liew V, Ghusn M, Crampton N, White S.
(2008) Laparoscopic inguinal hernia repair without mesh
fixation: early results of a large randomised clinical trial.
Surg Endosc 22(3):757–762
23. Olmi S, Scaini A, Erba L, Guaglio M, Groce E. (2007) Quan-
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differences between prosthesis fixation systems. Surgery
142(1): 40–46
24. Lovisetto F, Zonta S, Rota E, Mazzilli M, Bardone M, Bottero
L, Faillace G, Longoni M. (2007) Use of human fibrin glue
(Tissucol) versus staples for mesh fixation in laparoscopic
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25. Lau H. (2005) Fibrin sealant versus mechanical stapling for
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26. O’Dwyer PJ, Kingsnorth AN, Molloy RG, Small PK, Lammers
B, Horeyseck G. (2005) Randomized clinical trial assessing
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26:1472–1480
 34

Recurrence or Complication:
The Lesser of Two Evils? A Review
of Patient-Reported Outcomes
from the VA Hernia Trial
L. Neumayer
 252 Chapter 34 · Recurrence or Complication: The Lesser of Two Evils?
Introduction
Inguinal hernia is one of the most common disease
states affecting men worldwide. The direct and
indirect costs of this condition, with or without re-
pair, are great. Recent studies have questioned the
need for repair in asymptomatic patients; however,
in both of these studies, pain and discomfort were
the main reasons for a crossover to repair from the
»watchful waiting« group [1, 2].
Pain is now recognized as a common com-
plication after hernia repair. In this review we
intend to address, using previously reported data
[3–5], the issue of whether a recurrence–which is
viewed by most surgeons as a negative outcome–is
worse for the patient in the long term than pain
or other complications. Further, we review pre-
dictors of complications that may help guide sur-
geons in the choice of operation for individual
patients.
Methods
The methods of the U.S. Department of Veteran
Affairs (VA) hernia trial comparing laparoscopic
versus open tension free hernia repair, as well as
the analyses performed for evaluation of patient-
reported outcomes and predictors of complica-
tions, have been previously reported [3–6]. The
study was designed to detect a 3% difference in re-
currence at 3 years and to evaluate other surgeon-
34 centered and patient-centered outcomes (com-
plications/death, pain, functional status, activity
levels, caregiver burden, and cost). In addition, we
measured patient and surgeon satisfaction. As part
of this large study, two new instruments, the Surgi-
cal Pain Scale (SPS) and the Activities Assessment
Scale (AAS), were developed and validated [7, 8].
All results reported herein have been previously
reported [3–6]. This report serves as an amalga-
mation of prior analyses.
As a post hoc analysis, we also evaluated the
relationship between patient-reported outcomes
(PROs) and recurrence or complications [4]. In
particular, we sought to determine the impact of
recurrence and other complications on overall pa-
tient outcome as measured by the Medical Out-
comes Study Short Form 36 (SF-36). This analysis
was limited to patients who had both preoperative
and postoperative PRO assessment. Cumulative
rates of recurrence and complications were used.
Complications were further divided into four cat-
egories: (1) hematoma/seroma, (2) orchitis, (3)
neuralgia of the leg or groin, and (4) other. Patient-
reported outcomes included the SF-36, the SPS,
the AAS, and patient satisfaction. All of these out-
comes were measured at baseline and at 2 weeks,
3 months, 6 months, and 1 and 2 years postop-
eratively. (Patient satisfaction, however, was not
measured at 2 years.)
To evaluate the relationships between preop-
erative and postoperative PROs, we used Pearson’s
correlation coefficients. Univariate comparisons
among groups were performed using analysis of
variance for continuous variables and chi-square
or Fisher’s exact test for categorical variables. Re-
gression analyses were employed to determine sig-
nificant predictors of postoperative PROs.
As previously reported, we further analyzed
predictors of short-term and long-term complica-
tions and long-term pain by initially looking for
potential predictors with appropriate univariate
statistics. Our initial analyses revealed different
predictors for open and laparoscopic techniques,
so we modeled these separately. Only outcomes
with at least 50 occurrences and with p-values >0.2
in univariate comparisons were entered into re-
gression models to ensure relative stability in the
models [5].
Results
As reported previously 2,134 men were random-
ized to Lichtenstein or laparoscopic (totally ex-
traperitoneal or transabdominal preperitoneal)
repair of their inguinal hernias [3]. Although a
few patients did not undergo repair, 1,983 com-
pleted an operative intervention, and 1,696 were
available for 2-year recurrence assessment. Nearly
all of these patients (1,603) also had PRO data at
2 years (1,526 had PRO data at 1 year). Demo-
graphics of the patients with PRO data at 1 and
2 years were similar to those of the whole group
(⊡ Table 34.1) [3, 4].
Chapter 34 · Recurrence or Complication: The Lesser of Two Evils?
⊡ Table 34.1. Demographic and outcome data, adapted from Hawn et al. [5] and Matthews et al. [6] (PRO patient-
reported outcome)
Total study
N=1,983
Open Laparoscopic
N (%) N (%)
Recurrence 41/834 (4.9) 87/862 (10.1)
Neuralgia 99/950 (10.4) 71/943 (7.5)
Hematoma 17/950 (1.8) 50/943 (5.3)
Orchitis 7/950 (0.7) 11/943 (1.2)
Other 80/950 (8.4) 86/943 (9.1)
Patients with recurrence, a complication,
or both reported scores for the AAS, SPS, and
physical component portion of the SF-36 that
were significantly different on univariate analy-
ses (p<0.001) from those for patients without a
recurrence or complication. Patient satisfaction
also differed; 97% of patients who did not have
a recurrence or complication were satisfied with
their operation, whereas only 62% of those with a
recurrence and 89% of those with a complication
were satisfied.
After adjustments were made for baseline pre-
operative scores and patient demographics, a re-
currence did not affect the patient’s general health
status as measured by the SF-36. However, patients
with neuralgia or orchitis had significantly lower
PCS scores than patients who did not suffer those
complications. Patients with neuralgia had lower
mental component scores than those without neu-
ralgia.
After open repair, patients with a recurrence
had significantly more pain at rest and with activ-
ity than patients who had recurrence after laparo-
scopic repair. As would be expected, patients with
self-reported neuralgia had higher pain scores on
the SPS (10-mm difference at rest, 21-mm dif-
ference during work or exercise) compared with
patients without neuralgia. Younger patients had
more pain preoperatively and postoperatively than
older patients did, but the magnitudes of reduction
in pain scores were equivalent between younger
and older patients.
253 34
PRO subgroup at 2 years
N=1,603
Open Laparoscopic
N (%) N (%)
37 (4.6) 68 (8.5)
67 (8.4) 53 (6.6)
14 (1.8) 41 (5.1)
6 (0.8) 11 (1.4)
69 (8.6) 81 (10.1)
Younger patients who were not actively em-
ployed prior to operation reported more limita-
tions in activity during work or exercise as mea-
sured by the AAS. The presence of neuralgia,
orchitis, or other complications also limited activ-
ity during work or exercise, but the presence of a
recurrence did not limit activity during work or
exercise. When operative techniques were com-
pared, other complications after laparoscopic re-
pair were accompanied by limitations in patient
activity, whereas other complications after open
repair did not seem to limit activity.
Younger patients and those with a recurrence,
neuralgia, or other complications were signifi-
cantly less likely to be satisfied with the operation
or their total hernia care when analyzed by logistic
regression.
Predictors of Complications
As previously reported, complications were di-
vided into short term (occurring within 2 weeks of
operation) and long term (occurring at 3 months
and beyond) and occurred more frequently in
patients who had undergone laparoscopic repair
(39% vs. 33%, p=0.02) [3, 5]. The most com-
mon short-term complications in both the open
and laparoscopic groups were wounds/scrotal
hematomas/seromas and urinary retention. The
most common long-term complications were
seromas and chronic leg or groin pain. Wound
 254 Chapter 34 · Recurrence or Complication: The Lesser of Two Evils?

⊡ Table 34.2. Predictors of complications after open repair (multivariate analysis), adapted from Matthews et al. [6] (OR
odds ratio; CI confidence interval; MCS mental component score)

Complications Significant predictors Adjusted OR p-value

(c-index of model) (95% CI)

Short-term Type of hernia: recurrent 2.02 0.006

(0.655) (1.22, 3.32)

Hispanic ethnicity 2.94 0.043

(1.03, 8.35)

Hernia into scrotum 2.31 0.0005

(1.47, 3.94)

Long-term SF-36 MCS score: OR for each 3-unit increase 0.95 0.008
(0.624) (0.92, 0.99)

Age: OR for each 5-year increase 0.90 0.003

(0.84, 0.97)

⊡ Table 34.3. Predictors of complications after laparoscopic repair (multivariate analysis), adapted from Matthews et al.
[6] (OR odds ratio; CI confidence interval; BMI body mass index)

Complications Significant predictors Adjusted OR p-value

(c-index of model) (95% CI)

Short-term Enlargement of hernia in past 6 months 1.50 0.01

(0.644) (1.10, 2.05)

Duration: present for >1 year 1.59 0.004

(1.16, 2.18)

Hernia into scrotum 2.02 0.011

(1.18, 3.46)

Prostatism 1.94 0.0005

(1.34, 2.81)

Type of hernia: recurrent 2.04 0.003

34 (1.27, 3.27)

Long-term Prostatism 1.71 0.009

(0.631) (1.14, 2.57)

BMI: OR for each 1-unit BMI increase 1.07 0.006

(1.02, 1.12)

infection was infrequent at any time for both
types of repair, and no patient required mesh
removal.
For both techniques, having a recurrent hernia
repaired increased the likelihood of short-term
complications, as did the presence of a hernia ex-
tending into the scrotum (⊡ Tables 34.2 and 34.3).
Prostatism was a predictor for both short-term and
long-term complications in the laparoscopic group,
while younger age was associated with long-term
complications in the open group. Younger age was
associated with a higher likelihood of long-term
pain in both open and laparoscopic groups (the
adjusted odds ratio for each 5-year increase in age
was 0.82 in open repairs and 0.83 in laparoscopic
repairs) [5].
Chapter 34 · Recurrence or Complication: The Lesser of Two Evils?
Discussion
The VA hernia trial comparing laparoscopic and
open tension-free inguinal hernia repair in men is
one of the largest ever conducted. We planned to
be able to examine both surgeon-centered (recur-
rence, complications, and death) and patient-cen-
tered (SF-36 functional status, surgical pain, activi-
ties) outcomes for the duration of the study, which
included a minimum of 2 years of follow-up. Col-
lecting such massive amounts of data has allowed
analyses of many different outcomes. Our analysis
of the relationship of patient-centered outcomes
to recurrences and complications is one of the few
based on prospectively collected data rather than
recall data from patients mailed a survey years af-
ter their herniorrhaphy.
From these further analyses, we have con-
firmed the findings of others that chronic pain
is a significant and measurable adverse effect of
hernia repair and that it is more common long
term after open repairs and in younger patients.
We have further elucidated that for most patients,
chronic pain has a deleterious effect on overall
functional status, whereas recurrence, although
associated with pain, in and of itself does not
negatively affect functional status as measured
by the physical component score of the SF-36. In
our cost-effectiveness analysis, we showed that
laparoscopic repair was cost-effective for a uni-
lateral hernia; it is possible that the finding of a
decreased physical component score in patients
with chronic pain and no recurrence is respon-
sible for this finding [9].
In addition, we have identified some other pre-
dictors of complications, which will require fur-
ther investigation as to whether they themselves
are putative risk factors or surrogates for unmea-
sured factors.
The strength of the VA hernia trial is that
it was conducted in »real-life« practices, not in
highly specialized hernia or laparoscopic centers,
and therefore represents the current practice of
most general surgeons. As part of the trial, data
were collected prospectively, allowing analyses of
many secondary outcomes. A limitation is that the
study was performed within the Veterans Affairs
healthcare system, in which the majority of pa-
255 34
tients needing inguinal hernia repair are not »good
risk,« thus limiting to some extent the generaliz-
ability of our results.
References
1. Fitzgibbons RJ, Giobbie-Hurder A, Gibbs JO, Dunlop DD,
Reda DJ, McCarthy M, Neumayer LA, et al. (2006) Watch-
ful waiting vs repair of inguinal hernia in minimally
symptomatic men: a randomized clinical trial. JAMA
295(3):285–292
2. O’Dwyer PJ, Norrie J, Alani A, et al. (2006) Observation
or operation for patients with an asymptomatic inguinal
hernia. A randomized clinical trial. Ann Surg 244(2):
167–173
3. Neumayer L, Jonasson O, Fitzgibbons R, Henderson W,
Gibbs J, Carrico CJ, Itani K, Kim L, Pappas T, Reda D, Dun-
lop D, McCarthy, Hynes D, Giobbie-Hurder A, London MJ,
Hatton-Ward S. (2003) Tension-free inguinal hernia repair:
the design of a trial to compare open and laparoscopic
surgical techniques. J Am Coll Surg 196(5):743–752
4. Neumayer L, Giobbie-Hurder A, Jonasson O, Fitzgibbons
R, Dunlop D, Gibbs J, Reda D, Henderson W. (2004) Open
mesh versus laparoscopic mesh repair of inguinal hernia.
N Engl J Med 350(18):1819–1827
5. Hawn MT, Itani K, Giobbie-Hurder A, McCarthy M, Jonas-
son O, Neumayer LA. (2006) Patient reported outcomes
following inguinal herniorrhaphy. Surgery 140:198–205
6. Matthews RM, Anthony T, Kim LT, Wang J, Fitzgibbons
JR, Giobbie-Hurder A, Reda DJ, Itani KMF, Neumayer LA.
(2007) Factors associated with postoperative complica-
tions and hernia recurrence for patients undergoing in-
guinal hernia repair: a report from the VA Cooperative
Hernia Study Group Am J Surg 194(5):611–617
7. McCarthy M, Chang CH, Pickard AS, Giobbie-Hurder A,
Price DD, Jonasson O, Gibbs J, Fitzgibbons R, Neumayer
L. (2005) Visual analog scales for assessing surgical pain. J
Am Coll Surg 201(2):245–252
8. McCarthy M, Jonasson O, Chang CH, Pickard AS, Giobbie-
Hurder A., Gibbs J, Edelman P, Fitzgibbons R, Neumayer
L. (2005) Assessment of patient functional status after
surgery. J Am Coll Surg 201(2):171–178
9. Hynes D, Sroupe K, Luo P, Giobbie-Hurder A, Reda D, Kraft
M, Itani K, Fitzgibbons R, Jonasson O, Neumayer L, for the
Veterans Affairs Cooperative Studies Program 456 Inves-
tigators. (2006) Cost-effectiveness of laparoscopic versus
open mesh hernia operation: results from a Department
of Veterans Affairs randomized clinical trial. J Am Coll Surg
203(4):447–457
 35

Chronic Pain After Inguinal Hernia

Repair: The Choice of Prosthesis
Outweighs That of Technique
G. G. Champault
 258 Chapter 35 · Chronic Pain After Inguinal Hernia Repair: The Choice of Prosthesis Outweighs That of Technique
Introduction
The true incidence of chronic pain after inguinal
herniorrhaphy is unknown, and until recently it
was a secondary consideration, with the recurrence
rate being deemed of greater importance. The inci-
dence was reduced by the use of prostheses [1]. As
recurrences have declined, though, more attention
is now being focused on other measures of success,
particularly quality of life. Numerous recent studies
have examined the incidence of chronic pain after
operations. Grant et al. [2] reported that 9.7% of
their patients experienced chronic pain after surgery,
and other studies [3–6] have put the figure as high
as 34%. Typically, such complaints decrease over the
course of the first year [7], but a significant number
of patients do develop chronic and debilitating pain
[8]. With the recognition that this is more common
than was previously realized, numerous authors have
begun to investigate the impact of pain on quality of
life [9, 10]. Various factors have been examined to
determine the etiology of postoperative pain.
Patient age has been implicated, with the avail-
able data indicating that younger patients have a
higher likelihood of postoperative pain [5, 10]. But
a recent study [7] refuted this notion, finding that
the incidence of chronic pain is evenly distributed
among age groups.
Preoperative pain seems to be a risk factor,
with multiple studies [5, 6] showing that those
who report pain beforehand are more likely to de-
velop chronic pain afterward.
Certain individuals can be physiologically or
psychologically predisposed to develop chronic
pain. Courtney et al. [8] found that patients with
35 such symptoms after herniorrhaphy are more
likely than most other people to suffer from other
chronic pain conditions. Body habitus may play a
role here because obese patients can have a higher
incidence of postoperative inguinodynia [10].
Ferzli et al. [11] found that the probability of
developing chronic pain was more than twofold
higher in those undergoing ambulatory hernior-
rhaphy. The type of anesthetic administered has
been examined as a possible factor in this problem.
Nordin et al. [12] showed that local anesthesia was
associated with less chronic pain than regional or
general anesthesia.
Other risk factors for chronic pain include being
employed and having private health insurance [5].
Direct injury to nerves, resulting in either par-
tial or complete transection, can lead to neuroma
formation and subsequent development of chronic
pain. The ilioinguinal and iliohypogastric segments
of the genital branch of the genitofemoral nerves are
vulnerable to injury; when injured, they can pro-
duce pain syndromes that are refractory to narcotic
and multidisciplinary management techniques.
Some authors have also implicated the role
of mesh [13, 14]. Demirer et al. [15] showed that
when peripheral nerve tissue comes in contact
with polypropylene mesh, myelin degeneration as-
sociated with edema and fibrosis occurs. However,
multiple studies have examined this issue, and the
weight of the evidence seems to indicate that mesh
does not significantly increase the risk of chronic
pain [8, 10, 16].
Operative technique may also play a role. No
particular surgical approach has proved superior
in terms of subsequent pain, although data sug-
gest that the laparoscopic procedure [17] may be
more beneficial. Douek et al. [18] found that after
5 years, the transabdominal preperitoneal proce-
dure resulted in significantly less pain than an
open tension-free mesh repair (2% vs. 10%). In
contrast, the largest study [19] to date comparing
open techniques with laparoscopy found no differ-
ences after 3 months.
Multiple studies have examined the role of
mesh. The etiological factors include irritation or
damage of inguinal nerves by sutures or mesh [13],
an inflammatory reaction against the mesh [20],
or simply scar tissue. A recent systematic review of
mesh techniques compared with nonmesh meth-
ods pointed out that no strong evidence indicated
that the use of mesh increased the rate of chronic
pain [1]. Recent studies [3] have pointed out that
»mesh-induced pain« occurs more frequently than
reported, including in tension-free techniques.
Amid [21] identified »meshoma« as a radiologic
entity and pathologic cause of chronic pain. Me-
shoma occurs when the mesh prosthesis becomes
wadded into a ball because of nonfixation, insuf-
ficient fixation, or insufficient dissection to make
adequate room for the prosthesis. In other situa-
tions, the weight of the evidence seems to indicate
Chapter 35 · Chronic Pain After Inguinal Hernia Repair: The Choice of Prosthesis
that mesh does not significantly increase the risk
of chronic pain [10, 16, 18].
But research into alternatives to polypropylene
continues. Cobb et al. [22] have advocated the use
of newer lightweight polypropylene, which may in
theory result in less foreign body response and
would improve operative outcomes. Post et al. [23]
reported that after 6 months of follow-up, light-
weight polypropylene mesh is preferable to con-
ventional mesh for Lichtenstein repair of inguinal
hernia. After this study, two randomized studies
[24, 25] reported that use of a partially absorbable
lightweight mesh was associated with less chronic
pain than a nonabsorbable heavy mesh after 1 and
3 years. The frequency of recurrence was similar for
the two meshes. A recent laparoscopic study indi-
cated that fewer postoperative complications and an
improved quality of life can be achieved by reduc-
ing the amount of polypropylene in meshes used
for laparoscopic hernia repair [26]. Foreign body
sensations were also fewer for lightweight meshes
compared with conventional polypropylene mesh.
In this study, Horstmann et al. [26] followed their
patients only 1 year after surgery, when a foreign
body sensation is more common than after 2 years.
On the other hand, Paajanen [14] recently
compared three different meshes [partially absorb-
able polypropylene–polyglactin mesh, lightweight
polypropylene mesh (55 g/m2), and conventional
densely woven polypropylene mesh] in a random-
ized trial of 228 patients (232 hernias) treated by
Lichtenstein tension-free hernioplasty under local
anesthesia in same-day surgery by the same sur-
geon using exactly the same surgical technique. He
found no differences in pain or quality of life after
2 years of follow-up.
The nature and quality of prostheses have
evolved over the last 10 years, with polypropylene
being the most common material. Many prosthe-
ses have offered additional refinements: anatomi-
cal molding; inclusion of elements to reduce the
residual mass of nonresorbable material, thereby
diminishing complications; and, recently, coatings
of substances that assist in tissue acceptance and
integration.
We performed a study [27] to prospectively as-
sess the results at 2-year follow-up in patients who
underwent tension-free hernia repair by either the
259 35
Lichtenstein technique or laparoscopy, using two
types of prostheses: polypropylene and beta-D-glu-
can-coated polypropylene (Glucamesh, Genzyme
France). Glucan-coated prostheses are composed
of an unwoven polypropylene mesh that is coated
with beta–(1→3),(1→4)-D-glucan, a complex car-
bohydrate extract of oat. Oat beta-glucan is an
entirely (100%) natural plant product that has been
used in burn and wound care applications [28–30].
Beta-glucans have also been the subject of research
regarding their roles as immunomodulators [31–34]
and agents in wound healing [35, 36].
Patients and Methods
Patients
Between 2001 and 2003, 410 consecutive patients
(396 men, 14 women) of mean age 54 years (range
18–84) underwent repair of inguinal hernias, 96
(23%) of which were bilateral and 56 (13%) recur-
rent. Most patients (95%) were classified as Ameri-
can Society of Anesthesiologists (ASA) physical
status I or II [8], and 72 (17.5%) of them had a
body mass index (BMI) above 30.
Methods
All surgery was done under general anesthesia by
four surgeons. Thrombosis prophylaxis and anti-
biotic prophylaxis were used in all cases. Lichten-
stein repair was performed as first described [9].
The prosthesis was fixed at the inguinal ligament
with five to seven stitches of polypropylene. In lap-
aroscopic repair (totally extraperitoneal approach,
or TEP), the Retzius space was developed and
insufflated using three trocars. Prostheses were not
fixed. This technique was preferred for bilateral
hernias or for hernias that recurred after hernior-
rhaphy in young (20–45 years) active professionals
or sportsmen or women with no anesthetic risk
and a BMI under 30. All other patients underwent
Lichtenstein repair.
Two types of prosthesis were used: polypropyl-
ene of weight per unit area 105 g/m2 (Bard, Ethi-
con) and polypropylene of weight per unit area
 260 Chapter 35 · Chronic Pain After Inguinal Hernia Repair: The Choice of Prosthesis Outweighs That of Technique
50 g/m2 coated with beta-D-glucan (Glucamesh;
Genzyme France), a plant derivative (oat) that
promotes healing and has an immunomodulatory
effect.
Patients were randomly assigned to the two
groups depending on whether they agreed to be
included in a prospective study [10].
All patients were followed up prospectively
for at least 2 years by a surgeon not involved in
the study. Recurrence was confirmed by physical
examination or repeat surgery. Chronic pain was
assessed using a visual analog scale (VAS) and a
validated questionnaire [11]. Pain was considered
mild for a VAS score below 3, moderate below 5,
and severe or debilitating above 5.
Statistics
Quantitative values are given as means ± standard
deviation. The Kruskal–Wallis test or Wilcoxon
test was used for (nonparametric) comparison of
the two groups. For qualitative parameters, per-
centages were compared using the chi-square test.
Differences were considered statistically significant
for p-values <0.05. The statistical analyses were
done using SPSS 10.0 software for Windows.
Results
Lichtenstein repair was done in 273 (66.5%) pa-
tients, with polypropylene mesh in 215 (78.7%)
and Glucamesh in 58 (21.3%). Laparoscopic repair
was used in 137 patients, with polypropylene mesh
35 in 80 (58.4%) and Glucamesh in 57 (41.6%). In
⊡ Table 35.1. Two-year recurrence (n%) as a function of technique and mesh (ns not significant)
n Recurrence
Lichtenstein 232
Laparoscopy 117
Glucamesh 104
Polypropylene 245
Total 349
each of these two groups, the populations were
comparable in terms of age, gender, type of hernia,
ASA score, and incidence of obesity. The mean du-
ration of hospitalization was 2.82 days (range 1–5),
independent of the technique or mesh.
Two-year follow-up was possible in 85.1% of
patients (n=349: 117 TEP, 232 Lichtenstein) and
was comparable for the two techniques used.
At 2 years, recurrence had occurred in 10 cases
(2.8%) and was independent of the technique [TEP
n=2/117 (1.7%) vs. Lichtenstein n=8/232 (3.4%),
not significant] or of the type of mesh [Glucamesh
n=2/104 (1.9%) vs. polypropylene n=8/245 (2.4%),
not significant]. (⊡ Table 35.1).
At 2 years of follow-up, 69 patients presented
with residual mild (VAS<3) or moderate (VAS<5;
19.7%) pain and 11 with intense pain (VAS>5;
3.1%). Moderate pain (⊡ Tables 35.2 and 35.3) was
significantly less frequent (p=0.05) with Glu-
camesh than with polypropylene mesh (4.8% vs.
26.1%) irrespective of the repair technique (6.5%
vs. 27.2% for laparoscopy; 3.7% vs. 25.6% for Lich-
tenstein). There was no significant difference be-
tween the two techniques in the Glucamesh group
(6.5% vs. 3.7%) or the polypropylene mesh group
(27.2% vs. 25.6%). This was also true for chronic,
severe, debilitating pain (⊡ Tables 35.4 and 35.5).
Pain characteristics were comparable whatever the
repair technique (⊡ Table 35.6).
Discussion
There is no consensus concerning the repair tech-
nique for inguinal hernia. However, it is clear that
the use of prosthetic strengthening significantly
% p
8 3.4 ns
2 1.7 ns
2 1.9 ns
8 2.4 ns
10 28
Chapter 35 · Chronic Pain After Inguinal Hernia Repair: The Choice of Prosthesis
261 35
reduces the incidence of recurrence [37]. Tension- repair, which is now the most widespread tech-
free techniques may reduce the incidence of re- nique because of its advantages in terms of cost,
sidual pain [9, 10]. This explains the preference risk, and simplicity. Nonetheless, the indications
for the laparoscopic approach and for Lichtenstein for laparoscopic repair are still subject to debate.

⊡ Table 35.2. Incidence of chronic pain (n%) as a function of technique (ns not significant)

Laparoscopy Lichtenstein Total p

Glucamesh 3/51 (6.5%) 2/53 (3.7%) 5/104 (4.8%) ns

Polypropylene 18/66 (27.2%) 46/179 (25.6%) 64/245 (26.5%) ns

Total 21/117 (17.9%) 48/232 (20.6%) 69/349 (19.7%) ns

⊡ Table 35.3. Incidence of chronic pain (n%) as a function of mesh

Glucamesh Polypropylene p

Totally extraperitoneal approach 3/51 (6.5%) 18/66 (27.2%) p=0.02

Lichtenstein 2/53 (3.7%) 46/179 (25.6%) p=0.02

Total 5/104 (4.8%) 64/245 (26.5%) p=0.02

⊡ Table 35.4. Incidence of severe pain (visual analog score >5) as a function of technique (ns not significant)

Laparoscopy Lichtenstein Total p

Glucamesh 1/51 (1.9%) 0/53 (0%) 1/104 (0.9%) ns

Polypropylene 3/66 (4.5%) 7/179 (3.3%) 10/245 (4%) ns

Total 4/117 (3.4%) 7/232 (3%) 11/349 (3.1%) ns

⊡ Table 35.5. Incidence of severe pain (visual analog score >5) as a function of mesh

Glucamesh Polypropylene p

Totally extraperitoneal approach 1/51 (1.9%) 3/66 (4.5%) p=0.27

Lichtenstein 0/53 (0%) 7/179 (3.3%) p=0.02

Total 1/104 (0.9%) 10/245 (4%) p=0.02

⊡ Table 35.6. Location of pain (ns not significant)

Glucamesh Polypropylene p

Groin 67% 77% ns

Testicle 50% 34% ns

 262 Chapter 35 · Chronic Pain After Inguinal Hernia Repair: The Choice of Prosthesis Outweighs That of Technique
We used laparoscopy in young, nonobese patients
with bilateral or recurrent hernia who were ac-
tive professionally or in sports and who had no
anesthetic risk. We applied the same indications to
the laparoscopic and Lichtenstein groups, which
were therefore perfectly comparable. The reported
2-year recurrence rate is comparable for Lichten-
stein repair and laparoscopic repair (2–5%) [38,
39], which accords with our experience (2.8%) in
which this incidence was independent of the tech-
nique or the prosthetic mesh.
The choice of prosthesis is even less well
defined and subject to criteria that are often cost-
related and subjective or personal. The character-
istics of the ideal prosthesis are well defined: large
mesh, solid, flexible, low specific weight, ability to
become incorporated in tissues, and biologically
inert. Most meshes are made of polypropylene or
polyester. Using these principles, a great variety
of products have been developed and adapted to
techniques or practices (laparoscopy): composite,
two-faced meshes that are coated to promote
healing and facilitate tissue integration. Coat-
ing with animal collagen has proved effective
but carries a small biological risk (cattle) or is
subject to religious restrictions (pig). Beta-D-
glucan is an entirely natural plant product that
promotes healing and has an immunomodula-
tory effect [29, 31, 33, 34]. Beta-D-glucan-coated
meshes are effective in terms of recurrence, qual-
ity of life, and chronic pain [40, 41]. In the pres-
ent study, we have shown that the 2-year recur-
rence rate was the same regardless of technique,
mesh, or the mesh’s weight per unit area. Studies
of lightweight meshes have yielded contrasting
35 results [24, 42].
When they compared outcomes after laparo-
scopic TEP inguinal repair using new lightweight
(28 g/m2) and traditional (85 g/m2) heavyweight
mesh, Khan et al. [43] found less discomfort and
pain in the lightweight group at 3-month fol-
low-up. Severity of numbness was less with light-
weight mesh, suggesting less nerve interference
and less inflammatory response. Also, the use of
lightweight mesh for Lichtenstein hernia repair did
not affect the recurrence rate, but some aspects of
pain and discomfort were improved 3 years after
surgery [24].
Chronic pain after hernia repair has been stud-
ied extensively [3, 6, 17, 43] but is difficult to as-
sess. Specific validated questionnaires [42, 44] have
been developed to evaluate and compare quality of
life as a function of technique. Numerous factors
have been implicated: anatomical factors (nerves),
type of hernia, technique, surgical field, and also
the mesh and its fixation. In our practice, the
meshes used in TEP are not fixed, and those used
in Lichtenstein repair are fixed with a few sutures
on the inguinal ligament. At 2-year follow-up,
these techniques were identical in comparable
groups of patients, whatever the type of prosthesis
used. There was no difference in chronic pain, or
even in pain qualified as severe, between TEP and
Lichtenstein repair. There was, however, a signifi-
cant difference in favor of Glucamesh compared
with polypropylene mesh in the groups compared,
irrespective of the repair technique. These advan-
tages may stem from the low weight per unit area
of Glucamesh but above all from the quality of the
beta-D-glucan coating.
Conclusion
Our findings suggest that at 2-year follow-up, the
quality of hernia repair in terms of efficacy and
quality of life is determined more by the character-
istics of the prosthesis than by the technique used.
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36. Wolk M, Danon D (1985). Promotion of wound healing by
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37. Wrigland WW, Van Den Tol MP, Luijendijih RW, Hop WCP,
Busschbacht JJV, de Lange DCD, Van Geldere D, Rottier
AB, Vegt PA, Ijzermans JNM and Jeekel J (2002). Rando-
mized trial of non mesh versus mesh repair of primary
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38. Arvidson D, Berndsen FM, Larsson LG. Leijonmarck CE,
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 264 Chapter 35 · Chronic Pain After Inguinal Hernia Repair: The Choice of Prosthesis Outweighs That of Technique

39. Wara P, Bay Nielsen M, Jul P, Bendix J, Kehlet H (2005). cilitate the integration in the muscle and secondly
Prospective nationwide analysis of laparoscopic versus to avoid an adherence. And that is a paradox. In
Lichtenstein repair of inguinal hernia. Br J Surg 92, 1277–
the literature there is no A-level publication show-
1281
40. Barrat C, Seriser F, Arnoud R, Trouette P, Champault G ing the usefulness of collagens. And the company
(2004). Inguinal hernia repair with beta glucan coated (Covidien) have put the same prosthesis without
mesh: prospective multicenter study (115 cases). Prelimi- collagen on the market – to be in the prize only!
nary results. Hernia 8, 33–38 Post: You cannot differentiate the difference be-
41. Champault G, Barrat C (2005) Inguinal hernia repair with
tween the effect of lightweight and heavyweight
beta glucan coated mesh: results at two years follow up.
Hernia 9, 125–130 and the glucan. So it might be hypothesized that
42. Conze J, Kingsnorth AN, Flament JB, Simmermacker P, the only difference is due to the light weight and
Arlt G, Langer C, Shippers E, Hartley A, Schlumpelick V not to glucan. In your randomized trial you started
(2005). Randomized clinical trial comparing lightweight just now, do you compare the same lightweight
composite mesh with polyester or polypropylene mesh
with and without glucan?
for incisional hernia repair. Br J Surg 92, 1488–1493
43. Khan LR, Kumar S, Nixon SJ (2006). Early results for new Champault: It probably will be the next trial.
lightweight mesh in laparoscopic totally extraperitoneal Smeds: Very interesting results. In order to under-
inguinal hernia repair. Hernia 10, 303–308 stand the mechanisms more, I am just curious to
know whether you allocated the surgeons to the
different type of meshes. Did you have the poly-
Discussion propylene surgeons and the glucan surgeons? Be-
cause we know that there is a significant difference
Schumpelick: Thank you very much for this pre- if you are a high-volume surgeon or a low-volume
sentation, I think these are excellent results. How surgeon.
do you explain your results? How is glucan work- Champault: No, the same surgeons. In a previous
ing? study we have shown that the results of trainees
Champault: I think there are three explanations: are the same as the results of consultants or more
First, it’s a lightweight mesh. Second, there is no experienced surgeons. In this study, the repairs
fixation, because of adhesiveness. Especially in TEP were performed within the whole group of our
hernia repair we do not fix the mesh anymore. surgeons.
Schumpelick: Is glucan like a glue?
Champault: There is no glue on this mesh. But
when you use this mesh in TEP hernia repair and
you put the mesh directly on the muscle, you don’t
need any fixation or tacks. And when you perform
a Lichtenstein hernia repair, you only have to put
in the prosthesis. In this study we used the official
35 technique described by Amid with a running suture
on the inguinal ligament. And third, with regard to
the role of glucan, I have seen the use of glucan in
burned patients. There it is very efficient, and you
win many days in healing. Perhaps there is an action
in the integration of the prosthesis in the muscle and
possibly, as the experimental studies have shown, an
action of the inflammatory reactions.
Schumpelick: And then you mentioned in your
discussion the covering of meshes with collagen. Is
that not working anymore?
Champault: There is a problem with collagen be-
cause you use the same product of collagen to fa-
 36

The Effect of Polypropylene

Mesh on the Ilioinguinal Nerve
in Open Mesh Repair of Groin Hernia
S. D. Demirer, I. Kepenekci, O. Evirgen, O. Birsen, A. Tuzuner,
S. Karahuseyinoglu, M. Ozban, E. Kuterdem
 266 Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve in Open Mesh Repair of Groin Hernia
Introduction
Open or laparoscopic mesh repair of groin hernia
is one of the most common elective operations
performed by general surgeons. Because of low
recurrence rates, the concept of tension-free mesh
repair methods has gained wide acceptance. The
development of chronic pain after inguinal hernia
repair is a well-known long-term complication,
with the reported frequency of pain varying from
0% to 37% [1–11]. Some studies have reported
a lower incidence of pain, 2–2.5%, after laparo-
scopic hernia repair than after open mesh repair
[3, 4, 8, 11–15]. The complaint of chronic pain
following inguinal hernia repair can continue
for months or even years. Several risk factors as-
sociated with this have been identified, including
recurrent hernia repair, the patient’s insurance
status, day surgery, patient age less than 60 years,
intensity of early postoperative pain, experience
of the surgeon, and type of surgical procedure
used [3, 6, 9, 16].
Mesh inguinodynia was described as »a new
clinical syndrome« after inguinal herniorrhaphy.
The development of this chronic debilitating pain
after herniorrhaphy has been attributed to several
mechanisms, including injury or entrapment of
the sensory nerves (ilioinguinal, iliohypogastric,
genitofemoral, or lateral femoral cutaneous nerves)
and mesh inguinodynia [2, 3, 6–8, 17]. Partial or
complete division, neuroma formation, stretching,
contusion, crushing, electrical damage, or suture
compression can injure sensory nerves in close
proximity to the operative field and cause neu-
ralgia. Secondary damage to a sensory nerve may
also result from scar tissue compression or from ir-
ritation by an adjacent inflammatory process such
36 as a suture granuloma or mesh. Polypropylene
synthetic mesh causes inflammatory reaction and
formation of scar tissue [2, 6, 8, 11, 17, 18].
The ilioinguinal nerve is a sensory nerve that
is usually preserved during hernia repair, but it
can interfere with placement of the mesh and may
be traumatized inadvertently during operation. In
this experimental study, we aimed to evaluate dam-
age or entrapment of the ilioinguinal nerve caused
by polypropylene synthetic mesh after groin hernia
repair.
Material and Methods
Our study protocol was reviewed and approved by
the ethics committee of Ankara University School
of Medicine. All animals received humane care in
accordance with the Guide for the Care and Use
of Laboratory Animals prepared by the National
Academy of Sciences and published by the U.S.
National Institutes of Health (NIH publication No.
85–23, revised 1985).
Experimental Design
Twenty-four New Zealand rabbits weighing 2.4–
2.7 kg were included in our study. They were sub-
jected to 1 week of preliminary conditioning dur-
ing which time they received standard chow and
water ad lib. They were housed in a temperature-
and humidity-controlled environment, two per
cage, with a 12-h light–dark cycle.
Preoperative antibiotics (cefazolin 10 mg/kg)
were administered intramuscularly 30 min prior to
skin incision. The rabbits were anesthetized by an
intramuscular injection of ketamine hydrochloride
(35 mg/kg) and Xylocaine (5 mg/kg). The animals
were placed in a dorsal recumbent position, fol-
lowed by hair removal from the inguinal area. The
inguinal and scrotal regions were shaved and pre-
pared with Betadine solution. In all animals, the
inguinal areas were explored bilaterally through
an inguinal incision. The ilioinguinal nerve was
identified on both sides and synthetic polypropyl-
ene mesh placed on only one side (⊡ Fig. 36.1). The
ilioinguinal nerve was in touch with polypropylene
mesh on this side (⊡ Fig. 36.2). We designated the
right groin as the control and the left groin as the
experimental side in each animal. After the opera-
tion, the inguinal incisions were closed in anatom-
ical layers with 3-0 monofilament suture.
All rabbits tolerated the surgery well, and they
were followed until reexploration. Three months
after surgery, the animals were anesthetized using
intramuscular ketamine hydrochloride, and bilat-
eral inguinal exploration was performed again, with
samples of nerve tissue taken from both sides. The
samples of nerve tissue were divided into two groups
as control and experimental groups. An internation-
Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve
⊡ Fig. 36.1. Ilioinguinal nerve of the rabbit after dissection
⊡ Fig. 36.2. Polypropylene mesh was laid in close proximity to
the ilioinguinal nerve
ally accepted standard definition of pain persisting
beyond the normal tissue healing time, assumed to
be 3 months, was used in our study [19].
Histological Tissue Processing
For electron microscopic study, inguinal periph-
eral nerve specimens from the control and ex-
perimental groups were fixed in 2.5% glutaralde-
hyde in 0.1 M phosphate buffer and postfixed in
1% osmium tetroxide. Tissue samples were dehy-
drated through a graded series of ethanol and
propylene oxide embedded in araldite. Semithin
sections were stained with toluidine blue-Azure II
267 36
and examined under a light microscope (Zeiss
Axio Scope photomicroscope). After double stain-
ing with uranyl acetate and lead citrate, ultrathin
sections were examined and photographed using a
LEO 906E transmission electron microscope.
For light microscopic study, inguinal periph-
eral nerve tissues were fixed in 10% formaldehyde.
Samples were dehydrated by immersion in a series
of alcohol concentrations and embedded in paraf-
fin; 5-μm sections were stained with hematoxylin
and eosin (H&E) and Masson’s trichrome and
examined under a light microscope.
Morphometric Analysis
For morphometric analysis, photographic color
images from semithin sections of experimental
and control groups were obtained with the Zeiss
Axio Scope photomicroscope at ×250 magnifica-
tion. The measurements were obtained using Adobe
Photoshop 7.0 software. The graphic file format
of the images is JPEG, and resolution was set at
500 pixels per inch. Myelinated fiber diameter, axon
diameter, G-ratio (axon diameter/myelinated fiber
diameter), myelin thickness, and the numbers of
nerve fibers with diameters of ≤4 μm, 5–8 μm, and
≥9 μm were assessed in a blinded fashion using a
semiautomated procedure [20].
Statistics
Statistical analysis was performed using the ad-
justed Student‘s t-test for clustered data and the
adjusted chi-square test for clustered binary data,
comparing the mesh-laid side of each group to the
control side of the same group. A p-value <0.05
denoted a statistically significant difference.
Results
No intraoperative or postoperative deaths occurred
in the rabbits, and we observed no infective com-
plications in either the control or the experimental
sides during 3 months of follow-up. There was
 268 Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve in Open Mesh Repair of Groin Hernia

a statistically significant difference between the

mean operating times in the two groups (13 min
in the control group vs. 24 min in the experimental
group, p<0.05). During reexploration, we found
macroscopically dense fibrotic tissues encompass-
ing the polypropylene mesh and adhesions on the
study side 3 months after surgery. On the experi-
mental side, the floor of the inguinal region was
very tight, and dissection as well as removal of the
ilioinguinal nerve was difficult because of fibrotic
changes. The nerve had thickened and adhered to
the mesh and adjacent inguinal region. There was
minimal fibrosis on the control side; therefore, the
ilioinguinal nerve was divided and removed easily
on this side. a

Histological and Morphometric

Assessment

H&E-stained sections from the experimental group

after 3 months revealed inflammatory reaction
and increased connective tissue that formed ar-
eas of fibrosis around polypropylene mesh islands
(⊡ Fig. 36.3a, b). Light microscopic examination of
H&E-stained and Masson’s trichrome-stained sec-
tions of peripheral nerves from the control group
were normal in appearance (⊡ Fig. 36.4a, b), but the
nerve fascicles in the experimental group operated
with mesh showed axonal dilatation and mild to
severe loss of myelinated axons (⊡ Fig. 36.5a, b).
b
Examination of semithin sections of peripheral
nerve fascicles from the control group showed
⊡ Fig. 36.3. Experimental group at the 3rd postoperative
almost intact myelinated and unmyelinated fibers
month: interface of the mesh and recipient tissue (pmg po-
(⊡ Fig. 36.5c). The endoneurium of closely located lypropylene mesh graft). Double asterisks (**) indicate con-
myelinated fibers appeared to be normal. Most nective tissue around polypropylene mesh islands (patches)
of the myelin sheath layers and the thickness of forming fibrosis and inflammatory reaction. Arrowheads show
36 equal-size fibers were the same and showed nor- striated muscle. a Original magnification ×100. b Original ma-
gnification ×200. Hematoxylin–eosin staining
mal morphology.
Electron microscopic examination of semithin
and ultrathin sections of nerve morphology in the
experimental group operated with mesh exhibited bers in the experimental group showed undulation
endoneurial edema with thickening of both the toward the axoplasm and the endoneurium. In the
endoneurium and perineurium, causing separa- experimental group we also observed separation
tion of nerve fibers (⊡ Fig. 36.5d, d insert). A few of myelin layers from each other as a prominent
extra layers of connective tissue formation in some feature of myelin degeneration in nerve fibers.
nerve fibers of the experimental group suggested Axoplasms also exhibited edema and crystalliza-
early onion-bulb formations. Myelin sheaths of fi- tion (⊡ Fig. 36.6a–d).
Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve
269 36
Results of the morphometric assessment are
outlined in ⊡ Table 36.1. Fiber diameter and ax-
onal diameter were increased in the experimental
group compared with the controls as a result of
axonal dilatation, and this difference was statisti-
cally significant. The G-ratio, which is considered
normal in the range of 0.60–0.64, increased in the
experimental group compared with controls as a
result of myelin sheath thinning; the difference
was statistically significant. Myelin thickness was
decreased moderately on the mesh side compared
with the control side, but there was no statis-
tically significant difference between them. The
number of nerve fibers considered healthy, with a
diameter <9 μm, was higher in the control group
a
than in the experimental group (Pcontrol=0.783 vs.
Pmesh=0.570), and the difference was statistically
significant (p<0.001) with an adjusted chi-square
test for clustered binary data.

Discussion

It is usual to preserve the ilioinguinal nerve, but

b
⊡ Fig. 36.4. Light microscopic images of peripheral nerves of
control group. a Arrowhead axon; arrow Schwann cell nucleus;
E endoneurium; P perineurium; Ep epineurium. Original ma-
gnification ×400. Masson’s trichrome staining. b Arrowheads
axons; arrow Schwann cell nucleus. Original magnification
×400. Hematoxylin–eosin staining
it can interfere with placement of the mesh and
may be traumatized inadvertently during opera-
tion. The increased surface area of the mesh might
allow adherence of nerves or abrasion and account
for an increased risk of neuropathic pain.
Using prosthetic mesh for inguinal hernia re-
pair is well accepted. But despite favorable clinical
outcomes, patients who undergo mesh hernia re-
pair may complain of severe, debilitating pain and
pose a bothersome chronic management problem
[1, 21, 22]. Local analgesic or steroid injections,
various pharmaceuticals, behavioral therapy, cryo-
therapy, alcohol or phenol injections, neurectomy,
and mesh removal are frequently used in treatment
[2, 18]. Delayed presentations of mesh inguino-

⊡ Table 36.1. Peripheral nerve morphometry

Average fiber diameter, Average axon diameter, Average G-ratio, Myelin thickness,
mean ± SD mean ± SD mean ± SD mean ± SD

Mesh side 9.05±0.24a 6.17±0.11a 0.68±0.007a 1.98±0.11

Control side 6.91±0.14 4.17±0.09 0.59±0.004 2.73±0.06

ap<0.001
significant with adjusted Student’s t-test for clustered data
 270 Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve in Open Mesh Repair of Groin Hernia

dynia may occur, possibly secondary to chronic
scarring or neuroma formation. The mesh as a
foreign body induces a dense fibroblastic response,
creating scar tissue and imparting strength to the
floor. Despite wide acceptance of this technique,
there is little data regarding the effects of the mesh
bioprosthesis and its resulting fibrotic reaction on
adjacent structures such as the spermatic cord or
peripheral nerves in the inguinal region [23–28].
In our study we aimed to evaluate the local
effects of mesh on the ilioinguinal nerve. Histo-
pathological and morphometric changes of the

a b

36

d
c

⊡ Fig. 36.5. a,b Light microscopic images of experimental
group. a Asterisks axonal loss; P perineurium; Ep epineurium;
arrowhead Schwann cell nucleus; arrows axons. Original mag-
nification ×400. Hematoxylin–eosin staining. b Asterisks axonal
loss; arrow axon; arrowhead Schwann cell nucleus; P perineu-
rium; Ep epineurium; E endoneurium. Original magnification
×400. Masson’s trichrome staining. c, d, d insert Semithin
sections of peripheral nerves. c Arrow myelin sheath; asterisks
unmyelinated nerves; P perineurium. Original magnification
×1,000. Toluidine blue staining. d, d insert Arrowheads extra
collagen fiber layers (onion-bulb formation); asterisks separati-
on of myelin sheath; arrows undulation of myelin sheath; P peri-
neurium; Ep epineurium; double asterisks Schwann cell nucleus.
Original magnification ×1,000. Toluidine blue staining
Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve
271 36
ilioinguinal nerve in the mesh group (mentioned lowing inguinal hernia repair. But it is difficult
in the results section of this paper), such as axonal to make a definitive statement regarding the im-
dilatation, loss of myelinated axons, endoneurial pact of these histopathological changes on chronic
edema, separation of myelin layers, increased fiber pain because animal models, not human beings,
and axon diameters, and increased G-ratio, may were used in this experimental study. It is very
be implicated in the etiology of chronic pain fol- well known that pain is a subjective complaint;

a b

c d

⊡ Fig. 36.6. Transmission electron microscopic (TEM) images
of experimental group. a Axp axonal dilatations and axoplasm;
double asterisks myelin sheath separation; umyn unmyelinated
nerves; SCCy Schwann cell cytoplasm. TEM ×3,597. b Double
asterisks extra collagen fibers around endoneurium sugges-
ting onion-bulb formation; arrows myelin sheath degenera-
tion and separation; asterisks myelin undulation; ms myelin
sheath. TEM ×2,784. c c collagen fibers; double asterisks endo-
neurial edema; umyn unmyelinated nerves; SCCy Schwann cell
cytoplasm; myelin sheath. TEM ×4,646. d Axp crystallization of
nerve fibers in axoplasm; double asterisks endoneurial edema;
L lipid droplets; asterisks inclusion body in Schwann cell cyto-
plasm; SCCy Schwann cell cytoplasm; arrowhead degenerative
inclusions between myelin layers. TEM ×12,930
 272 Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve in Open Mesh Repair of Groin Hernia
certainly, scaling and establishment of correlation
with these histopathological changes cannot be
done in animal models.
Polypropylene mesh serves as a flexible lat-
tice supporting the ingrowth of connective tissues
from the base of the wound and is known to incite
a prompt fibroblastic response, imparting strength
to the repair. An extensive inflammatory and fi-
broblastic granulomatous reaction occurs in re-
sponse to the foreign material, which causes dense
adhesions when the material is placed adjacent to
visceral organs [29, 30]. According to our macro-
scopic and microscopic findings, the ilioinguinal
nerve was affected by the resultant fibrotic reaction
to the mesh (⊡ Fig. 36.3a, b). Peripheral neuropathy
following mesh herniorrhaphy was most likely due
to incorporation of adjacent nerve fibers in the
fibroblastic reaction incited by mesh. During the
reexploration, we performed extensive dissection
to find and ensure adequate mobilization for the
ilioinguinal nerve because of the fibrotic changes
in the experimental group. It has been argued that
several factors may contribute to the development
of chronic groin pain; one of these factors may
be nerve entrapment. The nerves may hinder the
dissection or may lie across the prosthetic mesh
on the posterior inguinal wall. Chronic groin pain
after hernia repair can possibly be caused by the
entrapment of peripheral nerves in the scar tissue
formed by the mesh [2–4, 6–8, 17].
Uzzo et al. [27] demonstrated that entrapment
of the ilioinguinal nerve or its branches by the
mesh reaction gave rise to a traumatic neuroma. In
our study, the light microscopic and ultrastructural
changes seen in peripheral nerves in the experi-
mental group operated with mesh suggest that me-
chanical compression of peripheral nerves is asso-
36 ciated with myelin degeneration, endoneurial and
perineurial edema, thickening of collagen layers
around axons (called onion-bulb formation), and
axonal loss that may cause chronic inflammatory
demyelinating peripheral neuropathy. We think
that inflammatory and fibrotic reactions occur-
ring in response to the foreign material may have
caused adhesions and mechanical compression of
peripheral nerves, and we conclude that a similar
mechanism may be responsible in part for chronic
groin pain in humans.
Placement of mesh in direct contact with ingui-
nal nerves is not recommended for avoiding groin
pain [2–4, 6–8, 17]. Tsakayannis et al. [31] reported
that even elective neurectomy is safe to perform
and is not associated with chronic inguinal pain.
Our study indicates that preservation of the ingui-
nal nerves is important in mesh herniorrhaphy be-
cause of the mesh-induced changes that occur. We
conclude that the sensory nerves in the inguinal
region should be better separated from the mesh
and preserved carefully in order to prevent chronic
groin pain when mesh repair is performed. Further
studies are needed to evaluate the effect of anatomi-
cal position and the relationship of mesh and sen-
sory nerves to chronic pain after herniorrhaphy.
References
1. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM. Cause
and prevention of postherniorrhaphy neuralgia: a proposed
protocol for treatment. Am J Surg 1988;155:786–790
2. Helse CP, Starling JR. Mesh inguinodynia: a new clinical
syndrome after inguinal herniorrhaphy? J Am Coll Surg
1998;187:514–518
3. Bay-Nielsen M, Perkins FM, Kehlet H. Pain and functional
impairment 1 year after inguinal herniorrhaphy: a nation-
wide questionnaire study. Ann Surg 2001;233:1–7
4. Callesen T, Bech K, Nielsen R, Andersen J, Hesselfeldt P,
Roikjaer O, Kehlet H. Pain after groin hernia repair. Br J
Surg 1998;85:1412–1414
5. Haapaniemi S, Nilson E. Recurrence and pain three years
after groin hernia repair. Vallidation of postal question-
naire and physical examination as a method of follow-up.
Eur J Surg 2002;168:22–28
6. Callesen T, Bech K, Kehlet H. Prospective study of chronic
pain after groin hernia repair. Br J Surg 1999;86:1528–
1531
7. Ravichandran D, Kalambe BG, Pain JA. Pilot randomized
controlled study of preservation or division of ilioinguinal
nevre in open mesh repair of inguinal hernia. Br J Surg
2000;87:1166–1167
8. Kumar S, Wilson RG, Nixon SJ, Macintyre IMC. Chronic pain
after laparoscopic and open mesh repair of groin hernia.
Br J Surg 2002;89:1476–1479
9. Poobalan AS, Bruce J, King PM, et al. Chronic pain and
quality of life following open inguinal hernia repair. Br J
Surg 2001;88:1122–1126
10. Courtney CA, Duffy K, Serpell MG, et al. Outcome of pa-
tients with severe chronic pain following repair of groin
hernia. Br J Surg 2002;89:1310–1314
11. The MRC Laparoscopic Groin Hernia Trial Group. Laparo-
scopic versus open repair of groin hernia: a randomized
comparison. Lancet 1999;354:185–190
Chapter 36 · The Effect of Polypropylene Mesh on the Ilioinguinal Nerve
12. Seid AS, Amos E. Entrapment neuropathy in laparoscopic
herniorrhaphy. Surg Endosc 1994;8:1050–1053
13. Liem MS, van der Graaf Y, van Steensel CJ, et al. com-
parison of conventional anterior surgery and laparo-
scopic surgery for inguinal hernia repair. N Eng J Med
1997;336:1541–1547
14. Dirksen CD, Beets GL, Go PM, et al. Bassini repair compared
with laparoscopic repair for primary inguinal hernia: a
randomized controlled trial. Eur J Surg 1998;164:439–447
15. Hay JM, Boudet MJ, Fingerhut A, et al. Shouldice inguinal
hernia repair in the male adult: the gold standard? A
multicenter controlled trial in 1,578 patients. Ann Surg
1995;222:719–727
16. Salcedo-Wasicek MC, Thirlby RC. Postoperative course af-
ter inguinal herniorrhaphy. A case controlled comparison
of patients receiving workers’ compensation vs. commer-
cial insurance. Arch Surg 1995;130:29–32
17. Bower S, Moore BB, Stephen MW. Neuralgia after inguinal
hernia repair. Am Surg 1996;62:664–667
18. Wantz GE. Testicular atrophy and chronic residual neural-
gia as risks of inguinal hernioplasty. Surg Clin North Am
1993;73:571–581
19. Classification of chronic pain. Descriptions of chronic pain
syndromes and definitions of pain terms. Prepared by the
International Association for the Study of Pain, Subcom-
mittee on Taxonomy. Pain 1986;3 (suppl):S1–226
20. Campadelli P, Gangai C, Pasquale P. Automated morpho-
metric analysis in peripheral neuropathies. Comput Biol
Med 1999;29:147–156
21. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh
repair for primary inguinal hernias: results of 3,019 opera-
tions from five diverse surgical sources. Am J Surg 1992;
58:255–257
22. Lichtenstein IL, Shulman AG, Amid PK, Montllor MM. The
tension-free hernioplasty. Am J Surg 1989;157:188–193
23. Amid PK, Shulman AG, Lichtenstein IL. Critical scrutiny
of the open tension free hernioplasty. Am J Surg 1993;
165:369
24. Arnould JP, Eloy R, Weill-Bousson M, et al. Resistance et
tolerance biologique de 6 prostheses insertes utilizes
dans la reparation de la paroi abdominale. J Chir 1977;
113:85–100
25. Usher FC, Wallace SA. Tissue reaction to plastic, a compari-
son of nylon, Orlon, Dacron, Teflon and Marlex. Arch Surg
1958:76:997–1003
26. Walker AP. Biomaterials in hernia repair. In: Nyhus LM,
Condon RE (eds). Hernia, 4th edn. Lippincott, Philadel-
phia, 1995:534–540
27. Uzzo RG, Lemarck GE, Morrissey KP, et al. The effects of
mesh bioprosthesis on the spermatic cord structures:
a preliminary report in a canine model. J Urol 1999;
161:1344–1349
28. Shin D, Lipshultz LI, Goldstein M, Barme GA, Eugene FF,
Nagler HM, McCallum SW, Niederberger CS, Schoor RA,
Burgh VM, Honig SC. Herniorrhaphy with polypropyl-
ene mesh causing inguinal vassal obstruction: a pre-
ventable cause of obstructive azoospermia. Ann Surg
2005;241:553–558
273 36
29. Lichtenstein IL. Herniorrhaphy Am J Surg 1987;153:553
30. Wagner M. Evaluation of diverse plastic and cutis prosthe-
ses in a growing host. Surg Gynecol Obstet 1970;130:1077
31. Tsakayannis DE, Kiriakopoulos AC, Linos DA. Elective
neurectomy during open tension free inguinal hernia
repair. Hernia 2004;8:67–69
Discussion
Amid: Many congratulations on your study. We
were inspired by your work and started doing
the same thing on human subjects. We are doing
exactly what you did on the nerves that you are
removing from patients who have pain. And our
preliminary result is completely consistent with
your report. The only thing is that because we are
doing it on humans, we know that these changes
are causing pain, whereas in your rabbits you do
not know if they are feeling pain. Your work was
inspiration for our ongoing work. On a micro-
scopic point of view, when you remove the mesh
with the nerve, did you observe some adhesions of
the nerves to the mesh?
Demirer: Yes, of course. After 3 months we ex-
plored again. Here we observed on the experimen-
tal side a very dense fibrotic tissue and adhesion
formation as compared to the control side.
Smeds: Did you check how far away from the ad-
hesion area the nerves were changed? Did you test
it outside of the operation field as well?
Demirer: No.
Ramshaw: How would you translate this research
in terms of clinical patient benefit?
Demirer: In my clinic we now only use polypro-
pylene meshes, and 2–5% of patients complain of
pain.
Schumpelick: What did the neuropathologists say
to you about these findings? Have they seen such
alterations of nerves before?
Demirer: We did not ask the neuropathologists.
Deysine: Have you considered conduction studies
on those pieces of nerves that you took out?
Demirer: In the next studies we should investigate
degenerative changes by nerve physiologists. In
this study we did not perform such analyses.
 37

Lightweight Macroporous Mesh

vs. Standard Polypropylene Mesh
in Lichtenstein Hernioplasty
S. Bringman
 276 Chapter 37 · Lightweight Macroporous Mesh vs. Standard Polypropylene Mesh in Lichtenstein Hernioplasty
Introduction
A standard polypropylene mesh used in Lichten-
stein’s operation induces a strong foreign tissue
reaction with potential harmful effects [1]. A mesh
with less polypropylene and large pores could pos-
sibly be beneficial [2]. This chapter summarizes a
randomized controlled trial comparing standard
mesh and lightweight mesh [3–5].
Patients and Methods
Six hundred men with a unilateral primary inguinal
hernia were randomized through a secure Web site
to be operated on with a Lichtenstein repair using
either a lightweight (LW) macroporous mesh (Vy-
pro II, Ethicon, Hamburg, Germany) or a standard
polypropylene mesh (Prolene, Ethicon, Hamburg,
Germany). All data were captured through the Web
site. The patients were blinded to which mesh they
received. Five Swedish and one Finnish hospital
participated in the study. The patients completed
a diary with SF-36 and visual analog (VAS) pain
scales during the first 8 weeks postoperatively. After
1 year, a questionnaire was sent to all patients. Pa-
tients who indicated a lump in the groin or another
complaint were examined. Three years postopera-
tively, the patients were examined by a blinded sur-
geon, and another questionnaire was completed.
Results
Of the total 600 patients, 301 were randomized
to standard mesh and 299 to LW mesh, and 591
were operated on as allocated. The first patient
was recruited in mid-December 2000 and the last
in April 2002. The groups were comparable with
37 regard to demographic data. There were no dif-
ferences between the groups concerning return
to work or normal activities, SF-36 scores, or VAS
pain scores up to 8 weeks or at 12 months. The
recurrence rate 3 years after surgery was 3.7% after
standard mesh and 3.6% after LW mesh repair.
The LW mesh group had less pain when rising
from a reclining to a sitting position (p=0.03). Sig-
nificantly, more men in the standard mesh group
than in the LW mesh group (p=0.025) stated that
they could feel the mesh in their groin.
Discussion
In this Internet-based, multicenter study, it was
demonstrated that no differences existed between
Lichtenstein’s operation with LW mesh or with
standard mesh up to 12 months after surgery.
However, after 3 years, some aspects of pain and
foreign body sensation were noted to be less in
the LW group without increasing the rate of her-
nia recurrence. Other authors have demonstrated
similar results concerning pain and foreign body
sensation [6, 7]. One study showed an increased
risk of recurrence in the LW group [6], which
was estimated to be due to factors in the operative
technique. In the present trial we used a technique
with a running suture, with 1-cm intervals between
the large bites in the mesh. We found no difference
concerning recurrences between the groups.
In conclusion, we found no difference between
the group that received LW mesh and the group
that received standard polypropylene mesh in Lich-
tenstein’s hernioplasty up to 12 months postopera-
tively. The LW mesh did not affect recurrence rates
compared with standard mesh, but some aspects of
pain and foreign body sensation were improved at
follow-up 3 years after surgery.
References
1. Klinge U, Klosterhalfen B, Muller M, Schumpelick V. For-
eign body reaction to meshes used for the repair of abdo-
minal wall hernias. Eur J Surg 1999; 165(7):665–673
2. Junge K, Klinge U, Rosch R, Klosterhalfen B, Schumpelick
V. Functional and morphologic properties of a modi-
fied mesh for inguinal hernia repair. World J Surg 2002;
26(12):1472–1480
3. Bringman S, Heikkinen TJ, Wollert S, Osterberg J, Smed-
berg S, Granlund H, et al. Early results of a single-blinded,
randomized, controlled, Internet-based multicenter trial
comparing Prolene and Vypro II mesh in Lichtenstein
hernioplasty. Hernia 2004; 8(2):127–134
4. Bringman S, Wollert S, Osterberg J, Smedberg S, Granlund
H, Fellander G, et al. One year results of a randomised
controlled multi-centre study comparing Prolene and
Vypro II-mesh in Lichtenstein hernioplasty. Hernia 2005;
9(3):223–227
Chapter 37 · Lightweight Macroporous Mesh vs. Standard Polypropylene Mesh
5. Bringman S, Wollert S, Osterberg J, Smedberg S, Granlund
H, Heikkinen TJ. Three-year results of a randomized clini-
cal trial of lightweight or standard polypropylene mesh in
Lichtenstein repair of primary inguinal hernia. Br J Surg
2006; 93(9):1056–1059
6. O’Dwyer PJ, Kingsnorth AN, Molloy RG, Small PK, Lammers
B, Horeyseck G. Randomized clinical trial assessing impact
of a lightweight or heavyweight mesh on chronic pain
after inguinal hernia repair. Br J Surg 2005; 92(2):166–170
7. Post S, Weiss B, Willer M, Neufang T, Lorenz D. Randomized
clinical trial of lightweight composite mesh for Lichten-
stein inguinal hernia repair. Br J Surg 2004; 91(1):44–48
Discussion
Kurzer: There are three trials now. And in the
European guidelines we are asking ourselves if the
books are closed on this subject. The recommen-
dation is that the use of lightweight [mesh] can be
considered in inguinal hernia repair to decrease
postoperative discomfort – but it is also stated
that possibly [would be] at the cost of more recur-
rences. What would be your recommendation?
Bringman: Well, I think that the Vypro II is not
the best large-pore material available now. If we
had UltraPro when we started the trial, we would
definitely have used that one. It is true that there
are only some aspects where we found a difference
in our trial. I also know that the Vicryl portion of
Vypro II provokes rather heavy inflammation. So I
would expect the results from an UltraPro study to
make it clearer in the future
Post: Congratulations on the nice study. You men-
tioned that the design was single-blinded. Does
that mean that the examiner knew which type of
mesh was implanted, or was the examiner was also
blinded?
Bringman: The examiner was blinded.
Miserez: I presume you now use lightweight in
your standard daily practice—and I have two ques-
tions on that. First, does this advantage outweigh
that of increased costs? Second, do you use it in all
patients, or are there patients with a large direct or
indirect hernia where you would not use a light-
weight mesh?
Bringman: In very large defects I would use a heavy-
weight mesh. Now I do very little Lichtenstein any-
more. I focus on laparoscopic hernia surgery.
277 37
Jacob: There is a study that was recently pub-
lished by Dr. Heniford and Dr. Matthews, and
they looked at Ki67 and the continuing cell turn-
over for the different mesh products—I think they
used a rabbit model. They found that the heavy-
weight product actually had continuing cell turn-
over at a year compared to the lightweight mesh,
where this process actually died off. And so one
of the possibilities was that there is an ongoing
cellular turnover with these heavyweight products
that is contributing to the ongoing symptoms
that you found. So the question is with this nerve
information from its contact with the mesh. One
of my partners opens the floor in all of his open
repairs and puts the mesh in the same location as
in laparoscopic repair and closes the transverse
fascia over so that there is no mesh in contact
with the nerves running through the canal. And
I wondered if anyone else had thought of or has
been doing that and what their outcomes are—so,
some sort of Lichtenstein repair in the preperito-
neal space.
Champault: You are describing an operation de-
scribed by my chief Jean Rives in 1963. Transingui-
nal preperitoneal prosthesis, and Volker said it was
TIPP, but for me it was the Rives operation.
Jacob: Maybe that is the direction where we have
to go back to again to avoid the nerve problem, by
putting the mesh to this place.
Desine: I was very impressed by the mathematical
description of your work—I was able to under-
stand it very well—but I am concerned that you
had a high incidence of testicular atrophy which I
cannot explain except because of technique. And
that is what has to be emphasized for the rest of
his training. The percentage of testicular atrophy
should be below 1%.
Bringman: I agree.
Schumpelick: When we first used lightweight
meshes in the Lichtenstein repair, we had prob-
lems in fixing this floppy mesh in front of the pu-
bic bone. Should we use a bigger overlap to avoid
a recurrence?
Bringman: We made big overlaps and a rather
short distance between the stitches.
Schumpelick: And additional stitches?
Bringman: Additional stitches starting about 2 cm
up on the medial side.
 38

Does the Choice of Prosthetic

Mesh Type Make a Difference
in Postherniorrhaphy Groin Pain?
B. P. Page and P. J. O’Dwyer
 280 Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy Groin Pain?
Introduction
Chronic pain is the most serious long-term compli-
cation of inguinal hernia repair. Up to one-third of
patients will complain of some sort of pain at 1 year
postoperatively, and in 3–4% of patients this pain
will be severe and disabling [1, 2]. The causes of
this pain are poorly understood, but factors such as
nerve and tissue injury may be important. Psycho-
logical factors are also implicated, and more recently,
the type of mesh used has been considered [3].
The most frequently used mesh type in inguinal
hernia repair is polypropylene based. These meshes
can be monofilament or multifilament with a closed
or open weave. In some patients they become very
stiff over time, and patients complain that they can
feel the mesh in their groin, while in others the
mesh causes pain [4]. To overcome this, products
have been designed that contain an absorbable and
a nonabsorbable component [5]. The nonabsorb-
able polypropylene left in situ usually weighs about
one-third that of conventional meshes.
The aim of this study was to compare a par-
tially absorbable (PA) product, Vypro II, with a
conventional nonabsorbable (NA) polypropylene
mesh. The primary end point of the study was pain
at 1 year following surgery. This was assessed by
visual analogue pain scores and a validated ques-
tionnaire [2].
Patients and Methods
Ethics committee approval was obtained in five
surgical units to randomise patients over 18 years
of age with an inguinal hernia to receive either
PA or NA mesh using the Lichtenstein repair [6].
Randomisation was computer generated with block
sizes that allowed balanced recruitment within each
centre. Patients were excluded if the hernia was
strangulated or irreducible or if they had under-
gone an open tension-free mesh repair previously
38 on the same side as the current hernia. Both pa-
tients and the staff conducting the postoperative as-
sessments were unaware of the treatment allocated.
The PA mesh used in this study was constructed
of multifilaments of polypropylene with additional
absorbable polyglactin (Vypro II, Ethicon, Ham-
burg, Germany). This mesh has a pore size of 4 mm
and weighs 82 g/m2 at implantation and 32 g/m2 af-
ter absorption of the polyglactin component, which
usually takes 56–70 days. The NA mesh has a pore
size of 1 mm and weighs 85 g/m2 (Atrium, Atrium
Medical, Schiphol-Rijk, Netherlands).
Before operation, pain scores on a visual ana-
logue scale (VAS) were measured in all patients
at rest and while moving, and all completed a
short-form (SF)-36 questionnaire. Patients under-
went open tension-free Lichtenstein mesh repair.
Operative details recorded included the hernia
type and size, any adverse events, and whether the
nerves were identified and preserved or divided.
All postoperative complications were recorded, and
patients were telephoned with set questions at 10,
20, and 30 days after surgery to determine the inci-
dence of wound infection and other wound-related
problems. Patients who reported a wound infection
or haematoma were recalled and examined clini-
cally. Hospital stay and time to return to work and
normal activities were recorded for all patients.
Patients were sent a VAS pain scale at 1, 3, and
12 months, as well as a modified SF-36 question-
naire. Modifications included questions about pain
of any severity at the site of hernia repair (none,
very mild, mild, moderate, severe, or very severe).
Patients were also asked whether the pain was
present all of the time, most of the time, some
of the time, a little of the time, or none of the
time. In addition, they underwent clinical review
and examination at 12 months for any evidence
of chronic wound problem, testicular atrophy, or
development of a recurrent or contralateral hernia.
Patients were also asked about any pain or numb-
ness at the site of hernia repair.
A sample size of 300 evaluable patients was nec-
essary to ensure an 80% power to detect a benefit of
the PA mesh of 15% for primary efficacy (incidence
of chronic pain at 12 months: NA mesh, 35%; PA
mesh, 20%) at the 5% level of significance using
a two-sided test. All subjects, regardless of their
compliance with the protocol, were included in the
analysis. For efficacy analysis, patients with missing
data for pain at 12 months were analysed using the
last valid observation, which was carried forward
for those who did not complete a questionnaire at
that time point. All statistical tests were interpreted
Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy
281 38
at the 5% significance level, and 95% confidence in- graphics and the anaesthetic and operating details
tervals (CIs) were calculated when appropriate. No were similar for the two groups (⊡ Table 38.1).
adjustment for multiple testing was made.

Primary End Point

Results
Altogether, 333 patients consented to participate in
the study. Two patients did not fulfil the inclusion
criteria, while 10 either withdrew consent or failed
to complete the preoperative assessments. This
left 162 patients in the PA mesh group and 159 in
the NA group (see ⊡ Fig. 38.1). The patient demo-
There were no differences in pain as rated by
the VAS at any of the time points in the study
(⊡ Figs. 38.2 and 38.3). Similar numbers of patients
reported severe pain in both groups. Pain of any
severity was found to be less in the PA group,
39.5% vs. 51.6%, a difference of 12.1% (95% CI:
-23.1 to -1.0, p=0.033; see ⊡ Table 38.2).

Consenting patients: 333

Randomised: 330

Partially absorbable (PA) group:N=166 Nonabsorbable (NA) group:N=164

Completed postoperative assessments: Completed postoperative assessments:

162 (97.6%) 159 (97%)

1-month questionnaire: 142 (85.5%) 1-month questionnaire: 135 (82.3%)

3-month questionnaire: 125 (75.3%) 3-month questionnaire: 129 (78.7%)

12-month questionnaire: 129 (78.7%)

12-month questionnaire: 137 (82.5%)

12-month clinic: 142 (86.6%)

12-month clinic: 142 (85.5%)

⊡ Fig. 38.1. Trial profile

 282 Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy Groin Pain?

⊡ Fig. 38.2. Visual analogue pain scores at rest in both patient groups preoperatively and 1, 3, and 12 months after surgery
(plots are means with 95% confidence intervals)

38

⊡ Fig. 38.3. Visual analogue pain scores on movement in both patient groups measured preoperatively and at 1, 3, and 12
months after surgery (plots are means with 95% confidence intervals)
Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy
283 38

⊡ Table 38.1. Patient demographics and anaesthesia and operating details for the partially absorbable (PA) and nonab-
sorbable (NA) groups

PA group, n=162 NA group, n=159

Age (years)a 55.7 (16.4) 57.3 (15.8)

Sex ratio (M:F) 156:6 154:5

a
Body mass index 25.5 (3.4) 25.7 (3.0)

Site of hernia: Right 80 (49.9%) 86 (54.1%)

Left 82 (50.6%) 73 (45.9%)

Type of defect: Direct 64 (39.5%) 51 (32.1%)

Indirect 77 (47.5%) 78 (49.1%)
Combined 21 (13%) 30 (18.9%)

Size of defect: <1.5 cm 27 (16.7%) 24 (15.1%)

1.5–3 cm 74 (45.7%) 68 (42.8%)
>3 cm 61 (37.7%) 65 (40.9%)

Type of anaesthesia: General 90 (55.6%) 94 (59.1%)

Local 64 (39.5%) 62 (39%)
Spinal 8 (4.9%) 3 (1.9%)

Operating time (min)a 42.5 (17.2) 42.9 (16.6)

Incision length (cm)a 7.4 (1.9) 7.4 (1.5)

Nerves identified: Ilioinguinal 145 (89.5%) 146 (91.8%)

Genital 74 (45.7%) 77 (48.4%)
Iliohypogastric 10 (6.2%) 68 (42.8%)

Nerves divided: Ilioinguinal 32 (19.8%) 32 (20.1%)

Genital 13 (8%) 16 (10.1%)
Iliohypogastric 10 (6.2%) 11 (6.9%)
aValues are mean (standard deviation)

common in the PA group (⊡ Table 38.4). There

⊡ Table 38.2. Pain at 12 months in the partially
absorbable (PA) and nonabsorbable (NA) groups
was no statistical difference between groups in
terms of occurrence of testicular atrophy, wound
Any paina Severe or very severe pain sinus, or contralateral hernia when examined at
PA 39.5% 3%
12 months.

NA 51.6% 4%
aDifference:
12.1% (95% confidence interval -23.1 to -1.0),
Costs to Health Service
p=0.033
In terms of costs, the PA mesh costs approximately
£14.32 more than the NA mesh, and these costs as
well as the costs of treating additional recurrences
Secondary End Points have been calculated in a United Kingdom context.
Given that about 70,000 inguinal hernias are re-
Return to normal activities was the same in both paired each year, this translates to a cost of about
groups (⊡ Table 38.3). There were six (3.7%) wound £1.4 million to the United Kingdom health service.
infections in the PA group and 10 (6.3%) in the NA This will increase to £6.4 million when the cost of
group. Hernia recurrence was significantly more treating the extra recurrences is factored in.
 284 Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy Groin Pain?

⊡ Table 38.3. Time to normal activities in days; values are median (interquartile range)

PA group NA group p-value (log rank test)

Paid work 21 (14–42), n=82 26 (10–49), n=77 0.375

Housework 10 (5–24), n=161 10 (4–21), n=154 0.579

Social life 10 (5–21), n=161 10 (4–24), n=154 0.622

Sex 28 (14 to >365), n=161 28 (14 to >365), n=154 0.649

Hobbies 20 (10–40), n=161 14 (7–31), n=154 0.283

⊡ Table 38.4. Hernia recurrence at 12 months in the partially absorbable (PA) and nonabsorbable (NA) groups

Number Recurrencea p (Fisher’s exact test)

PA 142 8 (5.6%) 0.037

NA 142 1 (0.7%)
aAnalysis performed with respect to those who completed the postoperative assessments

Discussion pylene mesh, underestimated the consequence of

This study shows that there was no difference in
pain scores at rest or with movement between
patients randomised to PA or to NA mesh. There
was also no difference in severe pain between the
two groups. It is likely that the small differences in
all types of pain reported in favour of the PA group
reflected differences in mild and very mild pain
in this study. This finding is in keeping with other
studies in which patients were less likely to feel a
foreign body in their groin after inguinal hernia
repair with Vypro mesh [4].
One of the disappointing results of this study
was a significant increase in recurrence rates in
the PA group. Subsequent investigation revealed
that the reason for this was that the suture pull-
out force in the knitted direction of the mesh
38 was low (⊡ Fig. 38.4). This may have caused or
contributed to the high recurrence rate in the
PA group. The manufacturer had stressed that
suture bites of at least 1 cm were required with
its product. Surgeons used to taking smaller bites
of mesh, as is routine with conventional polypro-
inadequate fixation with Vypro II. This may ex-
plain why most of the recurrences–five of eight–
were observed in one of the participating centres.
Surgeons in this centre admitted that they did not
adhere to taking suture bites of at least 1 cm with
the PA mesh.
The PA mesh used in this study was among
the first of its type to be investigated in a ran-
domised clinical trial. The perceived advantage
of leaving about one-third of the amount of poly-
propylene in situ after the polyglactin compo-
nent is absorbed has been exploited in other
products that maintain the tensile strength of
the absorbable component for a longer period
(e.g. Ultrapro [7]). These products may perform
better than Vypro II but need to be evaluated in
a similar fashion. Meshes with less polypropyl-
ene and a larger pore size, 3–4 mm, should also
be evaluated in randomised clinical trials. The
in vitro performance of these products may not
be matched by what happens in patients. New
products, such as polyvinylidene fluoride, that
have a similar weight to conventional polypro-
Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy
⊡ Fig. 38.4. Suture pull-out force
pylene meshes but a larger pore size also require
further careful evaluation in long-term follow-up
studies [8]. Biological products that are thought
to help stimulate growth of normal human blood
vessels and collagen have also had limited testing
in inguinal hernia repair [6].
One of the drawbacks of the many new prod-
ucts is the increased costs. Some of these products
are several times more expensive than conven-
tional polypropylene meshes. It follows, there-
fore, that a dramatic improvement in the patients’
quality of life, with similar or reduced recurrence
rates, would be required to justify their routine
use in inguinal hernia repair. While this seems
unlikely, the cost to the health service of a product
would be reduced if proven advantages resulted in
increased use.
This study demonstrates no clinical advantage
for using a PA mesh in inguinal hernia repair. The
significant reduction in mild discomfort that was
observed warrants further investigation with dif-
285 38
ferent products in larger multicentre controlled
clinical trials.
References
1. Bay-Neilson M, Perkins FM, Kehlet H. Pain and functional
impairment 1 year after inguinal herniorrhaphy: a nati-
onwide questionnaire study. Ann Surg 2001; 233:1–7
2. MRC Laparoscopic Groin Hernia Trial Group. Laparoscopic
versus open repair of groin hernia, a randomised compa-
rison. Lancet 1999; 354:185–190
3. Lagenbach MR, Schmidt J, Zirngibl H. Comparison of
biomaterials in the early postoperative period. Polypro-
lene meshes in laparoscopic inguinal hernia repair. Surg
Endosc 2003; 17:1105–1109
4. Post S, Weiss B, Willer M, Neufang T, Lorenz D. Ran-
domised clinical trial of lightweight composite mesh
for Lichtenstein inguinal hernia repair. Br J Surg 2004;
91:44–48
5. Junge K, Klinge U, Rosch R, Klosterhalfen B, Schumpelick
V. Functional and morphological properties of a modi-
fied mesh for inguinal hernia repair. World J Surg 2002;
26:1472–1480
 286 Chapter 38 · Does the Choice of Prosthetic Mesh Type Make a Difference in Postherniorrhaphy Groin Pain?

6. Lichtenstein IL, Shulman AG, Amid PK, Willis PA. Hernia had mistakes here, and we have to make more
repair with polypropylene mesh, an improved method. overlap. The question to Bringman was that with-
AORN J 1990; 52:559–565
out enough overlap at the pubic bone, we have
7. Cobb WS, Kercher KW, Heniford BT. The argument for
lightweight polypropylene mesh in hernia repair. Surg problems. We need an optimized technique for
Innov 2005; 12:63–69 these new meshes.
8. Klinge U. Mesh for hernia repair. Br J Surg 2008; 95:539– O’Dwyer: We need a product that is forgiving.
540 Simons: How can there be 60 randomized in one
group and only 48 in the other?
What kind of randomization system did you have?
Discussion O’Dwyer: It was a computer-generated randomiza-
tion by our statisticians. Every single patient was
Montgomery: You mentioned the mesh weight, entered again as a new entry—it was not a block
and you said there was a middleweight mesh of randomization.
85 g. I just wondered whether this group here has
a consensus on what is a lightweight mesh and
what a heavyweight mesh. Should we use or call
anything midweight meshes?
O’Dwyer: Just out of interest, one of our group
has decided that less than 40 g/m2 is truly light-
weight and between 40 and 80 is middleweight,
and if it’s greater than 80 it is heavyweight. But
you could also say that if it is lighter than 60 g/
m2 it’s light weight, and if it’s greater than 60, it is
heavyweight.
Montgomery: Is anyone here having sort of a
consensus on this topic? And should we count the
mesh weight together with the composite part of
it?
Hegarty: We have to distinguish between mesh
weight and pore size, don’t we? I am not bothered
about how much it weighs or about the diameter of
the filaments—I want a big-pore mesh.
Conze: I think it is not only the weight—forget
about the weight. There are meshes that are cer-
tainly more heavy than polypropylene. Say, PVDF
is more heavy. If you take a PVDF mesh with the
same size and the same pore size as a polypropyl-
ene mesh, it is going to be a heavyweight mesh. We
should focus more on pore size and even more on
surface area. And by doing that, we will get to a
new classification.
O’Dwyer: I think that makes sense. Pore size and
38 filament type are perhaps more important. Unfor-
tunately, we have gone down this route for the last
10 years.
Schumpelick: The question is if we need a new
technique for these lightweight flexible meshes.
We have learned that with the ventral hernia we
 39

New Understanding of the

Causes and Surgical Treatment
of Postherniorrhaphy Inguinodynia
and Orchialgia
P. K. Amid
 288 Chapter 39 · New Understanding of the Causes and Surgical Treatment of Postherniorrhaphy Inguinodynia

Introduction than dividing the nerve as it emerges from the

internal oblique muscle, as was our practice previ-
Advances in inguinal hernia repair, such as the use ously, the nerve was followed and severed proxi-
of prosthetic materials and new techniques, have mal to the surgical field of the original hernia
markedly reduced the postherniorrhaphy recur- repair. In 21 of those patients, the intramuscular
rence rate. However, chronic pain after hernia segment of the iliohypogastric nerve was scarred
repair is of continuing concern. According to the by perineural fibrosis or entrapped by sutures
Swedish Hernia Registry, the incidence of chronic placed when the so-called conjoined tendon was
pain postherniorrhaphy is greater than that of her- sutured to the inguinal ligament, plug, or flat
nia recurrence [1]. We have previously described mesh, depending on the method of the original
the causes, prevention, and surgical treatment of hernia repair. In less than 5% of patients, the il-
postherniorrhaphy chronic pain [2]. iohypogastric nerve is under the internal oblique
The current study of groin neuroanatomy has aponeurosis in the inguinal region. During hernia
resulted in new understanding of certain features repair in these patients, the subaponeurotic course
of postherniorrhaphy inguinodynia and orchialgia. of the nerve must be determined by noting the
Our series now stands at 465 patients who have
undergone operation for chronic post hernia repair
groin pain intractable to nonsurgical pain manage-
ment treatment. Recent observations of groin neu-
roanatomy have prompted a modification of our
neurectomy technique to include a more extensive
resection of the iliohypogastric nerve and, for pa-
tients with orchialgia, resection of nerves within
the lamina propria of the vas deferens as well.
These observations also illustrate methods to avoid
nerve injuries in the original hernia operation.

Methods
⊡ Fig. 39.1. Intramuscular segment of the iliohypogastric
Between 1995 and 2008, the triple neurectomy nerve exposed by splitting the muscle fibers (with sutures
operation was performed on 465 patients who retracting the edges of split)
did not respond to nonsurgical pain management
treatment. These patients either did not have pain
prior to their original hernia repair or, if they
did, their postoperative pain was different from
their preoperative pain and had the characteristic
features of neuropathic pain according to the In-
ternational Association for the Study of Pain. The
interval between the original hernia repair and
triple neurectomy was 2–5 years. In 210 patients
who underwent triple neurectomy from 2004 to
2008, attention was focused on the intramuscular
segment of the iliohypogastric nerve, the most vul-
39 nerable neural structure within the operative field.
A slit was made in the internal oblique muscle ⊡ Fig. 39.2. Point of simultaneous passage of a subaponeu-
fibers to expose the intramuscular segment of the rotic iliohypogastric nerve from both external and internal
iliohypogastric nerve (⊡ Fig. 39.1). Then, rather oblique aponeurosis
Chapter 39 · New Understanding of the Causes and Surgical Treatment of Postherniorrhaphy
289 39
location of its exit at the small point of attach-
ment between the internal and external oblique
aponeuroses (⊡ Fig. 39.2), and the surgeon should
avoid placing sutures or staples below the above-
mentioned point because the course of the nerve
under the internal oblique aponeurosis is inferior
and lateral (⊡ Fig. 39.3). During triple neurectomy,
the subaponeurotic iliohypogastric nerve can be
identified by splitting the internal oblique aponeu-
rosis immediately below the aforementioned point
(⊡ Fig. 39.3).
In early 2005, a patient was referred with
chronic groin pain and orchialgia, and a magnetic
⊡ Fig. 39.3. Subaponeurotic iliohypogastric nerve exposed by
resonance scan showed the vas deferens entrapped
splitting the internal oblique aponeurosis
by a plug (⊡ Fig. 39.4). At operation, the plug com-
pletely encircled the vas deferens (⊡ Fig. 39.5). Be-
cause the patient had undergone an earlier va-
sectomy, the entrapped segment of the vas was
resected during the triple neurectomy. Postopera-
tively, the patient’s groin pain and orchialgia disap-
peared, which was contrary to our experience with
other patients with both groin pain and orchialgia
who had undergone triple neurectomy alone. His-
tological study showed fibrosis and foreign body
reaction around the paravasal nerves within the
lamina propria of the vas (⊡ Fig. 39.6).
In 11 subsequent patients with groin pain and
orchialgia combined, a 2-cm segment of the lamina
propria of the vas was resected (without resecting
the vas) as proximal to the internal ring as pos-
sible. Histology showed perineural fibrosis in these ⊡ Fig. 39.4. Magnetic resonance image showing entrapment
patients as well. of vas deferens by a plug

Results

From 1995 to 2008, 460 patients with chronic

postherniorrhaphy pain underwent surgical treat-
ment at the Lichtenstein Hernia Institute in Santa
Monica, California. In 180 patients who had most
recently undergone triple neurectomy, particular
attention was paid to the intramuscular portion
of the iliohypogastric nerve. Adding resection of
the intramuscular segment of the iliohypogastric
nerve improved the success rate of triple neurec-
tomy compared with division of the iliohypogas-
tric nerve at the point of its emergence from ⊡ Fig. 39.5. Explanted plug along with the entrapped seg-
the internal oblique muscle. Furthermore, adding ment of vas from Fig. 39.4
 290 Chapter 39 · New Understanding of the Causes and Surgical Treatment of Postherniorrhaphy Inguinodynia
⊡ Fig. 39.6. Perineural fibrosis of paravasal nerves corresponding to Figs. 39.4 and 39.5
resection of the lamina propria of the vas to triple
neurectomy eliminated testicular pain.
Discussion
The definition of chronic inguinodynia, its diag-
nostic criteria, preoperative workup, and intraop-
erative verification, as well as the surgical treatment
and postoperative follow-up, have been described
previously [2]. Triple neurectomy is a proven sur-
gical treatment for chronic postherniorrhaphy
pain that is intractable to multidisciplinary pain
management. According to three major series, the
success rate of the operation ranges from 80% [3]
39 to 95% [2, 4]. Resecting the intramuscular portion
of the iliohypogastric nerve, instead of severing the
nerve at the point of its emergence from the inter-
nal oblique muscle, improves the outcome of triple
neurectomy. Although a firm conclusion should
not be drawn from such a small number of cases,
it seems that resection of the paravasal nerves is a
useful addition to triple neurectomy for patients
with orchialgia associated with inguinodynia.
Pain after placement of mesh in the parietal
compartment of the preperitoneal space (during
both open and laparoscopic hernia repair) presents
special problems. The main trunk of the gen-
itofemoral nerve, the preperitoneal segment of its
genital branch, and its femoral branch located
in the parietal compartment of the preperitoneal
space have no fascial coverage to protect them
from direct contact with nerves. This is in contrast
to the nerves in front of the transversalis fascia,
where the ilioinguinal and iliohypogastric nerves
are covered by the investing fascia of the internal
oblique muscle, and the inguinal segment of the
genital branch is covered by the deep cremasteric
Chapter 39 · New Understanding of the Causes and Surgical Treatment of Postherniorrhaphy
fascia. These covering layers protect the nerves
by acting as a barrier against the mesh. There is
experimental evidence that direct contact of mesh
with the nerves leads to certain ultrastructural
changes in the nerves; this evidence is consistent
with the preliminary results of our ongoing study
of the structural changes of nerves in patients
suffering from postherniorrhaphy pain. Also, be-
cause the nerves within the preperitoneal space are
not easily accessible during operative exploration,
surgical treatment of inguinodynia and orchial-
gia after preperitoneal hernia repair is less likely
to improve the patient’s symptoms. Therefore, we
reserve triple neurectomy for pain after laparo-
scopic hernia repair for patients in whom staples
or tacks were used and for those in whom com-
puted tomography or magnetic resonance imaging
shows meshoma. Recently we proposed a possible
treatment for neuropathy following open and lap-
aroscopic preperitoneal repair by transabdominal
retroperitoneal transection of periinguinal nerves
over the psoas muscle [5]. This approach, which
can be referred to as transabdominal retroperito-
neal triple neurectomy, is currently used for lap-
aroscopic aortic surgery. In light of these new find-
ings, the following recommendations are added to
those previously suggested for preventing posth-
erniorrhaphy inguinodynia [2]:
1. Avoid passing sutures through the internal
oblique muscle.
2. Avoid suturing the upper edge of the mesh to
the internal oblique muscle during Lichten-
stein tension-free hernia repair.
3. Avoid mesh implantation in the parietal com-
partment of the preperitoneal space; within
the inguinal canal a layer of fascia acts as a
barrier between the nerves and the mesh, but
in the parietal compartment of the preperi-
toneal space, there is no investing fascia to
protect the nerves from direct contact with the
mesh.
4. Avoid removing the cremasteric layer in order
to protect the inguinal segment of genital and
paravasal nerves from direct contact with the
mesh and thereby avoid postherniorrhaphy
inguinodynia, orchialgia, and the possibility
of infertility due to direct contact between the
mesh and the vas deferens.
291 39
Failing to identify and protect the nerves during
hernia repair significantly increases the incidence
of postherniorrhaphy pain [6–8]. Yet this issue
has not received due attention. According to the
Netherlands Hernia Registry, only 32% of surgeons
identified the iliohypogastric nerve during hernia
repair, and only 36% identified the genital branch
of the genitofemoral nerves. As has been reported
by many authors [9], identification and careful at-
tention to the groin nerves during hernia repair re-
duce the incidence of chronic pain to less than 1%.
References
1. Franneby U, Sandblom G, Nordin O, Gunnarsson U (2006)
Risk factors for long-term pain after hernia surgery. Ann
Surg 244:212–219
2. Amid PK (2004) Causes, prevention, and surgical treat-
ment of postherniorrhaphy neuropathic inguinodynia:
triple neurectomy with proximal end implantation. Her-
nia 8:343–349
3. Madura JA, Copper CM, Worth RM (2005) Inguinal neurec-
tomy for inguinal nerve entrapment: an experience with
100 patients. Am J Surg 189:283–287
4. Starling JR, Harms BA (1994) Ilioinguinal, iliohypogastric,
and genitofemoral neuralgia. In: Bendavid R (ed) Pros-
theses and abdominal wall hernia. RG Landes, Austin, pp
351–356
5. Amid P, Hiatt JR (2008) Surgical anatomy of the preperito-
neal space. J Am Coll Surg 207:295
6. Alfieri S, Rotondi F, Di Giorgio A, et al. (2006) Influence
of preservation versus division of ilioinguinal, iliohypo-
gastric, and genital nerves during mesh herniorrhaphy:
prospective multicentric study of chronic pain. Ann Surg
243:553–558
7. Wijsmuller AR, van Veen RN, Bosch JL, Lange JFM, Klein-
rensink GJ, Jeekle J, Lange JF (2007) Nerve management
during open hernia repair. Br J Surg 94:17–22
8. Aasvang EK, Mohl B, Bay-Nielson M, Kehlet H (2006) Pain
related sexual dysfunction after inguinal herniorrhaphy.
Pain122:258–263
9. Kingsnorth AN, Bowley DMG, Porter C (2003) A prospec-
tive study of 1000 hernias: results of the Plymouth Hernia
Service. Ann R Coll Surg Engl 85:18–22
Discussion
Klinge: Why do you believe that a proper fixation
can prevent the development of mesh shrinkage
or mesh migration or meshoma? We have seen so
many meshes after some times, despite thousands
 292 Chapter 39 · New Understanding of the Causes and Surgical Treatment of Postherniorrhaphy Inguinodynia

of tacks. Why do you think that some sutures can

prevent this development?
Amid: You are right. This usually happens in the
preperitoneal space, because the fixation is not
complete and the surface is not completely smooth.
Very rarely you can see these meshomas in front of
the transversalis fascia. And maybe light meshes
could prevent that. I do not know. But theoreti-
cally, it makes sense to assume that light meshes,
by creating less fibrotic tissue, may prevent me-
shoma formation.
Kehlet: You have operated on 460 patients now.
Do you find these abnormalities every time you
operate? What is the specific indication for these
operations? Secondly, neurosurgeons have done
neurosurgery for chronic pain for many years—
always disappointing. What is the follow-up here?
What happens with time? Do you really think that
you have solved the problem in the long term?
Amid: First, I tell you about the follow-up: We see
these patients 1 week and 1 month after the op-
eration and then up to 6 months. We contact them
by phone, and that is the end of our follow-up. I
admit, this is not a complete follow-up. After the
last telephone conversation—and they tell us they
are satisfied—if their pain comes back or becomes
more, they would contact us. I agree, that is not
scientific enough.
How often we find these pathologies? Almost all of
the time! The least thing that we find is very dense
fibrotic tissue—histologically, perineural fibrosis.
Now we study the structural changes of the nerves.
Penkert: With your large experience in these cases,
I wonder that you have success in all cases. So, we
must estimate preoperatively what kind of pain it
is. If it is neuroma pain, it works. But if it really is a
neuropathic pain, it is quite another thing. I am in
doubt. That is my comment.
Amid: The best indication for this operation is
when the previous operation is an anterior repair
without manipulation of the preperitoneal space.
If the preperitoneal space is manipulated, even by
placement of a plug or by placement of a PHS or
by a preperitoneal repair, then the pain could be
39 related to the nerves in front of the transversalis
fascia or behind the transversalis fascia. And there
is no way to find out what part is belonging to the
front and what part belongs to behind.
 40

Surgery for Chronic Inguinal Pain:

Neurectomy, Mesh Explantation,
or Both?
G. D. Arlt, U. Huhn, C.C. Kersten
 294 Chapter 40 · Surgery for Chronic Inguinal Pain: Neurectomy, Mesh Explantation, or Both?

Introduction
⊡ Table 40.1. Results of neurectomy for chronic groin
pain after inguinal hernia repair
Chronic inguinal pain is a rare but severe compli-
cation of inguinal hernia repair, with a prevalence n Mesh Success Follow-up
of disabling pain from 3% to 9% (Kehlet et al. Stulz and 23 0 70% ?
2002, Aroori and Spence 2007). Its exact cause and Pfeiffer 1982
lack of evidence-based treatment path presents
Starling et al. 30 0 83% ?
problems in the effective management of this sur- 1987
gical complication. Most cases may be treated con-
servatively with repeated injections of cortisone Kennedy et 23 0 63% 36–144
al. 1994 months
and a local anesthetic for a permanent local nerve
block. About 70–80% of the patients respond to Bower et al. 15 0 80% 66
the infiltration therapy to the point of maximum 1996 months
tenderness (Aroori and Spence 2007, Palumbo et Skandalakis 6 0 100% ?
al. 2007). In the others, different treatment strate- 1996
gies have been proposed, such as analgesics and
Heise and 9 100% 56% 16
antidepressants, transcutaneous electrical neural
Starling 1998 months
stimulation, or recurrent surgery with neurolysis
and neurectomy with or without removal of the Amid 2004 225 100% 80% –
mesh. Although the necessity of repeated surgery
Madura et al. 100 27% 72% 1–60
for chronic pain after mesh repair may be rather 2005 months
low, at about 0.35% (Delikoukos et al. 2008), there
Ducic et al. 19 100% 84% 12
is major disagreement concerning both the selec-
2008 months
tion criteria for recurrent surgery and the type of
surgery itself.
Considering the chronic postherniorrhaphy
pain syndrome in detail, two types of pain can In cases of chronic pain after mesh repair
be distinguished: 1) neuropathic pain caused by which cannot be assigned to a distinct nerve, the
entrapment of the ilioinguinal, iliohypogastric, or considered surgical approach is mesh removal with
genital branch of the genitofemoral nerve, and 2) or without additional neurectomy. Two small se-
nonneuropathic pain, which might be triggered by ries of mesh removal for pain after groin hernia
staples to the periosteum and/or compression and surgery have been published. In 1998 Heise and
scar formation around the implanted mesh materi- Starling described transinguinal mesh removal in
als. The latter type of pain may be further differ- 20 patients with severe groin pain following Lich-
entiated into nociceptive or somatic pain induced, tenstein or laparoscopic mesh repair. The outcome
for example, by staples, and visceral pain such as was excellent or good in 12 (60%) of the 20 cases.
dysejaculation or testicular pain (Loos et al. 2007, Aside from a tendency to see better results after
Kehlet 2008). additional neurectomy during mesh removal, they
In patients with neuropathic pain, a surgical were unable to identify other factors that could im-
approach with neurectomy of the involved nerves prove postoperative results or help select better pa-
seems rational. Several studies have been published tients for surgery (Heise and Starling 1998). Rosen
reporting the results of dual or triple neurectomy et al. presented their experience with mesh explan-
for chronic groin pain following inguinal hernia tation on the basis of 10 cases selected from 1998
surgery. Success rates vary from about 60% to 80% to 2004. The indication was chronic groin pain
in most series (⊡ Table 40.1). Unfortunately, several not responding to local anesthesia of the inguinal
of these studies are judged to be of poor quality nerves. The index operation was a Lichtenstein
due to nonstandardized selection criteria, short procedure in nine of the 10 cases. In contrast to
40 follow-up, and small sample sizes. Heise and Starling, they used a combined surgical
Chapter 40 · Surgery for Chronic Inguinal Pain: Neurectomy, Mesh Explantation, or Both?
procedure with transinguinal removal of the mesh
and laparoscopic repair of the hernia defect. Re-
sults were good or excellent in nine of 10 patients
(Rosen et al. 2006).
Our own experiences with indications, opera-
tive technique, and results of revision surgery for
chronic groin pain after inguinal hernia repair are
presented here.
Patients and Methods
Patient Selection
Patients with persistent or recurrent disabling pain
interfering with daily activities 3 months after the
index operation were judged as chronic pain cases.
Pain of other origin, including hernia recurrence,
was ruled out by pain history, clinical and ultra-
sound examination, and, in some cases, magnetic
resonance imaging. Initial treatment was conserva-
tive and consisted of oral analgesics and infiltra-
tion therapy with local anesthetics and steroids.
Those who did not respond to this treatment were
candidates for surgery. Patients with neuropathic
pain responding to diagnostic nerve block with
local anesthetics (10 ml of Xylocaine 1% at the
anterior superior iliac spine) were offered revision
surgery with dual or triple neurectomy. Those with
nonneuropathic pain exhibiting no significant pain
relief after nerve block were candidates for mesh
removal and neurectomy.
Patients
From October 1998 to December 2007, 87 patients
with chronic groin pain not responding to conser-
vative treatment were referred for further surgery
at the surgical department of the Park-Clinic in
Berlin-Weissensee, Germany.
Fifty-four patients with severe neuropathic
complaints following an inguinal hernia repair
were identified for recurrent surgery with double
or triple neurectomy: 34 men and 20 women with
an average age of 47 (range 14–77) years. Thirty-
one cases presented after primary repair, and 23
patients had had several hernia repairs. A non-
295 40
mesh procedure had been done in 29 patients, and
25 had had a mesh repair.
The nonneuropathic pain group consisted of
33 patients (26 male, seven female) with an average
age of 48 (range 14–71) years. They were offered
a mesh removal procedure. The mesh procedures
done previously were a transabdominal preperito-
neal or totally extraperitoneal repair in 23 patients,
a Lichtenstein repair in five, and a mesh-plug re-
pair in another five cases.
Several attempts at conservative treatment on
an outpatient basis had been made for all of the pa-
tients. In some cases, psychosomatic therapy had
been recommended. Patients with mild or moder-
ate symptoms responding to conservative therapy
were not included in this series.
Operative Technique
In patients dedicated for neurectomy, the lateral
part of the skin scar in the groin was opened and
the deep inguinal ring exposed. After exclusion of
a recurrent hernia, the ilioinguinal and iliohypo-
gastric nerves were identified lateral to the deep
ring. Both nerves were resected, and a 1-cm strip
of nerve tissue was harvested for histologic ex-
amination. The proximal ends of the nerves were
embedded in the internus muscle. In cases with
triple neurectomy, the genital branch of the gen-
itofemoral nerve was identified at the »blue line«
near the deep ring and was resected together with
the external spermatic vessels. The surgical tech-
nique of mesh removal has been described before
(Arlt et al. 2003).
Perioperative Care and Follow-Up
Informed consent was given by all patients regard-
ing an increased risk of intraoperative and post-
operative complications (estimated percentage of
ischemic orchitis about 5%, vascular injury about
5%, and recurrent hernia up to 10%). A single-shot
antibiotic prophylaxis was used in all operations.
All patients were mobilized within 4–6 h postop-
eratively. Patients were discharged according to
their own wishes between days 2 and 10. Physical
 296 Chapter 40 · Surgery for Chronic Inguinal Pain: Neurectomy, Mesh Explantation, or Both?
activity was restricted for 2 weeks after hospital
discharge.
All patients were followed for at least 6 months
postoperatively. The last follow-up examinations
with clinical assessment and ultrasound were done
in June 2008, with the follow-up interval ranging
from 6 to 86 months. Results were classified as
good for satisfied patients with complete pain re-
lief and no need for further analgesic medications.
Satisfied patients with some pain during physical
activity and the need for painkillers on demand
not more than once or twice a week were classified
as having a fair result. A bad outcome was quoted
in dissatisfied cases with persisting or recurrent
disabling pain after the revision surgery.
Results
Neurectomy
In the group having neurectomy surgery, no se-
vere intraoperative or postoperative complications
occurred. All 54 patients could be followed at
least 6 months postoperatively. Forty-two patients
showed a good result with no complaints and no
analgesic medication at the follow-up examina-
tion after 6 months. Another five patients were
also satisfied with the surgery but reported in-
termittent pain during physical activity requiring
analgesics once or twice a week. They were clas-
⊡ Table 40.2. Results of neurectomy in 54 patients
with neuropathic pain; cases with intermittent or per-
sisting pain (fair or bad results of surgery) were sum-
marized as nonresponders
Nonresponders 12/54 (22%)
After primary repair 3/31 (10%)
After recurrent repair 7/25 (28%)
Age >50 years 3/25 (12%)
Age <50 years 7/29 (24%)
Further surgery 6/54 (11%)
40 Secondary mesh removal 5/25 (2%)
sified as having a fair result. In seven cases, the
pain persisted or returned within 6 months after
the operation.
Detailed analysis of the cases with intermittent
or persisting pain showed that an adverse outcome
(fair or bad) was more likely in younger patients
and those who had repair for a recurrent hernia
(⊡ Table 40.2). Further surgery with a triple neurec-
tomy or a secondary mesh removal was done in
six patients. Consideration of the risk of further
surgery with mesh removal in patients with neu-
ropathic pain and a mesh repair in their history
showed a 20% risk for additional operations in this
subgroup (five of 25 cases).
Mesh Removal
In the group receiving mesh removal, complete
or near total explantation of the foreign body was
achieved in 32 of 33 patients. In one man with a
previous Lichtenstein repair, the mesh removal was
impossible due to extended scar formation at the
cord, indicating a high risk for testicular atrophy.
The surgery was restricted to a dual neurectomy
with a fair result 6 months after the operation.
In the other 32 patients, one case each of par-
tial resection of the bladder, resection of the small
bowel, suture of the femoral vein, seroma forma-
tion, and ischemic orchitis with testicular atrophy
were the major intraoperative and postoperative
complications. Reconstruction of the posterior
wall was done with a two-layer Shouldice proce-
dure in 25 cases and a Lichtenstein repair using a
lightweight mesh (Vypro II /Ultrapro) in six cases.
In a 57-year-old woman, the excision of the mesh–
fascia–muscle specimen resulted in a large defect
of the posterior wall, which had to be closed by a
Rives procedure with a Vypro II mesh.
Macroscopically, all mesh specimens showed
extended folding and shrinkage of 50–70% of
the surface (⊡ Figs. 40.1 and 40.2). Analysis of the
mesh material and the histopathologic examina-
tion of the explanted foreign bodies showed that
30 meshes were heavyweight (>90 g/m2) polypro-
pylene meshes and two were polyester meshes.
Chronic inflammation and apoptosis were regular
findings at the mesh–tissue interface.
Chapter 40 · Surgery for Chronic Inguinal Pain: Neurectomy, Mesh Explantation, or Both?
297 40
At follow-up 6 months to a maximum of 86
months postoperatively, two recurrent inguinal
hernias were found. Twenty-two patients had no
complaints and were completely satisfied (69%
good results). In seven cases, the patients were
satisfied but had intermittent pain during physi-
cal activity (22% fair results). In one of these
patients, a recurrence was found and repaired.
During further follow-up, this patient again had
a fair outcome. Three patients were dissatisfied
(9% bad results). One developed a testicular atro-
phy, another a symptomatic recurrent hernia, and
another complained of persisting disabling pain
(⊡ Table 40.3).

Conclusion
⊡ Fig. 40.1. Polypropylene Hernia System prosthesis from a
17-year-old girl 11 months after implantation
The series of 87 patients surgically treated for
chronic postherniorrhaphy pain shows that a good
or fair clinical result with a satisfactory outcome
can be achieved in up to 85% of cases. An impor-
tant supposition is careful selection of patients.
Indication should be restricted to cases with con-
servatively intractable symptoms. At present, the
distinction between neuropathic and nonneuro-
pathic pain on the basis of local nerve blocks can
be recommended.
The mesh removal operation is challenging,
and the surgeon should also be experienced in her-
nia and vascular surgery. Informed consent from
the patient concerning the increased risk of tes-
ticular and vascular complications is necessary. To
⊡ Fig. 40.2. Heavyweight small-pore polypropylene prosthe-
develop a standardized surgical approach regard-
sis 18 months after a transabdominal preperitoneal repair
ing chronic groin pain after hernia repair, a large
multicenter study would be indispensable.

⊡ Table 40.3. Results of mesh removal for chronic

pain: follow-up at 6–86 months
References
Follow-up in June 2008 (clinical n=32
exam/ultrasound) Amid PK (2004) Causes, prevention, and surgical treatment
of postherniorrhaphy neuropathic inguinodynia: triple
Recurrent hernia n= 2
neurectomy with proximal end implantation. Hernia
No complaints/satisfied n=22 (69%) 8:343–349
Arlt G, Lamm T, Klosterhalfen B (2003) Mesh removal in ingui-
Pain during physical activity n=7 (22%) nal hernia repair. Eur Surg 35:42–44
Aroori S, Spence RA (2007) Chronic pain after hernia sur-
Dissatisfied (testicular atrophy/ n=3 (9%)
gery–an informed consent issue. Ulster Med J 76:136–
recurrence/persistent pain)
140
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Bower S, Moore BB, Weiss SM (1996) Neuralgia after inguinal
hernia repair. Am Surg 62:664–667
Delikoukos S, Fafoulakis F, Christodoulidis G et al. (2008) Re-
operation due to severe late-onset persisting groin pain
following anterior inguinal hernia repair with mesh. Her-
nia 12:593–595
Ducic I, West J, Maxted W (2008) Management of chronic post-
operative groin pain. Ann Plast Surg 60:294–298
Heise CP, Starling JR (1998) Mesh inguinodynia: a new clinical
syndrome after inguinal herniorrhaphy? J Am Coll Surg
187:514–518
Kehlet H (2008) Chronic pain after groin hernia repair. Br J
Surg 95:135–136
Kehlet H, Bay-Nielsen M, Kingsnorth A (2002) Chronic posth-
erniorrhaphy pain–a call for uniform assessment. Hernia
6:178–181
Kennedy EM, Harms BA, Starling JR (1994) Absence of mal-
adaptive neuronal plasticity after genitofemoral-ilio-
inguinal neurectomy. Surgery 116:665–670; discussion
670–671
Loos MJA, Roumen RMH, Scheltinga MRM (2007) Classifying
postherniorrhaphy pain syndromes following elective in-
guinal hernia repair. World J Surg 31:1760–1765
Madura JA, Madura JA II, Copper CM, Worth RM (2005) Ingui-
nal neurectomy for inguinal nerve entrapment: an experi-
ence with 100 patients. Am J Surg 189(3):283–287
Palumbo P, Minicucci A, Nasti AG et al. (2007) Treatment for
persistent chronic neuralgia after inguinal hernioplasty.
Hernia 11:527–531
Rosen MJ, Novitsky YM, Cobb WS, Kercher KW, Heniford BT
(2006) Combined open and laparoscopic approach to
chronic pain following open inguinal hernia repair. Her-
nia 10:20–24
Skandalakis JE, Skandalakis LJ, Colborn GL (1996) Testicu-
lar atrophy and neuropathy in herniorrhaphy. Am Surg
62:775–782
Starling JR, Harms BA, Schroeder ME, Eichman PL (1987) Di-
agnosis and treatment of genitofemoral and ilioinguinal
entrapment neuralgia. Surgery 102:581–586
Stulz P, Pfeiffer KM (1982) Peripheral nerve injuries resulting
from common surgical procedures in the lower portion of
the abdomen. Arch Surg 117:324–327
Discussion
Deysine: It is evident that these are sometimes
true catastrophes, implying very difficult surgery.
I am not surprised about the complications that
you have. Referring to your paper and the paper of
Dr. Amid, there is an alternative thing that we can
teach to our residents when we do this hernia sur-
gery: that you do not need to tie knots extremely
40 hard so that you strangulate the tissue. If you teach
your residents to just approximate the mesh to
whatever structure you are using, if you have the
poor luck of having a nerve in between, it is not
going to be strangled, and the patient will not have
pain. Because otherwise, going after those nerves
is difficult. Again, the technique is a very impor-
tant aspect for having good results.
Schumpelick: I congratulate you. I think it is one
of the ugliest operations of all. You must inform
your patients about the loss of sensitivity, bleeding
of the vein, about the big hole you left and that
you have to close maybe with a new mesh. And
you must give him the message that at least 20%
will have pain. If patients agree with that, he really
must have pain. Even in younger people. In my
personal experience, they will even come if you say
that they might lose their testes. We have at least
once a month such a patient.
Champault: Two years ago, I saw a young man
with pain. I explained the risk of infertility because
he had a hernia on the other side when he was
2 years old. So he said okay, and he came back
2 weeks ago with a young boy. To sum up, he post-
poned the operation for one girl and one boy.
Kehlet: Apparently you did a local anesthetic block
to divide your indication toward neurectomy or
mesh removal. What is the rationale for that, be-
cause if you think the pain is coming from the
mesh, a local anesthetic block should also help?
Arlt: I do not believe that the pain always origi-
nates from the mesh.
Kehlet: Why did you remove it?
Arlt: Only in those cases where they had a me-
shoma, because when we started this series we
followed strictly the idea of having responders to
local anesthesia [receive] nerve cutting and non-
responders [receive] mesh removal. We saw that
we had five patients with pain responding to local
anesthesia who had to have a third operation to
take out the meshoma.
Kehlet: But my question is, if you believe that the
pain is coming from the mesh or the meshoma,
why shouldn’t a good anesthetic block work?
Arlt: Yes, it works, but only for some hours. It was
a diagnostic local anesthesia. We also do this injec-
tion therapy, and we have at least 60–70% of pa-
tients we do not have to operate on. Thirty percent
come again and again, despite injection therapy.
 41

Results of Tailored Therapy for Patients

with Chronic Inguinal Pain
M. Stumpf, D. Kämmer, U. Klinge
 300 Chapter 41 · Results of Tailored Therapy for Patients with Chronic Inguinal Pain

The onset of chronic inguinal pain has been in-

41 creasing in recent years, but therapeutic options
for these patients remain unclear. Different meth-
ods apart from conservative management have
been described for dealing with this problem.
These options include local revision of the scar
and the inguinal nerves, with the next step being
retroperitoneal triple neurectomy. Patients with an
implanted mesh have the option to have the mesh
material explanted, but this can sometimes be a
rather difficult operation.
We analyzed patients treated surgically for
chronic inguinal pain in the surgical clinic of the
University of Aachen (Germany) between 2005 ⊡ Fig. 41.1. Retroperitoneal triple neurectomy
and 2008. Thirty-three of these patients were in-
cluded in the study. All patients had to fill out a
structured pain questionnaire (Deutscher Schmer-
zfragebogen). In addition, immunohistochemi-
cal investigations of explanted nerves and meshes
were done. Most patients had experienced com-
plaints for more than 2 years. Seventy-five percent
of patients with chronic inguinal pain had had a
mesh repair in the past, mainly Lichtenstein or a
laparoscopic procedure.
The aim of the study was to analyze which
patients would benefit from an operative approach ⊡ Fig. 41.2. Explanted mesh plug and flat mesh
and to learn whether it is possible to distinguish
between two types of chronic inguinal pain and
whether there are any clinical implications for the
therapeutic strategy. ⊡ Table 41.1. Results after different operations
For treatment, we chose three different types
Local Explan- Neurec-
of surgery: local revision of the scar and nerves, revision tation tomy
retroperitoneal triple neurectomy (⊡ Fig. 41.1), or
explantation of the mesh. The explanted meshes Pain-free 0% 50% 25%
were mainly heavyweight flat meshes and plugs Improvement 50% 25% 50%
(⊡ Fig. 41.2).
Persistent pain 50% 25% 25%
The best results were achieved for patients
treated by complete mesh explantation: 75% were
pain free or had real improvement in their pain.
No patient was pain free after local revision, and those in group 2 had persistent pain after opera-
50% had persistent pain (⊡ Table 41.1). tion.
We then hypothesized that two types of Seventy percent of the male patients improved,
chronic inguinal pain exist. Type I is not curable but only 55% of the female patients did. There were
with operative intervention, but type II will pos- no statistically significant differences between the
sibly benefit from operative intervention. There- two groups with regard to age, obesity, duration of
fore, a differentiation was made among the pa- pain, days of hospital stay, or number of previous
tients: Group 1 patients were pain free or had an operations (⊡ Table 41.2). Looking at the types of
improvement in their pain after operation, and explanted meshes, it is interesting that all patients
Chapter 41 · Results of Tailored Therapy for Patients with Chronic Inguinal Pain
301 41
Stumpf: We fix the hernia as well. It depends on
⊡ Table 41.2. Differences between patients who
improved after surgery and those with persistent pain the age of the patients. If you have a young patient
with comparable stable tissue we do a Shouldice
Improvement Persistent repair. But after a TAPP or TEP hernia repair you
Age 51.16±13.93 43.17±13.97 mainly have a large defect of the abdominal wall.
In those cases we usually use large pore and low
Obese 8 4
weight meshes to fix it again.
Duration of pain 25±19.4 45±51.5 Köckerling: How do exclude a recurrence? And do
(months) you use a diagnostic laparoscopy?
Days at hospital 12.9±14.2 11.42±6.5 Stumpf: We use the ultrasound in every patient
with inguinal pain. However at first we try to
Former 1.8±1.0 1.58±1.0 diagnose a recurrence clinically followed by an
operations (n)
ultrasound. In case of an experienced investigator
you can objectify a recurrence very exactly. A diag-
nostic laparoscopy was used in some cases, but we
didn’t use it routinely.
with plug repairs were pain free after mesh explan-
tation. Both groups showed significant differences
in the immunohistochemical expression of CD68
and matrix metallopeptidase 2 (MMP2) at the
nerve tissue, which may hint at existing differences
in the ultrastructure of the two types of patients.
In conclusion, patients receive only minor ben-
efits from local revision of the scar and inguinal
nerves. The best results, yielding a high number of
pain-free patients after the revision, were reached
after mesh explantation. All patients who under-
went plug removal were pain free.
There might be a correlation between the type
of patient and the benefit experienced; patients
who were pain free after their operation showed
differences in immunohistochemical markers com-
pared with the patients who did not benefit from
surgery. Further investigation will be necessary
to elucidate these interesting findings concerning
chronic inguinal pain after hernia surgery.

Discussion

Gryska: When you do an explantation, are not also

doing at least a partial neurectomy?
Stumpf: Indeed, if you are doing a reoperation fol-
lowing a Lichtenstein hernia repair to also remove
the ilioinguinal nerve while the mesh explantation if
the nerve wasn’t dissected while the first operation.
Gryska: What are you doing with the hernia after
explantation of the mesh?
 IV

IV Risk for Adhesion

42 Adhesion as a Chronic Inflammatory Problem?

Risk for Adhesions, Migration, and Erosions? – 305

43 Biological Tissue Graft: Present Status – 317

44 IPOM Results of 344 Consecutive Patients with a

PVDF-Derived Prosthesis – 323

45 Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia

Repair: 14 Years of Patient Data Accrual – 331

46 Tissue Ingrowth, Adhesion, and Mesh Contraction – 345

47 Effect of Different Mesh Materials on Adhesion Forma-

tion – 353

48 Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh

Materials: An Updated Review of the Literature – 365

49 Porosity and Adhesion in an IPOM Model – 375

50 Benefit of Lightweight and/or Titanium Meshes? – 381

51 ePTFE Prostheses and Modifications – 393

52 The Role of Stem Cells in Abdominal Wall Repair – 401

 42

Adhesion as a Chronic Inflammatory

Problem? Risk for Adhesions,
Migration, and Erosions?
M. Binnebösel, K. Junge, C. D. Klink, J. Serno, J. Otto, J. Conze, A. P. Öttinger,
V. Schumpelick
 306 Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration, and Erosions?
Introduction
Peritoneal adhesions are common and develop
42 postoperatively in more than 90% of patients fol-
lowing abdominal surgery. Most adhesions are not
symptomatic, however. Even years after surgery,
adhesions can lead to undesirable outcomes such
as small bowel obstruction, infertility, abdomi-
nopelvic pain, and difficult reoperative procedures
[1–3]. In addition, adhesions have a substantial
impact on the national health economy. In a cur-
rent Swedish survey, the annual cost of adhesion-
related problems was estimated to be €39.9–59.5
million, and the cost of inpatient readmissions was
almost equal to that for gastric cancer [4].
The peritoneum is the largest serous mem-
brane, with a surface of 2 m2. It covers the vis-
ceral organs (visceral peritoneum) and lines the
abdominal cavity (parietal peritoneum) [5]. The
peritoneum is composed of a monolayer of me-
sothelial cells of mesenchymal origin, resting on a
continuous basement membrane supported by the
submesothelium. The submesothelial layer consists
of the extracellular matrix made up of different
types of collagen, glycoproteins, glycosaminogly-
cans, and proteoglycans [5]. Diffusion and resorp-
tion of fluid occur freely through the mesothelium
and submesothelial stroma. The luminal surface
of mesothelial cells has numerous microvilli, in-
creasing the peritoneal surface area up to 40 m2
for exchange between mesothelial cells and the
peritoneal cavity. Overall, the peritoneum must be
regarded as an organ that has a protective function
for the contents of the abdominal cavity.
Peritoneal defects during surgical procedures
result in a reduced supply of oxygen and nutrients
as well as an impaired ability to remove metabolic
byproducts [6]. Correspondingly, it has been sug-
gested that adhesions may act as vascular grafts
between healthy organs and areas of ischemic tis-
sue, reflecting the body’s attempt to overcome local
damage [7]. It is generally supposed that peritoneal
adhesions reflect a kind of modified regeneration
of the peritoneal surface, initially as tender and
fibrinous bands that are transformed to inert scar
tissue with fibroblasts and collagen bundles [1].
In accordance with Epstein et al. [8], we found
human peritoneal adhesions to be highly cellular,
well-vascularized proliferating tissue, indicating a
dynamic and persistent remodeling [8, 9]. Besides
plasmin, plasminogen activator, and plasminogen
activator inhibitor, other factors–including trans-
forming growth factor beta, matrix metallopro-
teinases, tissue inhibitors of metalloproteinases,
insulin-like growth factor 1, and platelet-derived
growth factor–have been revealed to be important
mediators involved in peritoneal healing, all inter-
acting with each other (⊡ Fig. 42.1) [10]. Currently,
the impact of inflammatory stimulants–including
chemoattractants [interleukin (IL)-8, monocyte
chemotactic protein-1] and cytokines (tumor ne-
crosis factor alpha, IL-1β, IL-6)–as products of
invaded polymorphonuclear granulocytes, mono-
cytes, and leucocytes is increasingly discussed as
an important factor in adhesiogenesis [1–13].
The aim of the first study was to investigate
whether human peritoneal adhesions reveal in-
flammatory activity and whether persistent ad-
hesions reflect a disturbed peritoneal cell dif-
ferentiation, proliferation, and migration. To test
this hypothesis, we focused on the appearance
of macrophages (CD68), B-lymphocytes (CD20),
and T-lymphocytes (CD45) as main representa-
tives of the cellular immune response. Further-
more, we measured the occurrence of cycloox-
ygenase-2 (COX-2) as a pivotal component of
inflammatory cell activity. Finally, we analyzed
the expression profiles of Notch-3, ß-catenin, and
c-myc as important mediators of cell differen-
tiation, proliferation, and migration involved in
wound healing.
The aim of the second study was to investi-
gate the kinetics of peritoneal adhesions in a rat
model with special regard to the cellular immune
response [T-lymphocytes (CD3) and macrophages
(CD68)], inflammatory cell activity (COX-2), and
cell differentiation, proliferation, and migration
(ß-catenin and c-myc).
Patients and Methods
Study I: Patient Information
Adhesions were prospectively collected from 40
patients undergoing laparotomy at the surgical
Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration
307 42

⊡ Fig. 42.1. Elementary steps and complementary factors involved in the adhesion formation process according to Duron [10]
(PA plasminogen activator; PAI plasminogen activator inhibitor; TGF transforming growth factor; FSP fibrin split products; MMP
matrix metalloproteinase; ECM extracellular matrix)

department of the RWTH Aachen University
Hospital, Germany. The study was approved by
the local ethics committee, and patients gave
written informed consent to participate in the
trial. The clinical parameters acquired included
age, gender, diagnosis, and surgical and medical
history. Adhesion maturity was calculated from
the date of the last previous abdominal surgery,
according to Herrick et al. [14]. In each patient,
one sample of 5–10 mm was excised from the
visceral peritoneum close to the intestine, and
another sample of 5–10 mm was excised from
the parietal peritoneum distant from the perito-
neum. Tissue specimens were immediately fixed
in 4% paraformaldehyde and embedded in paraf-
fin wax.
Study II: Animal Model and Surgical
Procedure
The animal experiment was approved by the Ani-
mal Care and Use Review Committee of the Rus-
sian State Medical University, Moscow. All animals
were housed in accordance with the requirements
of the German Animal Protection Act. For the
experiment, 60 male Sprague–Dawley rats with a
mean body weight of 380 g were used. All ani-
mals were kept under standardized conditions:
temperature 22–24°C, relative humidity 50–60%,
and 12 h of light following 12 h of darkness. The
animals had free access to food and water. Food
was withdrawn 12 h before and after surgery. All
operations were carried out under general anesthe-
 308 Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration, and Erosions?
sia and aseptic and sterile surgical conditions. The
surgical procedure (explantation of the adhesion
tissue) was done at the Joint Institute for Surgical
42 Research of the Russian State Medical Univer-
sity in Moscow. After introduction by isoflurane,
general anesthesia was achieved with a subcuta-
neous mixture of 0.3 mg/kg medetomidine and
100 mg/kg ketamine hydrochloride. The rats were
weighed, and their skin was shaved and disinfected
with a polyvidone–iodine solution. The animals
were fixed in a supine position. Laparotomy was
performed by a 4-cm midline incision, and then a
standardized peritoneal defect with a diameter of
2 cm at the cecal area was created. The abdominal
wall and skin were separately closed with continu-
ous absorbable 4/0 polyglactin sutures (Vicryl). No
additional antibiotic treatment was given before or
during the experimental setting.
On postoperative days 3, 5, 14, 30, 60, and
90, 10 animals, respectively, were sacrificed and
weighed for morphological, histological, and im-
munohistochemical observations. In each animal
the developed adhesion tissue, including parietal
and visceral peritoneum, was explanted, and tis-
sue specimens were immediately fixed in 4% para-
formaldehyde and embedded in paraffin wax.
Histological Assessment
Histological and immunohistochemical investiga-
tions were done at the Surgical Department of the
RWTH Aachen University Hospital, Germany, and
were performed on paraffin-embedded 3-μm sec-
tions using peroxidase-conjugated, affinity-isolated
immunoglobulins. All sections were routinely
stained with hematoxylin and eosin (H&E) and were
processed at the same time to reduce internal stain-
ing variations. Briefly, immunohistochemistry was
done subject to the avidin–biotin complex method
and according to the manufacturer’s instructions.
Macrophages (CD68) were identified by a 1:50
mouse monoclonal antibody from Dako (Glostrup,
Denmark), with microwave pretreatment three
times, citrate buffer pH 6, and rabbit antimouse
1:300 (Dako) as secondary antibody. For the detec-
tion of B-lymphocytes (CD20) and T-lymphocytes
(CD45, CD3), we used a mouse monoclonal pri-
mary antibody 1:100 (Dako), and as secondary
antibody we used rabbit antimouse 1:300 (Dako).
Cyclooxygenase-2 (COX-2) detection was carried
out by a 1:100 rabbit monoclonal antibody from
DCS (Hamburg, Germany), with microwave pre-
treatment three times, citrate buffer pH 6, and goat
antirabbit 1:300 (Dako) as secondary antibody. For
Notch-3 staining, we used a 1:50 rabbit polyclonal
antibody from Santa Cruz Biotechnology (Santa
Cruz, CA, USA), with microwave pretreatment
three times, citrate buffer pH 6, and goat antirabbit
1:500 (Dako) as secondary antibody. Beta-catenin
was analyzed by a ready-to-use rabbit polyclonal
antibody from Spring Bioscience (Pleasanton, CA,
USA) and goat antirabbit 1:500 (Dako) as second-
ary antibody. Furthermore, c-myc expression was
investigated by a 1:50 rabbit polyclonal antibody
(Santa Cruz Biotechnology) and goat antirabbit
1:500 (Dako) as secondary antibody.
The expression of immunohistochemical pa-
rameters was classified by two independent,
blinded observers using a semiquantitative im-
munoreactivity score according to the method of
Remmele and Stegner [15]. Intensity of staining
was scored as 0 (negative), 1 (weak), 2 (medium),
or 3 (intensive). The extent of staining was scored
as 0 (0%), 1 (1–20%), 2 (21–50%), 3 (51–80%), or
4 (81–100%), indicating the percentage of positive
staining in adhesion tissue. Multiplication of the
intensity score (0–3) and the extent score (0–4) re-
sulted in the immunoreactivity score, ranging be-
tween 0 and 12. Sections were examined by stan-
dard light microscopy (Olympus BX51, Hamburg,
Germany). For each sample, six regions (×400,
area 100×100 μm) were captured by a digital cam-
era (Olympus C-3030, Hamburg, Germany).
Results
Study I: Human Peritoneal Adhesion
Tissue
The mean patient age was 55±19 years, and 17
female and 23 male patients were included in the
study. Eighteen of the 40 patients had had one
previous abdominal operation, and 22 patients had
had two or more. The parameters measured were
Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration
309 42

a b

c d

⊡ Fig. 42.2. Immunohistochemical features of peritoneal adhesion specimens demonstrating specific nuclear staining for T-
lymphocytes (CD45) and macrophages (CD68). T-lymphocytes were evident in peritoneal adhesions younger than 12 months
(a) and even in adhesions older than 12 months (b) without significant differences. Views c and d illustrate the specific nuclear
staining of macrophages (CD68), with significantly higher expression in adhesions <12 months (c) compared with adhesions
>12 months (d). (Magnification ×400)

not significantly affected by the gender or age of the
patients or by the number of previous operations.
T-lymphocytes (CD45) and Macrophages
(CD68)
Investigation of the H&E-stained sections revealed
extended infiltrates of mononuclear round cells.
Subtyping of these cells by CD68 and CD45 dis-
played predominant macrophages and T-lympho-
cytes. They were colocalized within the entire spec-
imen, and the appearance of these cells correlated
significantly with each other (r=0.624, p<0.001).
Adhesions with an age <12 months showed a sig-
nificantly elevated expression level of CD68 (mac-
rophages) compared with adhesions >12 months
(p<0.05). The expression of CD45 revealed no sig-
nificant differences regarding adhesion maturity
(p>0.05). (See ⊡ Fig. 42.2.)
Analysis of COX-2, ß-catenin, c-myc,
and Notch-3
COX-2 showed a positive cytoplasmic staining
with a mean score of 3±2.4. Similarly, ß-catenin
was expressed in the cytoplasm of endothelial
cells of blood vessels and fibroblasts (mean score
3.5±1.9). C-myc (mean score 3.1±1.8) showed pos-
itive nuclear staining, both in mononuclear round
cells and in fibroblasts predominantly surrounding
 310 Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration, and Erosions?

42

a b c

d e f

⊡ Fig. 42.3. Immunohistochemical features representing protein expression levels in peritoneal adhesions. Expression of
Notch-3 (a), ß-catenin (b), and c-myc (c) in adhesions <12 months. Expression of Notch-3 (d), ß-catenin (e), and c-myc (f) in peri-
toneal adhesions >12 months. (Magnification ×400)

a b

⊡ Fig. 42.4. Percentage of CD3-positive-stained cells representing a continuous infiltration of macrophages in visceral (a) and
parietal (b) peritoneal adhesions
Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration
311 42

a b

⊡ Fig. 42.5. a Percentage of CD68-positive-stained cells demonstrating a significantly higher expression in visceral adhesions
on postoperative days 3 and 5. b A significantly higher infiltration of macrophages was measured in parietal adhesions on post-
operative days 60 and 90

blood vessels. Expression of Notch-3 (mean score
6.3±3.4) was pronounced in all specimens. Posi-
tive staining was detected in the nucleus as well as
in the cytoplasm of both mononuclear round cells
and fibroblasts (⊡ Fig. 42.3).
Study II: Experimental Data
During the observation period, none of the rats
died or exhibited signs of infection. All rats devel-
oped peritoneal adhesions.
T-lymphocytes (CD3) and Macrophages
(CD68)
Both at the parietal and the visceral sites of the
adhesions, T-lymphocytes could be detected. The
expression profile of CD3 was stable even until the
90th postoperative day. Neither over the course of
time nor when comparing the parietal to the vis-
ceral site were significant differences seen regard-
ing the expression of CD3 (⊡ Fig. 42.4). Likewise,
macrophages were detectable until the 90th post-
operative day. At postoperative days 3 and 5, the
infiltration of macrophages was significantly ele-
vated at the visceral site of the adhesions compared
with the parietal site. At postoperative days 60 and
90, significantly more macrophages were detect-
able in parietal adhesions compared with visceral
adhesions (⊡ Fig. 42.5).
Cyclooxygenase-2, ß-catenin, and c-myc
A significant expression of COX-2 was evident in all
adhesions, both at the parietal and visceral sites of
the adhesions even 90 days after the operation. Over
the course of time, COX-2 was significantly reduced
from the 3rd to the 90th postoperative days. The
expression of COX-2 at the visceral site of the adhe-
sions was significantly higher on postoperative days
3, 5, and 14 compared with the parietal adhesion
sites. The expression of COX-2 was significantly
elevated at the parietal site of the adhesions on post-
operative days 30, 60, and 90 compared with the
visceral site (⊡ Fig. 42.6). Both ß-catenin and c-myc
were detected at the visceral site of the adhesions.
Over time, the expression profile of both param-
eters showed no significant differences even 90 days
following the operative procedure (⊡ Fig. 42.7). At
the parietal site of the adhesions, ß-catenin was evi-
dent without significant differences over the course
of time. However, c-myc was not detectable at the
parietal site (⊡ Fig. 42.7).
 312 Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration, and Erosions?

42

a b

⊡ Fig. 42.6. Collectively, there was a continuously marked expression of COX-2 until the 90th postoperative day. a In visceral
adhesions, the expression was significantly higher on postoperative day 3, 5, and 14. b A significantly higher expression was
measured in parietal adhesions on postoperative days 30, 60, and 90

a b

⊡ Fig. 42.7. a Persistent expression of ß-catenin and its target c-myc in visceral adhesions. b A persistent expression of ß-catenin
was detected in parietal adhesions, although no expression of c-myc was found distant to the intestine

Discussion ological wound healing and with lack of infection,

Traumatic peritoneal defects are presumed to ini-
tiate adhesion formation, whereas the causation
of maintaining peritoneal adhesions has not been
previously revealed [16–19]. Analogous to physi-
a time-dependent termination of the inflammatory
activity and a transformation of transient perito-
neal adhesions into scar tissue has been suspected
[20, 21]. Analysis of human peritoneal adhesions
demonstrated that they were cell-rich, well-vascu-
Chapter 42 · Adhesion as a Chronic Inflammatory Problem? Risk for Adhesions, Migration
larized, and innervated tissue. In a previous study
we also found them to be high in adipose tissue,
fibroblasts, and mononuclear round cells such as
macrophages and T-lymphocytes, irrespective of
the adhesions’ maturity [3].
In 2007 Hoshino et al. demonstrated that peri-
toneal macrophages trigger the development of
peritoneal adhesions via the chemokine receptor 8
(CCR8) and its target, the chemokine ligand 1
(CCL1) [22]. Concordantly, we detected mac-
rophages in long-lasting peritoneal adhesions both
in a rat model and even in mature human peri-
toneal adhesions. The evidence of a significantly
higher infiltration of macrophages in the early
postoperative period supports the assumption that
macrophages trigger the development of peritoneal
adhesions. In quantity and quality, T-lymphocytes
were found to have no significant differences re-
garding adhesion maturity. Consequently, an on-
going persistent inflammatory process with a func-
tional impact of T-lymphocytes or T-lymphocyte-
synthesized chemokines in maintaining peritoneal
adhesion may be suspected.
Cyclooxygenase-2 (COX-2) is a regulatory
factor in the biosynthesis of prostanoids such as
prostaglandins, prostacyclin, and thromboxanes
[23–25]. COX-2 expression is induced by a variety
of growth factors and cytokines, and the expres-
sion increases rapidly in response to inflamma-
tory stimuli and tissue damage [26–30]. During
physiological wound healing, expression of COX-2
regularizes within weeks after injury [31]. Saed et
al. measured significantly higher levels of COX-2
in vitro in adhesion fibroblasts compared with nor-
mal peritoneal fibroblasts and assumed an altered
cell regulation in peritoneal wound healing [30].
In accordance with these findings, we detected an
expression of COX-2 in human peritoneal adhe-
sions that was irrespective of adhesion maturity.
Although a continuous decrease in COX-2 expres-
sion was measured over the course of time in our
rat model of adhesion formation, a substantial
expression was evident even 90 days following the
surgical trauma.
The consideration of adhesions as widely are-
active fibrotic bands has been challenged; actually,
adhesion formation may be regarded as a defec-
tive wound healing process and as a disturbed
313 42
in situ regeneration of the peritoneal surface [32].
Notch-3, ß-catenin, and c-myc are well-known
mediators in cell signaling pathways of prolifera-
tion and differentiation responses during normal
development and wound healing [33, 34]. Notch
proteins are single-pass transmembrane receptors,
playing a critical role in control and cell-fate deci-
sions during developmental processes [35]. Notch
favors cell proliferation and opposing cell differen-
tiation and is closely connected to Wnt signaling.
ß-catenin and its target c-myc are crucial media-
tors of Wnt signaling and are thereby involved in
the regulation of cell growth, cell differentiation,
and tissue remodeling [36–39]. Activation of the
ß-catenin/c-myc pathway contributes to impaired
healing by inhibiting cell migration and altering
cell differentiation [40]. In accordance, a marked
expression of Notch-3, ß-catenin, and c-myc could
be verified even in mature human peritoneal adhe-
sions, indicating disturbed differentiation, migra-
tion, and proliferation of mesothelial cells. Like-
wise, ß-catenin and c-myc were detected in the
rat model of adhesion formation, confirming the
assumption of a disturbance in peritoneal wound
healing.
In conclusion, peritoneal adhesions should be
regarded as a consequence of continuously mal-
functioning cell differentiation and proliferation
within a chronic inflammatory process. It remains
unclear whether the chronic inflammatory process
or the malfunctioning differentiation/prolifera-
tion is causative in adhesiogenesis. Influencing the
individual inflammatory response to peritoneal
trauma seems to be necessary to avoid or at least
reduce the formation of postoperative peritoneal
adhesions.
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315 42
Smeds: From the clinical point of view, I wonder if
you had information about the dynamics of the ad-
hesions and whether there is a correlation to pain.
Binnebösel: In our investigation we found no cor-
relation to pain. Interestingly, previous publica-
tions showed that the amount of adhesions will
increase with the number of previous operations—
but this was different in our investigation. At the
moment, it seems unpredictable.
Smeds: Do you think it is a mechanical traction
of the peritoneum and the adhesion that promotes
the pain?
Binnebösel: Yes, this is a possible explanation for
the pain.
Montgomery: Where did you get the biopsies? I
think it is difficult to get reproductive biopsies?
Binnebösel: Yes, this is a limitation of our study,
because we randomly took two biopsies in every
patient. It is very difficult to define macroscopi-
cally where it is best to take the biopsies.

Discussion

Franz: Even on the surface of the skin, it is difficult

to define what a chronic wound is. One way is to
look at the fibroblasts. For example, what about the
fibroblast function?
Binnebösel: But how should we investigate the
function of the fibroblasts? We have not done it.
Of course, it is a very important subject, but when
we looked at these adhesions there was a small
amount of fibroblasts.
Franz: So when you said »cell-rich,« you mainly
meant inflammatory cells?
Binnebösel: Yes
Schumpelick: Is the adhesion story a one-way
story, or is there a way back to normal tissue?
Binnebösel: At the moment, we just do not know.
We do not know whether peritoneal adhesions are
a reaction of everybody, and we do not know why
in some patients adhesions dissolve and in some
patients they do not. And we have to find a solu-
tion for this problem.
 43

Biological Tissue Graft: Present Status

C. Bellows
 318 Chapter 43 · Biological Tissue Graft: Present Status
Overview of the Disease
Reconstruction of abdominal wall defects is a chal-
lenging problem that many surgeons face, not only
in the elective setting but also during emergency
surgery. Deficiencies of the abdominal wall can
43 be acute or chronic in nature and can result from
trauma, cancer, infection, or hernia disease. In-
cisional hernias are the most common cause of a
chronic abdominal wall defect. Despite advances
in medical technology, treatment of these defects
remains controversial. In fact, the repair of ab-
dominal wall defects continues to be imperfect
and costly, resulting in serious, chronic healthcare
problems. Current practice guidelines and medical
evidence support the use of a permanent pros-
thetic mesh for the repair of hernias as a means to
reduce the risk of recurrent hernia. Patients who
are not repaired with mesh, either owing to clinical
complications or by surgeon choice, have a much
higher incidence of recurrent hernia compared
with patients who are repaired with mesh [1–3].
Consequently, multiple prosthetic meshes with
a variety of characteristics have been developed.
However, no single material has gained universal
acceptance or preference, and a number of compli-
cations have been associated with the use of these
permanent synthetic materials [4–8].
Most synthetic mesh strengthens the abdomi-
nal wall by inciting an intense fibroplastic response
to form a strong scar-plate interface. Although this
works well, the inflammatory response incited by
the plastic meshes can lead to potentially serious
complications such as bowel fistulation, mesh con-
traction, intraperitoneal adhesions, erosion into
the abdominal viscera, a sensation of being able
to feel the mesh, and increased stiffness of the
abdominal wall with loss of compliance. Addition-
ally, the U.S. Food and Drug Administration has
received numerous reports of other complications
associated with mesh, including chronic pain and
infection [9]. Indeed, mesh infections are one of
the most commonly reported complications and
represent a potential nightmare. An infection is
traumatic for the patient and time-consuming to
treat. Bacteria adhere avidly to the mesh polymers
and immediately lay down a biofilm, which pro-
tects them from host immunological defenses and
antibiotics and thereby ensures their long-term
survival and leads to chronic infection of the her-
nia wound [10]. The increased morbidity and costs
associated with infected mesh are so dire that sur-
geons avoid placing permanent mesh in grossly in-
fected fields. Moreover, surgeons are now avoiding
placing permanent mesh in clinical circumstances
in which the risk of infection is increased, such
as in patients with a prior wound infection. Pre-
dictably, strategies to address these complications
related to the implantation of synthetic materials
are now the focus of intense research by hernia
surgeons. An extensive search is ongoing for al-
ternative materials with which to not only achieve
tension-free repair of an abdominal wall defect in
a single-stage operation (especially in the setting
of a contaminated wound) but also to achieve a
functional abdominal wall and a better quality of
life for the patient after repair. This search has led
to an era of acellular biological tissue grafts (e.g.,
derived from natural materials).
Rationale and Indications for Using
Biological Tissue Grafts
The art and science of using tissue grafts from ani-
mal (xenogenic) and human (allogenic) sources for
abdominal wall reconstruction is nascent. However,
during the past few years, several biological tissue
grafts have been introduced and are available for
hernia repair. The rationale for using a biological
tissue graft for abdominal wall reconstruction is to
avoid acute and chronic mesh infection, unwanted
chronic inflammation, and scar tissue formation,
which occur frequently in response to permanent
synthetic materials after implantation. The poten-
tial benefits of these new materials are extremely
attractive and include superior biocompatibility
(i.e., minimum inflammatory response), reduced
adhesion formation, early vascular ingrowth, and
decreased risk of infection in contaminated or po-
tentially contaminated surgical fields.
From a pathophysiological viewpoint, there
are two different indications for biological tissue
grafts: One is to repair an acute abdominal wall
defect created by trauma, cancer, or infection, and
the other is to repair a chronic, progressive ab-
Chapter 43 · Biological Tissue Graft: Present Status
dominal wall defect (i.e., hernia disease) resulting
from a presumed defective collagen metabolism
or impaired wound healing (such as in steroid us-
ers). Whereas acute wound defects can be repaired
with a biological tissue graft as a scaffold to induce
normal tissue regeneration, such an approach may
lead to an inadequate and weak scar in patients
with chronic abdominal wall defects after remod-
eling is complete. However, as is the case with any
new medical device or product introduced into
clinical practice, experience and time will ulti-
mately define the utility and limitations.
Types of Biological Tissue Grafts:
Distinguishing Features
Biological tissue grafts are rendered acellular
through various methods of preservation and
fabrication and are offered as collagen-rich scaf-
folding that allows cellular ingrowth and tissue
remodeling and revascularization, thereby setting
the stage for an intact hernia repair. However,
the specific manufacturing processes that yield
modified collagen matrices vary significantly from
one product to another. Therefore, each product
can be classified according to the material source,
type of tissue, presence or absence of collagen
cross-linking, decellularization methods, and ter-
minal sterilization methods. Currently, the dif-
ferent donor species grafts, including human and
animal (porcine, bovine), are made of one of three
types of tissue: dermis, small intestine, or peri-
cardium. The various decellularization methods
include physical (dissection, agitation, sonication,
pressure, freeze–thaw), chemical (detergents, ionic
solutions, acid/bases), and enzymatic methods.
The various terminal sterilization methods include
gamma irradiation, ethylene oxide gas, and hydro-
gen peroxide plasma. A few materials also employ
a chemical cross-linking method in the preser-
vation/processing of their collagen tissue grafts.
Experimental studies have demonstrated that col-
lagen cross-linked with glutaraldehyde imparts a
high degree of stability to the collagen against the
activity of the degrading enzyme, collagenase [11,
12], thereby slowing or stopping the degradation
of the donor collagen. However, some investigators
319 43
believe that this chemical cross-linking leads to
nonincorporation and preclusion of immune cell
penetration, making these grafts unable to par-
ticipate in normal tissue remodeling. Instead, im-
mune cells encapsulate the grafts, consistent with a
foreign body response.
Based on the variety of tissue origins as well
as distinct processing and sterilization procedures,
experimental studies have demonstrated that cur-
rently available biological tissue grafts vary in per-
formance characteristics, such as cellular response,
strength, biodegradability, susceptibility to infec-
tion, and tendency to transmit diseases from donor
to recipient after implantation [13]. Therefore, the
use of biological tissue grafts for treating hernia
disease needs to be considered on a product-by-
product basis as additional knowledge from clini-
cal trials and clinical experience accumulates.
Biological Tissue Grafts: Clinical Data
The first biological tissue graft was approved for
soft tissue reconstruction in 1999. Since that time,
the number of different products and the use of
these materials in clinical practice have grown
rapidly for want of a better solution for difficult
hernia repairs. Currently, over 13 biological tissue
grafts are commercially available. However, after
many years on the market, some biological graft
materials have been the subject of dozens of peer-
reviewed publications, whereas a number of other
products have been reported on in few or no publi-
cations–clinical or preclinical–indexed in Medline.
For example, a recent Medline search revealed 33
published articles on small intestinal submucosa
grafts, 32 on acellular human dermis grafts, and
13 on cross-linked porcine dermis grafts [14]. In-
terestingly, most of this published experience with
biological grafts is in clean field cases rather than
in infected fields.
Despite some encouraging early results, several
clinical complications have been reported follow-
ing the use of these biological materials to recon-
struct abdominal wall defects, including degrada-
tion, laxity, lack of integration, and recurrence.
Although the companies developing and market-
ing biological tissue grafts make various claims for
 320 Chapter 43 · Biological Tissue Graft: Present Status
the superiority of their product over others, as of
this writing, there are no prospective, randomized
clinical trial data comparing one biological tissue
graft to another and no data demonstrating the
superiority of one particular biological tissue graft
over a synthetic graft.
43 Despite this lack of data, there is growing con-
cern that not all biological tissue grafts perform
uniformly after implantation in humans. Clini-
cal data suggest that outcomes may be related in
part to the material source and the processing
method of these different biological tissue grafts.
For example, a recent systematic review reported a
failure rate of 8% at 19 months for small intestinal
submucosa grafts when used for ventral hernia
repair [14]. By comparison, an aggregate failure
rate of 15% at 12 months was reported for non-
cross-linked acellular human dermis grafts and 8%
at 15 months for cross-linked porcine dermis [14].
These results may also be related to the implant
scenarios, the implantation technique, a relatively
short duration of follow-up for many of these stud-
ies, and underreporting of complications related
to the use of these products. For example, it is well
documented that using biological tissue grafts in
infected fields results in significantly higher fail-
ure rates than when they are implanted in clean
fields. Not only do these patients tend to be more
emergent or critically ill, but patients with infected
fields also present the additional factor of material
digestion by bacterial enzymes that may weaken a
biological graft. Importantly, there have been more
reports on acellular human dermis grafts used in
infected fields compared with small intestinal sub-
mucosa grafts [14].
The techniques used are also very important
in hernia repair outcomes, and implantation tech-
niques appear to be especially important with bio-
logical grafts. Currently, several publications have
reported on the use of acellular human dermal ma-
trix in hernia repair, suggesting that recurrences
are highest (80%) when the product is used as a
fascial bridge to repair the defect [15]. By com-
parison, when the same biological tissue graft is
used to reinforce a primary reapproximation of the
fascia, utilizing the component separation tech-
nique, recurrence rates as low as 0–5% have been
reported at 2-year follow-up [16]. Taken together,
these data suggest that the use of biological tissue
grafts may not be justified unless primary wound
closure can be achieved.
Summary and Conclusions
Abdominal wall integrity may be lost after trauma,
infection, herniation, or surgical resection. The
surgical repair of these abdominal wall defects has
changed considerably over the last decades. Cur-
rently, a wide variety of new implantable acellular
biological tissue grafts have been developed and
introduced into the clinical market for the repair
of tissue defects. The sudden and rapid emergence
of these grafts has provided surgeons with an im-
portant new tool in their surgical armentarium
for treating abdominal wall defects, especially in
contaminated or infected surgical fields.
When the complexity of the patients and the
implant scenarios is taken into consideration, bio-
logical grafts have demonstrated a good overall
success rate. However, at present the data from
prospective trials and case series are limited, with
mostly short-term follow-up of patients treated
with biological tissue grafts for abdominal wall
reconstruction. More clinical work is necessary to
determine which patients would benefit the most
from repair using a biological tissue graft. To date,
the best clinical outcomes reported with biologi-
cal tissue grafts for abdominal wall reconstruction
occur in patients in the absence of gross infection
and when the graft is used as a fascial reinforce-
ment. However, these first-generation biological
tissue grafts are far from ideal.
The ideal biological tissue graft may take one of
a number of possible forms in the near future. The
most economical and proficient graft would be
one derived from a plentiful source, thus making
it affordable. In addition, the ideal graft material
should have an adequate shelf life so that it can be
taken off the shelf and used immediately; it should
be 100% biocompatible; and it should resist infec-
tion. Degradation and replacement of the graft
material by host tissue should ultimately occur in a
manner that maintains or increases the strength of
the abdominal wall repair. It may also be hypoth-
esized that the composition of an ideal biological
Chapter 43 · Biological Tissue Graft: Present Status
tissue graft is able to restore normal wound healing
in hernia formers and thereby strengthens the re-
sulting scar. No biological tissue graft has yet been
shown to possess all of these ideal characteristics.
There is increasing evidence that biological
tissue grafts will become more customized or in-
dividually tailored for specific needs. An animal
can have its own tissues (such as myofibroblasts
or stem cells) harvested and seeded onto extracel-
lular matrices prior to being transplanted back
into its body. This approach primes or precondi-
tions the biological tissue graft with the intended
recipient animal’s own progenitor cells. Such an
approach could add to the overall effectiveness of a
biological tissue graft, making it more resistant to
bacterial colonization and accelerating the deposi-
tion of collagen, which may more rapidly increase
the strength profile [17]. Strategies to accelerate
neovascularization of transplanted biological tis-
sue grafts after implantation will facilitate their
engraftment through the early delivery of oxygen,
nutrients, host immune cells, and antibiotics. The
preseeding of stem cells or progenitor cells into
tissue grafts could also offer an advantage with
respect to the need for rapid revascularization, as
these cells are resistant to low oxygen conditions.
All of these approaches to create a »designer extra-
cellular matrix« are within reach in the near future.
Perhaps such an approach will be called »smart
biological tissue grafts.«
References
1. Luijendijk RW, Hop WC, van den Tol MP, et al. A compari-
son of suture repair with mesh repair for incisional hernia.
N Engl J Med 343:392–398 (2000)
2. Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaas-
donk EG, Jeekel J. Long term follow-up of a randomized
controlled trial of suture versus mesh repair of incisional
hernia. Ann Surg 4:578–585 (2004)
3. Sanchez LJ, Bencini L, Moretti R. Recurrence after lapa-
roscopic ventral hernia repair: results and critical review.
Hernia 8:138–143 (2004)
4. Carbonell AM, Harold KL, Mahmutovic AJ et al. Local
injection for the treatment of suture site pain after
laparoscopic ventral hernia repair. Am Surg 69:688–691
(2003)
5. Leber GE, Garb JL, Alexander AI, Reed WP. Long term com-
plications associated with prosthetic repair of incisional
hernias. Arch Surg 133:378–382 (1998)
321 43
6. Morris-Stiff GJ, Hughes LE. The outcomes of nonabsor-
bable mesh placed within the abdominal cavity: literature
review and clinical experience. J Am Coll Surg 186:352–
367 (1998)
7. Welty G, Klinge U, Klosterhalfen B, Kasperk R, Schumpelick
V. Functional impairment and complaints following incis-
ional hernia repair with different polypropylene meshes.
Hernia 5:142–147 (2001)
8. Klinge U, Klosterhalfen B, Birkenhauer V, Junge K, Conze
J, Schumelick V. Impact of polymer size on interface scar
formation in a rat model. J Surg Res 103:208–214 (2002)
9. Robinson TN, Clarke JH, Schoen J, Walsh MD. Major mesh
related complication following hernia repair: events re-
ported to the Food and Drug Administration. Surg En-
dosc 19:1556–1566 (2005)
10. Jansen B, Schumacher-Perdreau F, Peters G, Pulverer
G. New aspects in the pathogenesis and prevention of
polymer-associated foreign-body infections caused by
coagulase-negative staphylococci. J Invest Surg 2:361–
380 (1989)
11. Oliver RF, Grant RA, Cox RW, Hulme MJ, Mudie A. Histo-
logical studies of subcutaneous and peritoneal implants
of trypsin prepared dermal collagen allografts in rats. Clin
Orthop 115:291–302(1976)
12. Oliver RF, Barker H, Cooke A, Grant RA. Dermal collagen
implants. Biomaterials 23:38–40 (1982)
13. Sandor M, Xu H, Connor J, Lombardi J, Harper JR, Sil-
verman RP, McQuillan DJ. Host response to implanted
porcine-derived biologic materials in a primate model
of abdominal wall repair. Tissue Eng Part A 14:2021–231
(2008)
14. Hiles M, Record Ritchie RD, Altizer AM. Are biologic grafts
effective for hernia repair? A systematic review of the
literature. Surg Innov 16:26–37 (2009)
15. Jin J, Rosen MJ, Blatnik J, McGee MF, Williams CP, Marks J,
Ponsky J. Use of acellular dermal matrix for complicated
ventral hernia repair: does technique affect outcomes? J
Am Coll Surg 205:654–660 (2007)
16. Espinosa-de-los-Monteros A, de la Torre JI, Marrero I, An-
drades P, Davis MR, Vásconez LO. Utilization of human
cadaveric acellular dermis for abdominal wall reconstruc-
tion. Ann Plast Surg 58:264–267 (2007)
17. Lai JY, Chang PY, JN Lin. Body wall repair using small
intestinal submucosa seeded with cells. J Pediatr Surg
38:1752–1755 (2003)
Discussion
Read: This is an excellent paper. We need more of
these, and I think your suggestions are excellent.
Falagas: I was impressed by the fact that there
are 13 FDA-approved biological grafts. If it were
a medication or drug, the FDA would need two
randomized controlled trials with about 1,000 pa-
 322 Chapter 43 · Biological Tissue Graft: Present Status

tients to show the usefulness of the new product. first introduction of the material in the early ’90s.
But for a biological graft—how does the FDA ap- Actually, there is an FDA Web site where volun-
prove them? There were no randomized controlled tarily reported complications with these biological
trials? tissue grafts are recorded in a database. And the
Bellows: It takes a couple of animal experiments number one graft that has the most reported com-
to show that the material is safe, not carcinoge- plications was actually Permacol.
43 netic….Alloderm gets away with it because it is Schumpelick: There was a big difference with re-
a minimally processed tissue. But there are some gard to laparoscopic or open surgery. Is it because
companies now that are taking proactive stents, the abdomen is a black box and we do not see the
and actually they are doing prospective random- results, or is it because of different milieus?
ized trials, comparing the biologics to the synthet- Bellows: I do not think we have the answer yet.
ics in humans—but they are also selling the prod- Most people are not using these products lap-
ucts at the same time. aroscopically. Often the data is very rare and the
Falagas: Would you like to see comparisons of follow-up is very short, so I cannot make any con-
these materials before approval, or are you okay clusions on this subject.
with a few animal experiments?
Bellows: Of course not. If the companies do not
have any data, I do not use such materials.
Ma: Two years ago in Suvretta I presented data
about biological meshes in inguinal hernia repair.
But afterwards I realized two problems: First, can
we use biological meshes if the patient has a col-
lagen deficiency or a family history or a recurrent
hernia? Second: What about the bowels, e.g., pa-
tients with FAP?
Bellows: To your first question, yes, that is some-
thing that we need to know—whether these meshes
are indicated in patients with collagen disorders.
We do not have enough data. The inguinal hernia
stuff is a small number of patients. Second, I think
it is an indication for a biologic tissue graft. It is an
individual decision for each patient, taking into ac-
count whether there might be a contamination or
reoperation. Again, we do not have all the answers.
That is why we need prospective trials with com-
parisons of the different materials.
Kukleta: Among those first 250 reports to the FDA
about adverse effects of artificial materials, there
are quite a few on SIS. The first paper, as I remem-
ber, of 46 cases implanted in humans led to such
chaos that they went back to the manufacturer and
asked what was wrong with it and if it is really true
that it can be used in humans. And now, all of a
sudden, everybody thinks that things are getting
better. Do you have any explanation?
Bellows: I know Surgisis had a lot of problems, as
you mentioned. And they went back to the draw-
ing board and performed different types since the
 44

IPOM Results of 344 Consecutive

Patients with a PVDF-Derived Prosthesis
D. Berger, M. Bientzle
 324 Chapter 44 · IPOM Results of 344 Consecutive Patients with a PVDF-Derived Prosthesis
Introduction
Incisional hernias frequently occur after major ab-
dominal surgery [1, 2]. Today the repair should
be based on mesh augmentation of the abdominal
wall because suturing alone has proved to be inef-
fective [3–5]. Conventional techniques mainly use
meshes in an onlay or sublay position and some-
44 times intraperitoneally. The laparoscopic approach
is characterized by the intraperitoneal placement
of meshes and therefore requires a special kind
of mesh material. These meshes should provide
strong incorporation on one side and prevent ad-
hesions to visceral organs on the other side.
One approach is the use of a material that al-
lows the production of a foil with a smooth and a
rough surface, such as expanded polytetrafluoro-
ethylene (ePTFE), which was used in most cases
of laparoscopic ventral hernia repair reported in
the literature [6]. Another possibility is to cover
a mesh made of polyester or polypropylene with
a resorbable film that prevents adhesions [7, 8].
A third approach is represented by DynaMesh
IPOM, which is made of polyvinylidene fluoride
(PVDF) containing polypropylene on the parietal
side. An inert material such as PVDF, which does
not induce adhesions to visceral organs, can be
applied as a real mesh structure, with large pores
being a precondition of strong and rapid incorpo-
ration. The incorporation characteristics can be
improved by adding a small amount of polypropyl-
ene on the parietal side [9, 10].
This prospective study included 297 consecu-
tive patients with incisional hernias and 47 patients
with parastomal hernias treated laparoscopically.
The primary targets were the evaluation of the re-
currence rate and mesh-related complications.
Patients, Materials, and Methods
Patients
Between May 2004 and January 2008, 297 unse-
lected patients with incisional hernias and 47 pa-
tients with parastomal hernias were prospectively
treated and followed. The demographic data are
summarized in ⊡ Tables 44.1 and 44.2. The patients
⊡ Table 44.1. Demographic and surgical data of
patients with incisional hernias
 Median age: 65 years (22–92)
 Median body mass index: 29 (17–58)
 Median hernia size: 122.5 cm2 (2–420)
 Median mesh size: 600 cm2 (80–2,115)
 Median operating time: 77.5 min (30–230)
 Median hospital stay: 8 days (2–36)
 Median follow-up: 24 months (6–48 in
251/297=84%)
⊡ Table 44.2. Demographic and surgical data of
patients with parastomal hernias
 Median age: 69 years (54–92)
 Median body mass index: 28 (18–57)
 Median hernia size: 155 cm2 (12–400)
 Median mesh size: 825 cm2 (525–1,425)
 Median operating time: 115 min (65–230)
 Median hospital stay: 10 days (6–66)
 Median follow-up: 20 months (6–48 in 43/47=91%)
were clinically examined after 1, 3, 6, and 12
months and yearly thereafter.
Surgical Technique
Patients were always treated in the supine position.
The pneumoperitoneum was established with a
Veress needle in cases with an untouched upper
quadrant. In all other cases, an open approach was
preferred. Usually, three trocars in one flank and
one trocar on the opposite side were introduced.
Adhesiolysis was performed by sharp dissection
without any energy-driven device. Bleeding control
was achieved by bipolar coagulation. Routinely, the
whole original incision was covered by the mesh. In
patients with upper midline incisions, the falciform
ligament was dissected, and the space of Retzius
was opened as well in cases with lower midline in-
cisions. The mesh was fixed with six stay sutures at
the corners and in the midline between the corners
in the longest extension. Furthermore, spiral tacks
(Protack; Covidien, Mansfield, MA, USA) were
used every 3–4 cm. The overlap of the defect and
the whole original incision was at least 5 cm.
Chapter 44 · IPOM Results of 344 Consecutive Patients with a PVDF-Derived Prosthesis
The parastomal hernias were repaired by the
recently described sandwich technique [11]. Af-
ter complete adhesiolysis of the whole abdominal
wall as described above, a 15×15-cm mesh was
incised in a keyhole fashion and placed around the
stoma. The mesh incision was closed by transfas-
cial sutures and tacks. A further mesh covering the
midline incision and the stoma loop was also used.
The stoma loop was finally placed between the two
meshes and lateralized for at least 5 cm.
A single dose of cefuroxime and metronidazole
was generally given prophylactically.
DynaMesh IPOM was used in all patients.
It represents a real mesh structure that is warp-
knitted from polyvinylidene fluoride. It contains
a small amount of polypropylene on the parietal
side, providing good incorporation.
Results
Incisional Hernia
⊡ Table 44.1 demonstrates the demographic data,
and ⊡ Table 44.3 summarizes the main surgical re-
sults. Twenty-three percent (n=67) of our patients
with an incisional hernia had undergone previous
repairs.
Two patients developed a recurrence (0.6%).
One recurrence occurred after explantation of the
mesh. During surgical excision of the hernia sac,
because a persistent seroma caused pain, the mesh
was incised and the small bowel opened. A formal
laparotomy was necessary to repair the bowel in-
jury, and the mesh was removed. Another patient
developed a hernia at the lower border of the
mesh, which was originally implanted because of
a hernia after an upper midline incision. The new
defect was located in the midline between the um-
bilicus and the symphysis, despite a 5-cm overlap
of the lower end of the scar.
A persistent seroma was observed in seven pa-
tients (2.1%) who had in common a small fascial
gap and a major hernia sac. Three of these seven pa-
tients experienced major complications after punc-
ture or surgical removal of the sac: two infections
and one mesh explantation. However, all patients
with a deep wound infection as well as the patient
325 44
⊡ Table 44.3. Clinical outcomes of laparoscopic repair
of incisional hernias
 Recurrences: 1/297 (0.3%)
 Trocar hernia: 1 (0.3%)
 Conversion: 1 (0.3%)
 Bladder laceration treated by Foley catheter: 1
 Relaparotomy due to bleeding: 1
 Bowel fistula that healed after local revision and
vacuum-assisted closure therapy: 1
 Punctures due to seroma: 4, with 1 infection due to
the puncture
 Further revisions with resection of the hernia sac
because of persistent seroma or hematoma: 3, with
1 postoperative wound infection and 1 patient with
intraoperative enterotomy leading to mesh explan-
tation and recurrence
 Delayed defecation: 5 patients
 Local revision of a stay suture: 1
 Strong pain and additional medical treatment over 3
months: 6 patients
 Patient deaths: 1 due to pulmonary embolism
⊡ Table 44.4. Clinical outcomes of laparoscopic repair
of parastomal hernias
 Recurrence: 1/47 (2%)
 Revisions because of stenosis of the stoma: 2, with a
consecutive wound infection in 1 patient
 Local revision because of abscess in the hernia sac
after puncture of a seroma: 1
 Conversion: 1 (2%)
 Strong pain and delayed relief: 1 patient, but no
redo necessary because of pain
 No enterotomy
 No bleeding
 No further delayed defecation
 No deaths
with an unrecognized enterotomy had a complete
recovery without persistent mesh infection.
The only bladder injury healed after prolonged
transurethral drainage.
One patient died on the 7th postoperative day
because of pulmonary embolism.
Parastomal Hernia
Demographic data are given in ⊡ Table 44.2, and
the surgical results are shown in ⊡ Table 44.4. It
should be pointed out that 26% of the patients with
 326 Chapter 44 · IPOM Results of 344 Consecutive Patients with a PVDF-Derived Prosthesis
a parastomal hernia were primarily admitted with a
recurrent hernia. Only one patient (2%) developed
a recurrent hernia. One conversion was necessary
because no free abdominal cavity existed, and the
pneumoperitoneum could not be established.
The main problem, however, is the possibility
of producing a stenosis of the stoma loop, which
occurred in two patients. In both cases, a preexist-
44 ing subcutaneous prolapse of the stoma loop was
associated with a sharp angulation at the fascial
level, which was produced by the meshes. A lo-
cal revision with shortening of the subcutaneous
part of the stoma loop abolished the angulation
and reestablished the passage. In one of these pa-
tients, the intraabdominal part of the stoma loop
was perforated digitally. A formal laparotomy was
necessary for repair. The patient developed a deep
wound infection around the stoma as well as in
the midline incision. With subsequent vacuum-as-
sisted closure (VAC) therapy, the infected meshes
could be preserved.
Another patient developed an abscess in the
hernia sac after a persistent seroma was punctured.
Again, VAC therapy led to final preservation of the
mesh and cure of the infection.
Discussion
The precondition for laparoscopic intraperitoneal
onlay mesh (IPOM) repair of incisional and paras-
tomal hernias is the availability of meshes that
can be incorporated into the abdominal wall but
also prevent adhesions between the visceral organs
and the mesh itself [12]. Up to now, most patients
reported in the literature were treated with ePTFE-
derived meshes [6]. The visceral side, prevent-
ing adhesions, is smooth, and the parietal side is
rough or covered with polypropylene to provide
strong incorporation into the abdominal wall. Ex-
perimental data, however, sometimes demonstrate
strong adhesions between bowel and mesh [10,
13]. Furthermore, mesh shrinkage is pronounced,
leading to a 50% reduction of the original sur-
face area [10, 14]. Also, an overlap of two ePTFE
meshes does not make any sense because the scar
cannot grow through the meshes, which are in fact
a real foil.
The use of meshes made from polypropylene or
polyester with an antiadhesive coverage represents
a different approach. These meshes are effective
in terms of incorporation and prevention of adhe-
sions. The shrinkage has been shown to amount to
about 20% [10, 13, 15]. No data exist concerning
the incorporation behavior when two meshes are
used to overlap each other. Inert material that does
not adhere to visceral organs can be used as a real
mesh structure, allowing an overlap of two or more
meshes. The meshes can be trimmed to the ideal
size, which is not possible when covered meshes
are used.
PVDF is a very inert material that has long
been used as a suture material. Its long-term sta-
bility is even better than that of polypropylene.
The inflammation reaction on a cellular level is
reduced, and the amount of fibrotic tissue is lower
compared with any other mesh material. The
shrinkage is comparable to that for covered poly-
propylene structures [9, 10, 16]. From an experi-
mental point of view, PVDF-based meshes may be
clinically useful.
This prospective study demonstrating clinical
results in 297 patients with incisional hernias re-
veals promising results. The recurrence rate was
very low compared with the literature. This may be
explained by the size of the meshes used through-
out, which was more than double that described by
other authors [6, 17].
One patient developed a recurrence after ex-
plantation of the mesh. Another recurrence can
only be explained by a suture-associated fascial
defect, which has not been described in the litera-
ture. The pathogenesis may be similar to the tack-
associated hernias described by LeBlanc [18].
The laparoscopic repair of parastomal hernias
also showed very good results. As we recently
demonstrated, the sandwich technique, which
was used in the patients in the present study, is
superior compared with the original Sugarbaker
technique [11]. Despite some promising results in
the literature, our own series clearly showed that
the one-mesh technique according to Sugarbaker
is sufficient only for medial defects of the fascia
[19–21]. In cases of lateral or combined defects,
two meshes are needed to stabilize the abdominal
wall. A precondition of the sandwich technique is
Chapter 44 · IPOM Results of 344 Consecutive Patients with a PVDF-Derived Prosthesis
the availability of a mesh material that allows the
meshes to overlap each other, with stable incorpo-
ration of both meshes; ePTFE-derived meshes are
foils that completely prevent any ingrowth of scar
tissue in both meshes. On the other hand, the key-
hole technique seems to be an attractive and tech-
nically easier alternative. In fact, there is one study
with promising results [22], but the follow-up was
only 6 weeks. These results, however, could not be
confirmed in other studies [21, 23, 24].
Therefore, the sandwich technique seems to be
the most effective approach for the repair of paras-
tomal hernias. The only recurrence in our series
was due to a surgical correction of a preexisting
subcutaneous prolapse of the stoma loop. Dur-
ing a local revision, the subcutaneous part of the
stoma loop was shortened, and the intraabdominal
part with adherent small bowel loops was pulled
between the two meshes. After that procedure, the
patient suffered from strong pain starting immedi-
ately after any oral intake.
Another major issue concerns the resistance of
meshes against infection. ePTFE-derived meshes
must usually be removed if an infection occurs [25,
26]. To our knowledge, nothing is known about
the behavior of infected meshes covered with an
antiadhesive barrier. Four patients in our series
developed a deep wound and mesh infection after
puncture or early surgical revision. In all cases, the
meshes were preserved. Recently we published a
series of 25 patients prophylactically treated with
a PVDF-derived three-dimensional mesh. One pa-
tient of this series underwent early relaparotomy
because of an enterotomy leading to stercoral peri-
tonitis. After 5 days of daily revisions, the abdomi-
nal wall could be closed, and the intraperitoneal
mesh could also be preserved [27].
One patient developed a secondary bowel leak
due to unrecognized small bowel laceration with
a fistulization through the mesh, which healed
uneventfully after VAC treatment. Enterotomies
that had not been recognized during the primary
procedure occurred in about 2% of patients after
laparoscopic incisional hernia repair.
Seroma or hematoma can be observed in al-
most 100% of our patients because we perform
routine ultrasonography after 3–5 days. In a very
few patients (n=4) in this series, these seromas
327 44
needed to be punctured because of complaints.
Three patients underwent surgical excision of the
hernia sac because of a persistent seroma. These
patients had a major hernia sac and a small fascial
defect less than 30 cm2. According to the literature,
seroma or hematoma often occurs, but only ultra-
sonography reveals the real rate of that complica-
tion [6, 17, 28].
Further complications are summarized in Ta-
ble 44.4 and proved to be rare. The low overall
complication rate supports the view that laparo-
scopic repair of incisional and parastomal hernias
with modern meshes such as DynaMesh IPOM is
an effective and safe technique. The results seem to
be better than those obtained by open approaches
[17]. At the least, the open repair of parastomal
hernias is much more effective compared with
conventional techniques [29, 30].
In summary, DynaMesh IPOM was shown to
be a safe and effective mesh for the laparoscopic
repair of incisional and parastomal hernias. The
possibility of overlapping two or more meshes
provides an ideal overlap of the abdominal wall
in almost all situations and opens the way to the
sandwich technique for parastomal hernia repair,
which seems to be the best approach today. Infec-
tious complications occurring in our study dem-
onstrated the resistance of PVDF against infec-
tions. Experimental data exhibit excellent results
with regard to shrinkage and adhesion formation.
Overall, the described technique for laparoscopic
incisional and parastomal hernia repair using Dy-
naMesh IPOM provided satisfying results with no
mesh-related complications to date.
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15. Demir U, Mihmanli M, Coskun H, Dilege E, Kalyoncu A,
Altinli E, Gunduz B, Yilmaz B (2005) Comparison of pros-
thetic materials in incisional hernia repair. Surg Today
35:223–227
16. Conze J, Junge K, Wei BC, Anurov M, Oettinger A, Klinge U,
Schumpelick V (2008) New polymer for intra-abdominal
meshes–PVDF copolymer. J Biomed Mater Res B Appl
Biomater 87:321–328
17. Pierce RA, Spitler JA, Frisella MM, Matthews BD, Brunt
LM (2007) Pooled data analysis of laparoscopic vs. open
ventral hernia repair: 14 years of patient data accrual. Surg
Endosc 21:378–386
18. LeBlanc KA (2003) Tack hernia: a new entity. JSLS 7:383–
387
19. Sugarbaker PH (1985) Peritoneal approach to prosthetic
mesh repair of paraostomy hernias. Ann Surg 201:344–
346
20. Mancini GJ, McClusky DA, Khaitan L, Goldenberg EA,
Heniford BT, Novitsky YW, Park AE, Kavic S, Le Blanc KA,
Elieson MJ, Voeller GR, Ramshaw BJ (2007) Laparoscopic
parastomal hernia repair using a nonslit mesh technique.
Surg Endosc 21:1487–1491
21. LeBlanc KA, Bellanger DE, Whitaker JM, Hausmann MG
(2005) Laparoscopic parastomal hernia repair. Hernia
9:140–144
22. Hansson BM, de Hingh IH, Bleichrodt RP (2007) Lapa-
roscopic parastomal hernia repair is feasible and safe:
early results of a prospective clinical study including 55
consecutive patients. Surg Endosc 21:989–993
23. Muysoms F (2007) Laparoscopic repair of parastomal her-
nias with a modified Sugarbaker technique. Acta Chir
Belg 107:476–480
24. Safadi B (2004) Laparoscopic repair of parastomal hernias:
early results. Surg Endosc 18:676–680
25. Heniford BT F, Park AF, Ramshaw BJ, Voeller G (2003) Lapa-
roscopic repair of ventral hernias: nine years’ experience
with 850 consecutive hernias. Ann Surg 238:391–400
26. Berger D, Bientzle M, Muller A (2002) Postoperative com-
plications after laparoscopic incisional hernia repair. Inci-
dence and treatment. Surg Endosc 16:1720–1723
27. Berger D (2008) Prevention of parastomal hernias by pro-
phylactic use of a specially designed intraperitoneal onlay
mesh (Dynamesh IPST). Hernia 12:243–246
28. Susmalain S, Gewurtz G, Ezri T, Charuzi I (2001) Seroma
after laparoscopic repair of hernia with PTFE patch: is it
really a complication? Hernia 5:139–141
29. Carne PW, Robertson GM, Frizelle FA (2003) Parastomal
hernia. Br J Surg 90:784–793
30. McLemore EC, Harold KL, Efron JE, Laxa BU, Young-Fadok
TM, Heppell JP (2007) Parastomal hernia: short-term out-
come after laparoscopic and conventional repairs. Surg
Innov 14:199–204
Discussion
Deysine: How did you prove the low adhesion
activity?
Berger: These are only some experimental data.
And the PVDF is used for bacterial filtration. And
you can only use bacterial filters with low adhe-
sions of bacteria to the filter. If you do a sterile
filtration, you can use PVDF as material for the
filter.
Kukleta: You saw less pain after the implantation.
Don’t you think it is the number of the fixation
points that you use now? Do you use less than you
used before?
Berger: In fact, I use the same number of sutures,
but I do not use as many tacks as in previous
times.
Klinge: Some years ago we did experimental stud-
ies with our microbiologists and looked at the
Chapter 44 · IPOM Results of 344 Consecutive Patients with a PVDF-Derived Prosthesis
329 44
attachment of bacteria to different materials. We
quantified the amount of genetic material from the
bacteria of standard meshes that had been in con-
tact with various strains of bacteria. PVDF was not
free but belonged to materials where the amount of
genetic material was lowest.
Schumpelick: You used fewer tacks. Why?
Berger: The incorporation is better than with
ePTFE. At the beginning I was convinced that we
needed a permanent fixation. When I saw these
incredibly shrunken dual meshes of up to 75% and
all the tacks wandered with the mesh, I stopped
believing in any permanent fixation. I only want to
fix the mesh for a few days.
Schumpelick: How does it look after 2 years? Are
there long-term results available?
Berger: We have done some relaparoscopies and
relaparotomies and measured the mesh and found
shrinkage up to 10%—not more—and the mesh
was covered completely by a peritoneal layer.
Peiper: The material of the mesh is one thing. The
material of the fixation device is another thing.
Many adhesions occur not at the mesh area but
at the tacks. Do you have any experience with ab-
sorbable tacks?
Berger: I have started with absorbable tacks for
incisional hernia repair and always use absorbable
tacks for umbilical hernias. But the company sells
them for a very high price, and therefore I could
not decide to completely change to absorbable
tacks.
Kukleta: I was using Easy tacks for 3 years. If you
see adhesions, they are always at the tack, and the
adhesions will even pull out the tacks. So it is ex-
actly the same reaction that we have seen before.
I use the absorbable tacks now—maybe we can
afford a little more—but at the moment we do not
have any results, as they have been used only for 2
or 3 months.
 45

Pooled Data Analysis of Laparoscopic

vs. Open Ventral Hernia Repair:
14 Years of Patient Data Accrual
B. D. Matthews, R. A. Pierce, M. M. Frisella, L. M. Brunt
 332 Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair: 14 Years of Patient Data Accrual
Introduction
Incisional hernia is a common complication or con-
sequence of abdominal surgery. In recent published
series, the rate of incisional hernia after midline
laparotomy has been as high as 20% [23, 26, 29, 33].
Due to recurrence rates as high as 30%, incisional
hernias are not only associated with significant
morbidity but may represent a significant financial
strain on the healthcare system [10, 11]. Over the
last decade, mesh-based repair techniques have re-
45 placed primary suture repair for most incisional
hernia repairs because of an unacceptably high fail-
ure rate after primary repair [1, 6, 18, 19]. Neverthe-
less, open incisional hernia repair is often a major
operation, with the associated risks of wound- and
mesh-related infections and hernia recurrence. As
an alternative approach, laparoscopic incisional her-
nia repair was developed and first reported in 1991
[16]. This technique is now increasingly used in the
management of patients with uncomplicated as well
as more complex incisional hernias.
Thus far, nearly 100 studies have been published
on laparoscopic ventral hernia repair, although most
represent small series of patients in uncontrolled
and nonrandomized trials from single institutions.
The aggregate data from these studies have not been
carefully analyzed on a large-scale basis, and only a
single meta-analysis involving a total of eight stud-
ies has been published [13]. Prospective random-
ized trials comparing laparoscopic and open ventral
hernia repair are ongoing in the United States and
Europe. To better understand the current status
of laparoscopic ventral hernia repair and critically
compare it with open techniques, we examined the
published literature to evaluate studies reporting on
laparoscopic ventral hernia repair alone or in com-
parison with open ventral hernia repair.
Methods
Study Selection
A Medline search was performed to identify all
publications involving laparoscopic ventral her-
nia repair from January 1996 through January
2006. Publications containing the keywords ven-
tral hernia, incisional hernia, umbilical hernia, and
diastasis recti were identified and pooled. A similar
search was also done on the broad-based keyword
laparoscopy. These two groups were combined to
isolate those references common to both and were
further limited to studies conducted in humans
and published in English. This final limitation pro-
duced a total of 330 publications and their accom-
panying abstracts. A manual review of the bibliog-
raphies of several recent publications dealing with
laparoscopic ventral hernia repair did not identify
any additional citations within the defined time
frame that were missed. Studies were excluded
from consideration if they contained fewer than 20
laparoscopic cases or if laparoscopic ventral hernia
repair was not the primary focus of the article. As a
result, 78 published series that contained at least 20
subjects each and dealt primarily with laparoscopic
ventral hernia repair were further analyzed.
These 78 studies were separated into series that
compared patients who had undergone laparoscopic
or open ventral hernia repair within a given institu-
tion (»paired« studies) and series that described
only patients who had undergone laparoscopic ven-
tral hernia repair (»unpaired« studies). If a single
group or institution had published multiple studies,
then the largest series from the group was chosen
for inclusion unless the studies involved distinct,
nonoverlapping patient populations. If a group had
published both a paired and an unpaired study, then
the paired study was chosen for analysis. Each of
the 78 studies was then independently evaluated
by two of three reviewers. Data extracted from
each selected report included patient demographics,
hernia etiology characteristics, perioperative details,
postoperative complications, and hernia recurrence.
All studies that provided sufficient detail regarding
complications and recurrences were included in the
analysis, even if some variables (e.g., mean hernia
size) were missing. Any discrepancies were resolved
by consensus of all investigators after reviewing the
primary data again. This process led to the final
selection of 45 total studies (14 paired, 31 unpaired),
which are listed in Appendices 45.1 and 45.2.
Intraoperative parameters that were evaluated
included operating time, hernia and mesh sizes,
open hernia repair technique (mesh vs. primary
suture), open conversion for laparoscopic cases, and
Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair
complications. Postoperative information on hos-
pital length of stay (LOS), complications, follow-up
duration, hernia recurrence, mortality, and cost of
hospitalization were all recorded. Complications re-
lated to the surgical procedure, including wound
problems, mesh infection, trocar site hernia, seroma,
and need for early reoperation, were evaluated.
Other postoperative complications were classified
into the following categories: cardiac, pulmonary,
gastrointestinal, genitourinary, thromboembolic,
septic, neurologic/psychiatric, prolonged pain, and
miscellaneous. The perioperative mortality rate was
analyzed independently, but the principal cause of
death was also included as a complication.
Statistical Methods
Statistical analysis was performed by an indepen-
dent statistician. Two separate data sets were ana-
lyzed (paired studies comparing laparoscopic to
open ventral hernia repair and unpaired studies of
laparoscopic ventral hernia repair only). Data from
the paired studies were analyzed as the primary
evaluation and designated the »paired« analysis.
Additionally, data from the unpaired laparoscopic
ventral hernia repair studies were combined with
the laparoscopic ventral hernia repair data from the
paired studies to create a pooled laparoscopic ven-
tral hernia repair group. These pooled laparoscopic
ventral hernia repair data were then compared
with the open ventral hernia repair data from the
paired studies and designated the »pooled« analy-
sis. In three instances, a given group had published
both a paired study as well as a more recent, larger
unpaired study that appeared to incorporate the
laparoscopic ventral hernia repair cases from the
smaller paired study. In these situations, the lap-
aroscopic ventral hernia repair cases in the paired
study were included in the paired analysis, but they
were excluded from the combined analysis in lieu
of the larger unpaired cohort.
The strategy behind this dual analysis (paired
and pooled) was that the paired analysis should
have the greatest amount of internal validity, as the
same groups of surgeons were performing both the
open and laparoscopic cases and so it was much
more likely that the patients undergoing either
333 45
laparoscopic or open ventral hernia repair in these
studies would have been selected from the same
respective patient populations. In addition, com-
paring the results of the paired analysis to those
derived from the tenfold larger laparoscopic ven-
tral hernia repair group used for the pooled analy-
sis allows for external validation and extrapolation
to a more global patient population.
In several series, the patient populations were
split into smaller subpopulations, and mean values
were given for these subgroups. In these instances,
a conglomerate weighted mean was calculated and
used in the final analysis. Likewise, many of the
studies did not report standard deviations in their
statistical analyses, so weighted means were used to
perform the calculations. Accordingly, a two-tailed
t-test was used to compare differences in these
weighted means, and any studies that had missing
data points were taken into account when per-
forming the analysis. Because the raw numbers of
complications, recurrences, and deaths were avail-
able in all the studies that were evaluated, these pa-
rameters were amenable to more thorough statisti-
cal analyses. Thus, totals for these data points were
calculated for both the laparoscopic and open ven-
tral hernia repair groups, and differences between
them were determined using chi-square analysis.
Alternatively, Fisher’s exact test was used in the
event that the number of data points was too small
to allow for use of a chi-square algorithm.
Results
A total of 45 reports met the inclusion criteria,
including 14 paired and 31 unpaired studies. The
majority of these studies were retrospective (n=33;
73%), whereas three of the paired and nine of the
unpaired studies were done in a prospective fashion
(12 total; 27%). These reports encompassed a total
of 5,340 patients, including 4,582 (86%) who had
undergone laparoscopic ventral hernia repair and
758 (14%) who had open ventral hernia repair. Of
those 4,582 patients who underwent laparoscopic
ventral hernia repair, 619 (14%) were reported in
paired studies and 87% were from unpaired studies.
Demographic data from the 45 studies are shown
in ⊡ Table 45.1. The mean patient age was 55.3 years
 334 Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair: 14 Years of Patient Data Accrual

in the pooled laparoscopic group, 52.9 years in the
paired laparoscopic group, and 56.1 years in those
receiving open repairs (not significant). Only 19
series reported the body mass index (BMI), five of
which were paired studies. In the five paired series,
the weighted mean BMI was 30.5 for laparoscopic
cases and 29.5 for the open cases (not significant).
In the pooled group, the laparoscopic repair patients
had a somewhat higher mean BMI of 32.6 compared
with the open repair patients (p=0.0026).
Each study was also examined for the num-
45 bers of primary vs. incisional hernias and recurrent
hernias. Few series included all three data points;
however, 12 of the 14 paired and 27 of the 31 un-
paired studies documented the number of recurrent
hernias that were operated. Among the open group,
25.2% of the hernias were recurrent, compared to
27.5% of those done laparoscopically in only the
paired studies and 28.5% of cases from the com-
bined laparoscopic group. Two paired studies [12,
34] that focused solely on umbilical hernias were in-
cluded in the analysis. Both were paired studies, and
all of their open repairs were done using mesh. Con-
versely, two other paired studies [15, 28] reported
repairing some of their smaller ventral hernias using
a primary sutured technique. However, these 24
cases of primary closure represented only 4.4% of
the total number of open repairs. All laparoscopic
repairs were done using intraperitoneal mesh.
Operative data are shown in ⊡ Table 45.2. The
mean operating time for the laparoscopic cases in
the paired studies was 119.6 min, and 100.3 min
when all the laparoscopic procedures are consid-
ered. The mean operating time for open repairs falls
between these two times at 104.5 min. The hernia
defect size (70.8 cm2) and the size of the mesh used

⊡ Table 45.1. Patient demographics

Open Paired p-valuea Pooled p-valueb

repairs laparoscopic cases laparoscopic cases
Patient number (n) 758 619 4,582
Percent male 49 49 44
Age (years) 56.1 52.9 0.13 55.3 0.49
Body mass index 29.5 30.5 0.57 32.6 0.003
Length of stay (days) 4.3 2.4 0.015 2.4 0.0004
Follow-up time (months) 20.2 16.9 0.47 25.5 0.16
aCompares open group to paired laparoscopic ventral hernia repair group
bCompares open group to pooled laparoscopic ventral hernia repair group

⊡ Table 45.2. Operative data

Open Paired p-valuea Pooled p-valueb

repairs laparoscopic cases laparoscopic cases
Operating time (min) 104.5 115.0 0.40 100.3 0.61
Recurrent hernias (%) 25.2 27.5 28.5
Hernia size (cm2) 70.8 87.9 0.40 103.4 0.025
Mesh size (cm2) 170.1 260.9 0.27 295.2 0.009
Enterotomy rate (%) 1.2 2.9 0.022 2.1 0.11
Conversion rate (%) 3.9 3.5
aCompares
open group with paired laparoscopic ventral hernia repair group
bCompares
open group with pooled laparoscopic ventral hernia repair group
Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair
for repair (175.5 cm2) were smallest in the patients
undergoing open repair. The values are somewhat
larger (87.9 cm2 and 260.9 cm2) when compared di-
rectly to the patients undergoing laparoscopic repair
in the same set of paired studies. However, the larger
hernia and mesh sizes become even more apparent
when all the laparoscopic cases in the pooled group
are considered (103.4 cm2, p=0.025 and 295.2 cm2,
p=0.009, respectively). The enterotomy rate was
significantly higher in paired laparoscopic ventral
hernia repair cases compared to open ventral her-
335 45
nia repair (2.9% vs. 1.2%). Postoperative LOS was
significantly shorter for the laparoscopic repairs, av-
eraging 2.4 days in both paired and pooled laparo-
scopic ventral hernia repair groups compared with
4.3 days after open ventral hernia repair (p=0.015
and 0.0004, respectively).
Total complication rates were significantly
higher with open ventral hernia (41.6%) compared
to laparoscopic ventral hernia repair for both pooled
(22.7%) and paired (25.5%) analyses (p<0.0001;
⊡ Fig. 45.1). In the analysis of complications by or-

45
40
35 * p<0.0001
30
Incidence (%)

25 * *
20
15
10
5
0
OPEN PAIRED LAP POOLED LAP ⊡ Fig. 45.1. Total complications

⊡ Table 45.3. Organ system complications (NS not significant)

Open repairs (%) Paired p-valuea Pooled p-valueb

laparoscopic cases (%) laparoscopic cases (%)
Gastrointestinal 5.9 4.0 0.11 2.6 <0.0001
Cardiac 0.5 0 0.13 0.2 0.10
Pulmonary 1.7 0.8 0.14 0.6 0.0013
Septic 0 0 NS 0.02 1.0
Thromboembolic 0.3 0.2 1.0 0.1 0.20
Genitourinary 1.6 1.1 0.47 0.9 0.10
Neurological 0.1 0 1.0 0.02 0.26
Prolonged pain 0.9 1.0 0.93 2.0 0.047
Miscellaneous 1.9 1.0 0.18 0.7 0.0011
complicationsc
Mortality 0.3 0.3 1.0 0.1 0.32
aCompares
open group with paired laparoscopic ventral hernia repair group
bCompares
open group with pooled laparoscopic ventral hernia repair group
cIncludes fever, superficial thrombophlebitis, and psychiatric complications
 336 Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair: 14 Years of Patient Data Accrual

gan system, the pooled laparoscopic ventral hernia
repair studies reported significantly fewer wound,
pulmonary, and gastrointestinal complications
compared to the open ventral hernia repair series
(⊡ Table 45.3). Only total and wound complication
rates were significantly different in the paired study
comparison. No significant differences were noted
for rates of cardiac, thromboembolic, urologic,
or neurologic complications between any of the
study groups. In the pooled laparoscopic ventral
hernia repair group, prolonged postoperative pain
45 was reported in a significantly greater percentage
of patients (1.9%) compared to the open ventral
hernia repair group (0.92%); however, prolonged
pain rates were similar for the open and laparo-
scopic ventral hernia repair paired series. Mortality
rates were also similar between groups. Wound
infection rates were 4.6–8-fold higher in the open
versus laparoscopic ventral hernia repair series for
both pooled and paired study comparisons and
accounted for most of the wound-related complica-
tions (⊡ Table 45.4). The number of mesh infections
was also significantly higher with open ventral her-
nia repair for all comparisons. Interestingly, the
incidence of postoperative seroma was similar for
both open and laparoscopic series.
The rate of hernia recurrence (⊡ Fig. 45.2) was
significantly lower with laparoscopic ventral her-

14

12

10
Incidence (%)

8 * p<0.0001
6

4 * *
2

0
⊡ Fig. 45.2. Hernia recurrence OPEN PAIRED LAP POOLED LAP

⊡ Table 45.4. Wound complications

Open repairs (%) Paired p-valuea Pooled p-valueb

laparoscopic cases (%) laparoscopic cases (%)

Wound infection 10.4 2.3 <0.0001 1.3 <0.0001

Total wound 16.8 5.3 <0.0001 3.8 <0.0001

complicationsc

Mesh infection 3.2 1.5 0.039 0.9 <0.0001

Seroma 12.0 12.1 0.95 11.5 0.66

Trocar hernia 0 0.4

aCompares
open group with paired laparoscopic ventral hernia repair group
b
Compares open group with pooled laparoscopic ventral hernia repair group
cIncludes wound hematoma/bleeding, cellulitis, dehiscence, and fat necrosis in addition to wound infection
Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair
nia repair for both the pooled (4.3%) and paired
(3.1%) study cohorts compared to the paired
open ventral hernia repair series (12.1%, both
p<0.0001). Small variations existed in the length
of follow-up reported in the three groups of stud-
ies (25.5 months for pooled laparoscopic ventral
hernia repair, 16.9 months for paired laparoscopic
ventral hernia repair, 20.2 months for open ven-
tral hernia repair), but these differences were not
significant. The reported incidence of trocar site
hernia in the laparoscopic series was only 0.35%.
Discussion
Large, single, and multi-institutional series have re-
ported excellent results with few complications and
recurrence rates of generally <10% after laparo-
scopic ventral hernia repair [3, 4, 8, 14, 17, 22, 27,
32]. However, only one prospective, randomized,
controlled trial comparing laparoscopic to open
incisional hernia repair [7] and one looking at lap-
aroscopic versus open repair of Spigelian hernias
have been reported [21]. Despite the growing body
of knowledge in the field of laparoscopic ventral
hernia repair, published overviews of the topic are
largely review papers that have not pooled the data
and critically analyzed it as a whole [9]. A single
meta-analysis evaluating eight studies and three
data sets (perioperative complications, operating
time, and hospital LOS) has been published [13].
The most stringent statistical method for ana-
lyzing any published data from multiple sources
is a meta-analysis, requiring completeness and
uniformity in the data reporting methods. Any
studies that lack a data point of interest, or that
fail to report standard deviations along with their
means, must be excluded from analysis. Such
an approach in the area of ventral hernia repair
would exclude many potentially informative stud-
ies because of the variable reporting methods used
in these reports. A pooled-data analysis of lap-
aroscopic ventral hernia repair was performed in
order to encompass a broad range of papers and
achieve a more complete overview of the results
and outcomes. Dividing the study population into
»paired« and »pooled« groups allowed us to ex-
amine one cohort that should have a high degree
337 45
of internal consistency for comparison with open
ventral hernia repair (the paired studies only), as
well as a significantly larger group (the pooled
studies) that should give a broader view of the
field as a whole; this approach has proven useful
in similar past analyses [33].
In our analysis, we found the patient popula-
tions in both the pooled and paired laparoscopic
groups, as well as in the open surgery group, to be
demographically similar. All cohorts show a simi-
lar gender distribution, and the mean patient ages
across the groups of studies show little variation.
The vast majority of patients in the reported series
were clinically overweight or obese, not surprising
given that obesity is a strong predictive factor in
hernia formation and recurrence [24, 30, 31].
The analysis of perioperative data showed that
operative times were not significantly different for
open or laparoscopic approaches. However, there
was considerable variation across studies in the
laparoscopic operative technique used, with some
groups employing transfixion sutures routinely
and others using them in a limited fashion or
using only tacks. The variability in laparoscopic
technique and the fact that most series included
cases that were part of the institution’s early experi-
ence limit any definite conclusions about operative
time comparisons. The measured size of the hernia
defect and the size of mesh used, however, were
greater in the laparoscopic reports than for the
open patients, although these differences were sig-
nificant for the pooled laparoscopic studies only.
Possible explanations for these findings are that pa-
tients with larger defects are being selected for lap-
aroscopic repair, the laparoscopic series are mea-
suring sizes of all the combined defects whereas
open reports describe the size of the largest defect
only, additional defects are being detected and re-
paired with laparoscopic ventral hernia repair, or a
combination of these variables. Similarly, it is not
surprising that a larger mesh size was used with
laparoscopic ventral hernia repair because of the
technique of covering all defects with a single piece
of mesh without needing to dissect large tissue
flaps as with open ventral hernia repair.
Postoperative LOS for both the pooled and
paired laparoscopic groups averaged only 2.4 days
compared to 4.3 days for the open group. The
 338 Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair: 14 Years of Patient Data Accrual
reasons for shorter hospitalization with the laparo-
scopic approach are unclear but could be related
to fewer complications, as discussed below, among
other variables. A shorter hospitalization could
also be a factor in the potential economic impact
of laparoscopic ventral hernia repair, as recently
addressed by Earle et al. [11].
The primary outcome parameters were periop-
erative complications and hernia recurrences. The
analysis demonstrates that laparoscopic ventral
hernia repair was associated with a significantly
45 lower overall complication rate compared to open
ventral hernia repair in the paired analysis. This
difference was due primarily to more wound com-
plications in the open ventral hernia repair series.
Some differences were also seen in other organ sys-
tem complications when the pooled laparoscopic
ventral hernia repair data were compared to open
ventral hernia repair for gastrointestinal, pulmo-
nary, and miscellaneous other complications such
as fever and thrombophlebitis; however, these dif-
ferences did not reach statistical significance in the
paired comparison because of the smaller sample
size. Another explanation for the differences in
other organ system complications in the pooled
analysis is that groups reporting only on their lap-
aroscopic experiences (i.e., studies included only in
the pooled analysis) may have accumulated more
extensive experience and achieved better outcomes
with the laparoscopic procedure.
One of the main potential advantages of lap-
aroscopic incisional hernia repair is reduced
wound complications and mesh infections, and
the results of our meta-analysis support this. The
difference in wound complication rates between
laparoscopic versus open cases is largely a reflec-
tion of the decreased number of wound infections
seen in the laparoscopic group. Two major factors
likely contribute to a reduced infection rate. First,
open incisional hernia repair typically involves
extensive lateral dissection of tissue planes, with
a large subcutaneous dead space and potentially
altered blood flow. The mesh is often exposed to
the subcutaneous space, with the potential for sub-
sequent infection if a superficial wound infection
occurs. With the laparoscopic approach, there is
no flap dissection, and the mesh is placed intra-
peritoneally. Second, unlike laparoscopic ventral
hernia repair, during open ventral hernia repair
the prosthetic mesh is more likely to contact the
patient’s skin, with the potential for seeding by
residual dermal flora.
There was no difference in the rate of clinically
significant seroma formation between the laparo-
scopic and open ventral hernia repair groups.
One complication that occurred somewhat
more frequently in the laparoscopic group in the
paired analysis was enterotomy (2.9% laparoscopic
vs. 1.2% open). Enterotomy during ventral hernia
repair is a major complication with potentially life-
threatening consequences if unrecognized. The en-
terotomies recorded in this analysis included both
those that were recognized at the time of surgery
as well as those discovered later due to a subse-
quent complication. The occurrence of enterotomy
is probably related to multiple variables, including
surgeon experience, but most likely the primary
risk variable is the extent of intraabdominal adhe-
sions. The presence of prior mesh hernia repair
may also be a factor in the risk for enterotomy dur-
ing laparoscopic incisional hernia repair. In one
recent series, the incidence of enterotomy during
laparoscopic ventral hernia repair in patients with
prior mesh placed was 11.4% compared with no
enterotomies in patients who had not had previous
mesh repairs [25] .
Early postoperative pain was not evaluated in
this analysis, but prolonged pain was recorded in
a somewhat higher percentage of patients in the
pooled laparoscopic series compared to open, but
not in the paired analysis. These differences could
be accounted for in part by variable reporting
methods of prolonged pain as a »complication.«
However, unlike most other laparoscopic proce-
dures in which incisional pain is typically minimal,
laparoscopic incisional hernia repair is associated
with substantially more pain in the postoperative
period because of the methods of mesh fixation.
Specifically, the use of transfixion sutures for the
mesh has been associated with increased pain after
laparoscopic ventral hernia repair, but this issue
was not addressed in our analysis.
The most important measure of an effective
hernia operation is a low recurrence rate. In the
paired and pooled data sets, laparoscopic ventral
hernia repair was associated with significantly
Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair
fewer hernia recurrences. These results do not
appear to be explained on the basis of inadequate
or short follow-up periods (mean 17–25 months),
although longer-term studies with examination
at follow-up will ultimately be necessary to verify
these claims. Possible reasons for the lower recur-
rence rate with laparoscopic ventral hernia repair
are that wide areas of tissue–prosthesis overlap
can be obtained. This broad interface should
allow for better tissue–mesh integration and a
stronger repair with subsequent lower recurrence
rates. A laparoscopic approach also provides a
better opportunity to identify all hernia defects,
some of which could be missed with an open ap-
proach.
It is important to consider some of the limita-
tions of the data analysis. One potential shortcom-
ing of this study is the lack of complete statistical
analysis of all data points studied. This, however,
is largely due to inconsistent reporting of these
data points across the studies evaluated. All the
examined series reported their total number of pa-
tients; greater than 95% reported mean patient age;
and approximately 85–90% gave information on
gender breakdowns, operative times, hospital LOS,
and duration of follow-up. In contrast, only about
one-half to two-thirds of the studies gave informa-
tion on hernia and mesh size, and fewer than 50%
reported patient BMI values. Furthermore, only six
reports, all of them paired studies, gave any infor-
mation on the costs associated with the operative
procedure and/or the hospital stay [2, 5, 10, 15, 20,
35]. Even in instances in which these parameters
were reported, the values were sometimes given as
means and sometimes as medians, and they often
did not include standard deviations. Lack of such
detailed information limits the statistical analyses
that can be applied and precludes any formal me-
ta-analysis of the data points unless a large number
of studies with incomplete data are excluded.
Conclusions
An analysis of the published literature on lap-
aroscopic ventral hernia repair shows that this
procedure is associated with lower total complica-
tion rates and fewer wound and mesh infections
339 45
than with open ventral hernia mesh repair. Hernia
recurrence rates in short-term to medium-term
follow-up are acceptably low and are significantly
less than those reported in paired open ventral
hernia cases. Studies with longer-term follow-up
will be necessary to verify these results. Despite
the limitations of this pooled-data analysis, it ap-
pears that laparoscopic incisional hernia repair has
several distinct advantages over open approaches.
Laparoscopic repair should be strongly considered
by surgeons with appropriate advanced laparo-
scopic expertise for patients with noncomplex in-
cisional hernias.
Acknowledgments
The authors wish to thank Dr. Yan-Yan in the
Department of Surgery and the Siteman Cancer
Center, Washington University School of Medi-
cine, Barnes-Jewish Hospital, St. Louis, Missouri,
for statistical support.
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Appendix 45.1 Paired Series Included in
Study
1. Beldi G, Ipaktchi R, Wagner M, Gloor B, Candinas D (2006)
Laparoscopic ventral hernia repair is safe and cost effec-
tive. Surg Endosc 20:92–95
2. Bencini L, Sanchez LJ, Boffi B, Farsi M, Scatizzi M, Moretti
R (2003) Incisional hernia: repair retrospective compari-
son of laparoscopic and open techniques. Surg Endosc
17:1546–1551
3. Carbajo MA, Martin del Olmo JC, Blanco JI, de la CC,
Toledano M, Martin F, Vaquero C, Inglada L (1999) Laparo-
scopic treatment vs open surgery in the solution of major
incisional and abdominal wall hernias with mesh. Surg
Endosc 13:250–252
Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair
4. DeMaria EJ, Moss JM, Sugerman HJ (2000) Laparoscopic
intraperitoneal polytetrafluoroethylene (PTFE) prosthetic
patch repair of ventral hernia. Prospective comparison to
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14:326–329
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(2003) Laparoscopic versus open umbilical hernia repair.
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plasty. Surg Endosc 11:32–35
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and open ventral hernia repairs. Surg Endosc 17:1778–
1780
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incisional hernia repair: a comparison study. Surgery
124:816–821
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repair of large ventral hernias. JSLS 7:227–232
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13. Wright BE, Beckerman J, Cohen M, Cumming JK, Rodri-
guez JL (2002) Is laparoscopic umbilical hernia repair with
mesh a reasonable alternative to conventional repair? Am
J Surg 184:505–508
14. Wright BE, Niskanen BD, Peterson DJ, Ney AL, Odland MD,
VanCamp J, Zera RT, Rodriguez JL (2002) Laparoscopic
ventral hernia repair: are there comparative advantages
over traditional methods of repair? Am Surg 68:291–295
Appendix 45.2 Unpaired Series Included in
Study
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Laparoscopic tension-free repair of anterior abdominal
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sional hernia: a retrospective study of 159 patients. Surg
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3. Bamehriz F, Birch DW (2004) The feasibility of adopting
laparoscopic incisional hernia repair in general surgery
341 45
practice: early outcomes in an unselected series of pa-
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(2003) The experience with a modified technique for lap-
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Tech A 13:305–307
 342 Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair: 14 Years of Patient Data Accrual
20. Moreno-Egea DA, Martinez JA, Cuenca GM, Miquel JD,
Lorenzo JG, Albasini JL, Jordana MC (2004) Mortality fol-
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Laparoscopic repair of large incisional hernias. Am Surg
68:530–533
23. Perrone JM, Soper NJ, Eagon JC, Klingensmith ME, Aft
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Surgery 138:708–715
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erier F, Fanning A, Siperstein A (2003) Recurrence after
laparoscopic ventral hernia repair. Surg Endosc 17:123–
128
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laparoscopic ventral hernia repair: results and critical re-
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Technique and early results of outpatient laparoscopic
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584
28. Toy FK, Bailey RW, Carey S, Chappuis CW, Gagner M,
Josephs LG, Mangiante EC, Park AE, Pomp A, Smoot RT,
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30. Ujiki MB, Weinberger J, Varghese TK, Murayama KM, Joehl
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Discussion
Deysine: If I were a reviewer of this paper, I would
address the need of a pooled data analysis. How-
ever, it is very difficult to compare unpaired data.
So the valid comparison would be a data analysis
with paired groups. In the main table you pro-
duced, there was no major difference in several
outcomes between open and laparoscopic [proce-
dures], and you had to pull additional data without
comparative analysis to make a strong point in
favor of laparotomy.
Matthews: If you look at the pooled data, you
could say that is from laparoscopic experts, and is
that really applicable to the community surgeon
who does everything? So you are right. If you look
at the paired analysis, everything looks very simi-
lar in terms of those patient variables. Obviously,
there were some differences with the complica-
tions. You could argue that a laparoscopic ventral
hernia repair should be done by an expert hernia
surgeon. In a meta-analysis, you can work the data
however you want it to come out.
Kukleta: Concerning the prolonged pain, in the
pooled group you found an increase on the lap-
aroscopic side. Was there any possibility to take
a look at the technique of transfascial sutures and
the material used, because there are 25 U.S. papers
where, in most, ePTFE was used. Here fixation
must be stronger than everywhere else. Did you
find any correlation?
Matthews: You are absolutely right. Greater than
90% of our pooled data used an ePTFE mesh. So
there are some additional things that we can look
at.
Schumpelick: Is it really justified to compare
laparoscopic versus an open approach without
any functional results? After a laparoscopic ap-
proach, you have a defect of the muscles covered
by mesh. Sometimes there is a rectus diastasis in
the midline, and in the open approach you close
it. Therefore, we need a functional test of whether
there are differences or not. Have you seen such a
test? The story of Reeves and Flament was to close
the hernia to increase the muscle stability of the
abdomen.
Matthews: More and more surgeons in the U.S.
do not use the laparoscopic approach on every pa-
tient—and in my practice as well—because, from a
functional standpoint, some patients benefit from
an abdominal reconfiguration or reconstruction.
Flament: I was questioned about the selection of
patients. In Sevilla, Ramshaw said that hernias
with loss of domain are not suitable for laparo-
scopic treatment. Yesterday Predeep Chowbey said
we have to select our patients, as laparoscopy is not
Chapter 45 · Pooled Data Analysis of Laparoscopic vs. Open Ventral Hernia Repair
343 45
suitable for every patient. If so, the biggest hernias the large incisional hernias by the conventional
go to open surgery, and the smaller ones maybe go method, and when they come back with a recur-
to laparoscopic surgery. How can you introduce rence, which is usually a small hernia recurrence,
that in the analysis of the results? we handle it laparoscopically. That probably gives
Matthews: If you look at the results, the actual the best functional and anatomic results.
hernia size was much bigger in the laparoscopic
patients. So the selectivity, in terms of bigger ones
being done open and the smaller ones laparoscopi-
cally, did not really hold out in this analysis. I think
one of the things that actually really came out is
that, especially in the U.S., the average BMI of a
ventral hernia patient is morbidly obese—about
35—and so I have to consider that we are produc-
ing more morbidity and maybe increasing the
functional outcome, or is it a good trade-off? To
me, a lot of times that makes sense, and these are
the discussions I actually have with the patient.
We never discussed these things 5 or 6 years ago
with the patient. Selectivity has become more of
an issue.
Fitzgibbons: Actually, we are now usually recon-
structing the abdominal wall laparoscopically. I
routinely now close the defects. But to do that, of
course, you have to pick smaller hernias to some
extent. So we are individualizing. But you have
an enormous advantage of laparoscopy as you de-
crease the infection rate. In the right patient, it is
still a very good choice. And with regard to fixa-
tion with the tacks, my goal with the tacks is to seal
the polypropylene side of the prosthesis so that the
bowel cannot get in contact—not so much for the
fixation.
Deysine: You mentioned that patients were not
always operated by surgeons who were up to date
with the changes that have happened. You have
general surgeons doing this kind of operation,
sometimes with results that are not that great. The
essence of this conference should be spread to the
general surgical population until this becomes a
specialty.
Chowbey: As I mentioned yesterday, we have to
select the patients that we operate laparoscopically
or by conventional surgery with anatomical repair
reinforced by the mesh. And what we also empha-
size is that the recurrence after open surgery is
generally very small, and these small recurrences
can be very easily and comfortable managed lap-
aroscopically. That has been our policy. We treat
 46

Tissue Ingrowth, Adhesion,

and Mesh Contraction
S. L. Bachman, A. Ramaswamy, B. J. Ramshaw
 346 Chapter 46 · Tissue Ingrowth, Adhesion, and Mesh Contraction
Introduction
As is the case with almost every medical interven-
tion, the use of surgical prosthetics for hernia repair
is a double-edged sword. While mesh has allowed for
tension-free repairs and low recurrence rates, there
has been a long learning curve regarding how to
appropriately fabricate and use these materials. The
development of complications such as fistulas, pain,
mesh migration, and hernia recurrences are among
the complications our patients have suffered as mesh
and placement techniques continue to evolve.
It has become clear that mesh materials are
46 not inert; they both stimulate a reaction in the
organism and undergo changes over time while
implanted [1]. This paper examines three interac-
tions between the body and mesh: tissue ingrowth
into mesh and its effects, adhesions to mesh, and
mesh contraction in vivo.
Tissue Ingrowth
»Ingrowth« of a mesh refers to the interdigitation
of the mesh with fibrous tissue. This was histori-
cally considered a positive property of a material,
as the ingrowth of collagen (scar) incorporates the
mesh into the abdominal wall. However, it is also
recognized that if ingrowth occurs on the visceral
surface, such as on bowel or bladder, ingrowth is a
negative effect that can lead to mesh contamina-
tion and fistulas.
Multiple studies have examined the ingrowth
of materials in animal models; the outcome mea-
sures of these studies are varied, including histo-
logic examinations of the tissue–mesh interface,
measurements of the force required to disrupt
mesh from the abdominal wall, and sophisticated
imaging models.
Klinge et al. have demonstrated that mesh in-
corporation is the result of almost pure collagenous
tissue deposited around and between the mesh fi-
bers [2]. They demonstrated an acute inflammatory
response after mesh insertion that peaked at 7–14
days, with concomitant fibroblast infiltration and
a slow resolution of active cells in the wound bed
until 90 days postoperative, when only a physiologic
cell turnover of <1% was noted [2]. This study
compared monofilament heavyweight polypropyl-
ene with lightweight multifilament polypropylene
prosthetics. The heavyweight material had a more
intense inflammatory response with a correspond-
ing fibrosis. A dense plate of connective tissue com-
pletely embedded the mesh. In comparison, the
lightweight polypropylene material had a less pro-
nounced inflammatory and fibrotic response, with
eventual formation of a thin scar framework and
fatty tissue interspersed within the mesh pores [2].
Mesh was laparoscopically inserted onto the
abdominal wall in pigs and then examined at
28 days by Jacob et al. [3]. They found that three-
dimensional (3D) polyester mesh took more force
to be disrupted from the abdominal wall (4.15 N/
cm2) than oxidized regenerated cellulose-coated
lightweight polypropylene (3.11 N/cm2) or heavy-
weight polypropylene (2.96 N/cm2). Histology was
not quantified beyond demonstrating fibrous in-
growth between all mesh types [3].
A number of studies have looked at peel
strength as a proxy for integration. A comparison
in swine performed by McGinty et al. evaluated
heavyweight polypropylene, coated 3D polyester,
and expanded polytetrafluoroethylene (ePTFE)
mesh. They found that the force of disruption was
1.3 N/cm for ePTFE, 2.1 N/cm for heavyweight
polypropylene, and 2.8 N/cm for polyester [4].
Additional histology demonstrated fibrous tissue
between the pores of the polypropylene and poly-
ester weaves. There was fibrous tissue noted in the
micropores of the ePTFE surface, but there was no
growth through the solid ePTFE [4].
Gonzalez and Ramshaw reported on the histo-
logic differences between flat polyester, 3D polyester,
and heavyweight polypropylene meshes 25 weeks
after implantation [5]. They found that fibrous en-
capsulation of the polypropylene was twice that
of the polyester meshes, although polypropylene
had less foreign body reaction than either polyester
mesh. However, polypropylene had significantly less
connective tissue present than the polyesters did [5].
Histology demonstrated fibrous tissue within the
pores of the polypropylene and the polyester.
The long-term ingrowth of mesh was studied by
Novitsky at al., who examined four types of mesh
placed in an intraperitoneal location in rabbits [6].
Three barrier meshes–heavyweight polypropylene/
Chapter 46 · Tissue Ingrowth, Adhesion, and Mesh Contraction
ePTFE composite, dual-sided ePTFE, and light-
weight polypropylene/oxidized regenerated cellu-
lose (ORC) coating–were compared with macropo-
rous, uncoated, heavyweight polypropylene. The
strength of mesh incorporation into the abdominal
wall was measured by three differentiated variable-
reluctance transducers. No significant difference
was noted between the meshes in the force required
to disrupt the mesh from the tissue; however, the
compliance of the surrounding tissue was signifi-
cantly higher in the lightweight polypropylene [6].
Examination and measurement of the abdominal
wall after implantation of mesh in humans was per-
formed by Welty et al. [7] using ultrasound and 3D
stereography. Heavyweight monofilament polypro-
pylene mesh was compared to more elastic and low-
weight meshes. The patients with the heavyweight
monofilament mesh had more complaints of par-
esthesias and abdominal discomfort, as well as more
recurrences (although not statistically significant).
Three-dimensional stereography demonstrated in-
creased stiffness of all abdomens with mesh, but the
extent of the stiffness increased with mesh weight
and decreased pore size [7]. These findings support
the concept that a florid ingrowth around the mesh
can be detrimental to a hernia repair.
Thus, if the sequelae of fibrous reactions to mesh
are considered more detrimental (extensive fibrosis,
loss of abdominal wall compliance, pain) than ben-
eficial, it would be helpful to understand which
meshes will stimulate this reaction. An interesting
study by Sanders et al. [8] took the concept beyond
pore size and investigated whether the size of mesh
filaments affects the overall fibrotic ingrowth. Poly-
propylene fibers in four diameters ranging from
2.0 μm to 27.0 μm were implanted in rat soft tissue
for 5 weeks. After histology slides were obtained, the
thickness of the fibrous capsule surrounding each
filament was calculated. Fibers that were smaller
than 6.0 μm had no encapsulation in 87% of them,
and overall had significantly smaller capsules than
the fibers larger than 6.0 μm [8].
Mesh Adhesions
The same factors that promote ingrowth of the
muscular fascia of the abdominal wall, as described
347 46
above, are a potential problem when the mesh is
exposed to the abdominal viscera. Polypropylene
and polyester have been used since the 1950s [9,
10] and are two of the most frequently used types
of mesh in ventral hernia repair. They are struc-
turally macroporous and allow tissue, including
chronic inflammatory tissue, to grow through the
pores. Macroporous meshes have been coated with
substances to place against the abdominal viscera
to prevent ingrowth to bowel. However, when a
microporous (or solid) barrier is lacking between
the viscera and the macroporous mesh, such as
when titanium is used as the coating substance,
there is potential for ingrowth of bowel.
Human Studies
Evidence supports the contention that macropo-
rous mesh should not be placed into the peritoneal
cavity. Halm et al. [11] showed that reoperations
following intraperitoneal polypropylene mesh
placement are much more difficult and dangerous
than reoperations when mesh is placed outside the
peritoneal cavity. There was a 76% complication
rate when operating on patients with mesh previ-
ously placed in the abdominal cavity, compared to
a 29% complication rate in patients who had mesh
placed outside the abdominal cavity. In this retro-
spective study of 66 patients, all eight bowel resec-
tions and two enterocutaneous fistulas occurred in
the group of patients who had mesh placed in the
peritoneal cavity [11].
A common mesh used for laparoscopic ventral
hernia repair is ePTFE, which is designed for in-
traabdominal placement with a microporous side
placed toward the abdominal cavity. A retrospective
review reported the findings at reoperations in pa-
tients in whom ePTFE had been placed laparoscopi-
cally for ventral hernia repair [12]. The reoperations
in 65 patients showed that most patients (50/65) had
adhesions to the mesh; however, the adhesions were
mostly graded as easy to take down (44/50 were as-
signed a score of 1). It was also noted that no entero-
tomies occurred during lysis of adhesions [12].
Another human study evaluated postoperative
adhesions using a dynamic ultrasound technique
[13]. This study of 80 patients evaluated the inci-
 348 Chapter 46 · Tissue Ingrowth, Adhesion, and Mesh Contraction
dence of adhesion formation after open or laparo-
scopic ventral hernia repair using a polyester mesh
with an absorbable collagen coating designed for
intraperitoneal placement. Adhesions were present
at 1 year in 14% of patients by ultrasound exami-
nation [13].
The incidence of intestinal ingrowth when
using mesh coated with a solid microporous or
hydrogel-type barrier is unknown at this time.
Damage may occur during mesh manipulation or
fixation with tacks or sutures, which may strip off
the antiadhesive barrier and expose the macropo-
rous material to the abdominal viscera.
46
Animal Studies
There are numerous reports comparing mesh prod-
ucts placed in the abdominal cavity in animal ad-
hesion models [4, 14–28]. Various animal models,
including rat, rabbit, and pig, have been studied to
look at mesh adhesions. In these animal models,
mesh is placed in the abdominal cavity and fixed to
the peritoneal surface of the abdominal wall. The
peritoneum and/or abdominal contents, such as
small bowel or cecum, are abraded to induce injury
that would simulate an abdominal wall hernia re-
pair in humans. By abrading the bowel, this injury
induces adhesion formation more reliably than if no
peritoneal damage were induced. Although slight
differences in the specific adhesion rates for each
type of mesh are observed when comparing these
studies, all of the studies show that the meshes de-
signed for intraabdominal placement (either with a
solid microporous PTFE barrier or an absorbable
solid barrier) result in fewer adhesions compared
with macroporous meshes, including lightweight
macroporous meshes.
An important concept when discussing adhe-
sions to mesh is the fact that adherence alone is not
a major problem for surgeons who must reoper-
ate on a patient with a previous mesh placement.
An adhesion to mesh may rarely cause pain or
bowel obstruction for the patient, but long-term
complications and difficult reoperations occur if
there is ingrowth of the abdominal viscera into and
through the mesh (⊡ Fig. 46.1). This ingrowth of
viscera can lead to the difficult and dangerous re-
⊡ Fig. 46.1. Macroporous mesh being cut off the abdominal
wall but left on multiple loops of bowel due to ingrowth of
bowel into macroporous mesh
operations mentioned earlier and can result in late
bowel obstructions and fistulas that can harm pa-
tients (⊡ Fig. 46.2a, b). There are reports of fistulas
and bowel obstructions caused by intraperitoneal
placement of macroporous mesh up to 30 years
after implantation [28–32]. This evidence suggests
that even if macroporous mesh is no longer placed
into the peritoneal cavity after today, we as surgeons
will continue to face difficult reoperations and will
be managing enterocutaneous fistulas and bowel
obstructions due to macroporous mesh placed in
the abdominal cavity for many more decades.
Mesh Contraction
Surgeons who have had the occasion to remove
mesh from patients will be familiar with the phe-
nomenon of mesh contraction (⊡ Fig. 46.3a–c). The
acknowledgement of mesh contraction has led
to important changes in hernia repair technique.
An inadequate length of extension of mesh onto
healthy tissue may lead to recurrence if the mesh
retracts away from the hernia.
The phenomenon of mesh contraction has been
documented in experimental models, such as that by
Klinge et al. [33]. This canine study established that
mesh contraction occurs as early as within 4 weeks
after implantation. They noted that heavyweight
polypropylene was reduced to 54% of its original
size, and a reduced-weight polypropylene mesh was
Chapter 46 · Tissue Ingrowth, Adhesion, and Mesh Contraction
349 46

⊡ Fig. 46.2. a A mesh designed for intraabdominal placement b

[heavyweight polypropylene/polytetrafluoroethylene (PTFE)
composite] was used in a laparoscopic ventral hernia repair.
b A stitch was placed in the center of the mesh to help posi-
tion the mesh laparoscopically. The stitch apparently caused a
defect in the expanded PTFE, and an enterocutaneous fistula
developed a year after the operation

66% of its implantation size [33]. Many other inves-

tigators have also documented shrinkage of pros-
thetics in vivo. Coda et al. found that prosthetics
would shrink or even expand in response to being
bathed in different types of fluids [34]. Gonzalez
et al. explanted mesh from swine abdominal walls
3 months postoperatively and found that the mean
size of heavyweight polypropylene squares was 67%
of their original size, and flat polyester mesh was
87% of its original size [35]. They also studied tissue
integration and found that a higher force was neces-
sary to distract the polyester mesh (mean 194 N)
versus the polypropylene (159 N) [35].
c
⊡ Fig. 46.3. a A composite heavyweight/expanded polytetraflu-
oroethylene (ePTFE) mesh immediately after being excised from
the anterior abdominal wall. Note the scalloped edges that have
exposed the heavyweight component to the viscera. b An ePTFE
explant after tissue has been removed. The mesh is stiff and
contracted into this twisted shape. c A composite heavyweight
polypropylene/ePTFE mesh after explantation and cleaning
 350 Chapter 46 · Tissue Ingrowth, Adhesion, and Mesh Contraction
In another swine study, early explanation at
28 days demonstrated that 3D polyester mesh was
70.5% of its original size, heavyweight polypropyl-
ene was 74.7%, and lightweight polypropylene with
ORC was 66.4% of the initial size [3]. A study with
4-week explants found that heavyweight polypro-
pylene was 94% of its original size, 3D polyester was
79%, and ePTFE was 63% of the original size [4].
At 1 year postoperative, Novitsky et al. found that
ePTFE had contracted by a mean of 32.1%, ePTFE/
heavyweight polypropylene composite by 8.9%,
heavyweight polypropylene by 4.6%, and lightweight
polypropylene coated with ORC by 8.7% [6].
46 The early timeline of contraction implicates the
immediate wound-healing inflammatory response
as the mechanism. The initial deposition of collagen
by fibroblasts and the encasement of the mesh seem
to have a role. We tested this theory by administer-
ing a daily low dose of steroid to swine with three
types of mesh implanted on the anterior abdominal
wall. A second group of animals did not receive the
injection. Mesh was explanted at 3 months. There
was variable contraction between the groups, but all
three types of mesh in the steroid-treated animals
had 10% less contraction than the corresponding
untreated mesh (manuscript in preparation).
Surveying the literature on mesh contraction
leads to many contradictory results: Sometimes
heavyweight polypropylene contracts more, some-
times ePTFE, sometimes lightweight materials.
Some researchers have hypothesized that the loca-
tion of the mesh in the abdominal wall will influ-
ence contraction [36]. However, there does seem
to be a trend that an increased load of foreign
material will incite more inflammation and pos-
sibly contraction. An increased size of mesh pore
interstices also seems to reduce scar formation.
This kind of analysis is helping to drive the shift to
lighter-weight, lower-density prosthetics [37–39].
Conclusion
Mesh prosthetics undergo changes within the
body, and they incite an inflammatory response
as well. A body of research is accumulating in the
literature to try to better define these effects. New
mesh configurations are an attempt to minimize
the sequelae of scar plate formation around the
mesh while still obtaining the ingrowth that helps
secure the mesh’s position, diminish contraction,
and prevent adhesions to the visceral surface of the
mesh. We can expect to see more refinements of
the materials used in hernia repair in the future.
References
1. Costello CR, Bachman SL, Ramshaw BJ, Grant SA (2007)
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83B:44–49
2. Klinge U, Klosterhalfen B, Birkenhauer V, Junge K, Conze
J, Schumpelick V (2002) Impact of polymer pore size on
the interface scar formation in a rat model. J Surg Res
103:208–14
3. Jacob BP, Hogle NJ, Durak E, Kim T, Fowler DL (2007) Tis-
sue ingrowth and bowel adhesion formation in an animal
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5. Gonzalez R, Ramshaw BJ (2003) Comparison of tissue
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6. Novitsky YW, Harrell AG, Cristiano JA, Paton BL, Norton
HJ, Peindl RD, Kercher KW, Heniford BT (2007) Compara-
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growth, and textile properties of prosthetic meshes after
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Surg Res 140:6–11
7. Welty G, Klinge U, Klosterhalfen B, Kasperk R, Schumpelick
V (2001) Functional impairment and complaints follow-
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8. Sanders JE, Stiles CE, Hayes CL (2000) Tissue response to
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9. Usher FC, Ochsner J, Tuttle LL, Jr. (1958) Use of mar-
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10. Usher FC, Wallace SA (1958) Tissue reaction to plastics; a
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11. Halm JA, de Wall LL, Steyerberg EW, Jeekel J, Lange JF
(2007) Intraperitoneal polypropylene mesh hernia repair
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12. Koehler RH, Begos D, Berger D, Carey S, LeBlanc K, Park A,
Ramshaw B, Smoot R, Voeller G (2003) Minimal adhesions
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13. Aube C, Pessaux P, Tuech JJ, du Plessis R, Becker P, Caron
C, Arnaud JP (2004) Detection of peritoneal adhesions
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ton HJ, Kercher KW, Heniford BT (2007) Prospective his-
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21:1170–4
15. Bellon JM, Rodriguez M, Garcia-Honduvilla N, Gomez-Gil
V, Pascual G, Bujan J (2007) [Real-time monitoring of the
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16. Christoforoni PM, Kim YB, Preys Z, Lay RY, Montz FJ (1996)
Adhesion formation after incisional hernia repair: a ran-
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17. Alimoglu O, Akcakaya A, Sahin M, Unlu Y, Ozkan OV, Sanli
E, Eryilmaz R (2003) Prevention of adhesion formations
following repair of abdominal wall defects with pros-
thetic materials (an experimental study). Hepatogastro-
enterology 50:725–8
18. Matthews BD, Pratt BL, Pollinger HS, Backus CL, Kercher
KW, Sing RF, Heniford BT (2003) Assessment of adhesion
formation to intra-abdominal polypropylene mesh and
polytetrafluoroethylene mesh. J Surg Res 114:126–32
19. Gonzalez R, Rodeheaver GT, Moody DL, Foresman PA,
Ramshaw BJ (2004) Resistance to adhesion formation: a
comparative study of treated and untreated mesh prod-
ucts placed in the abdominal cavity. Hernia 8:213–9
20. Conze J, Rosch R, Klinge U, Weiss C, Anurov M, Titkowa
S, Oettinger A, Schumpelick V (2004) Polypropylene in
the intra-abdominal position: influence of pore size and
surface area. Hernia 8:365–72
21. Johnson EK, Hoyt CH, Dinsmore RC (2004) Abdominal wall
hernia repair: a long-term comparison of Sepramesh and
Dualmesh in a rabbit hernia model. Am Surg 70:657–61
22. Matthews BD, Mostafa G, Carbonell AM, Joels CS, Kercher
KW, Austin C, Norton HJ, Heniford BT (2005) Evaluation
of adhesion formation and host tissue response to intra-
abdominal polytetrafluoroethylene mesh and composite
prosthetic mesh. J Surg Res 123:227–34
23. Demir U, Mihmanli M, Coskun H, Dilege E, Kalyoncu A,
Altinli E, Gunduz B, Yilmaz B (2005) Comparison of pros-
thetic materials in incisional hernia repair. Surg Today
35:223–7
24. Kayaoglu HA, Ozkan N, Hazinedaroglu SM, Ersoy OF,
Erkek AB, Koseoglu RD (2005) Comparison of adhesive
properties of five different prosthetic materials used in
hernioplasty. J Invest Surg 18:89–95
25. Burger JW, Halm JA, Wijsmuller AR, ten Raa S, Jeekel J
(2006) Evaluation of new prosthetic meshes for ventral
hernia repair. Surg Endosc 20:1320–5
351 46
26. Harrell AG, Novitsky YW, Peindl RD, Cobb WS, Austin CE,
Cristiano JA, Norton JH, Kercher KW, Heniford BT (2006)
Prospective evaluation of adhesion formation and shrink-
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Surg 72:808-13; discussion 813–814
27. Bellon JM, Rodriguez M, Garcia-Honduvilla N, Pascual G,
Gomez Gil V, Bujan J (2007) Peritoneal effects of pros-
thetic meshes used to repair abdominal wall defects:
monitoring adhesions by sequential laparoscopy. J Lap-
aroendosc Adv Surg Tech A 17:160–6
28. Majeski J (1998) Migration of wire mesh into the intesti-
nal lumen causing an intestinal obstruction 30 years after
repair of a ventral hernia. South Med J 91:496–8
29. Fernandez Lobato R, Martinez Santos C, Ortega Deballon
P, Fradejas Lopez JM, Marin Lucas FJ, Moreno Azcoita M
(2001) Colocutaneous fistula due to polypropylene mesh.
Hernia 5:107–9
30. DeGuzman LJ, Nyhus LM, Yared G, Schlesinger PK (1995)
Colocutaneous fistula formation following polypropylene
mesh placement for repair of a ventral hernia: diagnosis
by colonoscopy. Endoscopy 27:459–61
31. Losanoff JE, Richman BW, Jones JW (2002) Entero-colo-
cutaneous fistula: a late consequence of polypropylene
mesh abdominal wall repair: case report and review of
the literature. Hernia 6:144–7
32. Costa D, Tomas A, Lacueva J, de Asis Perez F, Oliver I, Ar-
royo A, Sanchez A, Andreu J, Gallego JA, Calpena R (2004)
Late enterocutaneous fistula as a complication after um-
bilical hernioplasty. Hernia 8:271–2
33. Klinge U, Klosterhalfen B, Muller M, Ottinger AP, Schumpe-
lick V (1998) Shrinking of polypropylene mesh in vivo: an
experimental study in dogs. Eur J Surg 164:965–9
34. Coda A, Bendavid R, Botto-Micca F, Bossotti M, Bona A
(2003) Structural alterations of prosthetic meshes in hu-
mans. Hernia 7:29–34
35. Gonzalez R, Fugate K, McClusky D, 3rd, Ritter EM, Leder-
man A, Dillehay D, Smith CD, Ramshaw BJ (2005) Rela-
tionship between tissue ingrowth and mesh contraction.
World J Surg 29:1038–43
36. Garcia-Urena MA, Vega Ruiz V, Diaz Godoy A, Baez Perea
JM, Marin Gomez LM, Carnero Hernandez FJ, Velasco
Garcia MA (2007) Differences in polypropylene shrinkage
depending on mesh position in an experimental study.
Am J Surg 193:538–42
37. Klinge U, Klosterhalfen B, Conze J, Limberg W, Obolenski
B, Ottinger AP, Schumpelick V (1998) Modified mesh for
hernia repair that is adapted to the physiology of the
abdominal wall. Eur J Surg 164:951–60
38. Cobb WS, Kercher KW, Heniford BT (2005) The argument
for lightweight polypropylene mesh in hernia repair. Surg
Innov 12:63–9
39. Cobb WS, Burns JM, Peindl RD, Carbonell AM, Matthews
BD, Kercher KW, Heniford BT (2006) Textile analysis of
heavy weight, mid-weight, and light weight polypropyl-
ene mesh in a porcine ventral hernia model. J Surg Res
136:1–7
 352 Chapter 46 · Tissue Ingrowth, Adhesion, and Mesh Contraction

Discussion that there is some difference, but we do not know

what happens.
Deysine: The degradation is usually secondary to Ramshaw: I completely agree. Polypropylenes are
white cell proximity. I was wondering whether, in not the same; there are a lot of differences in the
some of the specimens that you removed, you tried way they are constructed; there is a high variability
to analyze the contained bacteria as the orthope- in the degree of degradation. Potential variables
dists do with their prostheses. They could not find are the length of time implanted, the bacterial mi-
the bacteria by normal ways. lieu, more degradation with infection, the different
Ramshaw: That is an excellent point. There will be types of fibers themselves. We are going to try to
an accelerated amount of oxidation in infection. In look at it as we start to correlate all of the variables
the infected meshes, we have not done any evalu- together in this large database.
ation of the bacteria. This is one of the things we
want to look at. We also want to look at the clinical
46 correlations from infection, chronic pain, recur-
rence, etc., and the patient characteristics such as
smoking, diabetes, and age. All we have done is
assess clinical signs of infection.
Franz: I particularly liked the distinction between
surface adhesion and ingrowth. With regard to bi-
ologics, if patients have a contaminated abdomen
or after failed synthetics, they are not interested in
another synthetic. Technique aside, do you think
cross-linking is good or bad?
Ramshaw: I could certainly give you the market-
ing point of view on it: If it’s a company without
cross-linking, cross-linking is bad because you
want regeneration, and the cross-linking will pre-
vent some of that cellular ingrowth or differentia-
tion. Companies that have cross-linking say that
non-cross-linking is bad because it is a risk for
early degradation. I think the answer is that we
have a lot of first-generation biologics, and we
really have not solved the real issue of getting
those cells to come in and differentiate into the
right types of material in the right patient. And
that is what I think the next generation of biolog-
ics may actually be better designed to do for our
patients.
Klinge: You described the degradation of polypro-
pylene. Usually, pure polypropylene is not suitable
to make filaments, and there are a lot of additives
and other substances which are mixed to the poly-
propylene. Unfortunately, we do not know what
these additives are. Did you see any differences in
the degradation process between the various poly-
propylenes? Some years ago, we saw in histological
analysis that some of the propylene heavyweight
meshes behaved better than expected. I believe
 47

Effect of Different Mesh Materials

on Adhesion Formation
S. Morales-Conde, J. Martín-Cartes, M. Socas
 354 Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation
Introduction
Because of the necessity of placing prosthetic
materials to reduce the high rate of recurrence
associated with conventional hernia repair with-
out mesh, aggressive dissection of tissues occurs
during conventional open repair. Laparoscopic
surgery has introduced a new technique for re-
pairing defects of the anterior abdominal wall
in order to avoid this large dissection, which is
associated with discomfort, the use of drains,
the possibility of contamination and infection of
the meshes used, and a long hospital stay for the
patient. These effects have led surgeons to accept
the laparoscopic approach as a valid option for
47 our patients [1].
Laparoscopic surgery and its application in
the treatment of ventral hernia have produced a
change in surgeon mentality. Before the advent of
this technique, surgeons always avoided placing
foreign materials in contact with intraabdominal
viscera in order to avoid adhesions.
Laparoscopic repair of ventral hernias is as-
sociated with the use of intraabdominal pros-
theses. This has improved the evolution of these
materials toward better ingrowth to the anterior
abdominal wall, but at the same time it has re-
duced the possibility of creating adhesions and
their potential complications, such as fistulas and
bowel occlusion [2].
The ideal mesh for intraperitoneal placement
has yet to be found. It should follow the principles
for any prosthetic material, such as being steril-
izable, noncarcinogenic, chemically inactive, and
resistant to physical manipulation, and it should
cause no inflammation, change in mesh character-
istics, altered tissue contact, or allergic or hyper-
sensitivity reaction. Moreover, the optimal mesh
should have certain characteristics when placed
intraabdominally: minimal pain and adhesion for-
mation, excellent tissue ingrowth with minimal
shrinkage, no formation of fistula or infection, and
minimal seroma formation. It is also important
that the prosthetic material cause no change in ab-
dominal compliance while at the same time being
easy to manipulate.
Factors Related to Adhesion Formation
with Prosthetic Materials
The formation of adhesions is an extremely complex
process that has not yet been completely explored.
As a result, many of the studies on this phenom-
enon are still empirical, but the results published so
far are promising. It is possible that we will be able
to control this process in the near future, whether
stimulating or inhibiting it, depending on the cir-
cumstances. The consequence of this could be the
possibility of applying these prosthetic materials for
intraabdominal use in laparoscopic surgery of the
abdominal wall with no risk of creating adhesions
and their subsequent consequences, such as fistulas
and bowel occlusion.
In the meantime, while we try to determine
the different factors involved in adhesion forma-
tion, the ideal materials and substances to prevent
adhesions are still far from being found. Different
studies performed so far have proved that it is pos-
sible to reduce the quantity and the quality of these
adhesions but not to prevent them completely. Full
tissue integration without adhesion formation is
still a challenge in the use of intraabdominal mesh
materials.
Different factors have been associated with the
process of adhesion formation, but the need of the
bowel and intraperitoneal organs to isolate foreign
agents (prosthetic materials, sutures, bacteria, etc.)
seems to play an important role. However, during
laparoscopic repair of ventral hernia, the presence
of intraperitoneal adhesions is a result not just
of the material itself; experimental studies have
related adhesions to the surgical technique used.
Spiral tacks, improper placement and fixing of the
mesh, and exposure of the sides of these materials
to the intraabdominal viscera could be related to
adhesion formation [3].
We also lack information about the healing
process involved in adhesion formation. It would
be interesting in the future to determine the criti-
cal moment when adhesions to prosthetic mate-
rials are formed. For that reason, some authors
have designed different studies using sequential
laparoscopy to monitor the real-time adhesion for-
mation process and the critical period when most
adhesions form [4, 5].
Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation
If we analyze the factors involved in adhesion
formation when a mesh in placed intraperitone-
ally, we can determine the following:
▬ Material: Different studies [6–12] have shown
that the porosity of the material is one of the
most important factors related to adhesion
formation and ingrowth. Large porosity has
been related to an increased number of ad-
hesions. Polypropylene mesh (PPM) is con-
sidered a high-porosity prosthetic material
that creates an important scar tissue involved
in adhesion formation. On the other hand, a
low-porosity material, such as expanded po-
lytetrafluoroethylene (ePTFE) [6–9, 13, 14],
produces a tissue capsule that covers the mesh
with a low rate of adhesions. Therefore, we
can conclude that the pore size of the mesh is
critical in the development and maintenance
of abdominal adhesions and tissue ingrowth.
It has been demonstrated, however, that re-
ducing the amount of material and increasing
the pore size result in better mesh biocompa-
tibility, with a potential reduction of adhesion
formations [15, 16], as some have tried to
demonstrate with the new lower-weight PPM.
These large-pore PPMs in the intraabdominal
position have shown a reduced inflammatory
tissue reaction, so they could be considered an
alternative for the development of intraperi-
toneal onlay meshes [17]. In fact, new studies
with reduced-weight PPM have demonstrated
less change in the adjacent tissue’s pliability/
compliance and less adhesion than conventio-
nal PPM [18].
In the future, these factors should also be ana-
lyzed with regard to the pore size of other
materials, such as PTFE. The larger-pore, thin-
ner meshes such as condensed PTFE (cPTFE)
have led to better tissue integration compared
with the other PTFE-based meshes or PPM.
Through hydrophobic chemistry, a low pro-
file, and increased pore size, cPTFE balances
the rapid resolution of the inflammatory and
wound-healing response to resist adhesion for-
mation, with efficient integration within the
surrounding abdominal tissue [19].
▬ Surgical technique for placing the mesh: An
experimental study conducted by our group
355 47
[20] has demonstrated the influence of the
surgical technique of mesh placement during
laparoscopic ventral hernia repair (LVHR). In
this study, most of the adhesions to the ePTFE
meshes were observed at the edges, compared
with the central part of this prosthetic mate-
rial. The potential reasons for these adhesions
were analyzed, and it could be seen how ad-
hesions formed to the undesired exposition of
the parietal face of the prosthesis or to tacks
improperly introduced into the mesh. These
issues demonstrate the need for a meticulous
technique to avoid complications related to
adhesions, such as bowel occlusion and perfo-
ration. The mesh must be properly extended
so that the parietal face is not exposed to the
bowel, and tacks should be introduced all the
way into the mesh to avoid their hanging from
the anterior abdominal wall.
▬ Fixation: As stated previously, adhesions to
spiral tacks may occur, and we have observed
these in experimental studies. Recent clinical
papers have even reported cases of obstruction
and/or perforation of the small bowel resulting
from a band adhesion caused by a displaced
spiral tack [21, 22].
▬ Surgical trauma: Surgical trauma to the bowel
or to the peritoneal surface of the anterior ab-
dominal wall during the process of adhesioly-
sis has some influence in adhesion formation,
even if the ideal intraabdominal mesh is used.
Adhesions result from the normal peritoneal
wound-healing response and develop during
the first 5–7 days after injury. Adhesion forma-
tion and adhesion-free reepithelialization are
alternative pathways. These both begin with
coagulation, which initiates a cascade of events
resulting in the buildup of a fibrin gel matrix.
If not removed, the fibrin gel matrix serves as
the progenitor to adhesions by forming a band
or bridge when two peritoneal surfaces coated
with it are opposed [23]. The band or bridge
becomes the basis for the organization of an
adhesion, especially if a foreign body reaction
is added to the process when a mesh is placed
intraabdominally, becoming of great impor-
tance to the surgical trauma on the bowel sur-
face [24].
 356 Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation
Analysis of the Influence of
Different Prosthetic Materials
on Adhesion Formation
Many prosthetic materials to be placed intraab-
dominally during LVHR are available on the mar-
ket, and new meshes are introduced regularly.
However, experimental and clinical documenta-
tion on safety, including information on adhe-
sions, fistulas, bowel occlusion, infection, and ef-
ficacy, are often not available to the clinician.
The choice of mesh may therefore be difficult in
clinical practice.
Regarding adhesion formation, different
experimental studies on animals show differ-
47 ent results (⊡ Table 47.1), and a mesh superior
to another in terms of adhesion formation in
one study may be inferior to the same mesh in
another study. If we analyze the different stud-
ies, the problem might be related to the fact that
they involved different implantation techniques
and were carried out in different animal mod-
els. In addition, the different factors analyzed
previously–such as manipulation of the abdomi-
nal viscera, fixation technique, size of the mesh,
size of the visceral face of the mesh in relation to
the parietal face (overlap), and management of
the abdominal wall area where the mesh is to be
placed–may influence the results of the various
studies, but in most cases, these factors are not
even described in the text.
A current review of the literature has been
published regarding safety measures such as ad-
hesions, fistulas, and infections after LVHR [25].
The only real concern based on this analysis
is about using pure PPM in the intraperitoneal
position. The use of intraperitoneal PPM to re-
pair incisional hernias has been demonstrated in
clinical and experimental studies to carry the risk
of adhesion and damage to the intraabdominal
viscera. Polypropylene is a material widely used
in surgery, but because of its association with the
formation of enterocutaneous fistulae and adhe-
sions, direct contact between mesh and intestine
is avoided. But, as has been analyzed previously,
the use of PPM may be reevaluated based on the
new studies of lightweight macropore meshes
to determine whether it could influence adhe-
sion formation. This study clearly points to very
few mesh-related complications after a proper
mesh is placed intraperitoneally and shows that
experimental studies and theoretical consider-
ations may argue for using a covered mesh (a
composite mesh or ePTFE) for LVHR in humans,
although it is stressed that no human data at the
moment support this. The only clinical informa-
tion available in the literature based on reopera-
tive findings concerning adhesions to prosthetic
materials placed intraabdominally was published
by Koehler et al. in 2003 [26]. They reported on
a multi-institutional study of adhesions to im-
planted ePTFE mesh at reoperation in patients
who had previously undergone laparoscopic in-
cisional hernia repair done with the same mesh
implantation technique. In this large series of
reoperations after LVHR, no or minimal adhe-
sion to implanted ePTFE mesh was observed in
91% of cases, and no severe cohesive adhesions
were found.
Regarding the two types of prosthetic materials
accepted for intraabdominal placement, it is im-
portant to consider the following factors:
▬ ePTFE: Traditionally, ePTFE is one of the
most widely used prosthetic materials for
repairing abdominal wall defects, but it has
been suggested that its behavior with respect
to the reparative process may depend on its
structure and that this factor should be con-
sidered to determine the capability to form
adhesions.
▬ Composite materials: Composite biomate-
rials designed for repairing abdominal wall
defects are usually composed of a reticular
component and a second component, or
barrier, which is laminar (absorbable or
nonabsorbable) and placed in contact with
the visceral peritoneum. Results on the
effectiveness of these membranes cover-
ing PPM or polyester mesh are related to
the membranes’ composition, but they are
contradictory: Studies with PPM covered
with materials such as polyglactin 910 mesh
(PGM), with the aim of avoiding contact
between the PPM and the intraabdominal
viscera, demonstrated that the interposition
of PGM did not alter adhesion formation
Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation
[27]. On the other hand, other studies de-
signed to evaluate how the composition of
this second component affects the biological
behavior of the biomaterial and the forma-
tion of adhesions have shown that physical
barriers seem to induce similar adhesions,
while adhesions formed to prostheses with
chemical barriers can vary considerably,
possibly depending on the chemical compo-
sition of the barrier [28]. Finally, the same
amount of adhesion despite the presence of
different protective barriers has been de-
monstrated with other polypropylene-based
meshes [29].
In conclusion, it is difficult to make a final state-
ment because the results of different studies are so
contradictory. Whereas some studies have demon-
strated the superiority of some composite meshes
over ePTFE [30–33], others showed ePTFE to be
related to less adhesion formation [18, 29, 34], and
there are even studies in which the two types of
mesh are similar [35]. The literature cannot give
general recommendations for the choice of mesh
based on randomized controlled trials. The final
choice of mesh for LVHR will therefore typically
be based on cost and the surgeon’s preference
while we await further data from randomized con-
trolled clinical trials.
Reducing Adhesion to Prosthetic
Materials
As already mentioned, meticulous technique is
one of the most important factors involved in
reducing adhesion formation: Avoid unnecessary
surgical trauma on the surface of the peritoneum
and the serosa of the bowel; avoid exposing the
parietal face of the mesh to the abdominal cav-
ity; and avoid letting spiral tacks hang from the
mesh because of improper introduction through
the prosthetic material.
But because these circumstances are not usu-
ally present, due to the process of adhesiolysis or
to a defect location that makes placement of the
mesh or tacks difficult, alternative methods to
avoid adhesion are under investigation. Efforts
357 47
to prevent or reduce adhesions have largely been
unsuccessful, hindered by the empirical basis,
the biochemical complexities of adhesiogenesis,
and the lack of good predictive animal models.
The two major strategies for adhesion preven-
tion or reduction consist of adjusting surgical
technique, as already proposed, and applying
adjuvants.
Different studies have been published that
used a variety of substances to prevent adhesion
formation to the prosthetic materials, with vary-
ing results. Hyaluronic acid/carboxymethylcellu-
lose (HA/CMC) membranes have been used as
an effective measure to prevent PPM-induced
adhesions; taurolidine 2% solution has been pro-
posed as a cost-effective alternative to HA/CMC
membranes when a PPM is placed in direct con-
tact with the abdominal viscera [36]; hyaluronate
sodium in the form of a bioresorbant membrane
has been demonstrated to significantly reduce
the development of intraabdominal adhesions
found after implantation of a PPM in the con-
text of surgical hernia repair [37]; and a colla-
gen foil has also been used to reduce adhesion
formation [38].
Looking for a cost-effective alternative to re-
duce adhesion formation to mesh placed intraab-
dominally during LVHR, we have conducted stud-
ies with two substances that can guarantee good
coverage of the complete surface of the mesh, even
if a large prosthetic material is used [39, 40]. These
two substances are fibrin glue (Tissucol; Baxter
Biosurgery, Vienna, Austria) and hyaluronidase
cream.
Both substances were able to decrease, in
an animal model, the number and quantity of
adhesions with PPM and ePTFE meshes. The
adhesion reduction with hyaluronidase cream is
a consequence of an acceleration in the normal
healing process needed to create adhesions. This
factor may also influence the reduction of adhe-
sions with fibrin glue, but it may be related to
other factors, such as the mechanical barrier that
the fibrin glue produces 3–5 min after its applica-
tion and the capsule of new tissue created by the
fibrin glue through a healing process different
from the inflammatory process necessary to cre-
ate an adhesion.
 47
358

⊡ Table 47.1. Experimental studies comparing adhesion formation of different prosthetic materials (lap laparoscopic; PP polypropylene mesh; ePTFE expanded polytetrafluoro-
ethylene; PHD glycerol-preserved human dura mater; PGA polyglycolic acid; PVDF polyvinylidene fluoride)

Year Author Animal N Meshes Open / lap Fewer adhesions More adhesions Time

1983 Jenkins et al. [41] Rats 196 PP (Marlex) Open Vicryl PP (Marlex ) 1, 2, 4, and 8 weeks
Vicryl PP (Marlex) + Gelfilm
ePTFE (STP)
Silastic
PHD
PP (Marlex) + Gelfilm

1993 Naim et al. [42] Rats PP + ePTFE (STP), Open PP + Interceed –

PP + Interceed
PP + Poloxamer

1996 Bellón et al. [43] Rabbits 24 PP (Marlex) Open ePTFE (Mycromesh) PP (Marlex) 14, 30, 60, and 90 days
ePTFE (MycroMesh)

1997 Baykal et al. [44] Mice 72 PGA Open PGA PP 5 and 14 days
PP

1998 Dasika and Widmann Rats 47 PP Open Vicryl PP 1, 2, and 3 months

[45] Vicryl PP +Vicryl
PP +Vicryl

1999 Bellón et al. Rabbits 48 ePTFE (STP) Open ePTFE (STP) – 14, 30, 60, and 90 days
[46] PP (Marlex) Lyodura
Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation

PP (Prolene)
Lyodura

2000 Vrijland et al. Rats 44 PP Open PP + Fluorosoft PP + Vicryl 60 days

[47] PP + Vicryl
PP + Fluorosoft

2000 Bellón et al. [48] Rabbits 8 ePTFE (MycroMesh) Open PP (Marlex) 3 and 7 days
ePTFE (DualMesh)
ePTFE (STP)
PP (Marlex)

2002 Bellón et al. [49] Rabbits 14 ePTFE (DualMesh) Open ePTFE (DualMesh) ePTFE (CV-4) 14 days
ePTFE (CV-4)

2002 Zieren et al. [50] Rats 40 ePTFE (DualMesh) Open No differences No differences 14 and 90 days
▼ PolyesterComposite
2003 Van ’t Riet et al. [51] Rats 91 PP Open Sepramesh PP 7 and 30 days
PP + Icodextrine Parietex PP + Icodextrine
Sepramesh
Parietex

2003 Matthews et al. [14] Rabbits 30 ePTFE (DualMesh) Open ePTFE (DualMesh) PP (Marlex) 1, 3, 9, and 16 weeks
PP (Marlex)

2004 Borrazzo et al. [52] Pigs 21 PP Lap Sepramesh 28 days

ePTFE (DualMesh)
Sepramesh

2004 González et al. [53] Rats 80 PP (Parietene) Open Parietex Composite PP (Parietene) 21 days
Parietex Composite Parietene Composite Sepramesh
Parietene Composite Composix E/X
Composix E/X ePTFE (DualMesh)
Sepramesh
ePTFE (DualMesh)

2004 Butler and Prieto [54] Guinea 19 PP (Prolene) Open PP (Prolene) + AlloDerm 4 weeks
pigs PP (Prolene) + AlloDerm

2005 Kayaoglu et al. [35] Rats 60 PP (Surgipro) Open Sepramesh 4 weeks

Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation

ePTFE (DualMesh) ePTFE (DualMesh)

Sepramesh
Vypro II
Parietex Composite

2005 Matthews et al. [29] Rabbits 30 ePTFE (DualMesh) Open ePTFE (DualMesh) 1, 3, 9, and 16 weeks
Composix E/X
Sepramesh

2005 Demir et al. [55] Rats 30 PP (Bard Mesh) Open PP (Bard Mesh) + 14 days
Composix E/X Interceed
PP (Bard Mesh) + Inter-
ceed
359

2005 McGinty et al. [30] Pigs 8 PP (Prolene) Lap Parietex Composite 28 days
ePTFE (DualMesh)
Parietex Composite

2005 Konstantinovic Rats 48 PP (Marlex) Open PP (Marlex) (30 days) 30 and 90 days
▼ et al. [56] Surgisis Surgisis (90 days)
47
 47
360

⊡ Table 47.1. Continued

Year Author Animal N Meshes Open / lap Fewer adhesions More adhesions Time

2006 Sikkink et al. [31] Rats 60 PP (Prolene) Open Sepramesh PP (Prolene) 2 months
PP (Prolene) + Hyalobar-
rier gel
PP (Prolene) + Tissucol
ePTFE (DualMesh)
Sepramesh
Parietene Composite

2006 Dilege et al. [57] Rats 30 PP (Prolene) Open PP + Interceed PP (Prolene) 28 days
PP + Interceed Sepramesh
Sepramesh

2006 Burger et al. [32] Rats 200 PP (Prolene) Open Sepramesh 7 and 30 days
ePTFE (DualMesh) Parietex Composite
Ultrapro
Timesh
Sepramesh
Parietex Composite
Proceed
Tutomesh

2006 Harrell et al. [34] Rabbits 60 ePTFE (DualMesh) Sequential ePTFE (DualMesh) PP (Marlex) 16 weeks
Composix E/X lap
Proceed
Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation

PP (Marlex)

2007 Kiudelis et al. [58] Rabbits 42 PP (Prolene) Open ePTFE Bard PP (Prolene) 30 days
Mersilene Proceed Mersilene
PP + Vicryl PP + Vicryl
ePTFE Bard
Proceed

2007 Jacob et al. [59] Pigs 10 Proceed Lap Parietex Composite PPL 28 days
Parietex Composite
PP

2007 Voskerician et al. [19] Rats cPTFE (MotifMESH) Open cPTFE (MotifMESH) PP (Marlex) 1 and 3 months
ePTFE (DualMesh) Composix
Composix
PP (Marlex)
▼ Proceed
2007 Novitsky et al. [18] Rabbits 20 PP (Marlex) Open ePTFE (DualMesh) PP (Marlex) 1 year
ePTFE (DualMesh)
Composix E/X
Proceed
2007 Bellón et al. [4] Rabbits 24 Parietex Composite Sequential Parietex Composite, Sepramesh 3, 7, and 14 days
Sepramesh lap PPL-PU 99
PP-PU 99
2008 Marcondes et al. [60] Rabbits 24 PP (Surgipro Mesh) Lap Sepramesh PP (Surgipro Mesh) 28 days
Sepramesh
Composix E/X
2008 Junge et al. [33] Rats 40 PVDF+PP (Dyna.Mesh) Open Parietene Composite PP 30 days
Parietene Composite
ePTFE (DualMesh)
PP
2008 Conze et al. [17] Rabbits co-PVDF Lap No differences No differences 7, 21, and 90 days
PP (Prolene)

 AlloDerm – Decellularized human dermis (LifeCell, Brachburg, NJ, USA)
 co-PVDF – Automanufactured mesh woven with PVDF polymer (Solvay, Brussels, Belgium)
 Composix – Nonwoven ePTFE (Davol, Cranston, RI, USA)
 Composix E/X – PP mesh sewn with PP stitching to a thin sheet of ePTFE (Davol, Bard,
Murray Hill, NJ, USA)
 Parietex Composite – Collagen-oxidized film-treated mesh (Sofradim, Trévoux, France)
 Poloxamer – Triblock copolymers consisting of a central hydrophobic block of polyethy-
lene glycol flanked by two hydrophilic blocks of polyethylene glycol
 PolyesterComposite – Polyurethane-covered Dacron mesh (Braun, Melsungen, Ger-
many)
Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation

 cPTFE (MotifMESH) – Nonwoven macroporous condensed PTFE (Proxy Biomedical, Gal-
way, Ireland)
 ePTFE (CV-4) – Automanufactured mesh woven out of ePTFE suture thread CV-4 (Gore &
Associates, Flagstaff, AZ, USA)
 ePTFE (DualMesh) – ePTFE (Gore & Associates, Flagstaff, AZ, USA)
 ePTFE (STP) – Gore-Tex Soft Tissue Patch, ePTFE with two laminar microporous surfaces
(Gore & Associates, Flagstaff, AZ, USA).
 Fluorosoft – Fluoropassivated polyester (Sulzer Vascutek, Renfrewshire, Scotland)
 Gelfilm – Pharmacia & Upjohn, a subsidiary of Pharmacia, Kalamazoo, MI, USA
 Hyalobarrier gel – Sterile, transparent, and highly viscous gel obtained by condensation
of hyaluronic acid (Fidia Advanced Biopolymers SRL, Abano Terme, Padova, Italy)
 Icodextrine – Iso-osmolar biodegradable –1,4-linked glucose polymer solution (Extra-
 PP (Marlex) – PP mesh (Bard, Murray Hill, NJ, USA)
 PP (Surgipro) – Monofilament PP mesh (AutoSuture, Norwalk, CT, USA)
 PP-PU 99 – Autodesigned prosthesis composed with a reticular PP mesh and a nonab-
sorbable 26-μm-thick polyurethane film
 Proceed – PP–polydioxanone composite with oxidated cellulose coating (Ethicon, So-
merville, NJ, USA)
 Prolene – PP mesh (Ethicon, Somerville, NJ, USA)
 PVDF + PP (DynaMesh) – Two-component (PP mesh and PVDF) monofilament mesh
(FEG Textiltechnik, Aachen, Germany)
 Seprafilm – Bioabsorbable translucent membrane composed of carboxymethylcellulose
and hyaluronic acid (Genzyme, Cambridge, MA, USA)
 Sepramesh – PP mesh coated on one side with a bioresorbable adhesion barrier (Sepra-
361

neal, Baxter Healthcare, Vienna, Austria)
 Interceed – Oxidized regenerated cellulose (Johnson & Johnson Medical, New Bruns-
wick, NJ, USA)
 Lyo-dura – Lyophilized dura mater (Braun-Dexon, Barcelona, Spain)
 Mersilene – Polyethylene terephthalate (Johnson & Johnson, Somerville, NJ, USA)
 MycroMesh – ePTFE (Gore & Associates, Flagstaff, AZ, USA)
 Parietene Composite – PP mesh bonded on one side to a collagen-oxidized film (Sofra-
dim, Trévoux, France)
film; Genzyme, Cambridge, MA, USA)
 Silastic – Polydimethylsiloxane prosthesis (Dow Corning, Midland, MI, USA)
 Surgipro Mesh – Single-layer PP mesh (U.S. Surgical, Norwalk, CT, USA)
 Surgisis – Derived from porcine small intestine submucosa (Cook, Strombeek-Bever,
Belgium)
 Tissucol – Fibrin glue (Baxter Healthcare, Vienna, Austria)
 Vicryl – Polyglactin 910 (Johnson & Johnson, Somerville, NJ, USA)
 Vipro II – PP/polyglactin 910 composite mesh (Johnson & Johnson, Somerville, NJ, USA)
47
 362 Chapter 47 · Effect of Different Mesh Materials on Adhesion Formation
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27. de Vries Reilingh TS, van Goor H, Koppe MJ, Bodegom
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31. Sikkink CJ, Vries de Reilingh TS, Malyar AW, Jansen JA,
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34. Harrell AG, Novitsky YW, Peindl RD, Cobb WS, Austin CE,
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35. Kayaoglu HA, Ozkan N, Hazinedaroglu SM, Ersoy OF, Erkek
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39. Martín-Cartes J, Morales-Conde S, Suárez-Grau J, López-
Bernal F, Bustos-Jiménez M, Cadet-Dussort H, Socas-
Macías M, Alamo-Martínez J, Tutosaus-Gómez JD, Mo-
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peritoneal adhesions in laparoscopic ventral hernia repair
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tacks. Surg Endosc. 2008;22(3):631–4
40. Martín-Cartes JA, Morales-Conde S, Suárez-Grau JM, Bus-
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363 47
of fibrin glue in the prevention of peritoneal adhesions in
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Reduction of postoperative adhesions to Marlex mesh
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50. Zieren J, Paul M, Osei-Agyemang T, Maecker F, Müller JM.
Polyurethane-covered dacron mesh versus polytetraflu-
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51. van ’t Riet M, de Vos van Steenwijk PJ, Bonthuis F, Mar-
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53. Gonzalez R, Rodeheaver GT, Moody DL, Foresman PA,
Ramshaw BJ. Resistance to adhesion formation: a com-
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abdominal wall reconstruction. Plast Reconstr Surg. Morales-Conde: No.

2004;114(2):464–73 Schumpelick: Did you remove a large area of peri-
55. Demir U, Mihmanli M, Coskun H, Dilege E, Kalyoncu
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thetic materials in incisional hernia repair. Surg Today. Morales-Conde: We have to analyze that in an-
2005;35(3):223–7 other study.
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57. Dilege E, Coskun H, Gunduz B, Sakiz D, Mihmanli M.
Prevention of adhesion to prosthetic mesh in incisional
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47 operative adhesion formation in the New Zealand White
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2008;12(1):58–61

Discussion

Kukleta: Did you observe in the last study more

seromas because you completely sealed the space
between the mesh and the defect?
Morales-Conde: The amount of glue is not even
2 cc for a 15×19 mesh. We are injecting this ex-
tra glue inside the sac. We saw a decrease of the
seroma.
Klinge: You mentioned that the fixation is respon-
sible for the pain. What do you think about the
importance of elasticity?
Morales-Conde: You have to think about the elas-
ticity of the mesh and of the capsule around the
mesh. We do not have that data as we never mea-
sured the elasticity of the abdominal wall in the
pigs.
Klinge: I think it is not only the capsule, but the
ePTFE without the capsule is not elastic at all.
Gryska: I am glad to see you recognizing that the
tackers can cause pain. Do you have experience
with gluing only without tacks?
 48

Tissue Ingrowth and Laparoscopic

Ventral Hernia Mesh Materials:
An Updated Review of the Literature
E. Honigsberg, D. Fowler, and B. Jacob
 366 Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials: An Updated Review of the Literature
Introduction
Laparoscopic ventral hernia repair (LVHR) is an
accepted means of treating incisional and ventral
hernias and has been associated with a number of
benefits, including low wound infection rates, low
recurrence rates, low postoperative pain rates, and
short hospital length of stay [1]. However, LVHR
requires the intraperitoneal placement of a mesh
prosthesis, which can increase the risk of visceral
adhesion formation and its sequelae [2]. In addi-
tion, there is a risk, although small, of recurrence
due to improper mesh fixation resulting from in-
adequate technique or inadequate adherence of the
mesh to the abdominal wall. Therefore, mesh used
for LVHR requires two unique properties: an anti-
adhesive side to minimize adhesions to the viscera
and a side that optimizes tissue ingrowth to mini-
48 mize recurrence rates and mesh migration. The
demand for this optimal two-sided prosthetic for
LVHR has led to the research and development of
a number of biomaterials specifically designed to
optimize adhesiveness to the peritoneum while de-
creasing adhesion formation to viscera. The focus
of this review article is to provide an updated lit-
erature review on the concept of fibrous ingrowth,
also known as tissue ingrowth, as it relates to the
use of two-layered mesh in LVHR.
Baseline intraabdominal pressures (IAPs) have
previously been studied in healthy humans us-
ing transduced pressures from transurethral blad-
der catheters [3]. While the mean pressure in the
supine position was 1.8 mmHg, the mean pres-
sures for sitting and standing were 16.7mmHg and
20.0 mmHg, respectively. The average pressure for
a cough was 107 mmHg. These are the estimated
pressures that an LVHR mesh would be exposed
to after insertion. Given the wide variety of mesh
products available for ventral hernia repairs, the
authors hypothesized that learning these baseline
IAP numbers could better direct the engineering
of mesh prosthetics and could arm surgeons with
the minimum benchmark pressures that a hernia
repair needs to withstand to avoid recurrence.
By studying the strength of tissue ingrowth
into the various mesh products, we can better
understand which materials can generate enough
ingrowth to stand up to daily IAPs and ultimately
prevent recurrences. We can also evaluate which
mesh products will not withstand normal pres-
sures and instead will require more permanent
fixation.
Physiology of Tissue Ingrowth
The optimal technique for mesh fixation to mini-
mize hernia recurrence rates remains debatable
and often focuses on the types and number of
sutures and tacks required [4]. In a porcine ca-
daver, the authors showed that the force required
to disrupt a single transfascial suture was sig-
nificantly greater than that required to disrupt a
spiral tack (67 N vs. 28 N, p<0.001). Although
the strength of a tack or a suture is interesting,
the published conclusions on mesh fixation in
human clinical studies usually fail to evaluate the
type of mesh used and that mesh’s ability to incite
tissue ingrowth from the peritoneal surface. The
mesh prostheses commonly used are known to
be both chemically and physically biocompatible;
however, they are not inert and instead induce a
multitude of host tissue responses, including tis-
sue ingrowth, that play a major role in a success-
ful LVHR [5].
Tissue ingrowth likely begins within hours of
the establishment of contact between the mesh
polymers and the peritoneal surface [5]. The initial
cellular events over the first 2 days are dictated
by an acute inflammatory response. Leukocytes,
macrophages, and mast cells are released and ac-
tivated. These inflammatory cells in turn release
growth factors and cytokines. By the 3rd day, this
process has lead to early angiogenesis from the
preexisting host microvasculature. Angiogenesis
continues with the formation of capillary buds
and sprouts that grow into and around the mesh
filaments. These sprouts ultimately interconnect
with each other and form a well-perfused micro-
vascular network. This neovasculature is required
for the formation of granulation tissue, which in
turn leads to incorporation of the mesh into native
tissue. After a period of only 2 weeks, the tissue
incorporation of the mesh implants continues on a
path of collagen synthesis similar to that found in
wound healing [5].
Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials
Animal studies have helped show that the tis-
sue ingrowth begins early and increases in strength
over time. In a porcine laparoscopic ventral hernia
model, Majercik et al. [6] demonstrated that the
bulk of tissue ingrowth occurs during the first
2 weeks after a polypropylene mesh is inserted, and
by 4 weeks the strength of the ingrowth has already
reached a strength equivalent to 95% of the peak
strength seen at 12 weeks [6]. By fixing sheets of
polypropylene/expanded polytetrafluoroethylene
(ePTFE) composite mesh to the abdominal walls
and then harvesting them at different time inter-
vals (2, 4, 6, and 12 weeks), the authors were able
to demonstrate a peel strength of 0.83 lb at 2 weeks,
1.06 lb at 4 weeks, and 1.13 lb at 12 weeks (5 N).
Histologic examination of specimens showed com-
plete cellular infiltration into and through the en-
tire layer of the polypropylene up to the ePTFE
layer. This study, which looked at the peel strength
of the polypropylene layer used in a heavyweight
polypropylene/ePTFE composite mesh, concluded
that the bulk of tissue ingrowth happens during
the first 2 weeks after implantation. At 4 weeks, the
strength then increases to a value that is equivalent
to 95% of the peak strength measured at 12 weeks
postimplantation.
It is now well accepted that this tissue in-
growth provides long-term adhesive strength to
the mesh. Interestingly, not all biomaterials are
equally incorporated into native tissue by this
cellular phenomenon. As early as 1995, Bellón et
al. published results that compared the cellular
response to, and subsequent tissue integration of,
two different mesh prostheses in a rabbit model
[7]. At the time, the two leading products were
made of only one material and were heavyweight
polypropylene and pure ePTFE. The authors sus-
pected that the two materials incited different lev-
els of inflammation and therefore implanted these
two meshes into the anterior abdominal wall of
rabbits, ensuring that each mesh was exposed to
the peritoneal cavity. Necroscopy was performed
at 14, 30, 60, and 90 days.
Microscopically, the host tissue response dif-
fered between the ePTFE and the polypropylene.
At the 2-week point, the ePTFE was encapsulated,
not infiltrated, with connective tissue, whereas
the polypropylene was infiltrated throughout
367 48
with loose scar tissue consisting mostly of mac-
rophages. Collagen fibers and strong evidence
of angiogenesis were not readily visible on the
ePTFE until 2 months after implantation, and by
3 months postimplantation, the connective tissue
was substantial and the cell population had stabi-
lized, consisting of mostly fibroblasts. In contrast
to the ePTFE, the polypropylene mesh demon-
strated complete integration into the host tissue.
The process of angiogenesis began within the first
2 weeks in the polypropylene mesh, and cells were
distributed within the interstices of the mesh. The
authors concluded that polypropylene incited a
more intense inflammatory foreign body reaction
and had superior tissue integration, and therefore
that ePTFE was more suitable for implantation
intraperitoneally, where it would be exposed to the
viscera, and polypropylene was better suited for
tissue integration [7].
After the development of two-sided (compos-
ite) mesh products, this variability of tissue inte-
gration among various mesh prostheses was again
demonstrated in a laparoscopic porcine model that
specifically looked at the tissue integration of the
same materials (polypropylene and ePTFE) but
in a two-sided mesh material [8]. By fixing sheets
of pure two-sided ePTFE mesh and of a heavy-
weight polypropylene/ePTFE composite mesh to
the abdominal wall in a porcine model, the authors
were able to study the differences in the strength
of tissue attachment to the two different materi-
als. Again, the meshes were evaluated at different
time intervals (2, 4, 6, and 12 weeks). The results
showed that the strength of tissue ingrowth was
significantly higher for the polypropylene com-
posite graft relative to the strength of ingrowth
into the pure ePTFE material at each time point.
For example, at 2, 4, and 12 weeks, the mean
peel strength for the ePTFE was 0.50 lb, 0.53 lb,
and 0.51 lb, respectively (0.51 lb equals 2.27 N).
This was significantly less (p<0.05) than the peel
strength of the polypropylene at 2, 4, and 12 weeks,
being 0.825 lb, 1.06 lb, and 1.12 lb, respectively
(equivalent to 3.68 N, 4.70 N, and 5.0 N).
The authors then looked at histology slides
and found that at 2 weeks, the polypropylene com-
ponent of the composite mesh was entirely in-
filtrated with fibroblasts and inflammatory cells,
 368 Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials: An Updated Review of the Literature
with collagen deposition occurring throughout the
polypropylene. The macroporous abdominal wall
surface of the ePTFE, however, showed no cel-
lular penetration through the ePTFE at 2 weeks.
The macropores were filled with benign-appearing
tissue, but no collagen deposition had occurred.
There were obvious differences in the histologic
reaction and peel strengths between the different
biomaterials, suggesting that tissue ingrowth and
peel strength were superior for the polypropyl-
ene layer of the polypropylene/ePTFE compos-
ite mesh compared with a pure ePTFE material
against the peritoneum [8].
The tissue ingrowth maturation process for
the polypropylene seems to reach 74% of its
maximum by 2 weeks and 95% of its maximum
by 4 weeks. Thus, the strength plateaus after a
12-week period of time in animal studies; how-
48 ever, there may be evidence that cellular turn-
over continues for up to a year, and the severity
of the continuing process may depend on the
type of mesh implanted. This degree of inflam-
mation produced in response to various LVHR
mesh products has recently been studied using
immunohistochemical testing for Ki-67, which
is an accepted and established marker of cell
proliferation and turnover [9]. In a rabbit study
that compared tissue ingrowth analysis between
a control of polypropylene and three mesh prod-
ucts–a heavyweight polypropylene/ePTFE com-
posite mesh (hPP), pure ePTFE, and a reduced-
weight polypropylene/oxidized regenerated cel-
lulose composite mesh (rPP)–the authors looked
at results 4 months and 12 months postimplanta-
tion. They found that the hPP mesh group had
significantly higher Ki-67 levels than the rPP
and ePTFE groups at 4 months. At 12 months,
a significant decrease in Ki-67 scores from the
4-month point was found in the rPP group only,
while the hPP group maintained elevated levels of
Ki-67. This interesting finding suggests that the
heavyweight polypropylene-based mesh material
incites an ongoing inflammatory process and scar
remodeling that lasts even 1 year later. This find-
ing was not seen with the lightweight polypropyl-
ene product or with the pure ePTFE. The way this
finding would translate into a human clinical set-
ting is unknown, but it may suggest that heavy-
weight polypropylene has relatively poor long-
term biocompatibility compared with lightweight
polypropylene and ePTFE. This poor biocompat-
ibility may lead to poor mesh compliance [9].
The compliance of the mesh implants may
change over time; the thicker the scar plate for-
mation that results from the fibrous ingrowth,
the less compliant the mesh may be in long-term
follow-up. Without a compliant mesh prosthesis,
the abdominal wall can become less pliable, and
clinically this may result in physical discomfort,
limitations in daily activities, and overall dissat-
isfaction. The group from Charlotte, North Caro-
lina, performed a rabbit comparison study and
within that study reported on mesh compliance
1 year after implantation [10]. Using a differenti-
ated variable reluctance transducer (DVRT) that
provided measurements of the axial forces re-
quired to stretch the mesh, the group reported
compliance data on pure polypropylene, a com-
posite mesh of polypropylene and ePTFE, pure
ePTFE, and a composite of lightweight polypro-
pylene and an oxidized cellulose layer. At 1 year,
they showed that the compliance of the pure
two-sided ePTFE mesh was superior to that of the
other three meshes.
Interestingly, using the same DVRT method to
then analyze the peel strength of the mesh products,
the group did not demonstrate a significant differ-
ence in peel strength among those four materials,
although the heavyweight polypropylene/ePTFE
composite trended toward having the greatest peel
strength. A number of rabbit studies published by
the same group showed no significant differences
in tissue ingrowth among ePTFE, lightweight poly-
propylene composite mesh, and heavyweight poly-
propylene composite mesh [10–12]. This finding
is not consistent with other published rabbit and
porcine studies that compared the same products
[8, 13], and it may be related to factors such as the
type of animal model used and the method of ob-
taining and calculating the peel strength.
In conclusion, while the polypropylene-based
mesh materials show superior tissue ingrowth and
superior peel strengths that may result in fewer re-
currences, the long-term compliance of the mate-
rial suffers, and this may have clinical sequelae yet
to be discovered.
Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials
Mesh Prostheses in Laparoscopic
Ventral Hernia Repair
Laparoscopic ventral hernia mesh is probably
best described as a foreign body, and it therefore
will be associated with a lifelong risk of potential
adverse host reactions [14]. Thus, it is important
to understand the different biomaterials currently
available in meshes designed for placement within
the abdominal cavity, along with the different reac-
tions they incite when placed intraabdominally. In
this review we will focus on polypropylene, polyes-
ter, and ePTFE, the three major materials used on
the peritoneal surface of these two-layered meshes.
A discussion of the newer bioabsorbable mesh ma-
terials is beyond the scope of this paper and can be
found in a more detailed review [15].
In 1958, Francis Usher introduced polypropyl-
ene mesh to the field of inguinal hernia repair [16].
Since then, polypropylene has become the most
frequently used mesh worldwide, and both heavy-
weight and lightweight polypropylene meshes are
in use [15]. Polypropylene is hydrophobic and con-
sists of a carbon backbone with alternating methyl
and hydrogen groups attached to the carbon chain.
It has been reported that in the long term, polypro-
pylene may be subject to oxidation, which in time
can change the compliance of the mesh material
[17]. In addition to polypropylene, polyester has
been widely used, and both two-dimensional (2D)
and three-dimensional (3D) polyester meshes are
available. Theoretically, a 3D weave provides more
scaffolding for tissue ingrowth. Polyester is a hy-
drophilic, carbon-based polymer that forms strong
fibers and, unlike polypropylene, has been shown
to resist oxidation [17]. If placed extraperitoneally,
either of these meshes can provide terrific tissue
ingrowth; however, in LVHR the mesh must be
placed intraperitoneally. Because of the significant
cellular ingrowth that these meshes incite, neither
polypropylene nor polyester should be used intra-
peritoneally, where they would be directly exposed
to the surface of the bowel. Instead, ePTFE is the
initial material that is safe to place against exposed
bowel [15]. It consists of a long carbon chain with
two side fluorine atoms per carbon. The two-sided
mesh of ePTFE has a microporous surface (3 μm
wide) on the visceral side and a macroporous
369 48
surface (>100 μm) on the peritoneal side. This
macroporous surface was engineered to encourage
maximal tissue ingrowth into a material originally
designed to minimize inflammatory responses.
The different mesh products can also be classi-
fied according to the physical properties of poros-
ity and pore size [16]. Macroporous meshes, such
as polypropylene and polyester, have pores >75 μm,
whereas microporous mesh such as ePTFE has
pores <10 μm in at least one dimension. The larger
pore size permits infiltration by macrophages, fi-
broblasts, blood vessels, and collagen fibers, al-
lowing for elimination of bacteria and rapid tis-
sue ingrowth. Macroporous mesh quickly becomes
fixed to tissue, whereas mesh with smaller pores
limits cellular infiltration and subsequent tissue
ingrowth [18]. A similar result was reported by
Klinge et al. in a rat model [19]. They found that
large-pore mesh was integrated in a loose net-
work of perifilamentary granulomas, leading to
improved integration and significantly less ongo-
ing inflammatory response, whereas smaller-pore
mesh was embedded only into granulomas, and
the scar tissue bridged the whole small pore, lead-
ing to less integration and intense ongoing chronic
inflammation. Their conclusions helped show the
advantages of a large-pore mesh material.
In addition to porosity, the structure of the
biomaterial plays a key role in the tissue reaction
to the prosthesis. Using a rabbit model, Bellón et
al. compared pure ePTFE in a laminar configura-
tion with a novel composite ePTFE made of the
same laminar layer but sewn to a reticular, wo-
ven parietal layer made of woven ePTFE suture
[20]. This allowed the authors to study ingrowth
differences between laminar ePTFE and reticular
(or woven) ePTFE. The results showed that after
14 days, the laminar mesh was encapsulated on its
subcutaneous aspect by dense scar tissue. Fibro-
blasts, macrophages, and other leukocytes were
present but colonized only the outer third of the
ePTFE sheet. Its visceral layer was associated with
a highly organized, thick neoperitoneum consist-
ing of connective tissue arranged in an even, par-
allel fashion. The reticular composite mesh had
a similar result for its laminar surface, but the
reticular surface was embedded in dense repair
tissue and demonstrated superior tissue ingrowth.
 370 Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials: An Updated Review of the Literature

⊡ Table 48.1. Commercially available two-layered mesh (ePTFE expanded polytetrafluoroethylene)

Composite mesh Visceral layer Parietal layer

DualMesh Microporous ePTFE Macroporous ePTFE

(Gore)

Proceed Surgical Mesh Oxidized, regenerated cellulose Reduced-weight polypropylene

(Ethicon) (encapsulated with polydioxanone polymer)

Parietex Composite Antiadhesive collagen (solution of oxidized Three-dimensional polyester weave

(Covidien) bovine atelocollagen type I, polyethylene
glycol, and glycerol)

Sepramesh Cellulose (carboxymethylcellulose) Polypropylene

(Genzyme)

C-Qur Omega-3 fatty acid bioabsorbable coating ProLite Ultra polypropylene

(Atrium)

Composix E/X Microporous PTFE Standard heavyweight polypropylene

(Bard)

48
Inflammatory cells extensively infiltrated the re-
ticular mesh filaments. As expected, with the use
of an Instron hydraulic-controlled tensiometer to
evaluate the peel strength of the tissue ingrowth,
the reticular mesh was significantly more adher-
ent than the laminar mesh (26.75 N vs. 14.11 N,
p<0.05) [20]. This finding shows that the type of
weave of the material, more so than the actual ma-
terial itself, is an important factor affecting tissue
ingrowth strength. This discovery helped lead to
the engineering of a number of other »composite«
or two-sided meshes.
The importance of both mesh porosity and
spatial structure to tissue ingrowth led to the de-
velopment of »second-generation« barrier meshes.
A summary of the two-layered mesh commercially
available today is provided in ⊡ Table 48.1.
Fibrous Ingrowth in Animal Models
Because it is difficult to evaluate fibrous ingrowth
in patients who have undergone LVHR, several
studies have focused on comparing tissue ingrowth
in different types of mesh prostheses in adhe-
siogenic rabbit or porcine laparoscopic ventral
hernia models. Several studies already mentioned
in this chapter compared pure two-sided ePTFE
mesh to heavyweight polypropylene/ePTFE and
lightweight polypropylene/carboxymethylcellulose
composite meshes. In a majority of the rabbit
models, no significant difference in peel strength
was found [9, 11], whereas in porcine models a
significant difference in peel strength was noted,
favoring the adherent strength of the heavyweight
polypropylene composite [8].
Recently, 3D polyester-based composite meshes
have also been used more often. One such compos-
ite mesh includes a 3D polyester parietal layer and
an antiadhesive barrier made of a polyethylene gly-
col, glycerol, and collagen mixture on the visceral
surface to prevent adhesions (Parietex Composite;
Covidien, Norwalk, CT, USA). A number of ani-
mal studies are available that compare it to other
leading mesh products currently in use [21–23].
In a porcine adhesiogenic laparoscopic ventral
hernia model, McGinty et al. compared the 3D
polyester/antiadhesive collagen composite mesh
to the pure two-layered ePTFE mesh (DualMesh;
Gore, Arizona), using heavyweight polypropylene
as a control [21]. After laparoscopic insertion and
survival for 4 weeks, the peel strength of the mesh
from the abdominal wall was analyzed using a
digital tensiometer and was found to be signifi-
cantly less for the pure ePTFE than for the poly-
ester/antiadhesive collagen composite mesh or the
Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials
pure polypropylene control (1.3 N/cm vs. 2.8 N/cm,
p=0.001, vs. 2.1 N/cm, p=0.05, respectively). His-
tologically there was excellent fibrous growth into
and through the polypropylene and the polyester
component of the composite mesh. There was no
tissue growth through the ePTFE. This finding sup-
ports the notion that complete tissue ingrowth can
be found in a 3D polyester mesh and that this leads
to superior adherence strength compared with the
peel strength seen with pure two-sided ePTFE.
In another study, the 3D polyester/antiadhe-
sive collagen composite mesh was then compared
to a heavyweight polypropylene/ePTFE composite
mesh (heavyweight polypropylene parietal layer)
[22]. The same porcine model was used. Again,
a pure polypropylene mesh was used as a control.
While the study reported on a number of variables,
regarding the issue of tissue ingrowth as measured
by the peel strength of the mesh from the abdomi-
nal wall, the authors concluded that the polyester
composite product and the polypropylene compos-
ite product were not significantly different regard-
ing abdominal wall adherence. This result suggests
that a 3D polyester mesh has fibrous ingrowth
properties similar to those of polypropylene mesh.
In yet another prospective randomized study
using the same adhesiogenic porcine model, the
3D polyester/antiadhesive collagen composite
mesh was compared to Proceed, a composite mesh
made of lightweight polydioxanone-polymer-en-
capsulated polypropylene on the peritoneal surface
and oxidized regenerated cellulose as the antiad-
hesive barrier on the visceral surface [23]. Again,
regular polypropylene was inserted as a control.
After 1 month the mesh was harvested, and as part
of the evaluation, peak peel strength was measured
using a digital force gage tensiometer (Omega
DFG51-10 microprocessor-based digital force
gage). The results showed that the peel strength
was significantly higher for the 3D polyester com-
posite mesh than for the encapsulated lightweight
polypropylene composite mesh (17.2 N vs. 10.7 N,
respectively; p<0.002). The authors concluded that
the 3D polyester composite mesh incited better
tissue ingrowth than the lightweight encapsulated
polypropylene composite mesh.
In a rabbit animal study, Judge et al. found
similar results when they compared the 3D poly-
371 48
ester/antiadhesive collagen composite mesh with
another composite mesh of lightweight poly-
propylene/carboxymethylcellulose (SepraMesh;
Genzyme) [24]. As part of their evaluation, they
reported the strength of mesh incorporation by
measuring the peel strength using an Instron 4502
tensiometer (Instron) at two time points, 1 month
and 5 months. They showed that the peel strength
of the 3D polyester/antiadhesive collagen compos-
ite mesh was superior to that of the lightweight
polypropylene/carboxymethylcellulose composite
mesh: 60.8 N vs. 42.6 N (p<0.001), respectively,
at 1 month and 70.9 N vs. 31.5 N (p<0.001) at
5 months. In their rabbit model, the 3D polyester
product had superior ingrowth at both time points
compared with the lightweight, nonencapsulated
polypropylene composite product.
Interestingly, most of the published animal
studies showed that the 3D polyester/antiadhe-
sive collagen composite mesh had significantly
more tissue ingrowth than the pure ePTFE and
two different lightweight polypropylene products.
However, the polyester composite mesh had no
significant difference in peel strength compared
with the heavyweight polypropylene composite
product. ⊡ Table 48.2 summarizes these extrapo-
lated peel-strength results from a select group of
animal studies that reported at least 4 weeks of
follow-up and also compared tissue ingrowth data
between two different mesh materials. Given such
terrific tissue ingrowth results for the 3D polyester
composite mesh, as were also found for the heavy-
weight polypropylene composite mesh, one might
be concerned about the long-term compliance of
this material. But to date, not enough data suggest
that the compliance of the polyester composite
mesh changes significantly over time.
Shortcomings of the Animal
Experiments
It is difficult to compare the tissue ingrowth re-
sults among the different animal studies. For one,
it is important to point out that the methods
used to obtain the peel-strength force varied. In
different studies, peel strength was obtained by
either a handheld microprocessor-based digital
 372 Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials: An Updated Review of the Literature

⊡ Table 48.2. Extrapolated peel-strength results from a select group of animal studies
(ePTFE expanded polytetrafluoroethylene; NS not significant)

First Animal Weeks Mesh 1 Mesh 2 Peel strength, Peel strength, Reported
author model (parietal layer) (parietal layer) mesh 1 mesh 2 p-value

McGinty Porcine 4 Pure ePTFE Polyester 1.3 N/cm 2.8 N/cm p=0.001
[21] composite

Duffy [22] Porcine 4 Heavyweight Polyester 5.1 N 4.8 N NS

Polypropylene composite
composite

Jacob [23] Porcine 4 Lightweight, Polyester 10.7 N 17.2 N p<0.002

coated composite
polypropyl-
ene composite

Iannitti [8] Porcine 12 Pure ePTFE Heavyweight 0.51 lb (2.27 N) 1.12 lb (4.98 N) p<0.05
polypropylene
composite

Judge [24] Rabbit 4, 20 Lightweight, Polyester 42.6 N, 31.5 N 60.8 N, 70.9 N p<0.001,
48 uncoated composite p<0.001
polypropylene
composite

tensiometry [21–23] , a servohydraulic-controlled
tensiometer made by Instron [8, 20], or a differ-
entiated variable reluctance transducer [9]. To our
knowledge, none of these peel-strength measur-
ing methods has been validated well, nor can the
reported results of each method be compared with
one another.
In addition to the different methods of obtain-
ing peel strength, the studies vary in the type of
animal model used. Some of the studies used a
rat or rabbit model and employed an open mesh
insertion technique, whereas other studies used
porcine models with either an open mesh insertion
or a laparoscopic mesh insertion technique. Some
of these models were »adhesiogenic,« and others
were not. If a mesh is inserted laparoscopically in
an adhesiogenic animal model, it can be assumed
that this would better represent the handling and
trauma that the material would be exposed to
during a human laparoscopic case. Some of the
models attempted to create a more adhesiogenic
environment by abrading the small bowel [21–23],
while other models did not [8–12].
Finally, the length of time a mesh was left in situ
before being analyzed varies among the studies.
Some studies evaluated the mesh at 1 month, and
others at a number of different time points up to
a year. Not shown in ⊡ Table 48.2 are the results
of the North Carolina group’s many rabbit studies
followed for up to a year, in which no significant
difference was found in the peel strength of the
various mesh products they tested [9–12]. These
findings that failed to show a difference in peel
strength may be attributable to factors related to
the animal species used, the method of obtaining
the peel strength, or the time the mesh was left in
place. Further, the results may not be reflective of
the behavior of the mesh in humans and are best
used to compare mesh material.
As mentioned earlier, the baseline IAP in hu-
mans when lying down, sitting, standing, and
coughing was shown in one study to be 1.8 mmHg,
16.7 mmHg, 20.0 mmHg, and 107 mmHg, respec-
tively [1]. While these baseline values are pressure
values reported in mmHg, as shown in this chapter,
most of the tensile strength data (the force required
to separate, or peel, the mesh prosthetic from the
tissue ingrowth formed on the peritoneal surface)
are shear-force values and are reported in either
pounds, newtons, or newtons per centimeter. Ac-
Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials
cording to standard physics conversion charts, a
pressure value (such as mmHg) cannot be con-
verted directly to or from a shear-force value (such
as newtons). Instead, to our knowledge, the for-
mula of pressure = force/area (N/m2) would need
to be employed. Therefore, the data reported in
most of these animal studies should be used only
to relatively compare the two or three mesh prod-
ucts within that particular study. The data should
probably not be extrapolated to make assumptions
about whether those measured peel-strength forces
are the same as the forces that would be required to
withstand the normal IAPs of daily living.
Conclusion
Armed with the knowledge of the varying levels
of tissue ingrowth and peel strength of the differ-
ent mesh products, the published clinical human
studies showing different recurrence rates may
make more sense. For instance, in a popular paper
published in 2003 that summarized a very large se-
ries of laparoscopic hernia repairs, Heniford et al.
reported a 4.7% recurrence rate after LVHR with
a pure ePTFE material [25]. Extrapolated in the
results is that approximately 20 of the 35 patients
with recurrences experienced these recurrences
for »unknown reasons.« It is certainly feasible that
some of these reasons were related to lack of ad-
equate tissue ingrowth through the ePTFE; more
permanent fixation is often required for that type
of mesh. Today, studies that neglect to comment
on the mesh material and its inherent proper-
ties to incite tissue ingrowth may be overlooking
an important early characteristic that reaches be-
yond the importance of whether to use a tack or
a suture. Of course, the ability of a mesh to stay
compliant over time may be just as important, if
not more so; therefore, the optimal prosthetic may
still be debatable.
As LVHR has become an accepted means of
dealing with a common surgical problem, the pur-
suit of an »ideal« mesh for intraperitoneal place-
ment continues. Animal studies suggest that the
different materials available today incite varying
levels of tissue ingrowth, which translates into
varying levels of adherence strength to the ab-
373 48
dominal wall. Both the 3D polyester composite
product and the heavyweight/ePTFE composite
product have superior adherence strengths com-
pared to reported results for the other materials.
That being stated, some evidence suggests that
the heavyweight polypropylene composite prod-
ucts incite long-term inflammatory changes and
even lose compliance over time, thus potentially
changing the long-term biocompatibility of that
product. Long-term compliance results following
the use of the polyester composite product are yet
to be reported.
The development of composite meshes is based
on the important physiologic phenomenon of fi-
brous tissue ingrowth, which is a well-described
cellular reaction to the placement of a mesh pros-
thesis. Many different animal studies illustrate well
the varying levels of tissue ingrowth and the long-
term results of that tissue ingrowth on the mesh
material. The ideal mesh must incite minimal ad-
hesions on its visceral aspect while also inciting
strong tissue ingrowth on its parietal surface and
avoiding continuous long-term scar remodeling
that may reduce its long-term biocompatibility.
References
1. Cobb WS, Kercher KW, Heniford BT (2005) Laparoscopic
repair of incisional hernias. Surg Clin North Am 85:91–103
2. Leber GE, Garb JL, Alexander AI, Reed WP (1998) Long-
term complications associated with prosthetic repair of
incisional hernias. Arch Surg 133:378
3. Cobb WS, Burns JM, Kercher KW, Matthews BD, Norton
HJ, Heniford BT (2005) Normal intraabdominal pressure in
healthy adults. J Surg Res 129:231–235
4. van’t Riet M, de Vos van Steenwijk PJ, Kleinrensink GJ,
Steyerberg EW, Bonjer HJ (2002) Tensile strength of mesh
fixation methods in laparoscopic incisional hernia repairs.
Surg Endosc 16:1713–1716
5. Laschke MW, Häufel JM, Thorlacius H, Menger MD (2005)
New experimental approach to study host tissue re-
sponse to surgical mesh materials in vivo. J Biomed Mater
Res A 74(4):696–704
6. Majercik S, Tsikitis V, Iannitti DA (2006) Strength of tissue
attachment to mesh after ventral hernia repair with syn-
thetic composite mesh in a porcine model. Surg Endosc
20(11):1671–1674
7. Bellón JM, Buján J, Contreras L, Hernando A (1995) Inte-
gration of biomaterials implanted into abdominal wall:
process of scar formation and macrophage response.
Biomaterials 16(5):381–387
 374 Chapter 48 · Tissue Ingrowth and Laparoscopic Ventral Hernia Mesh Materials: An Updated Review of the Literature
8. Iannitti DA, Hope WW, Tsikitis V (2007) Strength of tissue
attachment to composite and ePTFE grafts after ventral
hernia repair. JSLS 11(4):415–421
9. Novitsky YW, Cristiano JA, Harrell AG, Newcomb W,
Norton JH, Kercher KW, Heniford BT (2008) Immunohis-
tochemical analysis of host reaction to heavyweight-,
reduced-weight, and expanded polytetrafluoroethylene
(ePTFE)-based meshes after short-and long-term intraab-
dominal implantations. Surg Endosc 22:1070–1076
10. Novitsky YW, Harrell AG, Cristiano JA, Paton BL, Norton
HJ, Peindl RD, Kercher KW, Heniford BT (2007) Compara-
tive evaluation of adhesion formation, strength of in-
growth, and textile properties of prosthetic meshes after
long-term intra-abdominal implantation in a rabbit. J
Surg Res 140(1):6–11
11. Matthews BD, Mostafa F, Carbonell AM, Joels CS, Kercher
KW, Austin C, Norton HJ, Heniford BT (2005) Evaluation
of adhesion formation and host tissue response to intra-
abdominal polytetrafluoroethylene mesh and composite
prosthetic mesh. J Surg Res 123:227–234
12. Harrell AG, Novitsky YW, Cristiano JA, Gersin KS, Norton
48 HJ, Kercher KW, Heniford BT (2007) Prospective histologic
evaluation of intra-abdominal prosthetics four months
after implantation in a rabbit model. Surg Endosc
21(7):1170–1174
13. Greenawalt KE, Butler TJ, Rowe EA, Finneral AC, Garlick
DS, Burns JW (2000) Evaluation of Sepramesh biosurgical
composite in a rabbit hernia model. J Surg Res 94:92
14. Schumpelick V, Klinge U (2003). Prosthetic implants for
hernia repair. Br J Surg 90:1457–1458
15. Bachman S, Ramshaw B (2008) Prosthetic material in ven-
tral hernia repair: how do I choose? Surg Clin North Am.
88(1):101–112
16. Amid PK (1997) Classification of biomaterials and their
related complications in abdominal wall hernia surgery.
Hernia 1: 15–21
17. Costello CR, Bachman SL, Ramshaw BJ (2007) Materials char-
acterization of explanted polypropylene hernia meshes. J
Biomed Mater Res B Appl Biomater 83B(1):44–49
18. Gonzalez R, Ramshaw BJ (2003) Comparison of tissue in-
tegration between polyester and polypropylene prosthe-
ses in the preperitoneal space. Am Surg 69(6):471–476
19. Klinge U, Klosterhalfen B, Birkenhauer V, Junge K, Conze
J, Schumpelick V (2002) Impact of polymer pore size on
the interface scar formation in a rat model. J Surg Res
103:208–214
20. Bellón JM, Rodríguez M, Serrano N, San-Martín AC, Buján
J (2004) Improved biomechanical resistance using an
expanded polytetrafluoroethylene composite-structure
prosthesis. World J Surg 28(5):461–465
21. McGinty JJ, Hogle NJ, McCarthy H, Fowler DL (2005) A
comparative study of adhesion formation and abdominal
wall ingrowth after laparoscopic ventral hernia repair in a
porcine model using multiple types of mesh. Surg Endosc
19(6):786–790
22. Duffy AJ, Hogle NJ, LaPerle KM, Fowler DL (2004) Com-
parison of two composite meshes using two fixation
devices in a porcine laparoscopic ventral hernia repair
model. Hernia 8:358–364
23. Jacob BP, Hogle NJ, Durak E, Kim T, Fowler DL (2007) Tis-
sue ingrowth and bowel adhesion formation in an animal
comparative study: polypropylene versus Proceed versus
Parietex Composite. Surg Endosc 21(4):629–633
24. Judge TW, Parker DM, Dinsmore RC (2007) Abdominal
wall hernia repair: a comparison of Sepramesh and Pari-
etex Composite mesh in a rabbit hernia model. J Am Coll
Surg 204(2):276–281
25. Heniford BT, Park A, Ramshaw BJ, Voeller G (2003) Lap-
aroscopic repair of ventral hernias: nine years’ experience
with 850 consecutive hernias. Ann Surg 238(3):391–400
Discussion
Deysine: How could you standardize the opera-
tion? Were there histologic proofs of the peritoneal
defects?
Jacob: No, we have no histology of the small in-
testine and the peritoneum. We had only the stan-
dardized adhesiolysis.
Smeds: With regard to three-dimensional, is this
again a question of where we locate the prosthe-
sis?
Jacob: In this product, we think that there is
a difference between flat and three-dimensional
meshes. Is you look at electromicroscopy, you see
differences in neovascularization.
Franz: You really have two studies going on within
these experiments: one showing improved ab-
dominal wall ingrowth, breaking strength, and the
reduced adhesion on the peritoneal surface. Have
you thought whether they are related? Or do you
have an idea what the mechanism may be?
Jacob: I do not think they are related. I think that
the strong tissue ingrowth is a product of the mate-
rial construction, perhaps even the three-dimen-
sional quality; it clearly has a stronger adherence.
Whether or not this is clinically important to re-
duce recurrences we do not know. The companies’
task was to come up with the ideal mesh, maxi-
mize tissue ingrowth, and minimize adhesions. So
you can place the mesh intraperitoneally and feel
comfortable. I really believe, at least based on these
small studies, that this has done that.
 49

Porosity and Adhesion

in an IPOM Model
J. Conze, M. Binnebösel, C. Krones
 376 Chapter 49 · Porosity and Adhesion in an IPOM Model
As the advancing laparoscopic techniques for in-
cisional hernia repair depend on meshes suitable
for direct contact with the intestine, the search
for the ideal mesh for intraabdominal placement
continues. In the last decade, much effort has been
put into the search for the perfect intraperitoneal
onlay mesh (IPOM). The main problem in the
investigation of meshes is the complexity of adhe-
sion formation and the impossibility of measuring
this in the human body without further invasive
methods. Several meshes are available that pro-
vide some sort of adhesion barrier, but for each
of these meshes we have found counterexamples
of dense adhesions in our daily clinical routine. In
an experimental rat model investigating modern
meshes for IPOM repair, Junge et al. found an ad-
hesion area of more than 20% despite the kind of
adhesion barrier [4].
Meshes in the intraabdominal position must
always maintain a balancing act between tissue–
49 mesh ingrowth on the parietal side of the perito-
neum and mesh protection on the visceral side
of the peritoneum. To address the problem of
adhesion formation, two different approaches have
been followed to promote tissue ingrowth on the
parietal side and to minimize the formation of
intestinal adhesions on the visceral side.
One idea is the use of barriers involving physi-
cochemical pretreatment of a prosthesis, with the
aim of creating an interface between the bioma-
terial and its areas of contact. The pioneer of
this idea was Chevrel in 1982, when he placed a
polyglactin mesh between the mesh and the in-
testine. Since then, many different materials have
been introduced to reduce the adhesive potential
and to optimize the fibrocollagenous ingrowth,
including carboxymethylcellulose, amnion mem-
brane, phospholipids, hyaluronic acid, collagen,
and many more.
The other approach is the use of a composite
mesh made of several components, one of which is
designed to attenuate or even abolish the adhesion
formation process on the visceral side and enhance
the fibrocollagenous ingrowth on the parietal side.
Typical combinations of these composite meshes
include polypropylene with expanded polytetra-
fluoroethylene (ePTFE) or polyvinylidene fluoride
(PVDF).
So far, none of the available meshes can claim
to be completely antiadhesive. They can only re-
duce the quantity and grade of adhesions with-
out completely eliminating adhesion formation.
Kapische et al. analysed the literature and con-
cluded that there was no evidence demonstrating
the superiority of any of the available meshes for
intraabdominal placement [5].
The experimental models for investigations are
limited and the transferability from animals to hu-
mans confined. Moreover, most animal models do
not even mirror the clinical setting. These meshes
are usually experimentally implanted in a full-
thickness wall defect using the mesh in an inlay
bridging technique. Today this technique has been
abandoned because of too many complications.
Another drawback is that studies often try to com-
pare too many parameters within a single study. To
investigate the significance of a single factor, such
as pore size, the researchers should change only
this single factor and nothing else.
We have developed a standardised experimen-
tal model in the rabbit to investigate the adhesive
potential of intraabdominal mesh prostheses cor-
related with pore size [2, 3]. To study the adhesive
potential of intraabdominal meshes, it is important
to reduce other possible adhesive factors as much
as possible. One of the major factors is surgical
trauma; therefore, the meshes were placed by a
minimally invasive laparoscopic technique. The
laparoscopic incisions were placed in the lower
abdomen, with the mesh placed in the upper abdo-
men, far away from the incisions. The systematic
approach was realised by always changing only
one of the textile parameters in one experimental
line. Textile parameters that need to be considered
are the polymer (polypropylene, polyester, ePTFE,
PVDF), the filament diameter, the construction
(monofilament or multifilament), and the pore
size (⊡ Fig. 49.1).
Pore size has become one of the most im-
portant parameters in the world of lightweight,
large-pore meshes, first introduced by Klinge et al.
in 1996 [7]. The foreign body reaction is character-
ised by thickness of the perifilamental granuloma
around the mesh fibre. The smaller the pore size
and the more pronounced the granuloma that
develops, the more likely a bridging of these neigh-
Chapter 49 · Porosity and Adhesion in an IPOM Model
polymer Filament size Filament construction
Tensile strength Elasticity Weight
Mesh complications
Adhesions Shrinkage
bouring granulomas will occur, leading to a scar
bridging. It seems that every polymer itself has
its own bridging distance, e.g. polypropylene has
a bridging distance of approximately 1,000 μm.
Polypropylene mesh prostheses with a pore size
below 1,000 μm will inevitably lead to a complete
fibrocollagenous incorporation with a strong scar
plate formation.
Today there is some confusion due to mixing
up of the terms »lightweight mesh« and »large
pore.« Not every large-pore mesh is a lightweight
mesh, and not every lightweight mesh is a large-
pore mesh. This was well shown by Weyhe et al.,
who compared a heavyweight polypropylene mesh
with a lightweight polypropylene mesh, observ-
ing impaired biocompatibility for the lightweight
mesh due to its microporous construction [9]. A
pore size smaller than 200 μm is almost watertight;
above 200 μm, neovascularisation becomes possi-
ble, and only a pore size of more than 500–600 μm
allows ingrowth of soft tissue. The extent of fibro-
collagenous bridging has an impact of the quality
of the scar and its possible tissue contraction and
subsequent mesh area shrinkage.
Therefore, it is no longer sufficient to reduce
the description of meshes to weight alone. The
pore size or, more precisely, the porosity of meshes
is relevant for the biocompatibility in the host tis-
sue. Mesh porosity can be defined as a parameter
that provides the polymer-free space for tissue
ingrowth. Muhl et al. have recently published a
method to objectively measure the porosity of tex-
tile implants by an image analysis system, objecti-
fying in two dimensions the pores’ structure and
geometry [8]. This enables more empirical charac-
terisation of meshes. By adding the perifilamental
377 49
Pore size
Surface Handling
⊡ Fig. 49.1. Textile parameters of
synthetic meshes for hernia repair
Foreign body reaction and their influence on possible
complications
foreign body granuloma to the in vitro porosity of
meshes, the »effective porosity« can be defined.
Surgeons today must choose from more than
100 available hernia meshes. But mesh technol-
ogy has become a scientific world of its own, with
a terminology of its own. Many parameters have
an impact on the biocompatibility. The only at-
tempt at an internationally accepted classification
of meshes was undertaken by Amid back in 1997,
when the large-pore group was represented by
Marlex [1]. But today the large-pore meshes have
a pore size of up to 3,000 μm. Furthermore, we
now have new mesh polymers, such as PVDF, with
a monofilament structure but a molecular weight
much higher than polypropylene–heavyweight
meshes independent of the pore size.
There is no longer any reason to classify meshes
by their weight. What seems more important is the
amount of contact area between the mesh and the
host tissue surface. A multifilament mesh con-
struction increases the mesh surface by a factor
of 1.57 [6]. Enlargement of the pore size leads to
a reduction in total filament length and, therefore,
less mesh surface. There seems to be a correla-
tion between pore size/surface area and adhesive
potential. In our standardised IPOM rabbit model,
we placed pure polypropylene meshes of three dif-
ferent pore sizes (0.6 mm, 2.5 mm, and 3.5mm) in-
traabdominally by laparoscopy. We then measured
the amount of adhesion formation by planimetry
and evaluated the adhesions with a specific score
after 7, 21, and 90 days. We found a significant
difference in the degree of adhesion area and ad-
hesion score between the two large-pore mesh
constructions and the small-pore mesh for all time
points (⊡ Table 49.1).
 378 Chapter 49 · Porosity and Adhesion in an IPOM Model

⊡ Table 49.1. Influence of pore size (0.6 mm, 2.5 mm, 3.5 mm) on adhesion formation after 7, 21, and 90 days in a rabbit
model of laparoscopic intraperitoneal onlay mesh repair (PP polypropylene)

Planimetry (mm²) Score

n Mean SD Min Max n Mean SD Min Max

Material Days 5 1,121.7* 600.8 513.1 1,869.4 5 7.0* 2.0 5.0 9.0

PP 0.6 7

21 5 1,111.8* 484.9 568.8 1,696.5 5 7.8* 1.3 6.0 9.0

90 4 869.0* 499.8 396.2 1,538.5 4 7.5* 1.3 6.0 9.0

PP 2.5 7 5 244.2 135.4 125.1 410.4 5 3.0 0.0 3.0 3.0

21 5 351.9 190.9 45.8 565.7 5 3.0 0.0 3.0 3.0

90 5 141.6 112.0 0.0 307.1 5 2.4 1.3 0.0 3.0

PP 3.5 7 6 479.1 343.9 84.9 1,020.5 6 4.2 1.3 3.0 6.0

21 6 306.9 294.8 14.4 835.3 6 3.8 1.0 3. 5.0

90 5 4.9 10.9 0.0 24.4 5 0.6 1.3 0.0 3.0

49
It seems obvious that we need a new termi-
nology for modern meshes. Not all lightweight
meshes are lightweight meshes! A new parameter
to differentiate hernia meshes should consider the
mesh surface area and the effective porosity. The
influence of mesh construction (filaments, pore
size, geometry) is probably more important than
the polymer itself. In the experimental setting,
minimal-surface, large-pore meshes have shown a
reduced adhesive potential. Further studies should
focus on the right balance between fibrocollag-
enous ingrowth and adhesion formation.
References
1. Amid PK (1997) Classification of biomaterials and their
related complications in abdominal wall hernia surgery.
Hernia 1:15–21
2. Conze J, Junge K, Klinge U, Weiss C, Polivoda M, Oettinger
AP, Schumpelick V (2005) Intraabdominal adhesion for-
mation of polypropylene mesh. Influence of coverage of
omentum and polyglactin. Surg Endosc 19:798–803
3. Conze J, Rosch R, Klinge U, Weiss C, Anurov M, Titkowa
S, Oettinger A, Schumpelick V (2004) Polypropylene in
the intra-abdominal position: influence of pore size and
surface area. Hernia 8:365–372
4. Junge K, Binnebosel M, Rosch R, Jansen M, Kammer D,
Otto J, Schumpelick V, Klinge U (2009) Adhesion forma-
tion of a polyvinylidenfluoride/polypropylene mesh for
intra-abdominal placement in a rodent animal model.
Surg Endosc 23:327–333
5. Kapischke M, Schulz T, Schipper T, Tensfeldt J, Caliebe A
(2008) Open versus laparoscopic incisional hernia repair:
something different from a meta-analysis. Surg Endosc
22:2251–2260
6. Klinge U, Junge K, Spellerberg B, Piroth C, Klosterhalfen B,
Schumpelick V (2002) Do multifilament alloplastic mes-
hes increase the infection rate? Analysis of the polymeric
surface, the bacteria adherence, and the in vivo conse-
quences in a rat model. J Biomed Mater Res 63:765–771
7. Klinge U, Klosterhalfen B, Conze J, Limberg W, Obolenski
B, Ottinger AP, Schumpelick V (1998) Modified mesh for
hernia repair that is adapted to the physiology of the
abdominal wall. Eur J Surg 164:951–960
8. Muhl T, Binnebosel M, Klinge U, Goedderz T (2008) New
objective measurement to characterize the porosity of
textile implants. J Biomed Mater Res B Appl Biomater
84:176–183
9. Weyhe D, Belyaev O, Muller C, Meurer K, Bauer KH, Papa-
postolou G, Uhl W (2007) Improving outcomes in hernia
repair by the use of light meshes–a comparison of diffe-
rent implant constructions based on a critical appraisal of
the literature. World J Surg 31:234–244
Discussion
Deysine: I think we have not done enough investi-
gations about the capacity of collagen to contract.
Chapter 49 · Porosity and Adhesion in an IPOM Model
379 49
Conze: We have some data about the correlation of
foreign body reaction and shrinkage. The stronger
the foreign body reaction, the more shrinkage we
see.
Fitzgibbons: Don’t you think the reason why peo-
ple stick to ePTFE is because it has a long track
record? We have all these new adhesion barrier
materials now, but these materials are going to
break down; we will see the same problems as with
polypropylene. That is why the U.S. surgeons are
reluctant to move away from ePTFE.
Miserez: I have three questions: first, is there a
relationship between elasticity and pore size? Sec-
ond, how would monofilament polyester react?
Third, is there also a maximum size of the pores?
Conze: I have three answers: first, we have no idea
about the in vivo elasticity but I think the pore
size is of great importance. Second, again, it is just
a question of pore size. Monofilament polyester
with a large pore size could be a good material as
well. Third, that is a wonderful question! We saw
deformation and folding with 6-mm pore size in
mesh modifications – that was probably too much.
It depends on the memory effect of the mesh.
Schumpelick: Is it justified to make a two-dimen-
sional definition of porosity? Because we need a
definition for the three-dimensional meshes.
Conze: Yes, you are right.
 50

Benefit of Lightweight and/or Titanium

Meshes?
C. Schug-Paß, F. Köckerling
 382 Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?
Introduction
Despite numerous experimental investigations, the
search for an ideal mesh for laparoscopic intrap-
eritoneal use still has not concluded. Numerous
experiments, mainly conducted on open small ani-
mal models, have demonstrated the advantages of
meshes coated with absorbable materials, among
other things. But what are the characteristics of an
ideal intraperitoneal mesh? If we consider techni-
cal aspects, laparoscopic handling of the mesh
should be easy and safe. Meshes should have a per-
manent stability, but also a defined elasticity, and
they should resist infection. On the parietal side,
the abdominal wall flexibility should be preserved.
Maximal biocompatibility–that is, good integra-
tion into the surrounding tissue, with minimal
chronic inflammatory reaction–and minimal mesh
shrinkage, as well as low formation of adhesions to
intestinal structures, are required.
We know that heavyweight meshes with a
small pore size as well as polyester meshes induce
a strong inflammatory reaction with scar forma-
50 tion and, therefore, reduction in elasticity of the
abdominal wall. The development of lightweight,
large-pore, and monofilament polypropylene
meshes led to a reduction in chronic inflammation
and minimized the amount and strength of adhe-
sions to intestinal structures [1–3]. By comparing
composite meshes in a laparoscopic pig model,
McGinty et al. showed collagen-coated polyester
mesh (Parietex composite) to be the best biocom-
patible mesh so far, with good tissue integration
on one hand and only small adhesions to intesti-
nal structures on the other hand; this mesh was
compared with a heavyweight polypropylene mesh
and the DualMesh prosthesis made of expanded
polytetrafluoroethylene (ePTFE) for intraabdomi-
nal use [4].
Materials and Methods
Technical Data on the Meshes
First Experiment
Two different types of mesh were implanted, all of
them 10×15 cm:
1. DualMesh (Gore) is made of ePTFE. This is a
membrane-like prosthesis with a smooth and
a rough surface. The ePTFE meshes are tradi-
tionally used for the intraabdominal position.
2. TiMesh Light (GfE Medizintechnik) is made
of a monofilament lightweight (35 g/m2) and
large-pore (diameter about 1 mm) polypropyl-
ene mesh, which is titanium coated (thickness
about 30 nm). This coating makes the mesh hy-
drophilic and easy to place in the right position.
Second Experiment
Three different composite meshes, all 10×15 cm,
were implanted. All meshes consisted of a basic
structure made of a monofilament polypropylene
material in combination with various antiadhesive
components:
1. DynaMesh IPOM (Dahlhausen Medizintech-
nik) is a highly elastic polypropylene mesh
(28% at 32 N/cm) that is interwoven with a
polyvinylidene fluoride (PVDF) thread on
the visceral side. Based on the manufacturer’s
information, this material is endowed with an-
tiadhesive properties. The total weight of the
mesh was 108 g/m2.
2. Proceed (Ethicon) consists of a polypropylene
mesh (44 g/m2) and an absorbable coating
made of PDS (polydioxanone) and Interceed
(cellulose), with an absorption time of around
4 months.
3. Parietene Composite (Covidien Healthcare )
is a polypropylene mesh (73 g/m2) coated with
an absorbable film made of collagen, polyeth-
ylene glycol, and glycerol. This is absorbed
after 2–3 weeks.
Experimental Pig Model
A laparoscopic porcine model, which was officially
approved in accordance with the animal protec-
tion law, was used for comparing different meshes
for intraabdominal use. Six pigs in each group
were operated upon. The average weight of these
animals was 28 kg. Meshes were prepared with
10 1/0-ply polypropylene threads, and in the case
of ePTFE, with 10 one-ply ePTFE threads. The
implantation was accomplished using one 12-mm
Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?
383 50
and two 5-mm optic trocars. Meshes were intro-
duced into the abdominal cavity via the 12-mm
trocar, positioned in the middle/upper abdomen.
They were then fixed with transfascial sutures.
After 3 (first experiment) or 4 months (second
experiment), the animals were sacrificed. A di-
agnostic laparoscopy was performed. Afterwards,
the whole mesh, including the surrounding tissue,
was removed. Adhesion areas and the dimensions
of the mesh were measured in the fresh specimen.
The data were entered into the computer and sub-
mitted for planimetric analysis. a

Histology

Five specimens of each mesh were taken. After

fixation in formaldehyde, they were prepared with
different staining methods to analyse the partial
volume of inflammatory cells and the proportion
of macrophages, monocytes, and T-lymphocytes.
The apoptotic index was determined by immuno-
histochemistry with the aid of in situ end-labelling.
For quantification of the extent of cell prolifera-
tion, the sections were incubated with the antibody
b
Ki67. The morphometric analysis was performed
at the interface within a distance of 300 μm of the
⊡ Fig. 50.1. Results of first experiment. a The greater omen-
filament. tum adhered in a discrete manner to all implants (except for
one DualMesh case). b Titanium-coated meshes were in good
contact with the tissue and revealed little folding
Statistics

Graphic and statistical analysis was performed
with the SPSS 14.0 statistical program. The results
were presented as mean values and standard devia-
tions. Statistical analysis (analysis of variance) was
carried out to determine significance levels, show-
ing statistical significance for p-values <0.05.
Results
First Experiment
Macroscopic Results
In none of the cases did the diagnostic laparos-
copy reveal adhesions to the small bowel. With
the exception of one case (DualMesh), the greater
omentum adhered in a discrete manner to all im-
plants (⊡ Fig. 50.1a). In all cases, sharp dissection
was needed to separate the omentum from the
mesh surface. In particular, in the group receiv-
ing DualMesh, shrinkage as a result of folding was
already evident at laparoscopy and was even more
evident in the explanted specimen, whereas the
titanium-coated meshes were in good contact with
the tissue and revealed little folding (⊡ Fig. 50.1b).
On macroscopic inspection, the meshes were cov-
ered with a shiny layer in the adhesion-free areas,
but the underlying layer differed in consistency on
palpation. This induration was particularly seen
with the PTFE implants.
The morphometric evaluation of the preopera-
tive and postoperative mesh dimensions revealed a
 384 Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?

Planimetric data
100%

90% Shrinkage
Adhesions
80%

70%

60%

50%

40% a
43%
30%

20%
23%
10% 20%
9%
0%
TiMesh light DualMesh

⊡ Fig. 50.2. Macroscopic results of first experiment

50
significantly smaller contact area for the DualMesh,
due in the first instance to the pronounced folding
of the mesh. In contrast to the titanium-coated
polypropylene mesh, the remaining mesh area was
almost one-half of the initial area (57.0±13.1%).
The mean area of the titanium-coated mesh was
80.0±4.1% (p=0.006; ⊡ Fig. 50.2).
The area of adhesions to the greater omentum
was smaller for the titanium-coated polypropyl-
ene mesh–on average, 9.0±5.4%–compared with
23.2±13.8% for the DualMesh, but because of a
high standard deviation, this was not significant
(p=0.055; ⊡ Fig. 50.2).
Histology and Immunohistochemistry
The microscopic slides showed the polypropylene
meshes firmly integrated within the surrounding
tissue, with only mild scar formation and for-
mation of a neoperitoneum, with each individ-
ual fibre being surrounded by connective tissue
(⊡ Fig. 50.3a). As a result, the connective tissue
structures were not always uniformly arranged. No
foreign body giant cells were seen in the vicinity of
the meshes.
b
⊡ Fig. 50.3. Results of first experiment. a The polypropyle-
ne meshes were firmly integrated within the surrounding
tissue, with only mild scar formation and formation of a
neoperitoneum, with each individual fibre being surrounded
by connective tissue. b The polytetrafluoroethylene meshes
were embedded within scar tissue, and a strong inflammatory
reaction was seen. The connective tissue fibres were mainly
arranged in parallel
In the case of PTFE, the shrunken meshes
were embedded within scar tissue, and a strong
inflammatory reaction was seen. Owing to the
small size of pores in the membrane, however, a
permanent »through-growth« of connective tissue
had not taken place, so there was no firm fixation
to the peritoneum. Rather, the picture was of an
encapsulated membrane with additional calcifica-
tions also seen. As a result of the smooth surface
of the membrane, the connective tissue fibres were
mainly arranged in parallel (⊡ Fig. 50.3b).
Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?
385 50
Histopathologic data
40
PV (% )
Ki 67 29.2
30
AI (% )

20.3
20
14
a
9.3
10 7.5
3.3

0
TiMesh light DualMesh

⊡ Fig. 50.4. Histopathologic results of first experiment (PV

partial volume of inflammatory cells; AI apoptotic index)

With regard to the partial volume of the in-

flammatory cells, the median figures were lowest
for TiMesh Light (20.3±2.1%) and were signifi- b
cantly higher for DualMesh (29.2±5.5%, p=0.009;
⊡ Fig. 50.4).
Investigations with the proliferation marker
Ki67, a sign of cell activity, again showed the
highest figures for DualMesh (14.0±3.9%), which
were thus also significantly higher than for TiMesh
(7.5±3.3%, p=0.011; ⊡ Fig. 50.4).
Finally, evaluation of the apoptotic index as a
sign of cell turnover with consecutive cell death
again revealed the highest figures for the ePTFE
membranes. The figure here was 9.3±2.5%, which
was again significantly higher than for the titanium-
coated polypropylene meshes (3.3±2.7%, p=0.002; c
⊡ Fig. 50.4).
⊡ Fig. 50.5a–c. Results of second experiment. More or less wi-
despread adhesions to the greater omentum were noted for
Second Experiment all meshes; these were often seen around the mesh margins

Macroscopic Results
In no case did laparoscopic diagnosis show any
adhesions to the intestinal structures, but these
were seen in some cases to the parenchymatous
organs depending on the position of the mesh
and its contact with the liver and spleen. More or
less widespread adhesions to the greater omentum
were noted for all meshes. These were often seen
around the mesh margins (⊡ Fig. 50.5a–c).
 386 Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?

Adhesions

DualMesh 25.0%

TiMesh light 9.0%

Parietene Composite 12.8%

DynaMesh 33.2%

Proceed 31.6%
⊡ Fig. 50.6. Results of second
experiment: adhesions 0% 20% 40% 60% 80% 100%

Mesh surface at explantation

DualMesh 57.0%

TiMesh light 80.0%

Parietene Composite 86.0%

50
DynaMesh 85.0%

Proceed 75.0%
⊡ Fig. 50.7. Results of second experi-
ment: mesh surface at explantation 0% 20% 40% 60% 80% 100%

A reflecting surface, attesting to an intact neo-
peritoneum, was observed in those areas of the full-
wall specimens that did not harbour any adhesions.
Only by resorting to sharp dissection was it possi-
ble to detach, in particular, the greater omentum in
areas with adhesions. The density of adhesions did
not differ among the meshes. Parietene Composite
had the fewest adhesions. Planimetric analysis re-
vealed a 12.8±9% adhesion surface to the greater
omentum for Parietene Composite. As such, this
was markedly less than that evidenced by Proceed,
but this finding was not significant (31.7±18.5%,
p=0.06). Compared with DynaMesh IPOM, there
was a significant difference (33.2±11.9%, p=0.01;
⊡ Fig. 50.6).
There was no evidence of any major fold-
ing in any of the meshes on macroscopic inves-
tigation. The greatest reduction in mesh surface
was seen with Proceed (25.0±7.5%). This shrink-
age was significantly higher than in DynaMesh
IPOM (14.2±7.1%, p=0.03) and was likewise sig-
nificantly higher than in Parietene Composite
(14.0±8.6%, p=0.04), which produced comparable
values (⊡ Fig. 50.7). The results are summarised in
⊡ Table 50.1.
All meshes were completely integrated into the
abdominal wall.
Histology and Immunohistochemistry
Histology showed only minor signs of a chronic
inflammatory reaction. The polypropylene meshes
were all well integrated into the surrounding tissue.
Formation of the neoperitoneum was complete in
the adhesion-free areas (⊡ Fig. 50.8a–c).
Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?
a the DynaMesh IPOM and Parietene Composite
b
c
⊡ Fig. 50.8a–c. Results of second experiment. The polypro-
pylene meshes were all well integrated into the surrounding
tissue. Formation of the neoperitoneum was complete in the
adhesion-free areas
The partial volume of inflammatory cells
showed the lowest values for Parietene Composite.
With a value of 6.6±2.9%, this was significantly
lower than for Proceed, at 14.7±4.6% (p=0.006),
or for DynaMesh IPOM, at 19.7±7.8% (p=0.007).
The Ki67-positive cells in a proliferation stage were
also significantly lower for Parietene Composite, at
387 50
4.5±2.7%, than for Proceed (10.8±5.7%, p=0.04) and
were markedly, but not significantly, lower than for
DynaMesh IPOM (7.2±6.7%, p=0.4). The apoptotic
index, as a marker of cell death, was very low for
all meshes, and no significant differences were seen
(DynaMesh IPOM 1.2±0.4%, Proceed 1.5±0.8%,
Parietene Composite 1.7±0.8%; ⊡ Fig. 50.9).
Overall, Parietene Composite scored best in
the macroscopic as well as the histologic investiga-
tions. In terms of shrinkage of the mesh surface,
meshes scored equally well and were superior to
Proceed. Findings are summarised in ⊡ Table 50.1.
Discussion
Numerous publications, including those of an ex-
perimental nature, concentrate mainly on the ex-
tent and pathology of adhesions. In this regard,
polypropylene meshes have proven to be consid-
erably inferior to ePTFE meshes. In our study
we were able to show that the lightweight and
large-pore TiMesh Light is associated with fewer
adhesions than ePTFE mesh, and in no cases were
intestinal adhesions seen. This confirms that the
structure of the material employed is of decisive
importance for this phenomenon. The reduction
in material and increase in pore size represent
a considerable improvement over the original
heavier polypropylene mesh [1, 3, 5–7].
The adhesions of the intestine to the mesh de-
scribed in other publications [8–10] were not seen
in our experiments. A major factor here is certainly
the minimally invasive placement of the mesh and
the lack of previous adhesiolysis or injury of the
peritoneum. Adhesion reactions include that of
the tissue to foreign material, which, in the case
of intraperitoneal meshplasty, takes place at the
peritoneum–mesh interface.
As also borne out by our series of experiments,
the collagen-coated mesh has performed very well
in all tests. In most cases, Parietex Composite
mesh (with polyester) was used [4, 11–14], and in
some cases Parietene Composite mesh (with poly-
propylene) was used [14–17].
Proceed showed a higher rate of adhesions.
However, the cellulose-based coating, albeit in
 388 Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?

⊡ Table 50.1

Dynamesh IPOM Proceed Parietene Composite

Shrinkage rate (%) 14.2±7.1 25.0±7.5 14.0±8.6

(p=0.029 vs. Proceed) (p=0.041 vs. Proceed)

Adhesion rate of the greater 33.2±11.9 31.7±18.6 12.8±9.9

omentum (%) (p=0.01 vs. Dynamesh)

Partial volume of inflammatory 19.7±7.8 14.7±4.6 6.5±2.9

cells (%) (p=0.007 vs. Dynamesh)
(p=0.006 vs. Proceed)

Proliferation Ki67 (%) 7.2±6.7 10.8±5.7 4.5±2.7

(p=0.04 vs. Proceed)

Apoptotic index (%) 1.2±0.4 1.5±0.8 1.7±0.8

Macrophages/monocytes activity 12.5±2.2 5.5±2.9 3.8±2.2

(CD 68) (p=0.001 vs. Dynamesh) (p<0.001 vs. Dynamesh)

Extracellular matrix 55.8±35.2 37.4±22.4 20.8±8.8

TGF-ß

30

50 25

20

15 PV (%)
Ki67 (%)
AI (%)
10

⊡ Fig. 50.9. Histopathologic

results of second experiment 0
(PV partial volume of inflamm- DualMesh TiMesh light Parietene DynaMesh Proceed
atory cells; AI apoptotic index) Composite

combination with hyaluronic acid (Sepramesh),
appears to confer advantages in principle, as at-
tested to by some experimental studies [14, 16,
18–23]. It is possible that the combination with
the slowly absorbable PDS (polydioxanone) plays
a role because degradation of the material over
a 3–4-month period provokes an acute inflam-
matory reaction. However, by that stage, these
differences are reflected at a cellular level only
in terms of the partial volume of the inflamma-
tory cells. Apart from that, no significant differ-
ences were seen between Proceed and Parietene
Composite regarding the chronic inflammatory
reaction.
The adhesion rate of DynaMesh IPOM was
on a par with that of Proceed. The widespread
Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?
chronic inflammation no doubt played a role here.
To what extent this is also determined by the
surface structure (i.e. porous structure) or the
amount of material used is something that can be
conjectured only from other experimental find-
ings [24, 25].
Greater attention needs to be paid to the ef-
fect of shrinkage. The pathophysiological reac-
tions involved in this phenomenon are extremely
complex, with shrinkage of the material being
the last link in the body’s chain of reactions to
the foreign material. This reaction appears to be
clearly related to the site of mesh placement and
also to the amount and structure of the material
[2, 26–28]. This would also explain the observa-
tion that, over the long term, polypropylene mesh,
fixed in an identical manner, shows considerably
less tendency to shrink than does ePTFE. These
reactions appear to persist over a period of years,
as Klinge et al. were able to show in explanted
meshes [2, 27].
Because PTFE is not really a mesh, but rather
a membrane, it cannot be completely integrated
despite the texturing of the surface in contact
with the abdominal wall. The presence of pores
in the mesh makes it possible for the individual
mesh fibres to become incorporated within the
process of neoperitoneum formation. In contrast,
a capsule formed around the foreign material is
consolidated by the chronic inflammatory reac-
tion that occurs. The cellular reaction induced
by the material is considerably greater in the
case of implanted membranes in comparison with
lightweight structured meshes, as we were able
to demonstrate by examining the partial volume
of the inflammatory cells. Increased inflamma-
tory activity is accompanied by an increase in cell
proliferation. During the course of this process,
cell death (apoptosis) also rises, which is reflected
in an increase in the apoptosis index. All three
factors were significantly elevated with the ePTFE
membrane.
For the titanium-coated mesh, the average
shrinkage in the intraperitoneal position was only
18%, in contrast to 43% for the DualMesh.
In our second experiment, apart from Pari-
etene Composite, DynaMesh IPOM showed the
lowest shrinkage rate despite the fact that the re-
389 50
maining inflammatory parameters, including the
adhesion rate, were markedly higher than those of
Proceed or Parietene Composite. Presumably this
is attributable to the mesh’s very good elasticity,
which counteracts a shrinkage reaction.
As expected, mesh integration into the abdom-
inal wall was assured thanks to the textile structure
of the polypropylene material used in all meshes,
in the absence of any major chronic inflammatory
reaction. Through-growth of the individual poly-
propylene fibres confers a high degree of fixation
strength, which is preserved even after reduction
of the polypropylene material.
Conclusions
On the basis of our results, we must conclude
that the titanium-coated polypropylene mesh is
suitable for laparoscopic intraperitoneal repair of
abdominal wall and incisional hernias and that it is
comparable to DualMesh with regard to adhesions
but is clearly superior in terms of shrinkage. So
over the long term, it is likely to be associated with
a reduction in recurrence rates.
The collagen coating of the polypropylene
mesh appears to confer important advantages in
terms of biocompatibility, with implications for
the adhesion and shrinkage profiles of the mesh
material.
No doubt, improvements can still be made re-
garding handling, composition of the coating, and
tendency towards infection. Further research and
experimental investigations, as well as prospective
randomised clinical trials, are thus needed.
References
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50 190:271–280
9. Bellon JM, Contreras LA, Pascual G, Bujan J. Neoperitoneal
formation after implantation of various biomaterials for
the repair of abdominal wall defects in rabbits. Eur J Surg
1999; 165:145–150
10. Matthews BD, Pratt BL, Pollinger HS, Backus CL, Kercher
KW, Sing RF, Heniford BT. Assessment of adhesion forma-
tion to intra-abdominal polypropylene mesh and polytet-
rafluoroethylene mesh. J Surg Res 2003; 114:126–132
11. Bellon JM, Garcia-Carranza A, Jurado F, Garcia-Honduvilla
N, Carrera-San Martin A, Bujan J. Peritoneal regeneration
after implant of composite prosthesis in the abdominal
wall. World J Surg 2001; 25:147–152
12. Bellon JM, Garcia-Honduvilla N, Jurado F ,Garcia-Carranza
A, Garcia-Moreno F, Martin AC, Bujan J. Use of composite
prostheses in the repair of defects in abdominal wall:
prosthetic behaviour at the peritoneum. Eur J Surg 2001;
167:666–671
13. Bellon JM, Jurado F, Garcia-Honduvilla N, Lopez R, Car-
rera-San Martin A, Bujan J. The structure of a biomaterial
rather than its chemical composition modulates the
repair process at the peritoneal level. Am J Surg 2002;
184:154–159
14. Gonzalez R, Rodeheaver GT, Moody DL, Foresman PA,
Ramshaw BJ. Resistance to adhesion formation: a com-
parative study of treated and untreated mesh products
placed in abdominal cavity. Hernia 2004; 8:213–219
15. McGinty JJ, Hogle NJ, McCarthy H, Fowler DL. A compa-
rative study of adhesion formation and abdominal wall
ingrowth after laparoscopic ventral hernia repair in a
porcine model using multiple types of mesh. Surg Endosc
2005; 19:786–790
16. Schug-Paß C, Sommerer F, Tannapfel A, Lippert H, Kö-
ckerling F. The use of composite meshes in laparoscopic
repair of abdominal wall hernias–are there differences
in biocompatibility? Experimental results obtained in a
laparoscopic porcine model. Surg Endosc 2009; 23:487–
495
17. Sikkink CJJM, Vries de Reilingh TS, Malyar AW, Jansen JA,
Bleichrodt RP, van Goor H. Adhesion formation and reher-
niation differ between meshes used for abdominal wall
reconstruction. Hernia 2006; 10:218–222
18. van´t Riet M, Burger WA, Bonthuis F, Jeekel J, Bonjer HJ.
Prevention of adhesion formation to polypropylene mesh
by collagen coating: a randomized controlled study in
a rat model of ventral hernia repair. Surg Endosc 2004;
18:681–685
19. Alimoglu O, Akcakaya A, Sahin M, Unlu Y, Ozkan OV, Sanli
E, Erylmaz R. Prevention of adhesion formations following
repair of abdominal wall defects with prosthetic materials
(an experimental study). Hepatogastroenterology 2001;
50:725–728
20. Besim H, Yalcin Y, Hamamci O, Arslan K, Sonisik M, Kork-
maz A, Erdogan S. Prevention of intraabdominal adhesi-
ons produced by polypropylene mesh. Eur Surg Res 2002;
34:239–243
21. Burger JW, Halm JA, Wijsmuller AR, ten Raa S, Jeekel J.
Evaluation of new prosthetic meshes for ventral hernia
repair. Surg Endosc 2006; 20:1320–1325
22. Dilege E, Coskun H, Gunduz B, Sakiz D, Mihmanli M.
Prevention of adhesion to prosthetic mesh in incisional
ventral hernias: comparison of different barriers in an
experimental model. Eur Surg Res 2006; 38:358–364
23. Felemovicius I, Bonsack ME, Hagerman G, Delaney JP. Pre-
vention of adhesions to polypropylene mesh. J Am Coll
Surg 2004; 198:543–548
24. Kayaoglu HA, Ozkan N, Hazinedaroglu SM, Ersoy OF, Erkek
AB, Koseoglu RD. Comparison of adhesive properties of
five different prosthetic materials used in hernioplasty. J
Invest Surg 2005; 18:89–95
25. Bellon JM, Rodriguez M, Garcia-Honduvilla N, Pascual G,
Bujan J. Partially absorbable meshes for hernia repair offer
advantages over nonabsorbable meshes. Am J Surg 2007;
194:68–74
26. Weyhe D, Belyaev O, Müller C, Meurer K, Bauer KH, Papa-
postou G, Uhl W. Improving outcomes in hernia repair
by the use of light meshes–a comparison of different
implant constructions based on a critical appraisal of the
literature. Word J Surg 2007; 31:234–244
27. Klinge U, Klosterhalfen B, Müller M, Ottinger AP, Schum-
pelick V (1998) Shrinking of polypropylene mesh in vivo:
an experimental study in dogs. Eur J Surg 1998; 164:965–
959
28. Klinge U, Klosterhalfen B, Müller M, Schumpelick V. For-
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minal wall hernias. Eur J Surg 1999; 165:665–673
Chapter 50 · Benefit of Lightweight and/or Titanium Meshes?
391 50
Discussion

Amid: Adhesion formation is not as important as

what the intestine adheres to. Formation of intes-
tinal fistula is something very slow; the longest
reported period was 15 years. Now the decision
of which meshes to use depends on the adhesive
property. But what matters is what the bowel ad-
heres to.
Schug-Paß: In our experiment, we did not violate
the peritoneum. There were only adhesions to the
omentum and not to the intestine. We think that if
there is a neoperitoneum formation that covers the
meshes, there is no problem.
Kukleta: The mesh that you chose as the best one
was the first mesh that I used. But I left it because
of the number of adhesions in patients that I had
to reoperate. And if it is even covered with neo-
peritoneum, you cannot prevent adhesions with it.
Deysine: Is this a thin film of titanium on the
mesh?
Schug-Paß: It is a special technique invented by
GFE. The coating of the lightweight meshes makes
no difference, but it might be different with heavy
meshes. One advantage is that the titanium coat-
ing makes the polypropylene hydrophilic and thus
easier to handle.
Desine: I thought polypropylene was hydrophilic
on its own.
Schug-Paß: No.
 51

ePTFE Prostheses and Modifications

G. Pascual, J. M. Bellón
 394 Chapter 51 · ePTFE Prostheses and Modifications
Introduction
Expanded polytetrafluoroethylene (ePTFE) is a
microporous, laminar, hydrophobic prosthetic ma-
terial with a negative charge. It is composed of
compact nodules interlinked by fine fibers. The
length of these fibers determines the material’s
internodal distance and pore size.
The first report of the use of polytetrafluoro-
ethylene for the repair of abdominal wall defects
was that by Harrison in 1957 [1], whose results
were certainly promising. However, the perfor-
mance of this material in woven form as a prosthe-
sis was so disappointing [2] that its clinical use was
soon abandoned.
A few years later, in 1963, Oshige [3] described
a method of expanding polytetrafluoroethylene,
preserving its microstructure and increasing its
mechanical resistance. This process was refined
by Gore [4] and applied in the manufacturing of
vascular prostheses for clinical use. This was fol-
lowed by further significant expansion to provide
a layered material that could be used to repair her-
nias and other soft tissue defects. The first of these
prostheses used to repair parietal defects in the
51 abdomen was the Soft Tissue Patch (STP).
The behavior of ePTFE in the repair of abdom-
inal wall defects was initially studied in the labo-
ratory. The works of Elliot and Juler in 1979 [5]
revealed the good biological tolerance of this mate-
rial, and Sher et al. [6], in 1980, were the first to
describe its superior peritoneal behavior compared
with polypropylene. This finding was highlighted
by Lamb et al. [7], who observed that the inflam-
matory response to an ePTFE implant was mini-
mal. Subsequent experimental studies [8–11] con-
firmed the favorable behavior of the ePTFE patch
at the peritoneal interface. Taking advantage of this
particular behavior, Walker et al. [12] were the first
to elaborate a composite prosthesis in which poly-
propylene was combined with a layer of ePTFE on
the peritoneum-facing side of the implant. Using
similar composites, good results were reported in
experimental studies conducted by other authors
[13, 14] and even in clinical practice [15].
The work of Bauer et al. [16] introduced the
use of ePTFE in clinical hernia repair in the form
of the STP, although in earlier publications [17, 18]
the advantageous behavior of ePTFE had already
been described. These authors [16] reported that
in 28 operated patients, this material induced a
good tissue response as well as a minimal inflam-
matory response and infiltration of fibroblasts and
collagen in the interstices of the prosthesis. At
10.7%, their hernia recurrence rate was compara-
ble to those quoted later by other authors [19–22].
In a clinical study of patients with incisional
hernias, Van der Lei et al. [23] described the need
for prosthetic overlap of the tissue defect and a
double suture to fix the prosthesis to avoid rehernia-
tion. In addition, as had been described by others in
experimental studies, the favorable behavior of STP
at the peritoneal level was indicated. In subsequent
clinical trials [24, 25], this property of ePTFE was
confirmed and was soon to prompt the use of STP
in the laparoscopic approach to hernia repair.
A property of the ePTFE patch that we should
discuss is its behavior in the presence of infec-
tion. The studies by Law and Ellis [26] demon-
strated that other materials, such as polypropylene,
showed better tolerance to infection than ePTFE
did. These findings were corroborated by other
authors [27–30]. In clinical practice, it is generally
accepted that ePTFE is more prone to infection
than other biomaterials and that when infection
occurs, most ePTFE implants will need to be re-
moved [31, 32].
Structural Changes Suffered by ePTFE
Prostheses
The lack of good tissue incorporation [33] and
a sometimes considerable hernia recurrence rate
induced the first modifications to this prosthetic
material. The first of these was the introduction
of multiple perforations in the ePTFE patch in an
effort to achieve a prosthesis that, although still
laminar in structure, would have the properties of
a reticular mesh. The initial idea of converting the
STP into a macroporous prosthesis belonged to
Simmermacher et al. [11], who made multiple per-
forations in an ePTFE prosthesis to improve tissue
ingrowth. These authors even tried to modify the
prosthetic structure by pretreating the ePTFE with
ethanol to increase its porosity. They observed no
Chapter 51 · ePTFE Prostheses and Modifications
gain in mechanical strength attributable to such
modifications. Despite this, these experiments led
to the first modification of ePTFE in the form of a
prosthesis called MycroMesh (MM).
In an experimental study in our laboratory
[34], we observed no biomechanical benefits of the
new MM over conventional ePTFE in the form of
a patch (STP). Further, because of its lack of sur-
face smoothness due to the presence of multiple
orifices, greater adhesion formation was induced
when it was implanted over the peritoneum.
A further modification to the ePTFE patch
was the creation of a prosthesis with some sort of
barrier on its peritoneal side to prevent cell infil-
tration. This prosthesis was given the commercial
name of DualMesh (DM).
Further studies by our group [35] indicated the
practically identical behavior of this new prosthe-
sis to that of the classic ePTFE patches. Although
there was no cell ingrowth on one of its sides, this
did not seem to affect its behavior at the peritoneal
interface, and its mesothelialization and neoperi-
toneum formation were similar to observations
of STP. Furthermore, no changes were noted in
mechanical strength after implantation.
A final modification to DM took the form of
the Corduroy type, for which a rough surface was
created on its non-peritoneal-facing side. The ob-
jective was to improve tissue incorporation. How-
ever, studies by our group (unpublished results)
indicated that tissue infiltration with the Corduroy
mesh was similar to that for the other ePTFE
prostheses, with no improvement in mechanical
resistance compared with previous designs.
Modifications Involving Pretreatments
Infection of a prosthetic material continues to be
a significant problem in clinical practice. Given
the generally poor tolerance of ePTFE to infection,
determined by its microstructure, one of the in-
novations applied to ePTFE prostheses was their
pretreatment with substances that would inhibit
bacterial colonization during the initial moments
of implantation and thus prevent biofilm forma-
tion. This gave rise to modified prostheses with
bactericidal activity: MycroMesh Plus and DualM-
395 51
esh Plus. The antimicrobial agents used for pre-
treatment were silver carbonate and chlorhexidine
diacetate. Harrell et al. [36] recently demonstrated
the in vitro efficiency of these pretreatments.
Personal Experience with Experimental
and Clinical ePTFE Implants
Our experimental and clinical findings using a
New Zealand White rabbit implant model have
been as follows.
Macroscopic observations at the tissue–tissue
interface reveal that ePTFE becomes encapsulated
such that the mesh is enveloped by an organized
connective tissue to form a »sandwich.« When
the implant makes contact with the visceral peri-
toneum, correct mesothelialization occurs from
the first moments of implantation. Despite the
different modifications to the layer of ePTFE, its
macroscopic behavior fails to vary.
On microscopic observation, tissue incorpora-
tion is preferentially cellular. STP and DM show
similar behavior in that host cells are able to pen-
etrate as far as one-third of the mesh thickness.
In STP, this occurs on both surfaces; in DM, only
one surface is affected. Neoperitoneum formation
is similar for both prostheses, and observations
include the presence of mesothelial cells and a
well-organized peritoneum.
Using the MM variant, tissue ingrowth pro-
ceeds via the orifices created in the prosthesis such
that tissue bridges may be observed between the
two prosthetic surfaces, with the existence of cel-
lular integration as well. Unlike STP and DM, the
MM mesh induces angiogenesis in the perforation
zones.
For the rough-surface variant of DM, incorpo-
ration continues to be cellular, with tissue depos-
ited between the rough zones of the ePTFE surface
(⊡ Fig. 51.1).
On the peritoneal-facing side, adhesion forma-
tion is almost null, and when it occurs, as some-
times observed with MM, these adhesions are very
loose (⊡ Fig. 51.2).
An important feature to consider is the foreign
body reaction induced by the biomaterial. With
the use of a monoclonal antibody specific for rab-
 396 Chapter 51 · ePTFE Prostheses and Modifications

51

⊡ Fig. 51.1. Macroscopic appearance of the different prostheses tested (left). Diagrams (middle) and microscopic examinations
(right) of the implants showing tissue incorporation of the biomaterials 30 days after implantation. Both surfaces of the Soft Tis-
sue Patch (STP) implant have become encapsulated by host connective tissue. Cell colonization is detectable on both prosthetic
surfaces. Scar tissue surrounds the MycroMesh (MM) implant on both the peritoneal-facing and subcutaneous-tissue-facing
sides. The arrows indicate the neoformed tissue within the prosthetic MM perforations. In both MM and STP, cells penetrate
beyond one-third of the mesh thickness. Microscopic observation of the DualMesh (DM) and DM Corduroy implants indicates
no major differences with respect to the other implants; the only differences noted are the lack of fibrous colonization of the
nonporous DM surface (PS peritoneal side; SS subcutaneous side)

bit, macrophage counts were always the same for
all of the prostheses. These counts were higher at
the early implantation stage and thereafter under-
went a steady decrease (⊡ Fig. 51.3).
The mechanical strength of the different pros-
theses (STP, MM, DM, and DM Corduroy) failed
to differ significantly (⊡ Fig. 51.4). Thus, questions
arise regarding whether this similar tissue in-
growth induced by the ePTFE and all its modified
forms depends on the chemical composition, and
whether it can be modulated.
As already demonstrated by Amid et al. [13]
using other materials, when the spatial structure
of a prosthesis changes, its tissue behavior varies
despite its unchanged composition. In a prosthetic
design in which we used ePTFE suture thread
(Cv4) to construct a mesh [37], the mesh’s behav-
ior was similar to that of a reticular-type mesh.
Moreover, its mechanical behavior postimplanta-
tion varied appreciably to attain tensile strength
values comparable to those of a polypropylene
prosthesis. This design revealed the different tissue
Chapter 51 · ePTFE Prostheses and Modifications
397 51

⊡ Fig. 51.2. Macroscopic images of adhesion formation to the different prostheses. The percentage of adhesion formation is
greater for the MycroMesh (MM) prosthesis than for the other three (Soft Tissue Patch, DualMesh, and DualMesh Corduroy) pros-
theses. Adhesions appear in areas corresponding to the suture and perforations of the MM implant. Most of these adhesions are
very loose in consistency

50
Macrophage number

40

30

20

10

0
14 days 30 days 60 days 90 days

Soft Tissue Patch MycroMesh

DualMesh DualMesh Corduroy

⊡ Fig. 51.3. Number of macrophage cells recorded for the

different expanded polytetrafluoroethylene prostheses im-
planted in the abdominal wall of New Zealand White rabbits
for 14–90 days

incorporation of laminar relative to reticular-type
materials.
Another problem mentioned earlier is the issue
of prosthetic infection. In a model of experimental
infection, we were able to observe ultrastructural
⊡ Fig. 51.4. Postimplantation tensile strengths of the different
prostheses. Resistance to traction increased steadily, reaching
significance with respect to initial values 30–90 days after im-
plantation of the different prostheses. These values are similar
for the different types of expanded polytetrafluoroethylene
prostheses at the same study times
 398 Chapter 51 · ePTFE Prostheses and Modifications
changes in ePTFE induced by bacterial contamina-
tion. The microbes penetrated the interstitial zones
of the prostheses, where they settled. We observed
changes in internode fibers and in zones of an-
chorage to host tissue.
In clinical practice (1997), the behavior of the
ePTFE implants proved to be similar to that shown
experimentally. The same occurred in cases of pros-
thetic infection. In most cases of infection, the pros-
thesis must be replaced. We have no experience with
the use of pretreated ePTFE (MM Plus/DM Plus),
although the in vitro studies described above have
yielded promising results in settings of infection.
Conclusions
1. No modifications made to the earliest laminar
ePTFE prosthesis, or Soft Tissue Patch, have
resulted in any changes or improvement in tis-
sue incorporation or postimplantation biome-
chanical strength.
2. Only changes in the spatial architecture of a
biomaterial will alter the pattern of tissue in-
corporation and biomechanical strength.
51 3. When confronted with infection, ePTFE and
its variants respond in the same susceptible
way, with the exception of the pretreated pros-
theses.
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184:154–159
 52

The Role of Stem Cells in Abdominal

Wall Repair
M. G. Franz
 402 Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair
Introduction
Incisional hernias fundamentally result from acute
laparotomy wound failure. Evidence supports the
mechanism that gaps in the early laparotomy re-
pair progress to clinical incisional hernias [1, 2].
The linea alba is especially at risk for acute wound
failure because of the low number of repair fi-
broblasts and relative ischemia at this location of
the abdominal wall. Laparotomy wound-healing
failure occurs when there is (1) reduced quantity
or 2) impaired quality of collagen matrix synthe-
sis, recellularization, and, ultimately, tissue repair
[3]. Surgical and mechanical approaches to the
problem of incisional hernia formation and repair
may underestimate how the biological response to
injured tissue affects wound-healing outcomes.
Surgical wound-healing failure is defined at the
tissue, cellular, and molecular levels. A major nor-
mal mechanism is fibroblast activation from quies-
cence and progression of the repair cell cycle after
injury [3]. It is unknown whether wound failure of
the abdominal wall results from a primary inher-
ited defect in fascial fibroblast activation leading
to incisional hernia formation or, conversely, from
an abnormal wound milieu after mechanical fas-
cial wound failure that induces impaired fibroblast
52 function [3]. A combination of the two may exist.
One strategy to improve acute wound healing
and decrease surgical wound failure is the phar-
macological use of cytokine growth factors, which
increase skin incision strength and decrease the
incidence of incisional hernias in experimental
models [4–7]. In vivo growth factor therapy, how-
ever, is limited by short half-lives. Another strategy
is cell-based therapy. Stem cells and stem-cell-like
multipotent cells express the ability to differenti-
ate into different cell types that are important
for wound healing and tissue repair [8–10]. Stem
cells also secrete growth factors that signal paral-
lel cellular processes active during wound healing.
The sensor capability of cell sources of tissue re-
pair signals may result in more physiologic heal-
ing through signal combination and dose [9–11].
Amnion-derived cells express characteristics of
stem cells, including the ability to differentiate
into distinct cell types of varied tissue lineages [12,
13]. Amnion-derived cells also secrete cytokines
and growth factors in culture and are reported to
be nonimmunogenic [14–17]. Stem cell therapy
of abdominal wall wounds may therefore acceler-
ate and improve the gain in laparotomy breaking
strength and, in so doing, decrease the incidence
and severity of surgical wound failure and inci-
sional hernia formation.
Materials and Methods
AMP and GFP-labeled AMP Cells
Amnion-derived multipotent progenitor (AMP)
cells and AMP cells labeled with green fluorescent
protein (AMP-GFP) were provided by Stemnion
(Pittsburgh, PA, USA). Amnion cells were isolated
from placentas following cesarean section and were
processed by proprietary techniques.
Animal Model
The rat models of laparotomy healing and in-
cisional hernias have been previously described
[18–20]. Sprague–Dawley rats weighing 450 g were
acclimated and housed under standard conditions.
All animal care and operative procedures were
performed in accordance with the United States
Public Health Service Guide for the Care of Labo-
ratory Animals and were approved by the Univer-
sity of Michigan Committee on the Use and Care
of Animals.
Laparotomy Wound-Healing Model
Briefly, a ventral skin flap was raised through the
avascular prefascial plane, and a 5-cm laparotomy
incision was made through the linea alba. The lap-
arotomy was repaired with a running 4-0 polypro-
pylene suture. The skin flap was securely sutured.
Two groups were studied: (1) abdominal walls
treated with normal saline (NS) as the control
(NS-S control) and (2) abdominal walls treated
with NS-washed, human-amnion-derived multi-
potent progenitor cells (AMP-S group). In the
NS-S group, the midline of the abdominal wall
Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair
(linea alba) was injected over 5 cm with 200 μl of
NS. In the AMP-S group, 200 μl of NS containing
106 amnion epithelial cells was similarly injected.
Surgical-site priming was performed with a 22-g
hypodermic needle (0.7×38 mm) into the linea
alba. Soft tissue distribution of NS or AMP cell
suspension was achieved. After 5 min, the laparo-
tomy incision was made and repaired as described
above.
On postoperative days (PODs) 7, 14, and 28,
the rats were killed. Isolated abdominal wall mus-
cle and tendon strips and fresh biopsies of the
abdominal wall to the laparotomy wound-healing
interface were collected for mechanical and histo-
logical testing.
Laparotomy Wound Breaking Strength
and Mechanical Properties
Mechanical testing was done on abdominal wall
strips collected from the laparotomy wound-
healing model as previously reported [4, 19, 20].
Briefly, sutures were removed. Abdominal wall
strips were made perpendicular to the wound-
healing interface. A cutting template was used to
mark the abdominal wall to minimize the size
variability among specimens. Strips were cut
10 mm in width and 60–80 mm in length. Two
strips were collected from each rat, and testing was
performed within 6 h of necropsy. The thickness of
the fascial tissue strip at the wound and the length
between grips were measured with Digimatic cali-
pers. Force extension curves were generated for
each fascial strip with the use of an Instron tensi-
ometer equipped with a 50-N static load cell set at
a crosshead speed of 10 mm/min. The fascial strips
were mounted into the load frame with the use of
pneumatic grips, preloaded to 0.1 N with a gauge
length between the grips of around 10 mm. The
load frame applied testing loads to the fascial strips
until mechanical tissue disruption occurred. Force
and tissue deformation data were simultaneously
recorded and captured on a computer connected
to the load frame via a digital interface card. Data
analysis was performed with the use of the Merlin
materials testing software package (Instron, Can-
ton, MA, USA). Breaking strength, the maximum
load force (Fmax) at mechanical failure (N); tensile
strength, the maximum stress developed in the
403 52
specimen per unit area, calculated as Fmax/cross-
sectional area (N/mm2); energy at break (mJ);
yield strength (N); yield energy (mJ); and stiffness,
the slope of the linear elastic region of the force-
extension curve (N/mm), were generated.
Incisional Hernia Model
Incisional hernia models were used as previously
described [18, 20]. Again, a skin flap was raised,
and a 5-cm laparotomy incision was made through
the linea alba. To induce hernia formation, two
fast-absorbing 5-0 plain gut stitches were placed at
the cranial extent and midpoint of the laparotomy
incision. The skin flap was again secured. Groups
treated with NS (NS-H control) and human-amni-
on-derived multipotent progenitor cells (AMP-H)
were again used for this experiment. In the NS-H
control group, 200 μl of NS was injected along the
midline for 5 cm. In the AMP-H group, 200 μl of
NS containing 1.5×106 amnion epithelial cells was
injected along the linea alba for 5 cm. On POD 28,
the rats were killed, and the musculotendinous
layer of the abdominal wall was collected and ex-
amined for incisional hernias.
Measurement of Hernia Size
For hernia size measurement, hernia model rats
were killed on POD 28. The skin was dissected free
circumferentially, and a 5×10-cm section of the
abdominal wall muscle was excised. The muscle
was stretched out and pinned down on a dissect-
ing board at the four corners with the peritoneal
side up. A standardized digital picture was taken.
Software Spot version 4.5 for Windows was used
to calculate hernia size on digital pictures. Calibra-
tion was set up using the rule reference on each
picture. A circle was drawn along the hernia ring
to measure the hernia size in square centimeters.
Laparotomy and Incisional Hernia
Histology
Laparotomy wound or hernia sections were cut
and fixed in formalin for histology. Specimens were
stained with hematoxylin and eosin or trichrome.
 404 Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair

Viable AMP-GFP cells were also injected into the Results

linea alba as described above. These tissues were
embedded in O.C.T. compound and snap-frozen
immediately in liquid nitrogen. A piece of sagittal
fascial wound from the linea alba was fixed in 10%
formalin on ice for 6 h, dehydrated through graded
sucrose washes for 24 h, and finally embedded in
O.C.T. compound and snapped in liquid nitrogen.
Serial cryostat sections were made for fluorescence
microscopy to evaluate the distribution or localiza-
tion of GFP-positive cells.
Statistics
Statistical analysis was performed using GraphPad
Prism version 4.0 for Windows. A t-test was used
to compare the difference between the NS control
group and AMP-treated groups. This software was
also used to create the incidence curves of inci-
sional hernia at POD 28 for fractional hernia of
any particular hernia or wound defect size and to
compare the curves between the NS-H control and
AMP-H groups. The significance level was set at
P<0.05.
Viability of AMP in Laparotomy
Wounds and Hernias
Successful transplantation requires clinical viabil-
ity of the transplanted AMP. To test the survival
of AMP cells in our models, 2.5×106 AMP-GFP
cells were injected into the linea alba, and laparo-
tomies were performed. Rats were killed on PODs
7, 14, and 28, and laparotomy tissue was collected.
Frozen-tissue sections were prepared for fluores-
cence microscopy. AMP cells expressed GFP in
laparotomy wound sections on PODs 7, 14, and
28, confirming AMP cell viability over this time
course (⊡ Fig. 52.1).
AMP Cells Accelerate Laparotomy
Healing
Tensiometric measurements found significant dif-
ferences in mechanical properties of the NS-S and
AMP-S groups following laparotomy. All wounds
were disrupted at the fascia–fascia interface of

52

⊡ Fig. 52.1. Viability of human-

amnion-derived multipotent pro-
genitor cells labeled with green
fluorescent protein (AMP-GFP) in a b
laparotomy wounds. AMP-GFP
were injected in the rat linea
alba, and tissue was harvested at
postoperative days (PODs) 7, 14,
and 28. Frozen-tissue sections
of abdominal wall collected at
these three time points were
examined under a fluorescent
microscope. a POD 7. b POD 14.
c POD 28. d Frozen skin tissue
section adjacent to injection site
c d
collected on POD 7
Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair
the laparotomy wound. Wounds treated with 106
AMP cells developed increased breaking strength
by POD 7 (⊡ Fig. 52.2). Laparotomy scar tissue
sampled on POD 7 showed greater vascularization
and fibrosis in the AMP-S group compared with
the NS-S group (⊡ Fig. 52.2g, h). Wound strength
properties continued to increase until POD 28.
Differences in the recovery of wound-breaking
properties were less on PODs 14 and 28, which is
consistent with normal acute wound healing in the
NS control group.
AMP Cells Reduce Laparotomy
Dehiscence and Herniation
To test whether accelerated laparotomy repair us-
ing AMP cells prevented hernia formation, AMP
cells or NS was delivered to the linea alba in the
hernia model. The hernia or wound defect size in
the AMP-H group was significantly smaller than in
the NS-H group (0.82±0.16 cm2 vs 2.72±0.56 cm2;
⊡ Fig. 52.3). Histology of the healing laparotomy
(⊡ Fig. 52.3b) or hernia ring (⊡ Fig. 52.3c) showed
again that there was more vascularization and fi-
brosis in the AMP-H rats, suggesting accelerated
and improved laparotomy wound repair in the
AMP-H group. In the best clinical study of predict-
ing incisional hernias, it was found that a 12-mm
gap in the laparotomy closure on POD 30 results in
incisional hernia 94% of the time. Conversely, only
3% of defects less than 12 mm in size developed in-
cisional hernias over 3 years [1]. Small laparotomy
defects do not form incisional hernias, but bigger
ones do. The majority of AMP-treated animals
developed very small laparotomy defects, if at all.
The largest and smallest hernia or defect sizes were
1.88 cm2 and 0 cm2, respectively, in the AMP-H
group vs. 6.28 cm2 and 0.50 cm2, respectively, in
the NS-H group. AMP treatment therefore reduces
the incidence of laparotomy wound failure that
progresses to incisional hernia.
Discussion
The two fundamental mechanisms for laparotomy
wound failure leading to incisional hernia may
405 52
be summarized as follows: (1) A primary defect
or delay in repair cell activation and provisional
wound matrix crystallization during acute fascial
repair causes herniation, or (2) mechanical failure
and dehiscence cause a delay or deficiency in the
acute wound-healing process [3]. The first is an in-
herited biological mechanism, and the second is an
acquired biomechanical or biosurgical mechanism.
It is possible that both mechanisms are active in
a reinforcing cycle of surgical wound failure and
herniation.
Wound breaking strength is the mechanical
property of a laparotomy that determines its abil-
ity to resist distractive forces. Burst abdomens, or
acute fascial dehiscence with evisceration, are one
important extreme of laparotomy failure.
Studies report that amniotic cell therapy im-
proves spinal injury and does not induce an im-
mune rejection reaction [17, 21–23]. Human am-
niotic epithelial cells are not reported to express
surface HLA-A, -B, -C, or -DR antigens or beta
2-microglobulin [21]. Human amnion epithelial
cells are also reported to survive up to 7 weeks
in vivo after allogeneic transplantation without in-
ducing acute immune rejection. Other researchers
found no residual amniotic epithelium in humans
2–3 months after human amniotic cell implanta-
tion [24]. These findings support its therapeutic
safety.
There are several potential mechanisms by
which AMP cells improve healing of laparotomy
incisions. AMP cells may differentiate into mes-
enchymal, fibroblast-like repair cells to replace
or augment fibroblasts in the failing laparotomy
wound. It is also possible that a repair or regenera-
tion signal secreted by AMP cells directs acceler-
ated and/or normal fascial fibroblast repair [25].
Our group has already reported the use of indi-
vidual growth factors–TGF-B2, bFGF, and GM-
CSF–to accelerate laparotomy repair and prevent
incisional hernia formation [5, 26, 27].
Tissue growth factors are an important class
of tissue repair signaling peptides that are upregu-
lated during the lag phase of acute wound healing
[27]. However, 5–7 days are required before peak
levels of fibroproliferative growth factors such as
TGF-β are reached in acute wounds [28]. Acute
wound therapy with proliferative growth factors is
 406 Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair

A 12
NS AMP B 0.35
NS AMP
*
10 P=0.0109 * 0.30
P=0.0239

Tensile stress (N/mm2)

Maximum Load (N)

8 0.25

0.20
6
0.15
4
0.10
2
0.05
0 0.00
NS AMP NS AMP

45 D 3.5
C NS
** NS P=0.0559
40 3.0
AMP AMP
35
Energy at Break (mJ)

2.5

Stiffness (N/mm)
30 P=0.0027

25 2.0
20 1.5
15
1.0
10
0.5
5
0 0.0
NS AMP NS AMP

E 12
NS AMP
F 20
NS AMP
10 P=0.0276 P=0.0301 *
*
15
8
Yield Energy (mJ)
Yield Load (N)

6 10

4
5
52 2

0 0
NS AMP NS AMP

G H

⊡ Fig. 52.2. Tensiometric measurements and histology exam on postoperative day (POD) 7. Fascial mechanical breaking characteris-
tics were measured with an Instron tensiometer on POD 7 (a–f). Values are the mean ± SEM of six wound biopsies each from the nor-
mal saline (NS) control (NS-S) and the NS-washed human-amnion-derived multipotent progenitor cell (AMP-S) groups. A t-test was
used to compare the difference between the two groups [single asterisk (*): p<0.05; double asterisk (**): p<0.01]. Morphology of fascial
incisional wound at POD 7 from the NS-S (g) and AMP-S (h) groups. Hematoxylin and eosin staining was performed for histology
Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair
A 3.5 NS-H
3.0 AMPs-H
2.5 P=0.0042
Hernia size (cm 2 )
2.0
1.5
**
1.0
0.5
0.0
NS-H AMPs-H
B C
⊡ Fig. 52.3. Effect of human-amnion-derived multipotent
progenitor (AMP) cells on hernia healing. Hernia or wound
defect size was measured on postoperative day 28. Values are
the mean ± SEM of 11 hernia biopsies each from the normal
saline (NS) control (NS-H) and the AMP-hernia groups. [Dou-
ble asterisk (**): compared with NS-H, p<0.01]. Morphology
of hernia ring from the normal saline (NS) control (b) and NS-
washed AMP (c) groups. Hematoxylin and eosin staining was
performed on tissue sections
known to accelerate the appearance of fibroblasts
and collagen into the wound, thereby shortening
the natural lag phase for gain in injured tissue
strength. The preponderance of clinical and pre-
clinical evidence supports the concept that very
early laparotomy wound failure is the mechanism
of incisional hernia formation. Load-bearing lapa-
rotomy wounds fail at the weakest point on the
acute wound-healing trajectory at the same time
that surgical patients are recovering. Early wound
failure results in incisional hernia formation 94%
of the time [1, 2]. Well-performed, prospective
series of incisional hernia repairs report early re-
currences, most within 3 years of operation. It is
therefore increasingly accepted that the majority
407 52
of incisional hernias arise from occult fascial de-
hiscences, so a new emphasis is being placed on
improved laparotomy closure and healing, through
either biological manipulation or the use of pro-
phylactic soft tissue prostheses. Preclinical work
has confirmed that accelerated laparotomy repair
through priming with tissue repair growth factors
can significantly reduce the incisional hernia rate
[4, 5]. The problems with single-peptide wound
therapy remain drug delivery, dosing, and timing.
Histological samples of AMP-treated wounds
are consistent with accelerated repair compared
with controls. There is more fibroplasia and angio-
genesis, and it is also suggested that the intensity
of the wound inflammatory response is modu-
lated and less severe. Collagen fibrils appear to
be more organized along natural lines of tension,
and the peritoneal lining appears restored during
AMP treatment. A comprehensive examination of
remote organs and tissue found no migration or
trafficking of AMP cells beyond the wound (data
not shown). This supports the application of AMP
cells in wound therapy. The immune privilege of
amnion-derived cells permits their use as an al-
lograft, and the containment of these cells to the
wound suggests their safety.
References
1. Pollock AV, Evans M. Early prediction of late incisional
hernias. Br J Surg 1989;76:953–4
2. Burger JW, Lange JF, Halm JA, Kleinrensink GJ, Jeekel H.
Incisional hernia: early complication of abdominal sur-
gery. World J Surg 2005;29(12):1608–13
3. Dubay DA, Franz MG. Acute wound healing: the biol-
ogy of acute wound failure. Surg Clin North Am
2003;83(3):463–81
4. Dubay DA, Wang X, Kuhn MA, Robson MC, Franz MG.
The prevention of incisional hernia formation using a
delayed-release polymer of basic fibroblast growth factor.
Ann Surg 2004;240(1):179–86
5. Franz MG, Kuhn MA, Nguyen K et al. Transforming growth
factor β2 lowers the incidence of incisional hernias. J Surg
Res 2001;97(2):109–16
6. Robson MC, Dubay DA, Wang X, Franz MG. Effect of cy-
tokine growth factors on the prevention of acute wound
failure. Wound Repair Regen 2004;12(1):38–43
7. Mustoe TA, Pierce GF, Thomason A, Gramates P, Sporn
MB, Deuel TF. Accelerated healing of incisional wounds
in rats induced by transforming growth factor-α. Science
1987;237:1333–6
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8. Yamaguchi Y, Kubo T, Murakami T et al. Bone marrow
cells differentiate into wound myofibroblasts and accel-
erate the healing of wounds with exposed bones when
combined with an occlusive dressing. Br J Dermatol
2005;152(4):616–22
9. Han SK, Yoon TH, Lee DG, Lee MA, Kim WK. Potential of
human bone marrow stromal cells to accelerate wound
healing in vitro. Ann Plast Surg 2005;55(4):414–9
10. Chunmeng S, Tianmin C, Yongping S et al. Effects of
dermal multipotent cell transplantation on skin wound
healing. J Surg Res 2004;121(1):13–9
11. Robson MC. Cytokine manipulation of the wound. Clin
Plast Surg 2003;30(1):57–65
12. Fliniaux I, Viallet JP, Dhouailly D, Jahoda CA. Transforma-
tion of amnion epithelium into skin and hair follicles.
Differentiation 2004;72(9-10):558–65
13. Miki T, Lehmann T, Cai H, Stolz DB, Strom SC. Stem cell
characteristics of amniotic epithelial cells. Stem Cells
2005;23(10):1549–59
14. Tahara M, Tasaka K, Masumoto N et al. Expression of
messenger ribonucleic acid for epidermal growth factor
(EGF), transforming growth factor-alpha (TGF alpha), and
EGF receptor in human amnion cells: possible role of TGF
alpha in prostaglandin E2 synthesis and cell proliferation.
J Clin Endocrinol Metab 1995;80(1):138–46
15. Padowska E, Blach-Olszewska Z, Gejdel E. Constitutive
and induced cytokine production by human placenta and
amniotic membrane at term. Placenta 1997;18:441–6
16. Denison FC, Kelly RW, Calder AA, Riley SC. Cytokine secre-
tion by human fetal membranes, decidua and placenta at
term. Hum Reprod 1998;13(12):3560–5
17. Wu ZY, Hui GZ, Lu Y, Wu X, Guo LH. Transplantation of
human amniotic epithelial cells improves hindlimb func-
52 tion in rats with spinal cord injury. Chin Med J (Engl )
2006;119(24):2101–7
18. Franz MG, Smith PD, Wachtel TL et al. Fascial incisions
heal faster than skin: a new model of abdominal wall
repair. Surgery 2001;129(2):203–8
19. Dubay DA, Wang X, Adamson BS, Kuzon Jr WM, Den-
nis RG, Franz MG. Progressive fascial wound failure
impairs subsequent abdominal wall repairs: a new
animal model of incisional hernia formation. Surgery
2005;137(4):463–71
20. Dubay DA, Choi W, Urbanchek MG, Kuzon WM, Franz MG.
Incisional herniation induces decreased abdominal wall
compliance via oblique muscle atrophy and fibrosis. Ann
Surg 2007;245(1):140–6
21. Adinolfi M, Akle CA, McColl I et al. Expression of HLA
antigens, beta 2-microglobulin and enzymes by human
amniotic epithelial cells. Nature 1982 28;295(5847):325–7
22. Akle CA, Adinolfi M, Welsh KI, Leibowitz S, McColl I. Im-
munogenicity of human amniotic epithelial cells after
transplantation into volunteers. Lancet 1981 7;2(8254):
1003–5
23. Sankar V, Muthusamy R. Role of human amniotic epi-
thelial cell transplantation in spinal cord injury repair
research. Neuroscience 2003;118(1):11–7
24. Yeager AM, Singer HS, Buck JR et al. A therapeutic trial
of amniotic epithelial cell implantation in patients with
lysosomal storage diseases. Am J Med Genet 1985;
22(2):347–55
25. Steed DL, Trumpower C, Duffy D et al. Amnion-derived
cellular cytokine solution: a physiological combination of
cytokines for wound healing. Eplasty 2008;8:e18
26. Dubay DA, Wang X, Kirk S, Adamson BS, Robson MC,
Franz MG. Fascial fibroblast kinetic activity is increased
during abdominal wall repair compared to dermal fibro-
blasts. Wound Repair Regen 2004;12(5):539–45
27. Robson MC, Mustoe TA, Hunt TK. The future of recom-
binant growth factors in wound healing. Am J Surg
1998;176(suppl 2A):80–2
28. Cromack DT, Sporn MB, Roberts AB, Merino MJ, Dart LL,
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Discussion
Amid: Now we have more than 250 meshes, and
our challenge remains the same. So I think it’s time
to [take the] focus from the mesh to the host. And
that is what you are doing.
Franz: Thank you.
Klinge: I am not really convinced about the clas-
sification into big and small recurrences. I think if
you create a wound within the abdominal wound,
you always have an immigration of stem cells. Do
you have any information that in patients with
impaired wound healing it is this process of adult
local stem cells that is impaired? And correspond-
ingly, these patients would benefit from some ad-
ditional stem cells?
Franz: There is evidence in the literature that the
amount of defect in the primary laparotomy will
predict late incisional hernia—it was published in
the British Journal of Surgery in 1989. The authors
were able to predict the future incisional hernia
based on the size of the hernia defect. Thus, it may
matter.
Miserez: Congratulations on this wonderful lec-
ture. You used human stem cells in the rat model.
Should we work on interspecies in the future, or
should we stay in one species, with autologous
material?
Franz: It is possible. In practical surgery it is nice
to have a product that is available. It may not mat-
ter what the species is.
Chapter 52 · The Role of Stem Cells in Abdominal Wall Repair
Schumpelick: Have you done experiments with
fibroblasts?
Franz: No. There is a group from Israel that has
done that on mesh.
409 52
Conclusion of Session IV,
by A. Montgomery
The session included both experimental investi-
gations and studies and discussions. First of all,
we had a good overview of the pathophysiology
of the peritoneum and adhesion formation. Then
we had a discussion on meshes in general and on
biological meshes. I would say that the knowledge
of meshes today is a mess. We are talking about
shrinkage and expansion of meshes. The biological
meshes have brought something new; we now have
13 FDA-approved biological meshes. There are a
lot of things to study. What is the body’s reaction
to these meshes? When to use them? Or should we
use them at all?
There is a lot of work to be done. I would com-
bine that with a congratulation to the last lecture
on stem cell biology and the possible new think-
ing. It might be a combination for the biological
meshes—to overbridge a distance of about 20 cm
with stem cell formation. This might be a future
for the biological meshes. We also should concen-
trate on the effect of pore size. I also think that
the surface area was a very interesting key in the
discussion of meshes.
With regard to the clinical part and laparos-
copy, we could conclude that there is a total lack
of evidence for any mesh to be used and in what
situations. Better hernia classifications and hernia
registries would enable more precise research.
 V

V Risk for Migration and Erosion

53 Safety and Durability of Prosthetic Repair of the Hiatal Hernia:

Lessons Learned from a 15-Year Experience – 413

54 Mesh Migration into the Esophageal Wall After Mesh

Hiatoplasty – 421

55 Complications After Gastric Banding–Results in

Germany – 429

56 Alloplastic Implants for the Treatment of Stress Urinary

Incontinence and Pelvic Organ Prolapse – 439

57 Prophylactic IPOM Mesh To Prevent Parastomal

Hernias – 445

58 Laparoscopic Parastomal Hernia Repair:

Pitfalls and Complications – 451

59 Concept of Visible Mesh and Possibilities for Analysis

of Mesh Migration and Shrinkage – 457
 53

Safety and Durability of Prosthetic

Repair of the Hiatal Hernia: Lessons
Learned from a 15-Year Experience
P. von Ryll Gryska
 414 Chapter 53 · Safety and Durability of Prosthetic Repair of the Hiatal Hernia: Lessons Learned from a 15-Year Experience

Introduction

Laparoscopic fundoplication has emerged as the

gold standard for treating refractory reflux disease
and symptoms of gastric herniation. Surgical suc-
cess rates as measured by patient satisfaction and
symptom relief have been reported to be between
85% and 95% [1, 2]. However, as with any op-
eration, we should continue to critically examine
clinical failures in an effort to identify and correct
a
potential sources of technical weaknesses.
There are several important technical features
of standard hiatal hernia repair/fundoplication, in-
cluding hernia sac excision, mobilization of the
esophagus, return of the stomach and distal esoph-
agus to the intraabdominal position, and crural re-
pair and wrap. Each has been recognized as an im-
portant feature of a successful clinical outcome [3].
Breakdown of the hiatal hernia repair has also been
recognized as a common cause for clinical failure,
often within the first 2 years, leading to wrap her-
niation and paraesophageal herniation and contrib- b
uting to the slipped Nissen phenomenon [4–6].
During the last 15 years, we have focused on ⊡ Fig. 53.1. a Staples and suture to right crus after crural clo-
hiatal hernia repair as a source of technical failure. sure. b Staples and suture to left crus
A prosthetic patch of the esophageal defect or rein-
forcement of the crural closure was used on all pa-
tients. With experience, the technique has evolved diaphragm [7]. The next 105 patients (group B)
from a pure nontension patch of the hiatal defect to underwent hiatal hernia repair using an ePTFE/
partial crural closure with sutures reinforced with PTFE prosthesis (CruraSoft; Davol/Bard). Fixa-
53 an expanded polytetrafluoroethylene (ePTFE)/ tion of this prosthesis as part of the crural closure
PTFE prosthesis stapled and sutured into position evolved quickly to partial crural closure with one
to prevent motion, migration, or erosion. In short, to three sutures and fixation of the prosthesis with
the crural closure is treated as a hernia repair any- staples (EMS 20; Ethicon) and 2-0 silk sutures
where else on the abdominal wall. Presented here (⊡ Fig. 53.1). The prosthesis was positioned onto
are the lessons learned about the fixation, durabil- the crural closure so that none of the material was
ity, and safety of prosthetic mesh at the hiatus. abutting the esophagus. This required thorough
esophageal mobilization and complete dissection
of the crural columns posteriorly.
Materials and Methods The focus of the record review was on short-
term and long-term safety as well as durability
Records of 217 patients undergoing laparoscopic of the prosthetic crural repair. Postoperative dys-
Nissen fundoplication were examined. Each pa- phagia, stricture, integrity of the crural repair, re-
tient had a prosthetic closure of the hiatal hernia herniation, and development of long-term compli-
or reinforcement of the crural repair. The first 112 cations were examined. Continuing analysis and
patients (group A) had a nontension patch using retrospective review then permitted evaluation of
a PTFE mesh stapled into position with 3 cm of the crural repair and fixation techniques that led to
mesh overlapping beyond crural bundles onto the the best clinical outcomes.
Chapter 53 · Safety and Durability of Prosthetic Repair of the Hiatal Hernia
Results
Beginning in November 1993, 217 patients under-
went laparoscopic Nissen fundoplication with a
nontension prosthetic closure of the hiatal defect
(group A =112 patients) or prosthetic reinforce-
ment of the hiatal hernia repair (group B =105
patients).
Patient demographics are listed in ⊡ Table 53.1.
Of note is the large number of type II and type III
hiatal hernias, with 75 patients having »large«
hiatal defects >6 cm. Twenty-two patients (10%)
underwent concomitant cholecystectomy, and 11
patients were referred for recurrent hiatal hernias
(2–26 years postoperative).
Short-Term Safety
There were no deaths, no transfusions, and no in-
traabdominal or mediastinal infections. There was
no tearing or disruption of crural tissues. Place-
ment of the prosthetic patch or reinforcement took
3–5 min when staples alone were used. Adding
two sutures to the fixation process added roughly
8–10 min to the procedure.
Although most operations were class I, to-
tally clean procedures without violation of the
gastrointestinal tract, 10% of the patients had a
cholecystectomy at the same time. One gastro-
tomy occurred during a redo operation, which
was closed immediately without contamination,
and one Collis–Nissen esophageal lengthening was
performed. These events officially made these cases
class II, clean-contaminated operations. Three uri-
nary tract infections, two cases of cellulitis at an
intravenous line site, three pneumonias (in large
paraesophageal hernias), a port site infection, and
sinusitis were treated aggressively. Sixteen post-
operative fevers were related to atelectasis. There
were no complications related to PTFE mesh fixa-
tion with staples or sutures.
Dysphagia to solid foods occurred routinely
in the 1st month after surgery, and patients were
kept on a liquid or very soft diet. Dysphagia
requiring endoscopic dilation after 6 weeks oc-
curred in 36 patients (12%). Nineteen of these 36
patients had had preoperative dilatation for stric-
415 53
⊡ Table 53.1. Patient demographics
217 patients, 120 female, ages 19–87 (mean 57.5 years)
Mean operating time: 155 min
Pure paraesophageal hernias: 22 (10%)
Large hiatal defects ≥6 cm: 75 patients (34.5%)
Mean age with large defects: 69.7 years
Mean operating time (large defects): 205 min
ture disease. Five patients in group A required
two to four dilations. One patient developed a
fibrous stricture of the esophageal hiatus 4 years
after initial surgery and required reoperation.
This patient had no intraluminal pathology or
erosion. Five of 17 primary postoperative dys-
phagia patients were from group B, each requir-
ing only one dilation.
Long-Term Safety
There were 165 patients for whom data since No-
vember 1993 were available. Data were available
on all group B patients. The mean follow-up was
71 months (6–173 months). Barium studies on
90 patients done 1 day to 8 years postoperatively
(mean 38 months) found no impingement of the
prosthesis onto the esophagus or stomach, and
116 endoscopies on 86 patients (8 weeks to 8 years
postoperatively; mean 42 months) found no ero-
sion or impingement. In the years since their index
surgery, six patients have undergone cholecystec-
tomy, two for acute disease; two patients had ap-
pendicitis; and five patients have been treated for
diverticulitis. Nine other patients have had in-
traabdominal surgery, and two have had thoracic
surgery. One patient had an esophagectomy for
progressing Barrett’s, during which the pure mesh
prosthesis was found to be thoroughly ingrown to
the crus and required excision with scissors to al-
low room for the gastric tube [7]. Two patients had
full-term pregnancies, with one cesarean section.
There have been no mesh infections and no mesh
erosions.
 416 Chapter 53 · Safety and Durability of Prosthetic Repair of the Hiatal Hernia: Lessons Learned from a 15-Year Experience
Durability
Failure of the hiatal hernia repair as determined by
symptoms and/or x-ray findings of wrap herniation
occurred in three patients (1.4%). Two required
reoperation. Hiatal hernia disruption occurred, re-
spectively, at 5 days, 2 weeks, and 2 months after
surgery. The earliest failure, at 5 days, was a totally
nontension PTFE repair (group A) and occurred
after heavy lifting. The other two were technical
failures in which the preshaped PTFE/ePTFE mesh
was merely stapled to the left and right crus without
crural closure and without sutures. In all subsequent
patients (101 patients), the crura were closed par-
tially or tightly to a 58-Fr bougie, and the prosthesis
was secured in position with staples and sutures.
All 217 patients underwent laparoscopic Nis-
sen fundoplication after crural repair with a pros-
thesis. In total, there have been three reoperations:
one for stricture developing 4 years after the initial
surgery and two for disruption of the crural repair
with wrap migration.
The one late-occurring stricture and one crural
disruption occurred in group A, the totally non-
tension group. Two disruptions of the crural repair
occurred in group B before we learned to close the
crus as a backing for the prosthesis and to suture
as well as staple the prosthesis in place. Since the
development of crural closure and suture fixation
along with staples, there have been no crural dis-
53 ruptions or reherniations in the last 101 patients
(follow-up 6–55 months).
Discussion
It is recognized that disruption of the crural clo-
sure leads to wrap herniation and clinical failure.
It should not surprise us that a primary tension
closure of the crural pillars can fail. The crural pil-
lars are pure muscle: There is no substantial fascia,
no tendinous tissue, and no ligamentous fibers,
and nowhere else in surgery do we close muscle
to muscle and expect it to hold under tension.
The myriad of studies [8–11] that show improved
integrity of crural repair after prosthetic reinforce-
ment force us to examine the next step: how to do
it safely. Granderath et al. define the ideal mesh
as »easy to handle at laparoscopy, able to adhere
to the diaphragmatic surface on one side and be
benign to visceral surface on the other« [12]. The
next challenge is to position the prosthesis prop-
erly and then secure it properly.
Several authors have shown that disruption of
the crural closure occurs frequently in the early
postoperative months to years [13–16]. Filipi has
shown that various »stressors« or intraabdominal
pressures can predispose to crural disruption [17].
Meshed prostheses do become ingrown into the
crural muscle with time [7]. Our clinical failures
even with a prosthesis occurred within the first
2 months after a nontension repair and therefore
are considered failures of fixation.
In subsequent patients, then, the crus was
closed with one to three sutures, depending on
the size of the defect, to provide backing to the
mesh and to provide substrate for staples, and
sutures were added to the fixation to provide extra
strength and prevent prosthetic movement until
tissue ingrowth could occur.
The problem of erosion was not seen in this
series over 15 years, and yet there are scattered pub-
lished reports of such and anecdotal reports (un-
published) to this author. Erosion could result from
improper placement of the prosthesis, i.e., placing
the prosthesis too far anterior and abutting the
esophagus, which may not be mobilized fully from
its posterior position. Erosion could also result from
migration and motion of a free-floating prosthesis
(e.g., Angelchik). For these reasons, the prosthesis is
now fixed to a closed crural defect with sutures and
staples and is positioned so that the esophagus does
not touch any part of the prosthesis. The posterior
wrap then further pulls the esophagus anteriorly
and away from the crural repair.
Short-term safety and avoidance of infection
related to the prosthesis at the hiatus are really
a function of careful surgical technique and po-
sitioning of the prosthesis on well-vascularized
crural muscle. In our review, no intraabdominal
or mediastinal infections were encountered despite
24/217 clean-contaminated procedures and 10 pe-
ripheral postoperative infections.
Dysphagia after 6 weeks occurred, not sur-
prisingly, in 19 patients who had required dila-
tion preoperatively. In 17/217 patients, primary
Chapter 53 · Safety and Durability of Prosthetic Repair of the Hiatal Hernia
postoperative dysphagia was treated with dilation
and seemed more a consequence of the wrap and
postoperative scar retraction or motility issues
than narrowing of the esophageal hiatus. Among
group B patients, only 5/105 had late postoperative
dysphagia consistent with primary crural closure
or mesh at the hiatus. Only one patient had clini-
cally significant hiatal scarring, resulting in late
dysphagia at 4 years. This rare phenomenon is
known to occur historically with primary closure
alone and is poorly understood.
Long-term safety after 15 years is quite satisfac-
tory. Despite intraabdominal infections from sub-
sequent disease and other elective clean-contami-
nated operations, the prosthetic meshes placed at
the hiatus are not susceptible to bacterial seeding.
Just as prostheses on the anterior abdominal wall
are covered with a protective peritoneal covering,
so too is the prosthesis at the hiatus [18]. Proper
positioning and proper fixation of the prosthe-
sis have prevented migration, impingement, and
erosion into the esophagus. The smooth ePTFE
surface of the patch used on the most recent 105
patients prevents tissue ingrowth and thereby pre-
vents fistulization to the stomach.
In a primary crural closure, one would not
expect to see the top of the closure or the suture
impinging on the esophagus at barium study or
endoscopy. Similarly, with a properly placed pros-
thetic patch reinforcing the crural closure, no im-
pingement was seen on barium study (90 patients)
or endoscopy (116 endoscopies in 86 patients).
This, too, is a consequence of proper placement
and proper fixation of the prosthesis as well as
thorough mobilization of the posteriorly seated
intrathoracic esophagus. This mobilization is nec-
essary to return the distal 2–3 cm of the esophagus
to the intraabdominal position, and it helps lift the
esophagus anteriorly away from the crural closure
and any prosthetic reinforcement. The bulky pos-
terior wrap further holds the esophagus anteriorly
away from the top of the closure. Most often, the
prosthesis is placed below the top of the crural clo-
sure. The approximated hiatal closure provides a
substrate behind the mesh for both near-term fixa-
tion with staples and long-term tissue ingrowth.
The fixation with 15–20 staples (not tacks) and
the addition of two sutures to fix the mesh to the
417 53
crus in a full-thickness fashion further secure the
prosthesis and prevent long-term migration and
erosion (⊡ Fig. 53.1). Suturing of the stomach, the
wrap, or the esophagus to the prosthesis is to be
avoided.
Durability of the hiatal hernia repair using a
prosthesis has also been quite satisfactory in this
experience. In three patients, breakdown occurred
at 5 days, 2 weeks, and 2 months, respectively. Two
patients underwent subsequent repair with pros-
theses. The very early failure was a consequence
of extreme Valsalva at postoperative day 5 on a
nontension repair. The next two breakdowns were
a failure of proper fixation, in which the PTFE/
ePTFE prosthesis was merely stapled to the cru-
ral columns without closure (also nontension).
It quickly became apparent that crural backing
was necessary for secure fixation as well as for
long-term tissue ingrowth. The technique evolved
quickly and incorporated fixation sutures on ei-
ther side of the prosthesis, incorporating the full-
thickness crural column and the inner aspect of
the prosthesis (⊡ Fig. 53.1).
Now, after 15 years, 214 of 217 patients have
had successful long-term treatment of their hiatal
hernias. The hiatal hernia repairs remain intact
after initial experience using a nontension pros-
thetic repair (111 patients) or subsequent experi-
ence with 101 patients in whom a primary crural
repair was reinforced with a PTFE/ePTFE prosthe-
sis. The PTFE/ePTFE prosthesis was thought to be
safer with the ePTFE surface facing the viscera and
thereby preventing tissue ingrowth and erosion.
Seventy-five patients in this series had hiatal
defects measuring 6 cm or greater. This large per-
centage of type II and type III hernias (34%) re-
flects an aging population (the mean age of this
subset was 69 years), the increasing use of en-
doluminal therapies for small hiatal hernias, and
a continuing reluctance of gastroenterologists to
surrender pure reflux disease that can be medi-
cally managed. This 15-year experience hopes to
show that hiatal hernia repair can be made durable
with the use of prosthetic reinforcement and can
be done safely using lessons learned from other
prosthetic hernia repairs.
The superiority of prosthetic repair has been
demonstrated in numerous studies over the last
 418 Chapter 53 · Safety and Durability of Prosthetic Repair of the Hiatal Hernia: Lessons Learned from a 15-Year Experience
⊡ Table 53.2. Review articles of studies comparing pri-
mary crural closure vs. prosthetic hiatal hernia repair
Authors Year Number of patients
Targarona et al. [19] 2004 480
Granderath et al. [12] 2006 766
Johnson et al. [20] 2006 639
decade and includes three review articles (⊡ Ta-
ble 53.2) [12, 19, 20]. With thousands of patients in
hundreds of studies, ethically the time has passed
for randomization of primary repair versus pros-
thetic repair of hiatal hernia. Although there are
surgeons who are capable of tailoring crural repair
to the individual patient [21], it may be safer for
the general surgeon at large if we as a community
can further define the best practice. Prosthetic
reinforcement of the crural repair should now be
considered the standard of care. Remaining chal-
lenges include the ideal prosthesis, proper posi-
tioning, and proper fixation.
References
1. Terry M, Smith DC, Branum GD, Galloway K, Waring JP,
Hunter JG (2001) Outcomes of laparoscopic fundoplica-
53 tion for gastroesophageal reflux disease and paraesopha-
geal hernia. Surg Endosc 15:691–699
2. Cowgill SM, Gillman R, Kraemer E, Al-Saadi S, Villadolid D,
Rosemurgy A (2007) Ten-year follow up after laparoscopic
Nissen fundoplication for gastroesophageal reflux dis-
ease. Am Surg 73(8):748–752
3. Cuschieri A, Shimi S, Nathanson LK (1992) Laparoscopic
reduction, crural repair, and fundoplication of large hiatal
hernia. Am J Surg 163:425
4. Basso N, De Leo A, Genco A, Rosato P, Rea S, Spaziani E,
Primavera A (2000) 360 degrees laparoscopic fundopli-
cation with tension-free hiatoplasty in the treatment of
symptomatic gastroesophageal reflux disease. Surg En-
dosc 14(2):164–169
5. Kamolz T, Granderath FA, Bammer T, Pasiut M, Pointner
R (2002) Dysphagia and quality of life after laparoscopic
Nissen fundoplication in patients with and without pros-
thetic reinforcement of the hiatal crura. Surg Endosc
16:572–577
6. Frantzides CT, Madan AK, Carlson MA, Stavropoulos GP
(2002) A prospective, randomized trial of laparoscopic
polytetrafluoroethylene (PTFE) patch repair vs simple
cruroplasty for large hiatal hernia. Arch Surg 137(6):649–
652
7. Gryska PV, Vernon JK (2005) Tension-free repair of hiatal
hernia during laparoscopic fundoplication: a ten-year ex-
perience. Hernia 9(2):150–155
8. Turkcapar A, Kepenekci I, Mahmoud H, Tuzuner A (2007)
Laparoscopic fundoplication with prosthetic hiatal clo-
sure. World J Surg 31(11):2168
9. Müller-Stich BP, Holzinger F, Kapp T, Klaiber C (2006) Lap-
aroscopic hiatal hernia repair: long-term outcome with
the focus on the influence of mesh reinforcement. Surg
Endosc 20(3):380–384
10. Lee YK, James E, Bochkarev V, Vitamvas M, Oleynikov D
(2008) Long-term outcome of cruroplasty reinforcement
with human acellular dermal matrix in large paraesopha-
geal hiatal hernia. J Gastrointest Surg 12(5):811–815
11. Granderath FA, Schweiger UM, Kamolz T, Pasiut M, Haas
F, Pointner R (2002) Laparoscopic antireflux surgery with
routine mesh-hiatoplasty in the treatment of gastroe-
sophageal reflux disease. J Gastrointest Surg 6(3):347–
353
12. Granderath FA, Carlson MA, Champion JK, Szold A, Basso
N, Pointner R, Frantzides CT (2006) Prosthetic closure of
the esophageal hiatus in the large hiatal hernia repair
and laparoscopic anti reflux surgery. Surg Endosc 20:367–
379
13. Endzinas Z, Jonciauskiene J, Mickevicius A, Kiudelis M
(2007) Hiatal hernia recurrence after laparoscopic fun-
doplication. Medicina (Kaunas) 43(1):27–31
14. Hatch KF, Daily MF, Christensen BJ, Glasgow RE (2004)
Failed fundoplications. Am J Surg 188(6):786–791
15. Hunter JG, Smith CD, Branum GD, Waring JP, Trus TL,
Cornwell M, Galloway K (1999) Laparoscopic fundoplica-
tion failures: patterns of failure and response to fundopli-
cation revision. Ann Surg 230(4)595–606
16. Filipi CJ (2000) Laparoscopic hiatal hernia repair: why
they fail. Hernia 4:219–222
17. Kakarlapudi G, Awad Z, Haynatzki G, Sampson T, Stroup
G, Filipi CJ (2002) The effect of diaphragmatic stressors on
recurrent hiatal hernia. Hernia 6:163–166
18. Amid P, Shulman A, Lichtenstein I, Hakakha M (1994)
Biomaterials for abdominal wall hernia surgery and
principles of their applications. Langenbeck Arch Chir
379:168–171
19. Targarona EM, Bendaham G, Balague,C, Garriga J, Trias M
(2004) Mesh at the hiatus. Arch Surg 139:1286–1296
20. Johnson JM, Carbonell AM, Carmody BJ, Jamal MK, Maher
JW, Kellum JM, DeMaria EJ (2006) Laparoscopic mesh
hiatoplasty for paraesophageal hernias and fundoplica-
tions: a critical analysis of the available literature. Surg
Endosc 20:362–366
21. Granderath FA, Schweiger UM, Pointner R (2007) Laparo-
scopic antireflux surgery: tailoring the hiatal closure to
the size of the hiatal surface area. Surg Endosc 21:1900
Chapter 53 · Safety and Durability of Prosthetic Repair of the Hiatal Hernia
419 53
Discussion

Fitzgibbons: I did not hear your failure rate. You

told us a lot of information,but what was your
failure rate?
Gryska: Within this study I put the data together,
and we had a clinical success rate equivalent to
standard reflux surgery. We have a 92–93% clinical
success rate.
Fitzgibbons: The only thing I want to say is that
we recently presented 25 cases of erosion.
Gryska: I was unaware of that.
Fitzgibbons: We collected them from all around
the country.
Gryska: I found six in the literature and three an-
ecdotal.
Fitzgibbons: And we found all types of materials,
including biologicals. Surgisis, GoreTex, anything
you can imagine.
Gryska: We should take this message and pay at-
tention to hernia and keep the prosthetic away
from the esophagus.
Flament: I am glad that Dr. Fitzgibbons said this.
Because in our department within the last 2 years
we had two cases of prosthesis migrating, and I
cannot imagine having 25% of the world cases.
There are a lot of cases never reported, and that is
probably the case for most of the complications in
every field of surgery.
Gryska: I believe you are right. We just see the tip
of the iceberg and have not yet come across the
perfect mesh, the perfect way of fixating the mesh.
I think as hernia surgeons we have to think about
a better way.
Schumpelick: Thank you for the comments. The
reason we put this topic on the agenda was because
2½ years ago we had the topic of incisional hernia
here in Suvretta, and we had all the cracks of hiatal
hernia here, but we did not get a real solution on
how to handle it. Now we see good clinical results.
 54

Mesh Migration into the Esophageal

Wall After Mesh Hiatoplasty
M. Jansen and J. Otto
 422 Chapter 54 · Mesh Migration into the Esophageal Wall After Mesh Hiatoplasty

Introduction

Because of recurrence rates of up to 42% after Nis-

sen fundoplication, the implantation of prosthetic
material is recommended in cases of paraesopha-
geal herniation [1, 2]. Clinical studies of patients
with gastroesophageal reflux disease have shown
that the recurrence of symptoms is mainly caused
by intrathoracic herniation of the gastric wrap into
the mediastinum [3–5]. Since the first descrip-
tion of hiatal mesh implantation by Kuster and
Gilroy [6], many different techniques have been a

published [7]. Although large series of patients

were treated, a good understanding of indications,
mesh placement technique, mesh structure, and
mesh material is still lacking. Most studies deal
with the clinical outcome, such as dysphagia or
recurrence rate. Only a few case reports give an
account of mesh migration and perforation into
the esophagus [8, 9]. One current article by Desai
and colleagues deals with histological results 1 year
after bioprosthetic repair of paraesophageal her-
nia with a new small intestinal submucosal (SIS)
mesh. The authors found no evidence of erosion
of SIS mesh into the esophagus [10]. To examine
b
functional and histological changes in the distal
esophagus after implantation of two different al-
⊡ Fig. 54.1. a Polypropylene–polyglecaprone 25 composite
loplastic mesh materials, we performed an animal mesh fixed to the esophageal hiatus, intraoperative view.
study in rabbits. b Polypropylene mesh fixed to the esophageal hiatus, intra-
operative view

Materials and Methods

54
Animals and Anesthesia
A total of 20 female chinchilla rabbits (mean body
weight 2.5±0.3 kg) were included in this study.
The rabbits were randomly assigned to two dif-
ferent groups of equal numbers. The surgical pro-
cedure was performed under sterile conditions
and general anesthesia by intravenous administra-
tion of ketamine 10% (Sanofi-Ceva, Dusseldorf,
Germany) and xylazine (Rompun 2%; Bayer, Le-
verkusen, Germany) [11, 12].
The stomach and the distal esophagus were ex-
posed. Two different meshes–polypropylene (PP;
Prolene) and a polypropylene–polyglecaprone 25
composite (PP-PG; UltraPro)–were placed on the
hiatus as an anterior onlay patch overlapping the
hiatal crura with a circular distance to the esopha-
geal wall of 3 mm. The meshes had a diameter of
2 cm and were fixed to the diaphragm with four
polypropylene (6-0) single stitches (⊡ Fig. 54.1).
The abdominal cavity was closed with two running
sutures of 3-0 polyglycolic acid.
Functional Analysis
After 3 months the animals received general an-
esthesia again. A small gastric tube (6 Ch) was
inserted into the proximal esophagus, and water-
soluble iodine contrast medium was injected very
carefully into the esophagus until deglutition was
Chapter 54 · Mesh Migration into the Esophageal Wall After Mesh Hiatoplasty
423 54
initiated. The swallow was documented by con- Statistical Analysis
tinuous radioscopy.
All data are expressed as mean ± standard error of
the mean (SEM). Wilcoxon’s two-sample test was
Macroscopic Analysis used for statistical analysis. Differences were con-
sidered statistically significant when p<0.05.
The animals were killed by a lethal dose of pen-
tobarbital sodium (Narcoren; Rhone Merieux,
Laupheim, Germany). The abdominal cavity was Results
reopened via a U-shaped incision in the upper ab-
domen for complete exploration. Adhesions to the The initial surgical procedure was uneventful in all
mesh were examined and photo-documented, and animals. Sixteen rabbits survived the complete ob-
the severity was registered according to a scoring servation period of 3 months. Four animals (three
system [13, 14]. with PP, one with PP-PG) died of pneumonia. We
found no complications caused by the surgical
procedure.
Histochemistry and
Immunohistochemistry
Contrast Medium Swallow
The distal esophagus and the diaphragm includ-
ing the implanted mesh were resected en bloc and After 3 months we found a prolonged passage of
fixed in formaldehyde solution, and 5-μm sagittal contrast medium into the stomach in all oper-
sections were then stained with hematoxylin and ated animals, which was associated with a prest-
eosin (H&E). Light microscopy was used to evalu- enotic dilatation of the distal esophagus. However,
ate the foreign body reaction, localization of the fluid passage was possible in all cases. A complete
mesh as related to the esophageal wall, and extent stenosis was not observed. The dilatation aver-
of esophageal stenosis. aged 1.2±0.5 cm in the PP group compared with
The foreign body reaction was analyzed quan- 1.0±0.3 cm in the PP-PG group (p=0.37; ⊡ Fig. 54.2).
titatively by measuring the diameters of the for-
eign body granuloma surrounding the mesh fila-
ments. In brief, the granulomas were subdivided
into »inner ring« granuloma, representing the
inflammatory infiltrate, and »outer ring« granu-
loma, resulting from the fibrotic tissue reaction.
After five granulomas per sample were captured
with a digital camera (×400, Olympus C-3030,
Hamburg, Germany), separate measurements of
four quadrants of the inner and outer granuloma
ring were made with the help of digital image-
analyzing software (Image-Pro Plus; Media Cy-
bernetics, Silver Spring, MD, USA) [15]. The mi-
gration of the mesh into the esophageal wall was
characterized as follows: 0= no contact between
mesh and esophagus; 1= mesh migration into the
outer longitudinal muscle; 2= mesh migration into
the inner circular muscle; 3= mesh migration into ⊡ Fig. 54.2. Swallow of water-soluble iodine contrast medi-
the submucosal layer; 4= mesh migration into the um with esophageal dilatation due to polypropylene mesh
esophageal lumen. implantation
 424 Chapter 54 · Mesh Migration into the Esophageal Wall After Mesh Hiatoplasty

Histology
80

We measured the granuloma diameter at the graft– 70

tissue interface close to the esophagus as well as
close to the diaphragm in order to evaluate the ex- 60
tent of foreign body reaction. The diameter of the

Diameter [μm]
inner ring close to the esophagus, representing the 50
inflammatory infiltrate, was similar in both groups.
40
The mean diameter was 19.2±1.9 μm after implan-
tation of PP-PG mesh compared with 18.3±2.4 μm 30
for the PP mesh (p=0.4). In contrast, we observed a
significant increase in the outer ring of granuloma 20
in the PP group (76.5±8.0) compared with the
10
PP-PG group (64±8.5, p=0.002; ⊡ Fig. 54.3a, b).
a 0
inner granuloma outer granuloma
Mesh Migration Ultrapro Prolene

After 3 months, distinctive mesh shrinkage was ob- 90

served in all animals, and meshes lost up to 50% of
their original size (⊡ Fig. 54.4a, b). Because the con- 80

tiguity to the distal esophagus was of paramount 70

interest, we focused on the mesh migration into
60
the esophageal wall. Only one of the implanted PP
Diameter [μm]

meshes was located within distance of the esopha- 50

geal wall. Three (43%) meshes moved into the
40
outer longitudinal muscle layer. Two (29%) were
detected in the inner circular muscle layer. One 30
(14%) mesh had perforated the muscle layer and
20
migrated into the submucosa.
The results for the PP-PG meshes were signifi- 10
cantly different: Four (44%) meshes were located
b 0
54 outside the esophageal wall, while three (30%) inner granuloma outer granuloma
were detected in the outer longitudinal muscle and
Ultrapro Prolene
two (22%) in the inner circular muscle layer.
It must be pointed out that both types of mesh
⊡ Fig. 54.3. a Diameter of inner and outer granuloma at the
left their implantation bed and migrated into the diaphragm after implantation of polypropylene (Prolene)
esophageal wall (⊡ Fig. 54.5). and polypropylene–polyglecaprone 25 composite (UltraPro)
mesh. b Diameter of inner and outer granuloma at the eso-
phagus after implantation of polypropylene (Prolene) and
Discussion polypropylene–polyglecaprone 25 composite (UltraPro) mesh

Johnson et al. [7] reviewed the literature on lap-

aroscopic mesh hiatoplasty and concluded that
current data »tend to support the use of prosthetic
materials for hiatal repair.« Nevertheless, different
techniques (anterior–posterior, onlay interposi-
tion) and mesh materials (polypropylene [16–19],
polytetrafluoroethylene [20, 21], Surgisis [22], Al-
loderm) were used, and the current data focus only
on the clinical outcomes.
However, data concerning implantation of al-
loplastic material for repairing incisional hernias
Chapter 54 · Mesh Migration into the Esophageal Wall After Mesh Hiatoplasty
425 54

a a

b b

⊡ Fig. 54.4. a Polypropylene–polyglecaprone 25 composite
mesh 3 months after implantation; adhesion to the liver
and stomach was removed. b Polypropylene mesh 3 months
after implantation; adhesion to the liver and stomach was
removed
⊡ Fig. 54.5. a Hematoxylin and eosin (H&E) staining of the
distal esophagus (magnification ×40) with submucosal de-
tection of mesh fibers (polypropylene). b H&E staining of the
distal esophagus (magnification ×40) with detection of mesh
fibers (polypropylene–polyglecaprone 25 composite) within
the longitudinal esophageal muscle layer

show the superiority of reduced-material meshes
with large pores to minimize the inflammatory
response and scar formation [23–26]. Extensive
work has led to several mesh modifications to
adapt to physiological requirements and improve
biocompatibility [15, 27, 28]. In particular, the
drawbacks of PP mesh implantation have been elu-
cidated and have led to mesh modifications such as
combined mesh materials [28–30].
A new composite mesh consisting of a reduced
amount of polypropylene supplemented with poly-
glecaprone 25 minimizes the development of gran-
ulomatous chronic foreign body reaction. Polygle-
caprone 25 filaments were essentially degraded
84 days after implantation [31]. Requirements for
mesh materials used for the repair of hiatal hernias
have not yet been shaped. Case reports indicate the
problem of mesh migration into the esophagus,
and, to the author’s knowledge, several oral reports
on this topic were presented at different meetings
in recent years. These reports may underscore the
necessity to analyze the biological and functional
outcomes of meshes used for hiatoplasty [9, 32].
A first attempt at mesh modification was done
by Desai et al. [10]. The researchers found that
implanting a small intestinal submucosal mesh led
to good reinforcement of the hiatus with marginal
foreign body reaction and native ingrowth of con-
nective tissue and skeletal muscle. However, this
type of mesh is not used widely in clinics.
 426 Chapter 54 · Mesh Migration into the Esophageal Wall After Mesh Hiatoplasty
The results of our experiments clearly indi-
cate that circular implantation of meshes around
the esophagus leads to a high rate of mesh mi-
gration. Furthermore, heavyweight polypropyl-
ene meshes are less compatible compared with
lightweight composite mesh (PP-PG). We found a
higher rate of migration into the esophageal wall
and an increased extent of foreign body reaction
with PP mesh compared with the PP-PG mesh.
These results are consistent with the biology of
meshes used in the treatment of incisional her-
nias [33–35]. Although the data were generated in
rabbits and have limited impact on humans, our
presented animal model can be used to develop the
necessary requirements for mesh hiatoplasty. More
experimental data are necessary to assess the opti-
mal size, structure, and positioning of prosthetic
materials for mesh hiatoplasty [36, 37].
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16. Granderath FA, Kamolz T, Schweiger UM, Pointner R. Im-
pact of laparoscopic Nissen fundoplication with pros-
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17. Granderath FA, Carlson MA, Champion JK, Szold A, Basso N,
Pointner R, Frantzides CT. Prosthetic closure of the esopha-
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18. Granderath FA, Kamolz T, Schweiger UM, Pointner R. Pros-
thetic material for crural closure in laparoscopic antireflux
surgery. Surg Endosc 2004 Jan; 18(1):171–2
19. Keidar A, Szold A. Laparoscopic repair of paraesophageal
hernia with selective use of mesh. Surg Laparosc Endosc
Percutan Tech 2003 Jun; 13(3):149–54
20. Frantzides CT, Madan AK, Carlson MA, Stavropoulos GP. A
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21. Hui TT, Thoman DS, Spyrou M, Phillips EH. Mesh crural
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22. Oelschlager BK, Barreca M, Chang L, Pellegrini CA. The use
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23. Klosterhalfen B, Klinge U, Hermanns B, Schumpelick V.
[Pathology of traditional surgical nets for hernia repair
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24. Schumpelick V, Klinge U, Welty G, Klosterhalfen B.
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Arlt G, Langer C, Schippers E, Hartley M, Schumpelick V.
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27. Klinge U, Junge K, Spellerberg B, Piroth C, Klosterhalfen
B, Schumpelick V. Do multifilament alloplastic meshes
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surface, the bacteria adherence, and the in vivo con-
sequences in a rat model. J Biomed Mater Res 2002;
63(6):765–71
28. Klinge U, Klosterhalfen B, Ottinger AP, Junge K, Schumpelick
V. PVDF as a new polymer for the construction of surgical
meshes. Biomaterials 2002 Aug; 23(16):3487–93
29. Conze J, Junge K, Klinge U, Weiss C, Polivoda M, Oettinger
AP, Schumpelick V. Intraabdominal adhesion formation of
polypropylene mesh. Influence of coverage of omentum
and polyglactin. Surg Endosc 2005 Jun; 19(6):798–803
30. Conze J, Rosch R, Klinge U, Weiss C, Anurov M, Titkowa S,
Oettinger A, Schumpelick V. Polypropylene in the intra-
abdominal position: influence of pore size and surface
area. Hernia 2004 Dec; 8(4):365–72
31. Junge K, Rosch R, Krones CJ, Klinge U, Mertens PR, Lynen
P, Schumpelick V, Klosterhalfen B. Influence of polygle-
caprone 25 (Monocryl) supplementation on the biocom-
patibility of a polypropylene mesh for hernia repair. Her-
nia 2005 Oct; 9(3):212–7
32. Hergueta-Delgado P, Marin-Moreno M, Morales-Conde S,
Reina-Serrano S, Jurado-Castillo C, Pellicer-Bautista F, Her-
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Gastrointest Endosc 2006 Jul; 64(1):120
33. Klinge U, Klosterhalfen B, Muller M, Schumpelick V. For-
eign body reaction to meshes used for the repair of ab-
dominal wall hernias. Eur J Surg 1999 Jul; 165(7):665–73
34. Klinge U, Klosterhalfen B, Muller M, Ottinger AP, Schumpe-
lick V. Shrinking of polypropylene mesh in vivo: an experi-
mental study in dogs. Eur J Surg 1998 Dec; 164(12):965–9
35. Klinge U, Klosterhalfen B, Conze J, Limberg W, Obolenski
B, Ottinger AP, Schumpelick V. Modified mesh for hernia
repair that is adapted to the physiology of the abdominal
wall. Eur J Surg 1998 Dec; 164(12):951–60
36. Aly A, Munt J, Jamieson GG, Ludemann R, Devitt PG,
Watson DI. Laparoscopic repair of large hiatal hernias. Br J
Surg 2005 May; 92(5):648–53
37. Andujar JJ, Papasavas PK, Birdas T, Robke J, Raftopoulos Y,
Gagne DJ, Caushaj PF, Landreneau RJ, Keenan RJ. Laparo-
scopic repair of large paraesophageal hernia is associated
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Endosc 2004 Mar; 18(3):444–7
427 54
Discussion
Kukleta: I would like to make a comment on the
strategy of the team of Pointner and Granderath. It
is a pity that they are not here, because they repre-
sent a very big experience in this field. It is obvious
that they achieved good results with these very
small one to three hernias and a mesh placed pos-
teriorly, and they improved their recurrence rate
immensely. And the number three and four are
obvious too, because for the very large paraesopha-
geal hernia, this was not enough. So the condition
of the crura was responsible for the two branches.
If the crura are fine, they rely on the crural suture
repair, and then they packed it posteriorly.
The other ones are the desperate cases which
you nearly cannot suture, and nobody believes that
that region can be tension-free covered for such a
long time, but there are several papers from Italy
where they placed a mesh circularly. Especially in
the anterior part, the mesh gets very, very close to
the esophagus. In the posterior part you can get
the 1-cm distance, so you actually do not have any
contact from the mesh to the esophagus. And if
you do a fundoplication, it will cover the mesh.
Jansen: I totally agree, and I think the idea of
Granderath is not that bad. What I would like to
avoid is that the indication for mesh implantation
comes nowadays to the situation that you implant
a mesh in every case. I do not think that is nec-
essary. I totally agree that we have problems in
dealing with these huge hiatal hernias, and for this
indication a mesh is probably necessary.
Matthews: We actually have a clinical trial going
on right now with patients with type 1 hernias
and type 3 hernias and in which we performed a
biopsy of endoabdominal fascia. What we found
was that these patients have tissue abnormalities
that are different even between the type 1 and
type 3 hernias, and so we are trying to understand
more about the basics. Probably in the future we
will be able to selectively use a mesh, as in inguinal
hernia.
Jansen: When I look at the literature, it is very
interesting that people dealing with hiatal hernia
have never read the huge [amount of] literature
based on pathophysiological aspects of incisional
hernia. There are so many questions not answered
 428 Chapter 54 · Mesh Migration into the Esophageal Wall After Mesh Hiatoplasty

in this area concerning everything we discussed. probably 80–90% of normal hiatal hernias can
Everyone tries a new shape of mesh or places be treated without a mesh with a primary suture.
meshes which were intended for incisional hernia And there are 5–10%, large or paraesophageal
for a long time. We have to think about the basics. hernias, which need a mesh. If you take this figure
What is the anatomy, the physiology? We need as the tailored approach, yes, probably we have to
good experimental results before placing a mesh in propagate it. But we probably do not need three
every hiatal hernia. to five different meshes for three to five different
Schippers: On Wednesday we had a lot of discus- indications.
sion concerning animal models, looking for the Schüssler: I am the gynecologist in this room, and
influence of meshes on the cord. And at that time I am the least to give answers, but what I’d like to
we were wondering whether the rat model is the ask you is, we have these small babies with large
appropriate animal. Maybe you would have had diaphragmatic hernias being easily repaired by the
fewer reactions to the mesh if you would have had pediatric surgeons without mesh materials. Is there
bigger animals? anything to learn from them? Just an ignorant
Jansen: Yes, probably. question. Maybe they can help a little bit.
Klinge: In this area, can it be a good indication to Jansen: I think it is a different situation. Dia-
use biologicals? phragmatic hernia cannot be compared to hiatal
Jansen: Perhaps. hernias.
Klinge: Is there any information from the litera- Kukleta: Just one more question. Do you think
ture? large paraesophageal hernias, type 3, are for every
Jansen: I do not know any. Probably there is some general surgeon?
clinical work on it. What you cannot find is any Jansen: No.
experimental work on biologics at the hiatus. Most
of the studies are clinical and not basic scientific
work.
Chowbey: Repairing hiatal hernia, there is one
point we are not considering seriously: The food
bolus is coming from the esophagus, and it needs
its space to go down to the stomach. Also, we have
to keep in mind that there will be a certain amount
of stasis in the lower part of the esophagus. If we
keep these two points in mind, probably our repair
54 will be better.
Schumpelick: I would like to hear from the audi-
ence. Who is using a mesh in second-size hiatal
hernias? ... Just three. And who never uses a mesh?
… It is the majority.
Chowbey: We have to look at the literature. As
we moved on from suture to prosthetic repair in
incisional hernia, there is the same trend in hiatal
hernia.
Gryska: The question I ask you is about the tai-
lored approach. I fear that the average surgeon
doing hiatal hernia surgery does not think as much
as we do. Do you believe the tailored approach can
be translated to general surgeons?
Jansen: The question is, what is the definition
of the tailored approach? I think in most cases,
 55

Complications After Gastric

Banding–Results in Germany
C. Stroh and T. Manger
 430 Chapter 55 · Complications After Gastric Banding–Results in Germany
Introduction
Worldwide, approximately 1.7 billion people are
overweight or obese [16, 23, 63]. Morbid obesity
is associated with numerous comorbidities such as
diabetes, hypertension, cardiac diseases, sleep ap-
noea syndrome, and degenerative skeletal diseases.
Every year, about 2.5 million obese people die from
their comorbidities [62]. The costs of these comor-
bidities are estimated to exceed $117 billion per
year in the United States [9].
In the international comparison, the Federal
Republic of Germany is one of the countries with a
very high prevalence of obesity. For this condition,
gastric banding is the most frequently performed
bariatric operation in Europe [3, 4, 30]. Complica-
tions such as slippage, pouch dilatation, and band
disconnection can be treated by repositioning the
band or by performing a bypass in the case of its
failure, but band erosion always requires band
removal.
Neither the impact of the selected surgical
procedure on perioperative morbidity, weight loss,
and degree of decrease in comorbidities nor the
profile of long-term complications have yet been
investigated in prospective studies. Therefore, ex-
periences with postoperative complications are
presented with an emphasis on the necessity of
quality assurance in the surgical treatment of mor-
bid obesity in Germany.
Discussion
After Roux-en-Y gastric bypass, gastric banding
55 is the most frequently performed bariatric opera-
tion worldwide. According to data compiled from
meta-analysis, it is carried out in 95% of countries
performing bariatric surgery (⊡ Table 55.1) [8].
Meta-analysis reports the amelioration of co-
morbidities such as diabetes, hypertension, hyper-
lipidaemia, and sleep apnoea without any recom-
mendations regarding long-term complications. In
the literature, only a few prospective randomised
studies have been reported. These studies compare
gastric banding with other bariatric procedures,
especially with Roux-en-Y gastric bypass and
sleeve gastrectomy. Otherwise, randomised trials
⊡ Table 55.1. Incidence of gastric banding worldwide [8]
Patients Countries
Roux-en-Y gastric bypass 65.11% 88%
Gastric banding 24.41% 95%
Vertical banded gastroplasty 5.43% 79%
Biliopancreatic diversion or 4.85% 67%
duodenal switch
have compared low-pressure and high-pressure
bands. Reports in the literature on complication
rates come only from single centres. The patient’s
outcome after gastric banding is influenced by the
long-term complications: slippage, pouch dilata-
tion, band migration, and port-site complications.
Slippage and Pouch Dilatation
The incidence of slippage has decreased since
the introduction of the »pars flaccida« technique
(⊡ Figs. 55.1 and 55.2) [58]. Pouch dilatation is a
long-term complication after gastric banding. Its
incidence is influenced by the surgical approach
(open vs. laparoscopic) and the technique (peri-
gastric vs. pars flaccida). Opening the lesser sac
during open band placement leads to a higher in-
cidence of pouch dilatation than the laparoscopic
approach does, with the creation of a small retro-
gastric channel. Data in the literature on the inci-
dence of pouch dilatation are very heterogeneous
because most studies include different approaches
and techniques. Many reports have a follow-up of
less than 5 years (⊡ Table 55.2).
Band Migration
Intragastric band migration is characterised by a
»silent« migration of the band into the stomach
(⊡ Figs. 55.3 and 55.4) [57, 60]. Peritonitis symp-
toms are usually absent. Only very limited retro-
spective data obtained from long-term studies are
available [8, 10, 34, 53, 64]. The incidence of band
migration ranges from 0.6% to 11% according to
Chapter 55 · Complications After Gastric Banding–Results in Germany
431 55

⊡ Fig. 55.1. Slippage ⊡ Fig. 55.2. Slippage

⊡ Table 55.2. Literature review on pouch dilatation (BMI body mass index; PG perigastric; PF pars flaccida)

First author Year Technique n BMI (kg/m²) Pouch dilatation Maximum follow-
rate (%) up (months)

Forsell [19] 1999 PG 326 Unknown 0.6 78

Doldi [17] 2000 PG 172 46.3 5.8

Szould [53] 2002 PF 715 43.1 7.40 30

Steffen [43] 2003 PF 824 42.2 2.70 60

Celen [13] 2003 PG 625 40 5.6

Zinzindohoue [65] 2003 PG/PF 500 44.3 8.00

Weiner [59] 2003 PF 984 46.8 >3.7 99

Angrisani [4] 2004 PF 3,562 43.3 4.1 60 (16.1%)

Chevallier [11] 2004 PF 1,000 44.3 10.4 72

Martikainen [27] 2004 PG/PF 123 49 21.0 108

Ren [37] 2004 PF 445 49.6 3.1 18

Silecchia [41] 2004 PF 313 46.1 3.2 Unknown

Zehetner [64] 2004 PF 190 Unknown 2.60 72

Spivak [42] 2005 PF 500 45.2 9.6

Stroh [46] 2005 PG/PF 3,973 Unknown 7.3 120

Stroh [45] 2005 PG/PF 168 49.6 10.70 120

Michelotto [29] 2006 PG/PF 684 42.2 6.1 60

Schouten [39] 2006 PG/PF 177 44.6 10.7 94

Suter [52] 2006 PG/PF 317 43.5 6.3 96

Balsiger [6] 2007 PF 196 44 12.2 108

Faretti [18] 2007 PG/PF 1,791 46.2 3.9 147

 432 Chapter 55 · Complications After Gastric Banding–Results in Germany

the literature [11, 28, 33, 40] (⊡ Table 55.3). In a
few studies, band migration has been considered
a complication of the first 2 postoperative years,
caused by intraoperative gastric perforation [12,
13, 18, 24, 29, 55].
⊡ Fig. 55.3. Band migration
55
⊡ Fig. 55.4. Band migration
The data show an erosion rate of 60% in cases
of intraoperative gastric perforation versus 3%.
In our data, patients with a noncritical intake
of nonsteroidal antirheumatic agents, bronchos-
pasmolytic drugs, and anticoagulant substances
showed a higher incidence of band migration. In
53.3% of cases with intragastric band migration,
the patients had been treated with nonsteroidal
antirheumatic substances (26.6%), anticoagulant
substances (20.0%), or bronchospasmolytic agents
(0.6%). That is why, in our opinion, these medica-
tions should be considered a further cause of band
migration. Simultaneous cholecystectomy did not
significantly increase the erosion risk in our study.
Chronic inflammation at the tissue area cov-
ered by the band could be a further reason for
the development of erosion [1]. For example, in
our experience band migration occurs by 30–86
months postoperatively. Interestingly, the erosion
rate increased with long-term follow-up [44, 46,
48–50, 52].
Band erosion can lead to a life-threatening
condition in cases of upper gastrointestinal bleed-
ing and bowel obstruction [15, 54]. Therefore, cor-
rect diagnosis is essential. In our study we did not
seen any port infection in the first 3 months after
operation and after band filling. In the literature,
port infection has been reported to be the first
symptom of erosion [25, 44]. However, our own
data reveal varying intervals between the onset of
port infection and the occurrence of erosion.
The treatment depends on symptomatology
(⊡ Fig. 55.5) [41]. We favour band removal in cases
of complete erosion, using gastroscopy and the
AMI Band Cutter (CJ Medical, Buckinghamshire,
UK) [57]. Gastroscopy is recommended at several
time points to recognise complete erosion; we pre-
fer intervals of 8 weeks. In the literature, 4-month
intervals have been reported [41]; such intervals
require patient reporting of information on possi-
ble complications as well as an acceptable distance
between the patient’s residence and the hospital.
Laparoscopy with intraoperative gastroscopy
using the AMI Band Cutter is a safe method of
band removal. A lesion of the gastric wall can be
sutured, and a drain can be placed. In patients
with bleeding of the upper gastrointestinal tract
or abscess, the band has to be removed via lapa-
Chapter 55 · Complications After Gastric Banding–Results in Germany
433 55

⊡ Table 55.3. Literature review on incidence of band migration (BMI body mass index; OP operation; PG perigastric; O open;
L laparoscopic; SAGB Swedish Adjustable Gastric Bands; PF pars flaccida; HG Heliogast band)

First author Year n BMI Rate OP OP Type Follow-up Maximum

(%) rate (%) follow-up
(months)
Forsell [19] 1999 326 4.6 PG SAGB 97 78
Meir [28] 1999 122 1.6 O/L PG Lap-Band 88 60
Miller [30] 1999 158 43 0.6 L PG SAGB 98 46
DeJonge [15] 2000 91 44.7 3.3 L PG Lap-Band 100 24
Doldi [17] 2000 172 46.3 0.6 O/L PG Lap-Band 99.4 72
Weiss [57] 2000 211 1.9 L PG Lap-Band 33
Baldinger [5] 2001 714 1.0 L PG SAGB
Holeczy [22] 2001 36 45.6 0 L PG Lap-Band 24
Silecchia [40] 2001 148 44.2 7.5 L PG Lap-Band 831 54
Niville [34] 2001 301 42.5 1.66 L PG Lap-Band 984 73
Belachew [7] 2002 763 42 0.9 L PG Lap-Band 90 66
Gustavsson [21] 2002 90 43 14.4 O PG SAGB
Szold [53] 2002 715 43.1 0.5 30
Wolff [61] 2002 256 47 0.8 PG/PF Unknown 48
Steffen [43] 2003 824 42.2 1.6 L PF SAGB 97 60
Coskun [14] 2003 70 45.2 2.8 O/L Lap-Band 39
Vertuyen [56] 2003 727 45 1.4 PG Lap-Band Unknown
Weiner [59] 2003 984 46.8 0.3 L PG/PF Lap, HG, SAGB 972 99
Angrissani [4] 2004 3,562 43.4 2.1 L PG/PF 161 60
Chapman [10] 2004 8,504 0.6 Unknown
Chevallier [11] 2004 1,000 44.3 0.30 L Lap-Band 72
Martikainen [27] 2004 123 49.0 9.00 108
Mittermair [31] 2004 682 0.8 L PF SAGB 48
Silecchia [41] 2004 313 46.1 5.1 L PG/PF Lap-Band 90
Ren [37] 2004 445 49.6 0.2 L PF Lap-Band 18
Zehetner [64] 2004 190 Unknown 2.1 72
Abu-Abeid [2] 2005 754 2.1 L PF Lap-Band 40
Nocca [35] 2005 4,236 43.2 1.6 L PG/PF All
Stroh [46] 2005 3,973 1.0 O/L PF/PG All 120
Stroh [45] 2005 168 49.6 4.2 O/L PG/PF Lap-Band 120
Michelotto [19] 2006 684 42.2 1.1 O/L PG/PF Unknown 60
Suter [52] 2006 317 43.5 9.5 L PG/PF Lap/SAGB 81.5 96
Lattuada [26] 2007 571 42.9 0.52 L PG/PF Lap, HG, SAGB 100
Balsiger [6] 2007 196 44 1.5 L PF SAGB 108
Favretti [18] 2007 1791 46.2 0.9 L PG/PF Lap-Band 145
 434 Chapter 55 · Complications After Gastric Banding–Results in Germany

Symptoms

Nonspecific symptoms Port Bleeding Intraabdominal

Vomiting infection Bowel obstruction abscesses

Contrast swallow Abdominal ultrasound

Gastroscopy Computed tomography
Abdominal ultrasound to exclude intraabdominal

Removal of the port system

Band removal via gastroscopy Laparoscopic band removal Open band

using AMI Band Cutter (CJ and intraoperative gastroscopy removal
Medical, Buckinghamshire, UK) using AMI Band Cutter
after complete band migration

⊡ Fig. 55.5. Differentiated treatment of gastric band migration [44]

rotomy if laparoscopy fails. Tangential resection of
the gastric wall can become necessary in cases of
massive bleeding.
In the literature, a correlation of the erosion
rate to the band type (high-pressure vs. low-pres-
sure band) has not been described [20, 21, 54]. The
data presented here show that the erosion rate of
the LAP-Band (Inamed Health, Santa Barbara, CA,
55 USA) is higher than that of the Gastrobelt (MED-
ING, Germany) or Swedish Adjustable Gastric
Bands (SAGB; Obtech, Ethicon Endo-Surgery),
but SAGB have been used only for the last 2 years.
At the end of the 1990s, repositioning of the
band in cases of slippage and pouch dilatation was
widely performed, but the data from our study–
with a higher incidence of gastric band migra-
tion–as well as the data in the literature show dis-
appointing results [44, 45, 48]. That is why, in
accordance with the literature [52], we see no
indication for rebanding in cases of slippage or
pouch dilatation. Band removal and rebanding
performed in one surgical intervention have been
described in the literature [2]. Because of the dif-
ferent causes of band erosion and the significantly
higher migration rate following intraoperative gas-
tric perforation, and based on the currently avail-
able data, band removal in cases of erosion with
simultaneous rebanding should not be performed
since there is a potential risk of infection of the
new band. In addition, because of the high failure
rate after band revision, a conversion to Roux-
en-Y gastric bypass or biliopancreatic diversion
needs to be considered [31].
Since January 1, 2005, data collected in the
German multicentre observational study for qual-
ity assurance in obesity surgery for all bariatric
interventions and revisions have been available
online for assessing the surgical treatment of mor-
bid obesity [47]. Although patients are selected
according to the guidelines of the International
Federation for the Surgery of Obesity, the Eu-
ropean Association for Endoscopic Surgery, and
Chapter 55 · Complications After Gastric Banding–Results in Germany
the German Society for Surgery of Obesity [38],
substantial differences are encountered when com-
paring centres of bariatric surgery because of the
regionally varying incidences of morbid obesity
and the house policies of the different surgical de-
partments. For instance, age and body mass index
(BMI) of the surgically treated patients are sig-
nificantly higher in Germany compared with data
obtained in the meta-analysis on bariatric surgery
[8]. In addition, significantly more patients suffer
from type II diabetes mellitus and arterial hyper-
tension.
The possible consequence of a higher comor-
bidity rate is severe metabolic syndrome. The im-
pact of a high(er) preoperative BMI on weight
reduction needs to be investigated through a long-
term study. Data obtained in the German multi-
centre observational study for quality assurance
in obesity surgery also confirm the worldwide
tendency towards combined and malabsorptive in-
terventions to reduce both body weight and the
frequency of comorbidities. This effect is under-
scored by the very high BMI of German patients.
According to the literature, the reintervention rate
per year of follow-up after a stomach volume op-
eration is between 3% and 4% [6, 52]. Prospective
long-term trials are necessary to detect short-term
and long-term complications after different bariat-
ric procedures. The amelioration of comorbidities
should not be a single point of the studies because
the complication rate after bariatric surgery seems
to be higher than that reported in the literature.
Predictive factors for patients’ election for differ-
ent procedures should be evaluated to reduce the
complication and reoperation rates.
Conclusion
There are varying symptoms of band erosion.
Those such as weight regain, nonspecific epigas-
tric pain, and vomiting are less severe, but more
serious complications include bowel obstruction
and acute bleeding of the upper gastrointestinal
tract. Because some patients show only nonspecific
symptoms, the erosion rate is assumed to be higher
than reported [12, 24, 36, 54]. The increasing inci-
dence during long-term follow-up has not yet been
435 55
well described [41, 50, 52]. Through long-term
follow-up, researchers need to investigate whether
the advantages of the low-pressure bands also re-
sult in a decreased erosion rate. In addition, the
relevance of band manometry should be investi-
gated in studies [44]. Patient-related factors such
as the intake of nonsteroidal anti-inflammatory
drugs, bronchospasmolytic drugs, and anticoagu-
lant substances must be included in data analy-
sis and further studies. Band migration should
be treated according to symptomatology and the
patient’s specific condition. In our opinion, the
higher incidence of band migration after intraop-
erative gastric perforation is a contraindication to
replacing a new gastric band after band removal
because of erosion [34]. In this case, conversion to
either Roux-en-Y gastric bypass or biliopancreatic
diversion is recommended [32].
Furthermore, there are no data in the litera-
ture on specific criteria that would allow us to
select patients, either for restrictive or malabsorp-
tive procedures, to improve final outcomes. To
guarantee long-term success after bariatric surgery
and to avoid complications, particularly following
combined procedures, lifelong postoperative care
is required; this is a specific peculiarity of obesity
surgery. Because only low-level evidence is avail-
able, based on limited long-term follow-up data
obtained in a few single-centre studies, prospective
research enrolling all patients is indicated. This is
being done by the German multicenter observa-
tional study for quality assurance in obesity sur-
gery. In this study, weight reduction, amelioration
of comorbidities, and long-term complications are
registered annually as parameters that assess daily
practice in the surgical treatment of morbid obe-
sity in Germany [44].
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 438 Chapter 55 · Complications After Gastric Banding–Results in Germany

Discussion we just started a register, and we hopefully will

have some answers in a few years.
Gryska: Having a look at a reoperation rate of Schumpelick: Thank you very much for the com-
30%, do you think we should look at gastric band- ment.
ing as something we should do or should not do Klinge: Are there any analyses using Kaplan–Meier
anymore? curves showing the cumulative incidence rates of
Stroh: That is a big discussion. In Europe, the situ- complications? The reason is that, as in incisional
ation is that the rate of gastric banding performed hernia, we know that the means given in the lit-
is decreasing more and more. And malabsorptive erature have to at least be doubled over the long
procedures are increasing. But in the States, it is term.
quite different at the moment, because after the Schumpelick: You presented the data to the Ger-
FDA approval, bandings are performed more and man Surgical Society. What was the reaction?
more. But you should be careful having a look at Stroh: Moving away from the band.
the European data.
Franz: You are right. In my hospital I am required
to report every explantation and the reason why
I do so. This is a medical–legal protection for the
hospital. Are you required in Germany to report
explantations to somebody?
Stroh: No. That is a very big problem in Germany.
And a very big problem for the insurance system
as well.
Franz: Bruce. Do you have to report?
Ramshaw: Not at this point. The biggest question
is, who is going to fund this collection?
Chowbey: What approach do you use for place-
ment of the band?
Stroh: We are using the pars flaccida technique.
Chowbey: But most of the studies you showed
used the perigastric approach.
Stroh: This is why it is really difficult to show if
this complication is really increasing or just a com-
plication of an approach which nobody uses any-
more. We know that slippage is decreasing, and we
know that pouch dilatation is decreasing, but we
55 really do not know if migrating is really decreas-
ing. So we have used the pars flaccida technique
since 2000, and band migration is occurring after
10 years. So we really do not know today if this
complication is really decreasing as well.
Chowbey: In India we are moving away from the
band because we saw that 25–35% of the patients
need further operations or explantation of the
band.
Bringman: I work in Stockholm, where gastric
banding was invented, and we almost stopped us-
ing it due to its complications. Another comment
is that concerning registration of obesity surgery,
 56

Alloplastic Implants for the Treatment

of Stress Urinary Incontinence
and Pelvic Organ Prolapse
T. Kavvadias, U. Klinge, B. Schuessler
 440 Chapter 56 · Alloplastic Implants for the Treatment of Stress Urinary Incontinence and Pelvic Organ Prolapse
Introduction
Stress urinary incontinence (SUI) is the complaint
of involuntary leakage with effort or exertion or
with sneezing or coughing [1]. Urethral hyper-
mobility, which permits urethral opening during
stress, as well as insufficiency of the urethral
sphincter seem to be the two main contributing
factors that lead to the above mentioned symp-
toms [2]. Pelvic organ prolapse (POP)–which is
defined as protrusion of the anterior vaginal wall,
the vaginal cuff, and the posterior vaginal wall,
thus including the bladder, enterocele, or rectum–
often shows a strong correlation with lower uri-
nary tract symptoms in women [3]. Apart from
the objective findings, symptoms of POP are
heaviness, a dragging sensation, and the need to
digitally replace the prolapse in order to defecate
or micturate [1]. POP development is multifacto-
rial; vaginal childbirth, advancing age, and in-
creased body mass index seem to be the most
consistent risk factors [4].
The measured prevalence of urinary inconti-
nence varies widely among different populations
and age groups and is very sensitive to how the
survey was conducted and whether urodynamics
were performed. Reports of »any« incontinence or
»at least once in the past 12 months« are estimated
to apply to 25–45% of adult women, and SUI has
a percentage of 50% [5]. The prevalence of POP
seems to be around 29% of the female population,
according to the presence of symptoms [6].
Apart from the obvious high prevalence of SUI
and POP, they both have a significant impact on
a woman’s quality of life [2]. The symptoms affect
a woman’s everyday life in many ways, including
decreased physical and sexual activity, diminished
56 social and self-confidence, and low overall quality
of life and sense of well-being.
Today, surgery is the most promising and ef-
fective therapy for both SUI and POP, showing
high rates of subjective and objective cure and
strong improvement in terms of quality of life.
Lately there is an ongoing tendency to use meshes
in the surgical treatment of SUI and POP, with
the development of the »perfect« material and
technique being in focus. This chapter presents an
overview of mesh surgery in urogynecology (SUI
and POP) with special emphasis on the advantages
and unresolved issues.
Meshes in Stress Urinary Incontinence
Abdominal colposuspension was the procedure of
choice for surgical management of SUI until 1995,
when Ulmsten and Petros introduced the intra-
vaginal slingplasty using polypropylene mesh, a
procedure that was received with great enthusiasm
because of its simplicity and short operating time
[7]. In a controlled randomized trial, this proce-
dure was shown to have no inferiority in terms of
efficacy as well as in the long term. Success rates
reach 81%. Furthermore, it is advantageous in
terms of fewer postoperative complications and
less recovery time compared with colposuspension
[8]. However, although well manageable, bladder
injury caused by insertion of the trocar is more
common when using the sling procedure [9].
At present, the gold standard in SUI surgery
is the suburethral sling, using either the tension-
free vaginal tape (TVT) or the transobturator tape
(TOT) technique (⊡ Fig. 56.1). The two procedures
do not seem to differ in terms of efficacy, with
TOT being advantageous because of the lower rate
of bladder injuries [10].
The initial concern that the meshes used might
lead to high rates of erosion did not hold true
when macroporous polypropylene was used. In
two long-term trials, the erosion rate was 1.7% and
3.1%, respectively. Most of the erosion was into the
vagina [9, 11], whereas erosion into the urethra or
bladder was more or less anecdotal [12].
However, low erosion rates in SUI depend on
the selection of material. A prospective random-
ized controlled trial by Meschia et al. showed
that vaginal erosion of the Amid type III mesh
used for intravaginal slingplasty was as high as
9% in a 2-year follow-up, which is significantly
higher compared to 0% using the classical TVT
(type I macroporous, monofilament, polypropyl-
ene mesh) in the same trial [13]. This was sup-
ported by Baessler et al., who showed a series of
major complications, including erosion of this type
of mesh, in a case series of 19 women treated with
intravaginal slingplasty [14].
Chapter 56 · Alloplastic Implants for the Treatment of Stress Urinary Incontinence
⊡ Fig. 56.1. Routes for transobturator and retropubic slings
⊡ Fig. 56.2. Removal of an eroded transobturator Safyre sling
after dislocation of the right silicone arm under the vaginal
mucosa
⊡ Fig. 56.3. Accumulation of macrophages around the fila-
ments of a polypropylene mesh (suburethral sling)
441 56
The use of silicone also seems to increase ero-
sive complications. Kuschel et al. demonstrated
dislocation of the silicone column of the TOT-Sa-
fyre, a composite sling consisting of a macroporous
polypropylene mesh beneath the urethra and two
silicone arms anchoring the sling. The erosion rate
reached a percentage of 8.8%, mainly as a result of
dislocation of the silicone arm from its lateral posi-
tion beneath the vaginal mucosa (⊡ Fig. 56.2) [15].
With ongoing research and further develop-
ment of existing macroporous materials, incidents
such as the »rolling effect« of the suburethral
sling are more or less under control. However,
inflammatory reaction around the mesh cannot
be avoided. Macrophage accumulation around the
filaments of the tape, cellular proliferation, and
changes in collagen composition are present in
the vaginal wall, identical to the reaction found
in the abdominal wall after hernia mesh surgery
(⊡ Fig. 56.3) [16].
Although erosion is not a major complication
all in all, development of the right material is still
an issue. Overall, the properties and requirements
of the sling material that might guarantee high
success rates combined with fewer complications
can be defined as follows: pore size >1 mm, little
elasticity (<10%), and width ≥1 cm to prevent cut-
ting through the urethra under load. The tensile
strength must not necessarily be >2 N/cm, and the
tension by application should not exceed 3–5 kPa;
this limitation could eventually be objectified by
future intraoperative measurements. The biologi-
cal properties of the mesh should guarantee mini-
mal inflammation and fibrosis with little white cell
turnover and little shrinkage. Sharp-ending fibers
must be avoided because they may stimulate the
inflammatory response. Nonabsorbable, perma-
nent, and synthetic materials should be preferred
instead of collagen devices [17].
Meshes in Pelvic Organ Prolapse
Besides conservative options such as vaginal pes-
saries and physiotherapy, surgery is the mainstay
of POP treatment. Surgery in prolapse is a three-
target issue: (1) control of prolapse, (2) control
or avoidance of problems related to bladder and
 442 Chapter 56 · Alloplastic Implants for the Treatment of Stress Urinary Incontinence and Pelvic Organ Prolapse
bowel function, and (3) restoration or improve-
ment of cohabitation, without new dyspareunia
either for the female patient or her male partner.
Basically, there are two different approaches:
(1) transvaginal fixation of the vaginal cuff without
mesh and (2) abdominal cuff fixation with mesh,
which is necessary to bridge the vaginal cuff for
fixation at the hollow of the sacrum.
In a Cochrane review, Maher et al. compared
the surgical routes used in pelvic surgery. They
found that the vaginal approach offers less surgery
time, a quicker return to activities, and lower costs;
the abdominal approach showed lower recurrence
rates and less dyspareunia, at the expense of a
mean erosion rate of 3.2% [18].
Therefore, vaginal mesh techniques might be
able to combine the advantages of both procedures:
less surgery time, a quicker return to activities, and
lower costs from the traditional vaginal approach
and low recurrence and dyspareunia rates from
the abdominal route. Based on this, numerous
vaginal self-anchoring mesh »kits« have been in-
troduced, all using lightweight macroporous mesh.
The results today are derived primarily from the
Apogee and Perigee systems as well as the Prolift
system. Surprisingly, the results in terms of mesh
erosion (⊡ Fig. 56.4), dyspareunia, and pain so far
do not meet the expectations of many experts in
this field.
56
⊡ Fig. 56.4. Mesh erosion on the anterior vaginal wall
Hiltunen et al. (2008), in a randomized con-
trolled trial that included 202 women and used
the Sofradim mesh, reported an erosion rate of
17% and a recurrence rate of 6.7% in a 12-month
follow-up [19]. Collinet et al. [20] and Abdel-
Fattah et al. [21] reported high erosion rates of
12.2% and 10%, respectively, using the Prolift
mesh. Altman et al., using the same material and
a follow-up time of 2 months, reported an ero-
sion rate of 1.6% but a higher recurrence rate of
13% [22]. In the same study, pelvic pain was up to
5.2%. Many of the studies have not yet reported
on dyspareunia, although in an observational
study of Tayrac et al., this problem reached a per-
centage of 12.8% [23].
Unresolved Issues and Prevention
Strategies
In summary, there are three different problems
related to the mesh kits in use today: erosion,
pain, and dyspareunia, and all three result from
the implanted mesh. As far as erosion is con-
cerned, the fact that the same material used in
the abdominal approach shows better results in-
dicates that it is not just the material that causes
mesh complications but, apparently, the route
of application. This is substantiated by previous
data from Wu et al., who showed that the erosion
rate for abdominal sacrocolpofixation increases
when the mesh is introduced through the va-
gina [24]. Furthermore, this is supported by an
analysis of results and changes in surgical strategy
by Collinet et al., who showed that minimiz-
ing vaginal incision may lead to a reduction in
erosion [20].
Another unresolved issue is that of the mesh
as a pain initiator, particularly pain in the muscles
adjacent to the sacrum. One possible cause could
be the anchoring of the mesh in the pelvic muscles.
One solution might be to replace nonabsorbable
anchoring arms with absorbable material.
Dyspareunia is based on erosion (especially
if the partner has the problem) as well as mesh
shrinkage and the muscle pain caused by the an-
choring arms. Recent guidelines recommending
avoidance of vaginal mesh kits in sexually active
Chapter 56 · Alloplastic Implants for the Treatment of Stress Urinary Incontinence
women do not seem to be a valid solution, as this
would exclude the majority of patients [25].
In essence, because the rationale for the use of
mesh kits is intact, further developments in mesh
and anchoring material are needed, as well as a
better understanding of the vaginal wall reaction
to polypropylene meshes, especially regarding why
a small mesh surface, as used in TVT/TOT, shows
a behavior different from that of large surfaces of
the same material.
References
1. Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten
U, Van Kerrebroeck, Victor A, Wein A. Standardisation
Sub-Committee of the International Continence Society.
The standardisation of terminology in lower urinary tract
symptoms; report from the standardisation sub-com-
mittee of the International Continence Society. Urology
2003;61(1):37–49
2. Abrahams P, Cardozo L, Khoury S, Wein A. Incontinence.
Health Publications, Plymouth, UK, 2005
3. Buchsbaum GM. Urinary incontinence and pelvic organ
prolapse, Minerva Urol Nefrol 2006;58(4):311–19
4. Jelovsek J, Maher C, Barber M. Pelvic organ prolapse.
Lancet 2007 24;369(9566):1027–38
5. Minassian V, Drutz H, Al-Badr A. Urinary incontinence as
worldwide problem. Int J Gynaecol Obstet 2003;82(3):
327–38
6. Barber M, Neubauer N, Klein-Olarte V. Can we screen
for pelvic organ prolapse without a physical examina-
tion in epidemiologic studies? Am J Obstet Gynecol
2006;195(4):942–8
7. Ulmsten U, Petros P. Intravaginal slingplasty: an ambula-
tory surgical procedure for treatment of female urinary
incontinence. Scand J Urol Nephrol 1995;29(1):75–82
8. Ward K, Hilton P; UK and Ireland TVT Trial Group. Tensi-
on-free vaginal tape versus colposuspension for primary
urodynamic stress incontinence: 5-year follow up. BJOG
2008;115(2):226–33
9. Ward K, Hilton P; UK and Ireland TVT Trial Group. Prospec-
tive multicenter randomised trial of tension-free vaginal
tape and colposuspension as primary treatment for stress
incontinence. BMJ 2002;325(7355):67
10. Freeman R, Holmes D, Smith P, Hillard T, Yang Q, Agur
W, Abrams P. Is transobturator tape (TOT) as effective
as tension-free vaginal tape (TVT) in the treatment of
women with urodymamic stress urinary incontinence?
Results of a multicentric RTC [ICS abstract]. Neurourol
Urodyn 2008;27(7):573–4
11. Kuuva N, Nilsson C. Long-term results of the tension-free
vaginal tape operation in an unselected group of 129
stress incontinent women. Acta Obstet Gynecol Scand
2006;85(4):482–7
443 56
12. Werner M, Najjari L, Schuessler B. Transurethral resection
of tension-free vaginal tape penetrating the urethra. Obs-
tet Gynecol 2003;102(5 Pt 1):1034–6
13. Meschia M, Pifaroti P, Bernasconi F, Magatti F, Vigano
R, Bertozzi R, Barbacini P. Tension free vaginal tape and
intravaginal slingplasty for stress urinary incontinence: a
multicenter randomised trial. Am J Obstet Gynecol 2007;
195(5):1338–42
14. Baessler K, Hewson A, Tunn R, Schuessler B, Maher C.
Severe mesh complications following intravaginal sling-
plasty. Obstet Gynecol 2005;106(4):713–6
15. Kuschel S, Schuessler B. Results on function and safety
of the Safyre-t, a hybrid transobturator vaginal sling for
the treatment of stress urinary incontinence. Neurourol
Urodyn 2008;27(5):403–6
16. Kavvadias T, Kaemmer D, Klinge U, Kuschel S, Schuessler
B. Foreign body reaction in vaginally eroded and non ero-
ded polypropylene tension free sub-urethral tapes in the
human female: a case series. In: Abstracts from the 33rd
Annual Meeting of the International Urogynecological
Association 2008;19(Suppl 1):13
17. Klinge U, Binneboessel M, Kuschel S, Schuessler B. De-
mands and properties of alloplastic implants for the treat-
ment of stress urinary incontinence. Expert Rev Med
Devices 2007;4(3):349–59
18. Maher C, Baessler K. Glazener C, Adams E, Hagen S. Sur-
gical management of pelvic organ prolapse in women.
Cochrane Database Syst Rev 2004 18;(4):CD004014
19. Hiltunen R, Nieminen K, Takala T, Heiskanen E, Merikari M,
Niemi K, Heinonen P. Low-weight polypropylene mesh for
anterior vaginal wall prolapse: a randomized controlled
trial. Obstet Gynecol 2007;110(2 Pt 2):455–62
20. Collinet P, Belot F, Debodinance P, Ha Duc E, Lucot J, Cos-
son M. Transvaginal mesh technique for pelvic organ pro-
lapse repair: mesh exposure management and risk factors.
Int Urogynecol J Pelvic Floor Dysfunct 2006;17(4):315–20
21. Abdel-Fattah M, Ramsey I, West of Scotland Study Group.
Retrospective multicentre study of the new minimally
invasive mesh repair devices for pelvic organ prolapse.
BJOG 2008;115(1):22–30
22. Altman D, Vayrynen T, Engh M, Axelsen S, Falconer C,
Nordic Transvaginal Mesh Group. Short-term outcome
after transvaginal mesh repair of pelvic organ prolapse.
Int Urogynecol J Pelvic Floor Dysfunct 2008;19(6):787–93
23. de Tayrac, Devoldere G, Renaudie J, Villard P, Guilbaud O,
Eglin G, French Ugytex Study Group. Prolapse repair by
vaginal route using a new protected low-weight polypro-
pylene mesh: 1 year functional and anatomical outcome
in a prospective multicentre study. Int Urogynecol J Pelvic
Floor Dysfunct 2007;18(3):251–6
24. Wu J, Wells E, Hundley A, Connolly A, Williams K, Visco A.
Mesh erosion in abdominal sacral colpopexy with and
without concomitant hysterectomy. Am J Obstet Gynecol
2006;194(5):1418–22
25. Konsensuspapier der Operateure der Prolift-Trainingszen-
tren. Empfehlungen zur Rekonstruktion von Beckenbo-
dendefekten mit Prolift. Gynaekologie Aktuell; Ein Sup-
plement zum Frauenarzt, April 2008
 444 Chapter 56 · Alloplastic Implants for the Treatment of Stress Urinary Incontinence and Pelvic Organ Prolapse

Discussion Schüssler: That may happen with the TVT. But we

do not have many problems with the TVT. On the
Kukleta: Well, I was wondering when the TVT was other hand, if you do overtension, then the patient
coming up so that you do not have more infec- immediately has problems.
tions. Because we would probably never implant a
mesh under conditions as you do.
Schüssler: We also wonder about that. But infec-
tion is not a problem at all.
Fitzgibbons: You said that the infection rate is
very low but erosions are high. In our way of
thinking about prosthetic material, it is the same.
But my comment is that this area is probably
ideal for the biologicals if they can be put under
tension.
Schüssler: There are data out in the literature
with biological materials for both prolapse and
incontinence. But the results are not as good as we
expected them [to be].
Klinge: I was always fascinated about the similar
problems they have in the pelvic area that we
have for our normal hernias. And a lot of the
experiences we had, you had as well. Some years
ago they tried PTFE as a band, and it failed com-
pletely. And they tried small porous meshes and
had a high complication rate. So they changed
to the large porous meshes. They tried biologi-
cals and had the same problems. So there is the
problem that we have, and if we look to the last
talks here, the hiatal hernia, the gastric banding,
and this one. The common problem of all of them
is migration. Migration through tissue. And we
all know the problem. In all of these diseases, we
have the serious problem that if the prosthesis
shows some kind of migration, we have serious
problems. And therefore we have to look at what
is the reason for migration on the cellular level
and whether there any ideas for devices that have
56 a higher or lower risk of migrating through tissue.
So we should work together because we have the
same problems.
Schumpelick: But I think there are slight differ-
ences. Because we do it absolutely aseptically, and
they do it with physiologic contamination.
Kukleta: I know that you do not think about the
tension you put on. You just pull it out and cut it
off, and just the structure of polypropylene allows
it to stay in place. Do you think you induce local
ischemia by pressure?
 57

Prophylactic IPOM Mesh To Prevent

Parastomal Hernias
D. Berger and M. Bientzle
 446 Chapter 57 · Prophylactic IPOM Mesh To Prevent Parastomal Hernias
Introduction
After an ostomy is created, hernias are a common
complication [1, 2]. Sometimes the frequency
exceeds 50% after 1 year, especially if computed
tomography (CT) is used diagnostically [3]. The
parastomal hernia may be associated with stoma
care problems and so considerably limits the
social activity of the affected patient. The cor-
rect surgical technique when creating a stoma
is inevitable, but surgical dogmas have not been
unequivocally confirmed [1]. From a pathoge-
netic point of view, parastomal hernias may be
comparable with incisional hernias, explaining
the lacking efficacy of only technical approaches
[4–7]. If disturbed collagen synthesis is accepted
as the underlying problem, the use of synthetic
nonabsorbable meshes is mandatory for treating
and preventing hernias.
From a technical point of view, prophylactic
meshes can be used in ways known from therapeu-
tic procedures. An onlay, sublay, or intraperitoneal
positioning of the prophylactic mesh may be pos-
sible. Advantages of the intraperitoneal onlay mesh
(IPOM) technique are its technical convenience, its
easy performance by laparoscopy, and the reduced
infection rate as shown for laparoscopic incisional
hernia repair [8, 9].
The availability of a mesh with a central hole
and a dome made of a material allowing intraperi-
toneal use, DynaMesh IPST (FEG-Textiltechnik,
Aachen, Germany), was the precondition of a pro-
spective observational study to evaluate the rate
of parastomal hernias and other stoma-related or
mesh-related complications when the mesh was
prophylactically used in an intraperitoneal onlay
position.
57 Patients, Material, and Methods
Between March 2006 and May 2008, 33 patients
(14 female, 19 male) were enrolled and prospec-
tively followed every 3 months. Thirty colostomies
and three ileostomies were created. Two of these
patients underwent correction of a preexisting
ileostomy or colostomy. In two patients with a
preexisting stoma, a colectomy with a new stoma
⊡ Table 57.1. Demographic and surgical data
 14 female, 19 male patients
 Median age: 71 years (41–86)
 Median body mass index: 27 (17–37)
 Median operating time: 153 min (90–260)
 19 APRE, 12 Hartmann’s procedures (including two
colectomies), two patients with only correction of a
preexisting stoma
 30 colostomies, three ileostomies
 6/33 laparoscopic procedures
 24/33 malignant diseases, 9/33 benign diseases
 Median follow-up: 18 months (2–28)
was necessary. The only exclusion criterion was
an emergency procedure. Major contamination
did not occur during the primary procedure. De-
mographic and surgical data are summarized in
⊡ Table 57.1.
As also shown in ⊡ Table 57.1, the stomas were
predominantly created because of malignant dis-
eases. One patient suffered from ulcerative colitis,
and two patients had Crohn’s disease. Other un-
derlying diseases were otherwise untreatable se-
vere incontinence or problems with a preexisting
stoma.
DynaMesh IPST represents a real mesh struc-
ture warp-knitted by polyvinylidene fluoride
(PVDF) containing a small amount of polypropyl-
ene on the parietal side. It has been experimentally
proven that the mesh is well incorporated and
effectively prevents adhesions to the intestine. Fur-
thermore, PVDF is associated with a reduced in-
flammatory response and development of fibrotic
tissue compared with polypropylene or expanded
polytetrafluoroethylene [10–12]. The implantation
technique is easy and does not significantly pro-
long the procedure.
In short, the stoma loop is pulled through
the funnel, which is oriented to the abdominal
cavity. The funnel should fit tightly. Therefore, in
32 cases, meshes with a funnel diameter of 2 cm
were used. One patient received a mesh with a
funnel diameter of 3 cm. The mesh is fixed only
by tacks at the edges and around the stoma itself.
The stoma loop itself is not fixed at the mesh. Six
of 33 procedures were performed laparoscopi-
cally.
Chapter 57 · Prophylactic IPOM Mesh To Prevent Parastomal Hernias
Results
One patient with liver metastasis of an advanced
carcinoma of the sigmoid died in the early post-
operative period because of hepatic failure. Two
patients died after 6 and 15 months, respectively,
due to advanced cancer (n=1) and liver failure dur-
ing anti-inflammatory therapy of ulcerative colitis
(n=1). During a median follow-up of 18 months,
no parastomal hernia or stoma prolapse was de-
tected clinically. In 15 patients, a CT scan was per-
formed 1 year after the primary procedure, which
also excluded any parastomal herniation. Stomal
obstructions did not occur despite the fact that
in 32 out of 33 patients, a mesh with the smallest
diameter (2 cm) was used. Even in a patient with
a body mass index of 38, the smallest diameter
proved to be adequate without signs of obstruc-
tion. Therefore, it should be pointed out that the
funnel should fit tightly around the bowel to pre-
vent a prolapse. Meshes with larger diameters,
3 cm and even 4 cm, are available, but these need
to be reserved for very obese patients with a dra-
matically thickened mesocolon.
Primary mesh infections were not observed.
Two patients developed a secondary enteral leak
with peritonitis. Both patients were treated with
daily planned relaparotomies and lavage. After the
peritonitis had disappeared, the abdominal wall
was closed, leaving the mesh in situ. In both pa-
tients the healing process proceeded uneventfully.
After almost 2 years and 3 months, respectively,
there are no clinical signs, elevated blood cell
count, or elevated serum levels of C-reactive pro-
tein in either patient.
The time needed for implantation of the pro-
phylactic mesh was very low, never exceeding
5 min.
Discussion
As outlined above, parastomal hernia is a very
frequent and sometimes burdening problem for
the affected patients [1, 2]. Although the repair
of parastomal hernias seems to be effective today,
the only technique that yields good results remains
difficult and elaborate [13]. Furthermore, some
447 57
complications are associated with parastomal her-
nia repair, thus strongly supporting the claim that
parastomal hernias should be prevented.
In 2004 a randomized study demonstrated the
dramatically reduced incidence of parastomal her-
nias after prophylactic mesh implantation in a
retromuscular position [14, 15]. Since that time,
further studies have supported the view that pro-
phylactic use of a mesh may reduce the rate of
parastomal herniation [16–19]. The meshes were
implanted after being incised in a sublay or onlay
position. In these series, the infection rate proved
to be very low, and other complications were not
described. Therefore, a summary of all studies
dealing with the prophylactic use of meshes to pre-
vent parastomal herniation concluded that meshes
are effective and associated with a negligible over-
all complication rate [20]. However, these series
had in common the fact that the number of en-
rolled patients was low, which could explain the
low rate of complications.
In our study, the technique differed completely
from that used in the above-mentioned studies by
the intraperitoneal application of the mesh. Prefer-
ence for an IPOM technique is based on the fact
that it is more suitable for laparoscopic approaches.
Furthermore, the preparation of different abdomi-
nal wall layers, creating large wound areas, is no
longer necessary. At least for laparoscopic repair of
incisional hernias, it has been clearly shown that the
infection rate is lower compared with conventional
techniques, which is explained by the reduced tissue
trauma and the contact of the mesh with perito-
neum on both sides [8, 9]. Another aspect favoring
the intraperitoneal position is the possible overlap,
which is much greater than in a sublay position.
Sometimes the retromuscular space is quite re-
stricted because of narrow rectus muscles. In these
cases, sometimes only 2 cm of overlap is possible.
The overlap of intraperitoneal positioning is limited
only by the anatomical borders of the abdominal
cavity. Therefore, a width of more than 5 cm is al-
ways possible, leading to wide augmentation of the
abdominal wall around the stoma.
The shape of the mesh used in our study
provides further advantages compared with two-
dimensional meshes that are incised. The cross-
shaped incision is followed by a relevant impair-
 448 Chapter 57 · Prophylactic IPOM Mesh To Prevent Parastomal Hernias
ment of the mesh stability. On the other hand, the
funnel around the stoma loop should effectively
prevent any prolapse. The main precondition,
however, is the tight fitting of the funnel around
the stoma loop. However, a stenosis may also be
created if the funnel is too narrow. We did not ex-
perience any stenosis, but we systematically tested
the outlet digitally at the end of the procedure.
A further aspect sometimes raised is the risk
of infection if the contaminated end of the stoma
loop is pulled through a mesh. In our series at
least, there was no primary infection, and the
literature does not support that potential risk. On
the contrary, the infection rate published today
is astonishingly low [20]. The described course
of two patients with severe septic complications
clearly showed that the combination of the intrap-
eritoneal position and PVDF as the mesh material
effectively reduces the susceptibility to persistent
mesh infections.
In conclusion, the prophylactic use of Dy-
naMesh IPST to prevent parastomal hernias shows
promising results. No complications occurred dur-
ing a median follow-up of 18 months. In particular,
infectious complications were not observed. The
procedure can be easily performed laparoscopi-
cally as well as in conventional surgery for perma-
nent terminal colostomies and ileostomies.
References
1. Carne PW, Robertson GM, Frizelle FA (2003) Parastomal
hernia. Br J Surg 90:784–793
2. Israelsson LA (2008) Parastomal hernias. Surg Clin North
Am 88:113–125
3. Cingi A, Cakir T, Sever A, Aktan AO (2006) Enterostomy
site hernias: a clinical and computerized tomographic
evaluation. Dis Colon Rectum 49:1559–1563
4. Klinge U, Si ZY, Zheng H, Schumpelick V, Bhardwaj RS,
Klosterhalfen B (2001) Collagen I/III and matrix metallo-
57 proteinases (MMP) 1 and 13 in the fascia of patients with
incisional hernias. J Invest Surg 14:47–54
5. White B, Osier C, Gletsu N, Jeansonne L, Baghai M, Sher-
man M, Smith CD, Ramshaw B, Lin E (2007) Abnormal pri-
mary tissue collagen composition in the skin of recurrent
incisional hernia patients. Am Surg 73:1254–1258
6. Rosch R, Junge K, Knops M, Lynen P, Klinge U, Schumpe-
lick V (2003) Analysis of collagen-interacting proteins in
patients with incisional hernias. Langenbecks Arch Surg
387:427–432
7. Kasperk R, Willis S, Klinge U, Schumpelick V (2002) Update
on incisional hernia. Parastomal hernia. Chirurg 73:895–898
8. Pierce RA, Spitler JA, Frisella MM, Matthews BD, Brunt
LM (2007) Pooled data analysis of laparoscopic vs. open
ventral hernia repair: 14 years of patient data accrual. Surg
Endosc 21:378–386
9. Carlson MA, Frantzides CT, Shostrom VK, Laguna LE (2008)
Minimally invasive ventral herniorrhaphy: an analysis of
6,266 published cases. Hernia 12:9–22
10. Klinge U, Klosterhalfen B, Ottinger AP, Junge K, Schumpe-
lick V (2002) PVDF as a new polymer for the construction
of surgical meshes. Biomaterials 23:3487–3493
11. Conze J, Junge K, Wei BC, Anurov M, Oettinger A, Klinge U,
Schumpelick V (2008) New polymer for intra-abdominal
meshes–PVDF copolymer. J Biomed Mater Res B Appl
Biomater 87(2):321–328
12. Junge K, Binnebosel M, Rosch R, Jansen M, Kammer D,
Otto J, Schumpelick V, Klinge U (2009) Adhesion forma-
tion of a polyvinylidenfluoride/polypropylene mesh for
intra-abdominal placement in a rodent animal model.
Surg Endosc 23(2):327–333
13. Berger D, Bientzle M (2007) Laparoscopic repair of pa-
rastomal hernias: a single surgeon’s experience in 66
patients. Dis Colon Rectum 50:1668–1661
14. Jänes A, Cengiz Y, Israelsson LA (2004) Randomized clini-
cal trial of the use of a prosthetic mesh to prevent paras-
tomal hernia. Br J Surg 91:280–282
15. Janes A, Cengiz Y, Israelsson LA (2004) Preventing paras-
tomal hernia with a prosthetic mesh. Arch Surg 139:1356-
1358
16. Marimuthu K, Vijayasekar C, Ghosh D, Mathew G (2006)
Prevention of parastomal hernia using preperitoneal
mesh: a prospective observational study. Colorectal Dis
8:672–675
17. Gogenur I, Mortensen J, Harvald T, Rosenberg J, Fischer A
(2006) Prevention of parastomal hernia by placement of a
polypropylene mesh at the primary operation. Dis Colon
Rectum 49:1131–1135
18. Israelsson LA (2005) Preventing and treating parastomal
hernia. World J Surg 29:1086–1089
19. Nagy A, Kovacs T, Bognar J, Mohos E, Loderer Z (2004)
Parastomal hernia repair and prevention with PHSL type
mesh after abdomino-perineal rectum extirpation. Zent-
ralbl Chir 129:149–152
20. Helgstrand F, Gogenur I, Rosenberg J (2008) Prevention
of parastomal hernia by the placement of a mesh at the
primary operation. Hernia 12(6):577–582
Discussion
Schumpelick: Are you not afraid of long-lasting
bacteria in this field?
Berger: These two patients showed that this should
not be a big problem. But these are only two pa-
Chapter 57 · Prophylactic IPOM Mesh To Prevent Parastomal Hernias
449 57
tients, and we started to use it also in the emer-
gency situation.
Schumpelick: You know the study by Leber—that
it will take some years.
Berger: But you also know the opinion by Israels-
son. In his department, he always uses a mesh
even in the contaminated situations. And he uses
it retromuscularly.
Franz: It is outstanding. Have I heard it right?
Should we place the stoma more laterally than the
rectus muscle?
Berger: I found a lot of papers telling us you have
to perform it in the transrectal position, but I also
found papers that showed that there is no differ-
ence where to place.
Schippers: As far as I understand, you use your
technique for permanent stomas. So there will be a
lifelong device in the patient.
Berger: Yes.
Schippers: Any material you implant shows some
kind of migration. How can you be sure that this
will not happen to you?
Berger: I cannot be sure that there will not be any
kind of migration. But correction of migration in
the stoma is much easier than correcting a migra-
tion, i.e. the esophagus.
Schumpelick: That is an argument.
 58

Laparoscopic Parastomal Hernia Repair:

Pitfalls and Complications
B. Hansson, I. de Hingh, R. P. Bleichrodt
 452 Chapter 58 · Laparoscopic Parastomal Hernia Repair: Pitfalls and Complications

Introduction important issues such as perioperative morbidity

Parastomal herniation is a common complication
of stoma formation. The incidence varies signifi-
cantly and may be as high as 48% for colostomies
and 28% for ileostomies (⊡ Table 58.1) [1]. The dif-
ferent open surgical approaches for treating paras-
tomal hernias are shown in ⊡ Table 58.2 [1]. Stoma
relocation involves relaparotomy and replacement
of the stoma to the contralateral side. Besides the
problem of developing an incisional hernia at the
midline or at the old enterostomy site in 20–30%
of cases, the technique carries a recurrence rate
of up to 36.3%. Mesh repairs have a lower recur-
rence rate of approximately 7.8%. Unfortunately,
most studies are retrospective in design and in-
clude only small numbers of patients. Therefore,
it is impossible to draw definitive conclusions on
⊡ Table 58.1. Incidence of parastomal hernia [1]
Parastomal Follow-up
hernia (%)
Mean Range Range (months)
End colostomy 15.8 4.8–48.1 35–120a
Loop colostomy 4.0 0–30.7 2.2–96a
and mortality and long-term recurrence rates after
parastomal hernia mesh repair.
In 2002, we described a laparoscopic technique
for repairing parastomal hernias with a prosthetic
mesh [2]. To provide insight into the feasibility
and safety of this procedure, a prospective clinical
study was started in 2002 [3]. The perioperative
details and early results of the first 55 consecutive
patients included in the study are presented.
Laparoscopic Repair: A Prospective
Study
Between 2002 and 2006, adult patients older than
18 years with a symptomatic parastomal hernia
(severe pain, recurrent obstruction, poor fitting
of appliance, cosmetic problems) were asked to
participate in the study. The exclusion criteria were
pregnancy, cardiopulmonary contraindications for
laparoscopy, or life expectancy less than 2 years.
Besides other information, demographic data,
operative details, perioperative and postoperative
complications, time to mobilization, food intake,
stoma production, hospital stay, and 6-week fol-
low-up data were recorded on a standard form.

End ileostomy 6.7 1.8–28 2.6a –9.2b Surgical Technique

Loop ileostomy 1.3 0–6.3% 2–3.2a
a The patient is placed in a supine position. A finger
Mean
bMedian condom is inserted into the stoma and fixed with
a transparent adhesive drape so that a finger can
be introduced into the stoma during the operation
⊡ Table 58.2. Approaches and results of open parastomal
and to determine the vitality of the stoma. The
hernia repair surgeon and assistant stand contralateral to the
stoma site. The first trocar is introduced by the
Recurrence (%) Follow-up open Hasson technique, and a pneumoperitoneum
Mean Range Range is created to a pressure of 12 mmHg. A 30° laparo-
(months) scope is inserted, and two or three working ports
are placed under direct vision on both sides of the
58 Stoma relocation 36.3 0–76.1 15–85
camera. After adhesiolysis, the hernia contents are
Onlay mesh repair 2.9 0–33 reduced. The bowel loop that runs to the stoma is
Sublay mesh repair a a a identified and dissected free from the fascial edges.
The hernia opening is narrowed with two nonre-
a a a
Preperitoneal mesh sorbable sutures. A 15×19-cm expanded polytetra-
repair
fluoroethylene patch (e-PTFE; Gore-Tex DualM-
Chapter 58 · Laparoscopic Parastomal Hernia Repair: Pitfalls and Complications
esh Biomaterial, Gore & Associates, Flagstaff, AZ,
USA) is fashioned with a central keyhole of 2 cm
and two radial incisions of 5 mm (⊡ Fig. 58.1).
This enables a funnel-like shape. The mesh is then
inserted, unrolled, and tacked to the abdominal
wall following the double-crown technique. The
cylindrical part of the mesh forming a small collar
that surrounds the stoma loop is stitched to the
bowel wall.
Results
Fifty-five consecutive patients fulfilled the inclu-
sion criteria and were included in the study. Of
the 55 procedures, 47 (85.5%) could be completed
laparoscopically. The median operating time was
120 min. Conversion to laparotomy was indicated
because of dense adhesions prohibiting safe dis-
section in four patients and full-thickness bowel
injury in four. There was no in-hospital mortality.
Postoperative recovery was uneventful in 47
patients (85%). Patients were able to consume a
normal diet on day 1 (range 1–3 days), had stoma
production on day 2 (range 1–13 days), and could
⊡ Fig. 58.1. Keyhole repair of parastomal hernia with a sublay
patch. a An expanded polytetrafluoroethylene patch (Gore-
Tex DualMesh Biomaterial) is fashioned with a central keyhole
of 2 cm and two radial incisions of 5 mm to create a funnel.
b After the trephine size is narrowed with nonabsorbable
sutures, the patch is positioned around the stoma and (a)
fixed with staples using the double-crown technique. By over-
lapping the two parts of the keyhole in the patch, a funnel
is created (b) around the colon (c). The patch is fixed to the
colon with nonresorbable sutures
453 58
be released from the hospital on postoperative
day 4 (range 2–20 days). Postoperative complica-
tions occurred in eight patients (14.4%). Four pa-
tients had to be reoperated: one for bleeding from
the epigastric artery, one for a mesh infection, one
for peritonitis caused by a small bowel lesion, and
one for a leaking colon anastomosis. Nonsurgi-
cal complications were observed in another four
patients.
Follow-up at 6 weeks revealed an unevent-
ful recovery in 51 patients (93%). Four patients
reported pain at the site of the mesh. On physical
examination, one recurrent parastomal hernia was
diagnosed in one of the patients in whom conver-
sion to laparotomy was performed because of a
full-thickness bowel injury; the hernia was small
and asymptomatic. Most wound complications had
resolved. Only one residual hematoma was noted,
and persisting seroma at the site of the hernia was
noted in three patients.
Higher incidences of conversion, intestinal
damage, and reoperation occurred in the recurrent
hernia group, but the number of patients was too
small to reach statistical significance.
Discussion
Laparoscopic parastomal hernia repair is feasible
and seems to be safe since the results are similar
as in open parastomal repair. However, definitive
conclusions cannot be made because the experi-
ence with laparoscopic parastomal hernia repair
is limited; most publications are case series of
moderate quality, and long-term follow-up is lack-
ing. Moreover, prospective randomized trials com-
paring open repair with laparoscopic repair are
not available. Therefore, laparoscopic parastomal
hernia repair cannot be advocated as the standard
of care.
In the literature, six series of more than five
patients have been published, with 189 patients al-
together [3–8]. The median number of patients in
these studies is 22, ranging from nine to 66 (⊡ Ta-
ble 58.3). The most frequently used techniques for
parastomal hernia repair are the Sugarbaker tech-
nique (51%) and the keyhole-like technique (39%).
The Sugarbaker technique is a nonslit procedure
 454 Chapter 58 · Laparoscopic Parastomal Hernia Repair: Pitfalls and Complications

⊡ Table 58.3. Results of laparoscopic parastomal hernia repair in published series having more than eight patients

Authors, year, N Age Technique Surgical complications Follow- Recur-

design up rence
Intraoperative Postoperative

Safadi [4], 2005 9 63.5 Sugarbaker 0 None Reoperated 0 18–23 4

Retrospective (53–77) Keyhole 9 (44%)
Single center Other Conservative
Ileus 1

LeBlanc et al. 12 ? Sugarbaker 7 Enterotomy 1 Reoperated 20 1

[5], 2005 (42–89) Double patch 5 Delayed rec. 1 (3–39) (8%)
»Prospective« Conversion 0 Ileus 1
Single center
Conservative
Ileus 1
Seroma 1
Died 1

Hansson et al. 55 63 Keyhole 55 Enterotomy 5 Reoperated 6 weeks

[3], 2007 (27–87) Mesh infection 1
Prospective Conversion 8 Peritonitis 2
Single center Hemorrhage 1

Conservative
Ileus 2
Hematoma 5
Seroma 15

Mancini et al. 25 60 Sugarbaker 25 Enterotomy 1 Reoperated 0 19 1

[6], 2007 (41–85) (2–38) (4%)
Retrospective Conversion Conservative
Multicenter Ileus 2
Wound Infection 1
Mesh infection 1
Died 1

Berger et al. 66 70 Sugarbaker 41 Enterotomy 0 Reoperated 24 8

[7], 2007 (34–92) Sandwich 25 Mesh infection 3 (3–72) (12.1%)
»Prospective« Conversion 1 Stoma obstruc- 2
Single center tion
Ileus 2

Conservative
?

McLemore et 19 66+12 Sugarbaker 14 ? ?? Reoperated 20 2

al. [8], 2007 Keyhole 5 Conversion Mesh infection 2 (8–39) (10.5%)
Retrospective Stoma obstruc- 1
Single center tion
58
Conservative
None
Chapter 58 · Laparoscopic Parastomal Hernia Repair: Pitfalls and Complications
in which a mesh is used to cover the hernia open-
ing, with an overlap of 4 cm at each side, after the
stoma loop is lateralized. Lateralization may lead
to retraction, tilting, and obstruction of the stoma
due to bowel kinking, as was almost exclusively
found in patients treated with this or a similar
technique. The keyhole technique is a procedure
in which the patch is draped around the bowel
(⊡ Fig. 58.1). Berger developed the sandwich tech-
nique, which combines the advantages of both
methods [7]. Several biomaterials such as polypro-
pylene mesh and e-PTFE have been used for paras-
tomal hernia repair, and most parastomal hernias
can be repaired laparoscopically. The conversion
rate in the literature is less than 1%, compared to
8.5% in our series of patients [3–8]. Most conver-
sions in our series were in patients who were reop-
erated for a parastomal hernia. The mortality was
less than 1%.
The main problems associated with laparo-
scopic parastomal hernia repair are accidental en-
terotomy, postoperative ileus or stoma obstruction,
mesh infection, and reherniation. In our series, 9%
of patients had an accidental enterotomy. In four
other series, 1.8% accidental enterotomies were
reported for 112 patients altogether [4–7]. In 2007,
three reviews were published about laparoscopic
hernia repair [9–11]. Müller-Riemenschneider et
al. [9] reported accidental enterotomies in 3% of
patients who underwent laparoscopic incisional
hernia repair. Pierce et al. [10] and LeBlanc et al.
[11] reported an enterotomy incidence of 2.9%
and 1.8%, respectively, during laparoscopic ventral
and incisional hernia repair. Especially if unrec-
ognized, bowel perforations represent a serious
and potentially life-threatening complication [11].
Accidental enterotomies are recognized in 82%
of cases during the first operation and are associ-
ated with a mortality of 1.7%. Eighteen percent of
enterotomies are diagnosed in the postoperative
period and have a significantly higher mortality of
7.7% [11]. With laparoscopy, the risk of accidental
enterotomy seems to be higher than in open sur-
gery. To prevent full-thickness bowel lesions, adhe-
siolysis should be performed by sharp dissection,
without the use of electrocautery or ultrasonic
devices. Sharp dissection has the advantage that
a serosal bowel lesion can be recognized immedi-
455 58
ately because of local bleeding, and lesions are not
sealed by electrocautery or ultrasonic devices.
Stoma obstruction or (prolonged) ileus were
reported in 12 (6.3%) of the 189 patients in the
literature. Six patients were reoperated, three for
an obstructed stoma and three for an ileus. Two
patients died as a result of aspiration pneumonia,
which may have been associated with bowel ob-
struction. Stoma obstruction is reported only in se-
ries that used the (modified) Sugarbaker technique.
Probably, the lateralization and coverage of the
stoma cause kinking and obstruction, especially if
the prosthesis is fixed tight to the abdominal wall.
Mesh infection was reported in 3.7%, similar
to infection rates in laparoscopic hernia repair and
lower than in open hernia repair, which may be a
benefit of the laparoscopic approach [9].
References
1. Carne PWG, Robertson GM, Frizelle FA. Parastomal hernia.
Br J Surg 2003; 90:784–793
2. Hansson BME, van Nieuwenhoven EJ, Bleichrodt RP. Pro-
mising new technique in the repair of parastomal hernia.
Surg Endosc 2003; 17:1789–1791
3. Hansson BME, de Hingh IH, Bleichrodt, RP. Laparoscopic
parastomal hernia repair is feasible and safe: early results
of a prospective clinical study including 55 consecutive
patients. Surg Endosc 2007; 21:989–993
4. Safadi B. Laparoscopic repair of parastomal hernias. Surg
Endosc 2004; 18:676–680
5. LeBlanc KA, Bellanger DE, Whitaker JM. Laparoscopic pa-
rastomal hernia repair. Hernia 2005; 9:140–144
6. Mancini GJ, McCluskz III DA, Khaitan L, et al. Surg Endosc
2007; 21:1487–1491
7. Berger D, Bientyle M. Laparoscopic repair of parastomal
hernias. A single surgeon’s experience in 66 patients. Dis
Colon Rectum 2007; 50:1668–1673
8. McLemore EC, Harold KL, Efron JE, et al. Parastomal hernia
short term outcome after laparoscopic and conventional
repairs. Surg Innov 2007; 14(3):199–204
9. Müller-Riemenschneider F, Roll S, Friedrich M, et al. Medi-
cal effectiveness and safety of conventional compared to
laparoscopic incisional hernia repair: a systematic review.
Surg Endosc 2007; 21:2127–2136
10. Pierce RA, Spitler JA, Frisella MM, et al. Pooled data analy-
sis of laparoscopic vs. open ventral hernia repair: 14 years
of patient data accrual. Surg Endosc 2007; 21:378–386
11. LeBlanc KA, Elieson MJ, Corder JM 3rd. Enterotomy and
mortality rates of laparoscopic incisional and ventral her-
nia repair: a review of the literature. JSLS 2007; 11(4):408–
414
 59

Concept of Visible Mesh and

Possibilities for Analysis of Mesh
Migration and Shrinkage
J. Otto, N. Krämer, G. A. Krombach, I. Slabu, M. Hodenius, M. Baumann,
U. Klinge
 458 Chapter 59 · Concept of Visible Mesh and Possibilities for Analysis of Mesh Migration and Shrinkage

After incorporation, textile meshes change their constructed (SF mesh). To compare this mesh with
appearance markedly because of tissue ingrowth a conventional UltraPro mesh, they were both
and integration into scar tissue. Migration and placed in a phantom model consisting of two
erosion, shrinkage and deformation, and fistula pieces of meat surrounded by water to evacuate
formation are rare but severe complications. To air. ⊡ Figure 59.4 shows a coronal slice of the two
appreciate the clinical relevance, we have to keep meshes. Only the nanoparticle-containing SF mesh
in mind that 1.5 million meshes are implanted
per year worldwide [1]. After mesh implantation,
a significant number of patients will present to a
doctor with mesh-related problems sooner or later.
Among these may be either newly developed pain
in the groin, functional problems in the hiatus if
the mesh was placed around the oesophagus, or
manifestation of fistulas to the intestines.
To decide whether to monitor the complaints,
surgically correct the position of the mesh, or
explant the mesh, a central question must be an-
swered: Is a dislocation of the mesh causing the
current complaints?
X-ray, ultrasound, computed tomography (CT),
and magnetic resonance imaging (MRI) are the
main radiological imaging methods at hand for pos-
sibly answering this question. However, X-ray is not
able to show the mesh itself; only the metal surgical
clips used for fixation may be visible (⊡ Fig. 59.1).
With ultrasound, the mesh cannot be distin-
guished from the ambient structure if the mesh has
been incorporated with no seroma, infection, or
scar formation because the signal differences are
too small to separate the mesh from the surround- ⊡ Fig. 59.1. X-ray after mesh implantation; mesh fixation with
ing tissues (⊡ Fig. 59.2). metal tacks (arrows)
Computed tomography and MRI struggle with
the same problem: In the case of mesh incorpora-
tion with no complications, it is almost impossible
to identify the mesh and reveal its exact localisa-
tion. Only in exceptional cases, if the mesh is sur-
rounded by fluids or fat, can the fine structure of
the mesh be delineated [2–4] (⊡ Fig. 59.3). Besides
these exceptions, X-ray, ultrasound, CT, and MRI
usually fail to directly visualise the mesh device.
To achieve an MR-visible polymer device, we
use superparamagnetic nanoparticles of ferrofluids
[5]. These superparamagnetic iron oxides are also
used as MR contrast media. On MRI, the nano-
59 particles cause a signal decrease by disturbing the
magnetic field, resulting in a hypointense signal.
A new textile mesh made from polyvinylidene
fluoride with superparamagnetic particles has been ⊡ Fig. 59.2. Mesh (arrow) surrounded by seroma (star)
Chapter 59 · Concept of Visible Mesh and Possibilities for Analysis of Mesh Migration
could be visualised by the desired susceptibility ar-
tefacts. These artefacts enabled an increased differ-
entiation from the tissue, which was not possible
using UltraPro mesh.
Based on these results, a prototype of the »vis-
ible« mesh was implanted as an inlay into the
abdominal wall of a dead rat. Again, it was possible
⊡ Fig. 59.3. Computed tomographic image after mesh hiato-
plasty. It is not possible to see the mesh beside the metal tacks
459 59
to identify and locate the mesh (⊡ Fig. 59.5) on MR
images. With the aid of a dedicated small animal
receiver coil and an imaging sequence providing
high resolution, even the pores of the mesh could
be delineated. However, this is possible only with
long data acquisition.
If the concentration is too high, the signal will
strongly exceed the diameter of the mesh fibre. Af-
ter proving that textile structures can be visualised
using MRI by adding superparamagnetic particles,
future work should optimise the particle size, the
concentration in relation to the fibre size, and
the MRI sequences. Knowledge of the magnetic
properties of the mesh is important for developing
models of MR signalling behaviour. On account of
this, the magnetic susceptibility will be determined
by superconducting interference device (SQUID)
measurements. The final goal will be to find a
method to image the mesh with a clear delinea-
tion of its surrounding structures. Because neither
air nor susceptibility artefacts provide signals, a
method to differentiate air from susceptibility arte-
facts with positive contrast is desirable.
Such a visible mesh will be helpful both for de-
ciding whether a revision operation of the mesh is
necessary and as a tool for constructing improved
⊡ Fig. 59.4. Magnetic resonance
image (MRI): Visible mesh vs. Ul-
trapro. No signal can be detec-
ted from the UltraPro mesh; the
SF mesh causes mild signal loss
(open arrow). Macroscopy: Upper
arrow indicates UltraPro with
blue stripes. Lower arrow indi-
cates colourless mesh of fibres
that include superparamagnetic
ferroparticles (SF mesh). Both
meshes were placed between
air-filled plastic tubes
 460 Chapter 59 · Concept of Visible Mesh and Possibilities for Analysis of Mesh Migration and Shrinkage

⊡ Fig. 59.5. Magnetic reso-

nance image of abdominal
wall replacement with visib-
le mesh in a rat model

meshes that, it is hoped, will have less shrinkage
and less risk of migration, particularly for areas
with a lot of mobility, such as the hiatus and the
pelvic floor.
5. Hodenius MA, Niendorf T, Krombach GA, Richtering W,
Eckert T, Lueken H, Speldrich M, Gunther RW, Baumann
M, Soenen SJ et al. Synthesis, physicochemical charac-
terization and MR relaxometry of aqueous ferrofluids. J
Nanosci Nanotechnol 2008, 8:2399–2409

Acknowledgements
Discussion
This work was supported by the German Fed-
eral Ministry of Education and Research (BMBF Schumpelick: Are you sure that every surgeon
01EZ 0849). would be glad to know where his mesh is?
Otto: Probably not.
Fitzgibbons: Are none of the others visible?
References Otto: It depends on the contrast. Just very thick
meshes in cases of seromas are able to see.
1. Junge K, Klinge U, Rosch R, Mertens PR, Kirch J, Klosterh-
Schumpelick: And what about nanoparticles? Any
alfen B, Lynen P, Schumpelick V. Decreased collagen type
I/III ratio in patients with recurring hernia after implanta-
dangers to their use?
tion of alloplastic prostheses. Langenbecks Arch Surg Otto: They are already in use.
2004, 389:17–22
2. Crespi G, Giannetta E, Mariani F, Floris F, Pretolesi F, Ma-
rino P. Imaging of early postoperative complications after
polypropylene mesh repair of inguinal hernia. Radiol Med
(Torino) 2004, 108:107–115
3. Di MM, Runfola M, Magalini S, Sermoneta D, Gui D. Rip-
pled mesh: a CT sign of abdominal wall ePTFE prosthesis
infection. G Chir 2006, 27:384–387
59 4. Fischer T, Ladurner R, Gangkofer A, Mussack T, Reiser M,
Lienemann A. Functional cine MRI of the abdomen for
the assessment of implanted synthetic mesh in patients
after incisional hernia repair: initial results. Eur Radiol
2007, 17:3123–3129
 VI

VI Strategy to Improve Results

60 Who Has the Major Role in Hernia Surgery:

The Surgeon or the Material? – 463

61 Two Controversial Concepts: Standard Procedure

in a Standard Patient Versus Tailored Surgery with
Procedures Adjusted to Individual Patients – 467
 60

Who Has the Major Role in Hernia

Surgery: The Surgeon or the Material?
R. C. Read
 464 Chapter 60 · Who Has the Major Role in Hernia Surgery: The Surgeon or the Material?
Introduction
Astley Cooper (1804), in the preface to his classic
monograph on the anatomy and surgical treatment
of hernia [1], wrote, »No disease of the human
body belonging to the province of the surgeon,
requires in its treatment a greater combination of
accurate anatomical knowledge with surgical skill,
than hernia in all of its varieties.« More recently, in
1989 George Wantz stated, »The outcome of an in-
guinal hernioplasty is more dependent on the skills
and experience of the surgeon than on the type of
repair« [2]. In 2006, Gilbert et al. [3] averred, »The
use of any mesh product to repair a hernial defect
will never supplant the need to fully know and
utilize the layers, planes and spaces of the abdo-
men.« The purpose of this chapter is to document
evidence supporting these judgments.
Sutured Repair
The importance of the surgeon’s experience in pre-
venting recurrence after hernia repair is exempli-
fied by the trend toward making herniology a sub-
specialty of general surgery. Glassow [4], in a 1970
review of 50,000 groin herniorrhaphies performed
at the Shouldice Hospital, pointed out that the in-
cidence of recurrence fell from 17% to 1% within
two decades after this herniological institute was
founded (1945). The improvement was attributed
to modifications made to the original Shouldice
procedure in the 1950s and to specialization. The
first detailed analysis of the relationship between
a surgeon’s operative experience of groin hernio-
plasty and recurrence was provided by Kingsnorth
et al. in 1981 [5]. Consultants and senior registrars
who had performed more than six such proce-
dures had a 2.5% recurrence rate, whereas the
figure for registrars with less experience was 9.4%
(calculated to be 28% in 25 years). The authors
therefore recommended careful supervision, by a
consultant, of six herniorrhaphies before juniors
could become principal operators. A subsequent
study in 1992 [6] also involved registrars who
were supervised while performing their first six
Shouldice operations. Their later high recurrence
60 rate of 4.5% was blamed on inexperience, indicat-
ing that this period of supervision was inadequate.
The authors point out that at the Shouldice clinic,
new staff surgeons receive close supervision for
their first 50 herniorrhaphies and do not operate
independently until they have repaired 100. A final
assessment of their technique is made after 1,000
hernias have been operated upon.
A similar finding of junior staff incurring a
high incidence of early recurrence after inguinal
herniotomy in children was reported by Harvey
et al. [7]. Poor technique was considered to be
responsible. The authors recommended that the
practice of placing hernia cases at the end of the
operating room list, thereby allowing junior staff
to work on them unsupervised, be discontinued.
Prostheses [8]
Reinforcement of sutured repairs in the groin using
metallic filigrees began soon after Bassini intro-
duced his cure (1887). During World War II, they
were replaced with plastic meshes by Aquaviva
and Bounet. The Lichtenstein procedure (1984),
using onlay polypropylene, became the gold stan-
dard for inguinal herniorrhaphy in the 1990s. It
supplanted the Shouldice operation because the
recurrence rate was significantly less. Because the
approach was anterior, through familiar anatomy,
there seemed to be no need for a specific training
period.
Positioning of mesh behind the transversalis
fascia is more difficult because the preperitoneal
space is unfamiliar territory. The open posterior
approach to both groins was pioneered by Cheatle
and Henry [9]. McEvedy introduced the unilateral
procedure in 1950 [9]. Stoppa [10] employed the
bilateral access for prosthetic repair and, in his early
experience, had a high rate of recurrence. Similarly,
Wantz, with this operation, reported a figure of
11.6% in his first 40 patients [11]. Subsequently,
this rate fell to 1.9%. Fernandez-Lobato et al. [12]
believed the Stoppa technique required an initial
learning curve of 20–30 cases. Kurzer et al. [13], us-
ing Wantz’s unilateral posterior preperitoneal repair
for anterior groin recurrences and thereby avoiding
scar, had 25% of their operations recur in their first
20 patients. Later, the figure was 1%.
Chapter 60 · Who Has the Major Role in Hernia Surgery: The Surgeon or the Material?
Schroder et al. [14] found a recurrence rate of
18.2% in their first 36 patients who received the
Kugel patch preperitoneal hernioplasty. The later
incidence was 2.9%. The overall results with open
posterior preperitoneal prosthetic repair indicate
that there is a learning curve during which com-
plications, including recurrence, are more likely.
Schroder et al. [14] considered its extent to be 40
cases, and Van Nieuwenhove et al. [15], in a study
of 450 Kugel repairs, estimated a training period of
25–35 patients, depending on the surgeon’s experi-
ence with the anatomy. Similar learning curves
were developed for incisional herniation and hiatal
herniae, the latter for open [16] and laparoscopic
repair [17].
The principles of open anterior or posterior
preperitoneal mesh herniorrhaphy apply to laparo-
scopic repair. Therefore, experience with the former
facilitates performance of the latter, which is tech-
nically demanding and therefore requires an ex-
tended learning curve if initial recurrences are to be
avoided. Wright and O’Dwyer [18] suggested that
30–40 supervised cases are needed for the groin.
Beets et al. [19] quoted a consensus of 50 repairs,
while DeTurris et al. [20] cited 30–50. Neumayer
et al. [21], comparing the results of open mesh and
laparoscopic repair of inguinal hernia in male vet-
erans, found that general surgeons who were super-
vised for their initial 25 laparoscopic hernioplasties
had a later recurrence rate that plateaued only after
250. It appeared that an inexperienced surgeon em-
ploying this new and demanding technique requires
more training. However, in a later report [22], these
authors raised the question of whether, despite ex-
perience, aging affects a surgeon’s performance, es-
pecially using newer, more challenging techniques,
such as laparoscopy and robotics.
Conclusions
In summary, pioneers in herniology have, over the
last two centuries, asserted that a surgeon’s skills and
experience are more important than the material
used to cure abdominal herniation. These senti-
ments encouraged the development of herniology
as a subspecialty of general surgery. The Shouldice
clinic [4] introduced learning curves for new staff so
465 60
that they could avoid initial complications, includ-
ing recurrence. Kingsnorth [5] did likewise for reg-
istrars. Later, the new gold standard for groin repair,
the Lichtenstein operation, was exempted because
its rate of recurrence was significantly less than
that of the supplanted Shouldice procedure. Prep-
eritoneal prosthetic repair required more training
(20–30 cases). A similar learning curve was recom-
mended for the repair of incisional and hiatal herni-
ation, open or laparoscopic. Laparoscopic repair of
inguinal herniae required a more extended learning
curve (30–50 cases). However, in 2004 a multicenter
Veterans Administration study [21] indicated that
for general surgeons, even this figure was inad-
equate. A later follow-up in 2005 [22] raised the
question of whether aging countered the value of
surgical experience when sophisticated technology,
i.e., laparoscopy, is employed. These data support
the axioms of pioneering herniologists.
References
1. Cooper AP (1804) The anatomy and surgical treatment of
inguinal and congenital hernia [preface]. Cox, London
2. Wantz GE (1989) The Canadian repair: personal observa-
tions. World J Surg 13:516–521
3. Gilbert AI, Graham MF, Young J, et al. (2006) Closer to
ideal solution for inguinal hernia repair: comparison bet-
ween general surgeons and hernia specialists. Hernia
10(20:162–168
4. Glassow F (1970) Recurrent inguinal and femoral hernia.
BMJ (1):215–216
5. Kingsnorth AN, Britton BJ, Morris PJ (1981) Recurrent
inguinal hernia after local anesthetic repair. Br J Surg
68:273–275
6. Kingsnorth AN, Gray MR, Nott DM (1992) Prospective
randomized trial comparing the Shouldice technique and
plication darn for inguinal hernia. Br J Surg 79(10):1068–
1070
7. Harvey MH, Johnstone MJS, Fossard DP (1985) Inguinal
herniotomy in children: a five year survey. Br J Surg
72:485–487
8. Read RC (2004) Milestones in the history of hernia sur-
gery: prosthetic repair. Hernia 8(1):8–14
9. Read RC (2001) Use of the preperitoneal space in ingu-
inofemoral herniorrhaphy: historical considerations. In:
Bendavid R (ed) Abdominal wall hernias: principles and
management. Springer, New York, pp 11–15
10. Stoppa RE, Warleumont CR (1989) The preperitoneal ap-
proach and prosthetic repair of groin hernia. In: Nyhus
LM, Condon RE (eds) Hernia, 3rd edn. Lippincott, Philadel-
phia, pp 199–216
 466 Chapter 60 · Who Has the Major Role in Hernia Surgery: The Surgeon or the Material?

11. Wantz GE (1989) Giant prosthetic reinforcement of the

visceral sac. Surg Gynecol Obstet 169:408–417
12. Fernandez-Lobato R, Tartas-Ruiz A, Jimenez-Miramon FJ
(2006) Stoppa procedure in bilateral inguinal hernia. Her-
nia 10(2):179–183
13. Kurzer M, Belsham PA, Kark AE (2002) Prospective study
of open preperitoneal mesh repair for recurrent inguinal
hernia. Br J Surg 89:90–93
14. Schroder DM, Lloyd LR, Boccaccio JE, et al. (2004) Inguinal
hernia recurrence following preperitoneal Kugel patch
repair. Amer Surg 70:132–136
15. Van Nieuwenhove Y, Vansteenkiste F, Vierendeels T, et al.
(2007). Open preperitoneal hernia repair with the Kugel
patch: a prospective multicenter study of 450 repairs.
Hernia 11(1):9–13
16. Orringer MB, Skinner DB, Belsey RH (1972) Long term
results of the Mark IV operation for hiatal hernia and
analyses of recurrences and their treatment. J Thorac
Cardiovasc Surg 63:25–33
17. Puri V, Kakarlapudi GV, Awad ZT, Filipi CJ (2004) Hiatal
hernia recurrence: 2004. Hernia 8(4):311–317
18. Wright D, O’Dwyer RJ (1998) The learning curve for lapa-
roscopic hernia repair. Semin Laparoscop Surg 5(4):227–
232
19. Beets GL, Dirksen CD, Go PMNYH, et al. (1999) Open or
laparoscopic preperitoneal mesh repair for recurrent in-
guinal hernia? Surg Endoscop 13:323–327
20. DeTurris SV, Cacchione RN, Mungara A, et al. (2002) Lapa-
roscopic herniorrhaphy: beyond the learning curve. J Am
Coll Surg 194 (15):65–73
21. Neumayer L, Giobbie-Hurder A, Jonasson O, et al. (2004)
Open mesh versus laparoscopic mesh repair of inguinal
hernia. N Engl J Med 350(18):1819–1827
22. Neumayer LA, Gawande AA, Wang I, et al. (2005) Pro-
ficiency of surgeons in inguinal hernia repair: effect of
experience and age. Ann Surg 243 (3):344–352

60
 VII

VII Pro and Contra

62 In Support of a Standard Technique for Inguinal

Hernia Repair – 475

63 In Support of Individual Selection of Technique as

Related to the Patient–Improvement by Better Selection
of Patients Who Can Be Offered a Less Risky Technique:
Groin Hernia – 479

64 In Support of Standard Procedure in Abdominal

Hernia Repair – 485

65 In Support of Individualized Procedures in Abdominal

Wall Hernia Repair – 493

66 In Support of Standard Procedure in Hiatal Hernia

Repair – 503

67 Strategy To Improve the Results? In Support of

Individualized Procedures in Hiatal Hernia Repair – 513

68 Questionnaire – 521
 61

Two Controversial Concepts:

Standard Procedure in a Standard
Patient Versus Tailored Surgery with
Procedures Adjusted to Individual
Patients
U. Klinge and A. Fiebeler
 468 Chapter 61 · Two Controversial Concepts: Standard Procedure in a Standard Patient Versus Tailored Surgery
Introduction
61
Surgeons have been working for decades to improve
their technique and to develop better procedures.
In doing so, they try to prove the effect of every
modification by clinical randomized controlled tri-
als (RCTs). The process should result in a best
technique that can then be considered the gold stan-
dard. This recommendation is outlined in so-called
guidelines offering evidence-based knowledge to
every physician. However, although RCTs have been
performed with increasing efforts, these often fail
to confirm any significant differences between the
groups involved. Furthermore, after replication by
other investigators, the overall results differ con-
siderably in outcome, making interpretation of the
results rather complicated. Even the collection of
several trials in meta-analyses often does not ease
interpretation. It appears that for some questions,
the RCT instrument needs some support to verify
the superiority of one procedure over another.
What might be the reason that even marked ex-
pansion of cohort size frequently does not show clearer
results? For explanation, it may be helpful to look at
our general concepts of disease in more detail.
Different Concepts of Disease
A disease is assumed to be best treated in a stan-
dardized way, and its impact on the outcome can
be tested by an RCT. An RCT is based on the as-
sumption that the disease process is uniform in
every patient. Individual patients are considered
as average patients since their individual differ-
ences will be compensated for by randomization.
This first concept of assuming one disease treated
by one standard therapy is the domain of the
RCT and usually does not offer serious problems.
This is true for many experimental settings with a
limited and known number of influencing effects.
However, for others the number of factors relevant
to the prognosis seems to be uncountable. Besides
technical aspects, an increasing number of biologi-
cal reasons seem to interfere with the results, e.g.,
gene polymorphism or functional imbalances in
the proteosome. Unfortunately, we do not know
which of the 40,000 genes (or all?) and the even
more numerous proteins have to be considered.
Furthermore, if a relevant impact of these biologi-
cal conditions is suspected, it is obviously impos-
sible to control all of these components in detail.
Consecutively, on the molecular level it has to be
accepted that every patient will react and respond
a little bit differently than another. Thus, this sec-
ond concept assumes relevant differences between
every individual and consequently results in an
individual disease that requires individualization
of therapies. The second concept may best reflect
the true diversification of diseases; however, it is
unsuitable for developing practical approaches to
treat our patients. The resulting picture of thou-
sands of individual diseases and treatments is too
complex to derive principles and guidelines that
can be taught to our students and residents.
A compromise between the two extremes can
be a third concept that considers several subgroups
of patients with prognostic differences in disease
progress, each demanding specific stage-related
therapies. This concept is already well established
for cancer therapy; cancer surgery is adapted to
the tumor stage to provide comparable subgroups,
which can then be tested by RCTs. Instead of the
first concept being applied, tumor patients are con-
sidered to be nonhomogeneous and are grouped
according to certain influencing constellations con-
cerning their prognosis for survival. According to
defined risk factors, different therapies are tailored
to each individual patient, forming a decision tree
for selecting the individualized best therapy.
In the following, we discuss whether the opti-
mal therapy for hernia can be derived from apply-
ing the first concept or whether better results can
be achieved by using the latter concept, which is
also referred to as a »tailored approach.« Further-
more, general remarks are given on how to identify
therapies with a clear causal impact on the result as
predicted by the first concept and how to test the
quality of a tailored approach.
A Century of Seeking the Best Standard
Procedure To Repair a Hernia?
The surgical repair of groin hernia started with
Bassini in 1884 as a suture repair, was modified
Chapter 61 · Two Controversial Concepts: Standard Procedure in a Standard Patient
by Shouldice in 1944, and changed toward mesh
repair with the introduction of the Lichtenstein
repair in 1986 and the laparoscopic procedures
at the beginning of the 1990s. Since Bassini, the
recurrence rate for suture repair had been <5% in
selected patients, but the long-term recurrence rate
was widely constant around 10–15%. Treatment
of recurrent hernia had been more difficult, with
recurrence rates of up to 30–50%. Reinforcement
of tissue with meshes improved the results, with
recurrence rates of <1% in selected patients [1], a
long-term rate of 5–10%, and a rerecurrence rate
of 10–20% [2]. Several meta-analyses concluded
that meshes reduce the recurrence rate by half,
regardless of whether they are implanted in open
surgery or laparoscopically [3]. In the guidelines
of many countries (including the United Kingdom
and the Netherlands), Lichtenstein mesh repair is
claimed to be the standard operation for primary
hernia in the adult patient [1].
Incisional hernia of the abdominal wall is even
more difficult to treat. Despite countless attempts
to improve the standard technique for closing a
laparotomy, the long-term incidence for develop-
ing an incisional hernia is up to 20%, and for
parastomal hernia it is even higher, up to 50%.
The rerecurrence rate after suture repair is >50%.
Again, reinforcement with meshes markedly re-
duces the recurrence rate to <10% [4]. To date,
there is no evidence regarding whether the onlay
position is as good as the sublay position in all
cases, but mesh repair is regarded as the standard
for repair of incisional hernia.
After more than 100 years of improving our
technical skills, we can state that reinforcement of
tissues by meshes hinders recurrence. However,
despite many attempts to identify the best closure
technique, we still do not know how to close a lap-
arotomy sufficiently. And up to now, no RCT has
proven any beneficial effect of a new technique.
What might the technical challenge be when ap-
proximating just two layers of the abdominal wall?
Until now, despite the clear and evident supe-
riority of mesh techniques proven by many RCTs
(and even several meta-analyses), we are still op-
erating on 10–15% of our patients with a groin
hernia because of a recurrent hernia–for decades
without any sign of reduction even though we are
469 61
using meshes in the huge majority of our patients.
What might be the reason that we could not solve
this simple technical problem, and why did many
RCTs fail to lead to significant improvement of our
techniques?
Recurrence as a Technical Failure?
From an engineer’s technical point of view, ab-
dominal wall hernia repair needs any adequate
procedure to simply close the hernia gap. A perfect
technique and procedure should be decisive for the
result and should permanently prevent recurrence.
However, in some cases a technical failure may
occur and will result in recurrence. For a group
of comparable cases, this should manifest after a
mean delay of some months or years (± standard
deviation). If a procedure is used that works better,
there may be either fewer recurrences or the recur-
rence should appear later (⊡ Fig. 61.1).
As a consequence, the outcome curve will show
an S-shaped configuration with its transflexion
point at the time of peak incidence. This is well
known for engineers and is in accordance with car
breakdowns due to certain technical defects [5].
Correspondingly, if we assume that every patient
with any kind of hernia is treated with a standard
procedure, in the case of a standard patient with a
standard hernia we should expect that recurrences
develop after a standard delay ± standard deviation.
Recurrence
Time
⊡ Fig. 61.1. Incidence of a technical failure (recurrence; red
solid line) and its cumulative incidence curve (blue dotted line)
 470 Chapter 61 · Two Controversial Concepts: Standard Procedure in a Standard Patient Versus Tailored Surgery
Do we have data to support such courses of
61 hernia recurrences? No, clearly this is not the rule.
Studying incisional hernia in a long-term survey,
Luijendijk et al. found unexpectedly high rerecur-
rence rates even after mesh repair: >60% after
suture and >30% after mesh repair [6, 7]. Many of
these recurrences developed after a long delay from
the previous operation, and even more intriguing,
the courses showed cumulative incidences that
formed curves with a roughly linear shape. Similar
courses are seen in the cumulative rate of opera-
tions for recurrence depicted from epidemiological
databases. In contrast to the expected peak inci-
dence with an S-shaped outcome curve, for groin
hernia [1] as well as for incisional hernia [8], the
cumulative incidence rises constantly over time,
not showing any S-shaped inflexion or reaching a
plateau at the end.
Is this really worth thinking about? And does
it help addressing the problem of standard versus
tailored treatment?
Regarding the linear rise of a cumulative recur-
rence rate, the best explanation is still that there
is not one specific reason but that there are many
of them. Conclusively, the development of a re-
currence cannot be related to one (i.e., technical)
problem that can be overcome by one technical
solution. In other words, it is unlikely for one stan-
dard procedure to address all of these problems
and to improve all results significantly.
Consequently, if we do not see a standard fail-
ure with a standard delay resulting in an S-shaped
outcome curve, it must be suspected that the basic
assumption of a standard patient with a standard
hernia is not advantageous. Recent investigations
of wound healing confirm the evidence that recur-
rence in hernia patients is a problem of a defective
biological network rather than a technical failure.
Because the defective scarring process is triggered
by a complex network of biological interferences, it
is not surprising that the causally relevant reason
may differ with each patient. The superimposi-
tion of all the many different possible reasons with
their different incidence peaks will result in a
linear rise of the outcome curve, as in fact is seen
in patients after hernia repair (⊡ Fig. 61.2). Not the
least consequence of this model is that it questions
the role of RCTs. These require either (sub)groups
Time course of failure with linear rise
due to accumulation of many incidences
1
Incidence of damage
cumulative »survival«
0
Time
⊡ Fig. 61.2. Incidences of several possible failures (red solid
line) and their superimposition toward a linear rise in the cu-
mulative incidence curve (blue dotted line)
comparable in their failure risk or a mechanism to
be tested that has an undoubted causal relevance
for the occurrence of a failure. Neither may be as-
sumed in the case of linear outcome curves. In the
case of linear cumulative incidences, an alternative
therapy may show a reduced rate of complications
at any time point; however, without having reached
a plateau, it is only a delayed manifestation of the
problem. Furthermore, if the results are not cor-
rected for age-related morbidity, every delay per se
will suggest a reduced number of complications.
In summary, the configuration of epidemio-
logical outcome curves indicates that recurrences
should not be regarded as simple technical failures
but rather as a complex problem of biology, and
that we should not look for a standard failure in a
standard patient.
Technical Solution for a Complex
Biological Problem
Currently, the technical solution to the biologi-
cal problem means reinforcement of tissue with
meshes. One way to overcome poor-quality scar-
ring in patients is to supply an extended sub-
duction of the mesh underneath healthy scar-free
tissue. The important question for the surgeon is
whether the overlap that can be achieved by a stan-
Chapter 61 · Two Controversial Concepts: Standard Procedure in a Standard Patient
dard technique is independent of the patient’s indi-
vidual type of hernia or whether it is necessary to
tailor various techniques to the individual patient.
We present some considerations that all indicate
that the procedure must at least be selected in view
of hernia size and location.
A larger hernia gap needs a larger mesh. How-
ever, in the case of a large mesh, even small shrink-
age of <15% may reduce the absolute width of the
mesh by >4 cm and thereby cut the overlap in half!
Next, surgeons should consider that positioning
the mesh on fat tissue is more likely to result in
slippage of the mesh and shortening of the over-
lap; thus, larger meshes will be advantageous in
such cases. This is in accordance with the clinical
results of increased recurrence rates in adipose
patients when the mesh had been placed in the
preperitoneal fat [9]. Furthermore, there are some
areas of concern where anatomy makes it difficult
to supply a sufficient overlap, such as close to bony
structures (e.g., the iliac crest or costal arch). In
these locations, intraperitoneal onlay mesh tech-
niques may provide greater overlap than meshes in
the onlay position. Because the various techniques
differ considerably in the mesh size used and the
overlap that is achievable by dissection, we must
tailor the procedure to the patient. This means we
have to select the technique that fits best and that
provides the biggest overlap with the lowest risk
for the patient.
Principle and Quality Control
of Tailored Surgery
The concept of tailored surgery does not mean
treating patients according to some vague expert’s
opinion. Quality control is required, just as for ev-
ery other therapeutic concept, although the evalu-
ation of a decision tree requires studies other than
the RCT.
The final goal of any tailored approach is to
achieve the best result in all patients, while using
various techniques in nonhomogeneous groups of
patients. First of all, we have to define criteria for
such a decision tree regarding which patient should
receive which technique. Checking the results after
x time and analyzing the complications in relation
471 61
to the procedure must show whether any problems
were caused by poor technique in the right patient
or by good technique in the wrong patient. If tech-
nical failure is suspected, surgical skills need to be
improved. If a technical failure can be excluded
and the problem was simply the wrong technique
for the patient concerned, the decision tree needs
to be modified such that the next similar patient
will receive a more appropriate technique. After
some time, all results have to be checked again.
Furthermore, all results need to be compared with
other clinics and other decision trees. Finally, it is
likely that decision trees with the best results will
be rather similar; however, it will be possible to
achieve good results with several different decision
trees in different target groups of patients.
Not the least advantage is that for this tailored
approach, no patient has to be randomized; there-
fore, every surgeon and every clinic can take part in
a comprehensive comparison of patients’ outcomes.
Even in theory, a tailored approach will lead
to superior results if corresponding subgroups can
be identified. Whereas for an entire cohort two
therapies may have a similar complication rate,
this may be eliminated if the procedure is tailored
to subgroups with less risk for a specific therapy
(⊡ Fig. 61.3).
The previous remarks focus on recurrence;
however, the principal aspects of a tailored ap-
proach should be applied for many other treatment
regimens, such as for curing infection, pain, etc.
Further, it is necessary to weight the importance
and relevance of the complications, advantages,
and disadvantages to the patient and the surgeon
as well as to the institution.
Conclusion
Although we may not feel comfortable with it,
we have to accept that there is no easy scientific
answer [10] that offers the one golden solution.
Only in the case of S-shaped outcome curves we
are allowed to assume that we are treating standard
patients with standard procedures, and in this
case we are right to expect standard results. In the
case of linear outcome curves, we should consider
whether a tailored approach is more appropriate.
 472 Chapter 61 · Two Controversial Concepts: Standard Procedure in a Standard Patient Versus Tailored Surgery

Assumption szenario III: „tailored approach“

61
Technique 1: laparoscopical Technique 2: open

5% A B A B 5%

B A

Technique 2 (open) A B Technique 1 (laparoscopical)

for patients of group A for patients of group B
(suprasymh., subxiphoid.) (lateral, close to bones)

⊡ Fig. 61.3. Two different techniques, each with 5% complications. For technique 1 it manifests in subgroup A, whereas for tech-
nique 2 it occurs in subgroup B. A tailored approach with treatment of A with technique 2 and of B with technique 1 will even
be able to eliminate all complications

However, once we have identified subgroups of 6. Luijendijk RW, Hop WC, van den Tol MP, et al. (2000) A
patients with identical risk profiles for a complica- comparison of suture repair with mesh repair for incisio-
nal hernia. N Engl J Med 343:392–8
tion, S-shaped outcome curves should be available
7. Burger JW, Luijendijk RW, Hop WC, et al. (2004) Long-term
for these patients, and those subgroups then should follow-up of a randomized controlled trial of suture ver-
be compared with RCTs. If not, we should try to sus mesh repair of incisional hernia. Ann Surg 240:578–83;
improve the quality of our decision tree for the discussion 583–5
tailored approach. Nevertheless, there is no doubt: 8. Flum DR, Horvath K, Koepsell T (2003) Have outcomes of
incisional hernia repair improved with time? A populati-
Every procedure has to be performed carefully and
on-based analysis. Ann Surg 237:129–35
correctly according to the well-established stan- 9. Rosemar A, Hana N, Ulf A, Staffan H, Pär N (2008) Groin
dards–which means, tailor your standards! hernia surgery and body mass index: a study based on a
national register (S). In: Proceedings of the 30th Congress
of EHS GREPA, Sevilla, Spain, 7–10 May 2008
10. Klinge U, Dahl E, Mertens P (2007) Problem poser–how
References to interpret divergent prognostic evidence of simultane-
ously measured tumor markers? Comput Math Methods
1. Schumpelick V, Fitzgibbons R (2007) Recurrent hernia– Med 8:71–75
prevention and treatment. Springer, Berlin
2. Eklund A, Rudberg C, Leijonmarck CE, et al. (2007) Recurrent
inguinal hernia: randomized multicenter trial comparing la-
paroscopic and Lichtenstein repair. Surg Endosc 21:634–40
3. McCormack K, Scott NW, Go PM, Ross S, Grant AM (2003)
Laparoscopic techniques versus open techniques for in-
guinal hernia repair. Cochrane Database Syst Rev 2003
(1):CD001785
4. Klinge U, Krones CJ (2005) Can we be sure that the mes-
hes do improve the recurrence rates? Hernia 9:1–2
5. Klinge U, Binnebösel M, Rosch R, Mertens P (2006) Hernia
recurrence as a problem of biology and collagen. J Minim
Access Surg 2:151–4
 62

In Support of a Standard Technique

for Inguinal Hernia Repair
M. P. Simons
 476 Chapter 62 · In Support of a Standard Technique for Inguinal Hernia Repair

Introduction
⊡ Table 62.1. Factors that influence the possibility of
using one standard technique in inguinal hernia repair
Is standardisation of treatment of inguinal hernia (ASA American Society of Anesthesiologists)

62 necessary? Yes, it is necessary because the vast

Patient-related
majority of surgeons are not dedicated hernia sur-
 Gender
geons, so they need guidance and training. Look-  Obesity
ing for a »standard« technique that is (relatively)  ASA class
easy to learn, safe, cheap, reliable, and reproducible  Prior groin surgery
is important.  Comorbidity
 Type of anaesthesia
In this chapter, factors that influence the choice
 Preference
of technique are discussed, and the European
Guidelines are used to demonstrate that standardi- Type of hernia
sation is indeed possible and recommended.  Indirect
 Direct
What is a standard technique? We know that  Combined
specialists such as Amid use a Lichtenstein tech-  Recurrence (prior technique?)
nique for almost all repairs. The same can be said  Femoral hernia
of other techniques such as Shouldice, Stoppa, and
Surgeon-related
endoscopic repair techniques. We, sadly, also know  Specialist in hernia centre
that many surgeons do not use the technique as  Specialist in general practice
described by the originator. »Choose the surgeon,  Laparoscopic surgeon
not the technique« is a known adagium. Is a »stan-  General surgeon (dedicated?)
dard« technique truly standard in most cases? And Resident
do surgeons who state that they use a standard
technique deviate from this standard in some (or
many) cases?
Before we can be pro standard technique, fac- Comorbidity: As with ASA class, some patients re-
tors influencing the possibility of stating this must quire a low-risk technique under local anaesthesia.
be identified. The type of hernia, type of patient,
type of surgeon, and the setting in which he or she Type of anaesthesia: Endoscopic surgery requires
operates are discussed (⊡ Table 62.1). general anaesthesia.

Preference: Although little data are available on

Patient-Related Factors this subject, nobody will contradict the fact that
some patients prefer a technique under local an-
Gender: Female patients have a higher rate of aesthesia whereas other patients request a mini-
chronic pain and a higher risk of femoral hernia. mally invasive technique.

Obesity: Morbidly obese patients require an indi-

vidualised approach. Type of Hernia

American Society of Anesthesiologists (ASA) The normal distribution (as measured in large
class: In many cases, ASA 3 and 4 patients have studies and national databases) of inguinal hernias
contraindications to general anaesthesia, preclud- is as follows:
ing the use of certain techniques. Indirect 50–55%
Direct 30–35%
Prior groin surgery: Prior groin surgery, prior Combined 10–15%
lower abdominal surgery, radiation, and other fac- Bilateral 10–15%
tors greatly influence the choice of technique. Recurrent 10–15%
Chapter 62 · In Support of a Standard Technique for Inguinal Hernia Repair
477 62

⊡ Table 62.2. Differences in hernia repair among countries

Types of inguinal hernia repair

Country Year Conventional Open mesh Endoscopic Other

Netherlands 2006 4% 78% 19%

Denmark 2006 2.5% 82.5% 15%

Finland 2006 7% 81% 8% 3%

France 2006 14.9% 46% 34% 4.6%

Poland 2006 38% 60% 1%

Austria 2006 76% 24%

Hungary 2007 60% 34% 6%

Sweden 2006 8.5% 82% 9%

The distribution shown precludes the use of one
standard technique in inguinal hernia. It is a fact,
though, that around 70–75% of inguinal hernia
repairs are for unilateral primary cases. For these
cases, a standard approach (either by anterior or
endoscopic approach) is feasible.
But a standard »Lichtenstein surgeon« will
have difficulty treating a complex third recur-
rent hernia after open techniques or bilateral large
recurrent hernias. A »laparoscopic surgeon« will
have difficulty when a patient specifically requests
an operation under local anaesthesia or has a dif-
ficult recurrence after prior preperitoneal repair.
Level of the Surgeon
Expert surgeons use a standard technique for most
cases and agree that surgeons need proficiency
in at least two techniques–preferably an anterior
technique and a posterior technique–to be able to
treat all cases.
Laparoscopic surgeons will state that almost
all cases can be treated by laparoendoscopic tech-
niques. But there are contraindications to these
techniques, including previous lower abdominal
surgery, radiation, prior mesh implantations, and
inability to undergo general anaesthesia.
Guidelines advise teaching residents both ap-
proaches (anterior and posterior).
Is Hernia Surgery Standardised?
Many techniques are being used, and the literature
shows that the differences among countries are sig-
nificant (⊡ Table 62.2). There is a growing indica-
tion that in European and North American coun-
tries, a majority of inguinal hernias are treated by
a Lichtenstein technique. Endoscopic repair varies
from 1% to 24%. Miscellaneous other techniques
are used in 5–20% of cases, but one could postulate
that these are standard procedures (for example,
Prolene Hernia System, Kugel, plug-and-patch), as
is the Lichtenstein.
In the Netherlands, guidelines in 2002 rec-
ommended a Lichtenstein repair (as a standard)
for unilateral uncomplicated inguinal hernia, an
endoscopic repair for bilateral hernias (if the
expertise was available), and a tailored approach
for recurrent hernias. An implementation study
was performed. In 2001, all inguinal hernia sur-
geries in 73 hospitals (70% of the total) were
analysed after 1 year of follow-up (charts only). A
few years after implementation of the guidelines
(2006), the study was repeated. Results are shown
in ⊡ Table 62.2.
It is postulated that the increase in mesh (pre-
dominantly Lichtenstein) has decreased the per-
centage of reoperations for recurrence from 14%
to 11%.
 478 Chapter 62 · In Support of a Standard Technique for Inguinal Hernia Repair
What Do the European Guidelines
Recommend?
62 Guidelines are developed to improve practice, es-
pecially general practice. Those involved in devel-
oping the European Guidelines have, after consid-
ering the following factors, come to the following
recommendations regarding the following:
▬ Risk of recurrence
▬ Safety (risk of complications)
▬ Postoperative recovery and quality of life
(resumption of work)
▬ Grade of difficulty and reproducibility (lear-
ning curve)
▬ Costs (hospital and societal)
Level A
All male adult (>18 years) patients with a symp-
tomatic inguinal hernia should be operated on
using a mesh technique.
When a nonmesh repair is considered, the
Shouldice technique should be used.
The open Lichtenstein and endoscopic ingui-
nal hernia techniques are recommended as best
evidence-based options for repair of a primary
unilateral hernia, providing the surgeon is suffi-
ciently experienced in the specific procedure.
Level D
For large scrotal (irreducible) inguinal hernias,
after major lower abdominal surgery, and when
no general anaesthesia is possible, the Lichtenstein
repair is the preferred surgical technique.
It is recommended that in the case of a re-
current inguinal hernia following an anterior ap-
proach, a preperitoneal mesh should be placed,
preferably by means of an endoscopic technique.
It is recommended that an anterior approach
be used in the case of a recurrent inguinal hernia
that was treated with a posterior approach.
Because evidence is scarce, a tailored approach is
recommended for female patients and young adults.
What Does the Literature Recommend?
Most trials describe results between standard pro-
cedures, but there is, of course, an inclusion bias
in trials. Specific patient categories are not ran-
domised, usually because they require a tailored
approach. O’Dwyer’s MRC trial is an example of a
study in which an endoscopic »standard« operation
was compared with a »tailored open approach.« In
the open group, around 20% of patients were oper-
ated on with a nonmesh technique and 80% by a
Lichtenstein technique. There was no difference in
recurrence after 2 years.
Conclusion
After analysing the arguments discussed above,
this author concludes that an approach using one
standard technique for all inguinal hernias is not
feasible. It is possible, though, to use one stan-
dard technique for the 70–75% primary unilateral
cases. This can be an open mesh technique such
as Lichtenstein. Some patients will prefer an en-
doscopic approach! This can also be a »standard«
endoscopic approach. Some patients will have con-
traindications for this technique, and it cannot be
performed under local anaesthesia.
Recurrent inguinal hernia requires an individ-
ualised approach with at least two and maybe even
three techniques, depending on prior technique
and patient factors.
It is important to determine for which type of
surgeon how this situation should be handled. A
specialist surgeon will be used to individualising
treatment and will master different techniques. On
the other hand, in a teaching hospital, surgeons
and residents should start by teaching/learning
one »standard« technique well for uncomplicated
cases. This leaves 20–25% of the cases, such as bi-
lateral hernias, recurrent hernias, female patients,
and young patients, for which dedicated or (sub)
specialised surgeons should be prepared to choose
between an open anterior or a posterior approach
(author’s opinion). The posterior approach can be
performed endoscopically or via an open approach.
In certain cases, a mesh might not be necessary. Ev-
idence is unclear whether females and young adults
with an indirect primary hernia require mesh.
 63

In Support of Individual Selection

of Technique as Related to the
Patient–Improvement by Better
Selection of Patients Who Can
Be Offered a Less Risky Technique:
Groin Hernia
B. D. Matthews
 480 Chapter 63 · In Support of Individual Selection of Technique as Related to the Patient–Improvement
Introduction
Dr. David Sackett of McMaster University in On-
tario, Canada, defined evidence-based medicine
as the judicious use of the best current evidence in
making decisions about the care of the individual
63 patient. He further remarked that evidence-based
medicine is a means to integrate clinical expertise
with the best available research evidence and pa-
tient values. Clinical outcome research in surgery
is commonly criticized for a lack of prospective
randomized trials to compare alternative surgi-
cal techniques or operative versus nonoperative
treatment when the option of avoiding surgical
intervention is considered appropriate. Despite
these shortcomings, there is perhaps no area in
surgery in which more level I evidence is available
to guide clinical practice and surgical decision
making than in the care of patients with inguinal
hernias.
Because the cumulative incidence of inguinal
hernias in males is approximately 14% at a median
follow-up of 18.2 years, as reported in a recent
publication from the first National Health and Nu-
trition Examination Survey, the application of clin-
ical outcome studies to inguinal hernia patients is
critical to guide surgeons toward appropriate care
of this common surgical problem [1]. Minimiz-
ing recurrent hernias, chronic inguinodynia, and
additional postoperative morbidities and decreas-
ing postoperative recovery to facilitate a return to
self-reliance are paramount. Despite an enormous
quantity of clinical outcome data comparing open
tension-free to primary tissue repair techniques
and open tension-free to laparoscopic inguinal
hernia repair, controversy persists regarding the
use of a standard versus a tailored approach to the
management of groin hernias. Patient care guide-
lines for inguinal hernia repair were published by
the Society for Surgery of the Alimentary Tract in
2006 and the National Institute for Clinical Excel-
lence for the NHS (United Kingdom) in 2004, but
they are vague in regard to the use of laparoscopic
inguinal hernia except for the need for appropriate
training and experience in a minimally invasive
approach.
Many techniques exist, including primary tis-
sue repair, open tension-free anterior or retroperi-
toneal repair, and laparoscopic transabdominal
(TAPP) or total extraperitoneal (TEP) inguinal
hernia repair. Watchful waiting for asymptomatic
or minimally symptomatic inguinal hernias is also
considered standard of care. Primary tissue repair
is infrequently performed, but it is often done for
incarcerated and/or strangulated inguinal her-
nias when wound contamination is a concern.
A Cochrane Database review in 2001 reported
a 50% reduction in inguinal hernia recurrence
when a tension-free repair was performed, pro-
viding additional evidence of the shortcomings of
primary repair [2]. Nevertheless, familiarity and
experience in primary tissue repair is important
when a surgeon is faced with an incarcerated and/
or strangulated hernia or unique circumstances
when a mesh-based repair is deemed inappropri-
ate. A tailored approach to the individual patient
using evidence-based medicine will allow for the
integration of surgical expertise and approach
with unique patient characteristics. This chapter
discusses important patient and surgeon variables
to consider in order to optimize patient outcomes
through selection of an appropriate technique
for patients undergoing elective inguinal hernia
repair.
Watchful Waiting Versus Inguinal
Hernia Repair
Upon initial evaluation of a patient with an in-
guinal hernia, the surgeon must decide whether
inguinal hernia repair is required. A doctrine that
the presence of an inguinal hernia, even if asymp-
tomatic, is an indication for repair to prevent an
acute hernia emergency from incarceration and/
or strangulation has been challenged by two re-
cent prospective randomized trials. O’Dwyer et
al. reported only one (1.3%) patient out of 78
who developed an acute incarceration at a median
follow-up of 574 days [3]. The rate of crossover
to inguinal hernia repair was 26% at 15 months.
Two patients in the observation group who subse-
quently underwent surgery suffered a myocardial
infarction and cerebrovascular accident, respec-
tively. The authors concluded that observation
may only delay surgical intervention. Neverthe-
Chapter 63 · In Support of Individual Selection of Technique
less, watchful waiting would be appropriate for
high-risk patients since an acute hernia accident
is quite rare. In a comparable study, Fitzgibbons
et al. reported the frequency of acute incarcera-
tion to be 1.8 per 1,000 patient-years inclusive
of patients followed for as long as 4.5 years [4].
The probability of crossover from watchful wait-
ing to inguinal hernia repair was approximately
23% at 3 years of follow-up. Delaying repair of an
asymptomatic or minimally symptomatic inguinal
hernia did not have adverse effects on subsequent
operative intervention or postoperative outcomes
[5]. Why would watchful waiting decrease patient
morbidity? A population-based questionnaire in
the Netherlands of consecutive patients who un-
derwent inguinal hernia repair over 68 months
reported that 40.2% of patients had »some degree
of pain,« with 21% being confronted with some
degree of limitation in daily functioning and 1.9%
experiencing severe pain [6]. Therefore, due to a
high incidence of chronic pain, watchful waiting is
particularly relevant for patients with asymptom-
atic or minimally symptomatic hernias.
Laparoscopic Versus Open Inguinal
Hernia Repair
Over 40 prospective randomized single-institution
or multi-institutional studies comparing laparo-
scopic (TAPP and TEP) inguinal hernia repair to
open tension-free inguinal hernia repair have been
reported worldwide. A recent review by Takata
and Duh summarizing these publications dem-
onstrated that laparoscopic inguinal hernia repair
has a beneficial role in decreasing chronic inguin-
odynia and recurrence rates and is associated with
shorter convalescence and a faster return to work
and activities in patients with recurrent, bilateral,
and primary inguinal hernias [7]. In a prospective
randomized trial of laparoscopic inguinal hernia
repair and anterior tension-free repair for recur-
rent inguinal hernias, patients experienced less
postoperative pain and fewer days of sick leave
after a laparoscopic approach. Cumulative 5-year
recurrence rates were equivalent [8]. Indeed, lap-
aroscopic inguinal hernia repair is most often
performed for bilateral and recurrent hernias. As
481 63
a consequence, laparoscopic techniques account
for only 20–30% of inguinal hernia repairs in
the United States. Reasons to not perform lap-
aroscopic inguinal hernia repair for a unilateral
primary hernia include surgeon preference, lack
of expertise in minimally invasive techniques,
complexity of the hernia (e.g., inguinoscrotal, in-
carcerate), and cost. Laparoscopic inguinal hernia
repair is almost always performed under general
anesthesia, certainly limiting its use. Ideally, all
patients would receive the treatment that provides
the most durable repair with the least amount of
perioperative morbidity (pain, quality-of-life limi-
tations, and cardiac, pulmonary, and non-hernia-
related complications). Although a few risks as-
sociated with hernia recurrence and even chronic
pain have been established, patient-specific and
hernia-specific factors associated with postopera-
tive complications and hernia recurrences are be-
ing defined. There is a possibility that minimally
invasive techniques are underutilized or, alterna-
tively, not performed in the appropriate patient.
Even though the majority of inguinal hernia re-
pairs are day cases, risk stratification of periop-
erative morbidity in addition to recurrence and
chronic pain after laparoscopic and open inguinal
hernia repair would be useful in determining an
appropriate surgical approach.
The Patient Safety in Surgery (PSS) Study, a
collaboration between the U.S. Department of Vet-
erans Affairs (VA) National Surgical Quality Im-
provement Program and the American College of
Surgeons and funded by the Agency for Healthcare
Research and Quality, took 97 different periopera-
tive variables (patient demographics, preoperative
risk factors, preoperative laboratory values, op-
erative values, and postoperative outcomes) and
cross-referenced them to the top 10 most frequent
current procedural terminology (CPT) codes [9].
In the VA system, open inguinal hernia repair (the
1st most common code), recurrent inguinal her-
nia repair (6th), and laparoscopic inguinal hernia
repair (8th) are represented. The PSS Study has
evolved to include private sector hospitals, with
open inguinal hernia repair being the 2nd most
common CPT code. Because the aim of the PSS
Study is to minimize postoperative morbidity and
mortality and to risk-adjust adverse events for
 482 Chapter 63 · In Support of Individual Selection of Technique as Related to the Patient–Improvement
common procedures in order to compare different
hospital systems, information on inguinal hernia
repair will allow surgeons to appropriately risk-
stratify patients for open and laparoscopic inguinal
hernia repair.
Matthews et al. have identified risk factors
63 associated with complications and recurrences
in patients undergoing laparoscopic and open
inguinal hernia repair and have developed a risk-
assessment model for hernia recurrence using the
data from the VA Cooperative Studies Program
trial that compared open and laparoscopic surgi-
cal techniques for tension-free inguinal hernia
repair [10]. Independent patient-specific and sur-
gery-specific variables that predict postoperative
complications and recurrence have been defined.
Many predictors of complications (e.g., recur-
rent hernia, inguinoscrotal hernia) were similar
between open and laparoscopic inguinal hernia
repair, although several variables (e.g., prostat-
ism, surgeon experience) differed based on the
surgical approach. Risk for recurrence after an
open inguinal hernia repair included a recurrent
hernia, preoperative activity level of the patient,
American Society of Anesthesiologists class, and
whether the hernia had enlarged recently. Using
regression analyses, Matthews et al. have also
developed predictive models for perioperative
outcomes. These models can be used to deter-
mine an appropriate surgical approach for an
individual patient to reduce the risk of recurrence
and complications.
Additional studies have reported a predictive
risk score for infection after inguinal hernia repair
as well as patient characteristics associated with
an increased risk of postoperative hematoma fol-
lowing herniorrhaphy. Pessaux et al. developed a
global infection score (GIS) dependent on risk fac-
tors for infection (age, obesity, and use of a urinary
catheter) as determined by multivariate analysis
from a database of 1,254 patients [11]. The use
of prophylactic antibiotics in patients with a high
GIS and/or a laparoscopic inguinal hernia repair
appears to be a better option in these patients.
Smoot et al. reported that preoperative Coumadin
usage was a significant risk factor for postop-
erative hematoma [12]. Intuitively, a laparoscopic
inguinal hernia repair with the potential for bleed-
ing into the widely developed preperitoneal space,
or even intraabdominal bleeding, seems a poor
choice compared with an anterior tension-free
repair in which postoperative bleeding could be
managed with less morbidity. As additional studies
are reported and risk stratification becomes more
reliable, surgeons will need to alter their operative
approach to inguinal hernia repair to ensure that
they reduce the risks of postoperative morbidity
and recurrence.
One factor that has not been evaluated is lap-
aroscopic inguinal hernia repair for a recurrent
hernia in a patient who has undergone an ante-
rior tension-free preperitoneal inguinal hernia
repair. A strategy to repair a recurrent hernia by
an opposite approach from the index operation
is obscured when the preperitoneal space has
been disturbed and used for mesh placement,
albeit by an anterior approach. Although laparo-
scopic transabdominal and extraperitoneal ingui-
nal hernia repair can successfully be performed
after previous abdominal and/or pelvic surgery,
additional investigation of laparoscopic inguinal
hernia repair after the anterior placement of pre-
peritoneal mesh needs to be done. In addition,
differentiation of whether laparoscopic transab-
dominal and extraperitoneal inguinal hernia re-
pair reduce hernia recurrences, chronic pain, or
perioperative morbidity has not been elucidated
through clinical trials.
Evidence is accumulating that experience is
important in determining outcomes with regard to
hernia recurrence, not only for laparoscopic ingui-
nal hernia repair but also for open inguinal hernia
repair [13, 14]. Anterior tension-free preperitoneal
inguinal hernia repairs such as the Prolene Hernia
System (Ethicon, Somerville, NJ, USA) and Kugel
(Davol, Cranston, RI, USA) repair require specific
training and an awareness of preperitoneal anatomy
and the nuances of mesh placement. Arbitrary case
volumes have been projected to define the learning
curve, but they do little to define appropriate train-
ing. Surgeons need to honestly assess their clinical
outcomes and level of technical expertise with any
type of inguinal hernia repair and properly choose
an approach that places the patient at the least risk
for perioperative technique-related complications,
recurrence, or chronic pain.
Chapter 63 · In Support of Individual Selection of Technique
Conclusions
A tailored approach to the individual patient with
an inguinal hernia integrates surgical expertise and
evidence-based medicine to optimize patient out-
comes through the selection of an appropriate tech-
nique. As predictors of complications after open and
laparoscopic inguinal hernia repair are more clearly
defined through large multi-institutional prospec-
tive registries, the frequency of chronic pain and
the incidence of recurrent inguinal hernias can be
reduced, and the relationships between outcomes
and patient comorbidities, hernia characteristics,
and surgeon experience will be revealed.
References
1. Ruhl CE, Everhart JE (2007) Risk factors for inguinal hernia
among adults in the US population. Am J Epid 165:1154–
1161
2. Scott N, Go PM, Graham P, et al. (2001) Open mesh versus
non-mesh for groin hernia repair [review]. Cochrane Data-
base Syst Rev (3):CD002197
3. O’Dwyer PJ, Norrie J, Alani A, et al. (2006) Observation
or operation for patients with an asymptomatic inguinal
hernia: a randomized clinical trial. Ann Surg 244:167–173
4. Fitzgibbons RJ, Giobbie-Hurder A, Gibbs, JO et al. (2006)
Watchful waiting vs repair of inguinal hernia in mini-
mally symptomatic men: a randomized clinical trial. JAMA
295:285–292.
5. Thompson JS, Gibbs JO, Reda DJ, et al. (2008) Does delay-
ing repair of an asymptomatic hernia have a penalty? Am
J Surg 195:89–93
6. Loos MJA, Roumen RMH, Scheltinga MRM, et al. (2007)
Chronic sequelae of common elective groin hernia repair.
Hernia 11:169–173
7. Takata MC, Duh QY (2008) Laparoscopic inguinal hernia
repair. Surg Clin North Am 88:157–178
8. Eklund A, Rudberg C, Leijonmarck CE, et al. (2007) Recur-
rent inguinal hernia: randomized multicenter trial com-
paring laparoscopic and Lichtenstein repair. Surg Endosc
21:634–640
9. Khuri SF, Henderson WG, Daley J (2007) The Patient Safety
in Surgery Study: background, study design, and patient
populations. J Am Coll Surg 204:1089–1102
10. Matthews RD, Anthony T, Kim LT, et al. (2007) Factors
associated with postoperative complications and hernia
recurrence for patients undergoing inguinal hernia repair:
a report from the VA Cooperative Hernia Study Group. Am
J Surg 194:611–617
11. Pessaux P, Lermite E, Blezel E, et al. (2006) Predictive risk
score for infection after inguinal hernia repair. Am J Surg
192:165–171
483 63
12. Smoot RL, Oderich GS, Taner CB, et al. (2008) Postopera-
tive hematoma following inguinal herniorrhaphy: patient
characteristics leading to increased risk. Hernia 12:261–
265
13. Neumayer L, Giobbie-Hurder A, Jonasson O, et al. (2004)
Open mesh versus laparoscopic mesh repair of inguinal
hernia. N Engl J Med 350:1819–27
14. Wilkiemeyer M, Pappas TN, Giobbie-Hurder A, et al. (2005)
Does resident post graduate year influence the outcomes
of inguinal hernia repair? Ann Surg 241:879–84
Discussion
Kurzer: Perhaps we should get away from saying
that recurrence is the only thing we are interested
in; some of us have alluded to that. I get patients
who come to me and ask if it will last forever,
but they don’t really expect the lack of recurrence
to last forever. You can’t just operate to get rid
of recurrence at all costs, and maybe we have to
take into consideration operations that are more
likely to cause pain in certain patients. In English,
they say that to the man who has a hammer, ev-
ery problem is a nail. Clearly, if you are a hernia
surgeon, you can’t have just one hammer, and you
have to have other tools to deal with other hernias.
There are clearly different hernias, different prob-
lems, different patients.
Schumpelick: Could it be that the hernia centers
tend more in the direction of standard procedures
and that the general surgeons who do [operate on]
some hernias take a tailored approach?
Kurzer: No, I do not think so… probably more the
other way round. I think the general surgeons are
the ones who would go through life with just one
operation that they use for everyone. It’s perhaps
not a bad thing, if the general surgeon has only one
procedure that he can do, as long as he recognizes
when he sees a patient who has something he can’t
deal with and as long as he is happy to send it to
someone who can. If he sees someone with a bilat-
eral recurrence and he can only do a Lichtenstein,
he sends that patient away to someone who can do
a TEP; he doesn’t try to do it himself. I think that
is important.
Schumpelick: Is it likely that someone who is not
used to doing a TAPP or TEP will send the patient
away? I have seldom heard about that.
 484 Chapter 63 · In Support of Individual Selection of Technique as Related to the Patient–Improvement

Deysine: I have a double experience. I worked at of strength—or divide the omentum with Ultra-
the Bellevue Hospital in New York, in a popula- cision or some device, make a small incision in
tion of malnourished alcoholics, and then I went the scrotum, and mobilize and remove the hernia
to work at the VA Hospital in Northport with a lot content. So this is a combination of imagination
of different people with different kinds of malnu- and expertise. The ultimate bottom line is that the
trition. And then I went to work in my neighbor- patient should not be harmed. Give the best for
63 hood, where the income is extremely high, and your patient; do whatever is best for him.
people usually eat very well and they exercise. Fitzgibbons: I think that is a very reasonable ap-
These are three different types of human beings; proach, individualizing to some extent, but, as you
they all are going to heaven but in different condi- said, not too far.
tions. So if you try to standardize and you use for Chowbey: In a strangulated inguinal hernia, we
everybody the same procedure, you are going to go transabdominal with a pneumoperitoneum, re-
find different results. Surgeons who came from duce the bowel, and look at the viability of the
New York Hospital, a very rich environment, and bowel. In a few situations where we were not sure
operated in Bellevue using the techniques they about the viability of the bowel, we did not mind
used at the New York Hospital were a disaster. leaving a small 5-mm trocar and putting in an
You have to have in your pocket two or three tech- optic and looking at the viability of the bowel after
niques you can use, and [you have to] analyze very a few hours under local or short sedation. If the
carefully the biology of the patient you are going bowel is not viable, just open the patient and do a
to deal with. resection. This way, you can extend your expertise
Chowbey: I think it is very important to under- to different degrees.
stand that the technique depends on the expertise
of the surgeon, a group of surgeons of a depart-
ment, who have developed an expertise in a par-
ticular technique of hernia repair. For example, in
our department, we do mainly TEP in the majority
of our patients. But at the same time, the group
should have a sense of responsibility where they do
not stretch their imagination too far, do not stretch
their technique too far so as to harm the patient.
So if there is a patient after a radical prostatectomy
and you find that TEP is going to be difficult, it is a
good idea to do an anterior approach.
Schumpelick: How important is the wish of the
patient when they come to you and say that they
want this technique? Today our patients are quite
well informed by newspaper and the Internet.
Chowbey: This will not happen in our situation.
When a patient comes to us, he only comes to us
for endoscopic technique because we are known
for his technique. So even when a patient comes
with a huge, obstructed hernia with half of the
omentum in the scrotum, it is our responsibil-
ity to modify our technique. For example, in this
particular situation, we would still do an extra-
peritoneal approach. We know it is irreducible;
either we do a TAPP and reduce the hernia and
then go extraperitoneally—because that is our idea
 64

In Support of Standard Procedure

in Abdominal Hernia Repair
J. B. Flament
 486 Chapter 64 · In Support of Standard Procedure in Abdominal Hernia Repair
Introduction
The incidence of incisional hernia (usually defined
as a chronic postoperative defect of the abdominal
wall through which intraabdominal viscera pro-
trude beneath the skin). has been reported to be
as high as 11–13% of all laparotomies [1, 2]. Surgi-
cal repair is difficult in cases of large abdominal
64 defects when the herniated viscera have »lost their
right to reside« in the abdominal cavity; it must be
remembered that surgical repair of an incisional
hernia has nothing in common with closure of
a laparotomy. The weakening of the abdominal
wall and the consequences of decreased abdominal
pressure on diaphragmatic mobility and respira-
tory function are important factors [3]. Surgical
repair requires placement of a prosthetic mesh.
Without mesh, the recurrence rate is high and pro-
hibitive because it may vary from 30% to 60% [1].
Retromuscular prefascial placement of the mesh,
which we will describe as a standard procedure,
has been proposed by Rives and used in our de-
partment since 1966. Let us remember its basic
principles:
▬ A macroporous mesh
▬ Placed in an extraperitoneal site
▬ With fixation by transfixing stitches
▬ Under a tension sufficient to give normal
physiology to the abdominal wall
▬ With a good cosmetic result
Described as early as 1973 [3], this technique
was clearly demonstrated in 1977 in the French
Encyclopedia of Surgery [4]. The drawings were
later reproduced in the first and second editions
of Chevrel’s Hernias and Surgery of the Abdomi-
nal Wall [5]. They have also been reproduced by
Kingsnorth [2] and, with minor modifications, by
Wantz [6], Stoppa et al. [7], and Bauer et al. [1].
This technique is considered the gold standard for
repair of midline incisional hernias [8].
Clinical features are evident, and the diagnosis
is obvious at the first look. The bulge is seen when
the surgeon asks the patient to push or cough, in-
creasing the abdominal pressure. Palpation identi-
fies the edges of the musculoaponeurotic defect,
but precise measurement of the defect’s dimensions
may be difficult in very obese patients. Therefore,
computed tomography (CT) scanning is very use-
ful to assess the dimensions of the defect, the
retraction of the lateral muscles of the abdominal
wall, and the volume of the mushroom-like mass of
bowel exteriorized from the abdominal cavity [9].
As a consequence of the extraabdominal pro-
trusion of the viscera, the decrease in intraab-
dominal pressure leads to general and local distur-
bances. The recti and lateral muscles are infolded
because they have lost their midline insertion on
the linea alba. Wylie [10], as early as 1887, had un-
derstood this, writing that »most operators entirely
overlook the fact that the deep fascia which divides
and forms the sheath of the recti muscles, and
unites in the median line to form the linea alba,
is in reality the tendon of the transverse abdomi-
nal muscles; that is the fascia, and not the recti
muscles, which gives the abdominal walls their
transverse strength.« The recti abdominis are sag-
ittalized, and flat lateral muscles (external oblique,
internal oblique, and transversus) are retracted
and become fatty and sclerotic. The skin is also
involved in the abdominal wall disease: Trophic ul-
cerations are often observed in large tumefactions.
They are located over the midline and the apex of
the protrusion, resulting from the weakening of
the subcutaneous cellular tissue and the flattening
of blood vessels due to visceral pressure [11].
Perhaps more important are the respiratory
consequences related to the disappearance of the
normal contribution of the abdominal muscles and
diaphragm in respiration [3]. These disorders must
be evaluated by appropriate respiratory function
tests in order to avoid a catastrophic postoperative
course. In some cases, the herniated organs have
lost their »right to reside« in the abdomen, and
herniation cannot be reintegrated into the abdo-
men. These cases require specific preparation with
therapeutic preoperative pneumoperitoneum [12].
Preoperative Care
On initial contact with the patient, respiratory
function must be assessed (history of smoking,
cough, expectorations). Preparation includes respi-
ratory physiotherapy, withdrawal of tobacco, and,
if possible, weight loss. In cases of hernias with
Chapter 64 · In Support of Standard Procedure in Abdominal Hernia Repair
loss of domain, as evaluated by preoperative CT
scanning [9], the technique of preoperative thera-
peutic pneumoperitoneum is useful. Air is injected
into the peritoneal cavity until the patients feels
discomfort (scapular pain). The amount of air that
can be injected during each session varies greatly
according to the patient, from half a liter to more
than a liter. These pneumoperitoneum sessions
are repeated every 2 or 3 days, and the patient is
monitored with X-rays (subdiaphragmatic air im-
ages). With this technique, the patient’s tolerance
to reintegration of the herniated viscera can be
assessed. The diaphragm is readapted to work in
physiological conditions and is able to accept the
postoperative increase in intraabdominal pressure.
Surgical Treatment
The objectives of the operation are to place a
prosthetic material in the retromuscular prefascial
space. The prosthesis must be sutured under ten-
sion. We use transfixing sutures. This procedure of
fixation can lead to recuperation of lateral muscle
function since the physiological tension lost be-
cause of the middle detachment of the muscle is
reestablished. But when there is a risk of septic
complication (opening of an old abscess, acciden-
tal opening of the bowel), the use of a nonabsorb-
able mesh must be forbidden.
In most cases of huge incisional hernias that
we deal with, there is a loss of domain because the
487 64
herniated organs are no longer able to reside in
the abdominal cavity and cannot be reintegrated
into the abdomen. In this situation, there are really
two abdominal cavities. This concept of a second
abdominal cavity was first described by Rives et al.
in 1977 [4]. CT scanning gives a clear view of the
protruded viscera compared to the volume of the
residual abdominal cavity [9].
A general description of the procedure can be
easily given looking at a transverse cross-section of
the abdominal wall (⊡ Figs. 64.1–64.4) [12, 13]. The
prosthesis is placed in the rectus sheath, in contact
with the muscular fibers of the rectus muscle,
between the muscle and its sheath. The posterior
layer of the rectus sheath, strictly closed, prevents
any contact of the prosthesis with the bowel loops.
Lateral fixation by transfixing stitches, placed
through buttonhole stab wounds, prevents any
displacement of the prosthesis and recreates the
physiological tension of the lateral muscles of the
abdominal wall [14].
The direction of skin incision is chosen ac-
cording to the previous incision or to the major
axis of the tumefaction. We usually perform a large
resection of fat and skin (dermolipectomy or pan-
niculectomy) since the hernial sac always adheres
to the skin. In cases of cutaneous ulceration, the
resected area should be as large as possible, ex-
tending well behind the zone of infected lymphatic
reticulum [12]. After opening of the sac, adherent
bowel loops, which are often present (mainly in
cases of multirecurrent hernia), must be freed.
⊡ Fig. 64.1. The posterior rectus
sheath is opened near the linea
alba to expose the posterior layer
of the rectus muscle. (From Chevrel
and Flament [13], with permission
from Elsevier)
 488 Chapter 64 · In Support of Standard Procedure in Abdominal Hernia Repair
The margins of the orifice must be carefully
identified. Secondary orifices must be searched
for carefully (usually, these are diagnosed on sag-
ittal three-dimensional CT scan reconstruction)
and should be open; residual aponeurotic bands
extending from one margin to the other have no
structural value and cannot be used for repair.
When the abdominal cavity is free, by lib-
64 eration of bowel adhesions, the posterior rectus
sheath is opened–either with a sharp knife or
electrocautery–near the linea alba, to expose the
posterior layer of the rectus muscle (Fig. 64.1).
The area of mesh insertion must be as large as
possible. Suturing the mesh to the margins of the
defect offers no guarantee and usually results in
hernia recurrence because of lateral detachment
of the mesh. Accordingly, the mesh should extend
widely beyond the limits of the myoaponeurotic
orifice. An overlap of at least 5 cm is necessary.
The dissection of the retromuscular space is real-
ized with a swab or scissors. It is a blunt dissec-
tion and bloodless because it runs in an avascular
space. The dissection must be pushed to the lateral
margins of the rectus muscle, easily recognizable
by the perforating branches of intercostal neuro-
vascular bundles [15] (⊡ Fig. 64.2).
Below the arcuate line there is no posterior
layer of the rectus sheath, so the prosthesis will be
placed in the so-called preperitoneal or properito-
neal space (Retzius space medially, Bogros space
laterally). The dissection must be careful because
branches of the inferior epigastric artery cross
the operative field and may cause postoperative
⊡ Fig. 64.2. The dissection is pu-
shed to the lateral margins of the
rectus muscle, easily recognizable
by the perforating branches of
intercostal neurovascular bundles.
(From Chevrel and Flament [13],
with permission from Elsevier)
hematomas if injured. In this case, they may be li-
gated. The dissection must be pushed to the pubic
symphysis medially and to the Cooper’s ligament
laterally. Thus, stitches may be passed through the
Cooper’s ligament. Such stitches are a trick that
takes only a few seconds and prevents any slippage
of the mesh that would lead to suprapubic recur-
rences. This dissection may be difficult in cases of
previous prostate or bladder surgery.
The peritoneal cavity must be closed before
the mesh is implanted. In most cases, suturing of
the fascial margins can be achieved when the pos-
terior rectus sheath has been correctly and widely
freed. When fascial closure cannot be achieved, we
close the defect with a patch of absorbable mesh.
Omentum, when present, can also be used to pro-
tect viscera from any contact with the prosthesis;
the posterior surface of the omentum allows good
peritonization, while its anterior surface offers a
surface of granulation tissue that granulates into
the prosthesis.
Preparation of the Prosthesis
The choice of prosthesis is based on the physi-
cal and biological properties of the material to
be used. The ideal material must be a fairly open
mesh structure so that a rapid fibroblastic re-
sponse is able to invest the prosthesis, facilitating
its insertion. The ideal material must also be light,
with a certain degree of elasticity and suppleness;
elasticity allows the prosthesis to conform freely
Chapter 64 · In Support of Standard Procedure in Abdominal Hernia Repair
to the curvatures of the visceral sac. According
to the classification given by Amid [16], we use
either a type III (macroporous with microporous
components; Mersuture) or a totally macroporous
prosthesis (Prolene). The force of the abdominal
pressure holds the prosthesis against the deep sur-
face of the muscle, achieving a sort of »suture by
apposition.« However, this pressure-induced ap-
position is not sufficient to maintain the prosthe-
sis correctly during the first postoperative week.
Therefore, it is necessary to ensure solid peripheral
suturing of the prosthetic material. Sutures are
placed near the edge of the prosthesis; the two
ends of a nonabsorbable stitch are passed through
a fold (⊡ Fig. 64.3).
To pass the stitches through the abdominal
wall, we use a Reverdin needle when the subcuta-
489 64
neous fat is very thick (as is usually the case in our
patients). Each limb of the suture is passed through
the abdominal wall separately, but through the
same buttonhole stab wound (⊡ Fig. 64.4). In some
cases when the abdominal wall is not too fatty, an
ordinary stitch with a straightened needle, held
by a strong needle holder, may pass through the
abdominal wall, from outside to the retromuscular
space previously dissected; take a bite of the pros-
thesis; and pass again through the abdominal wall
from inside to outside. (It is interesting to note
that a company, Gore & Associates, has designed
a »suture passer« for celioscopic use that is very
similar to a straight Reverdin needle.) So each
stitch transfixes the abdominal wall twice, through
a cutaneous buttonhole stab wound that will be
closed at the end of the procedure by a single cuta-
⊡ Fig. 64.3. Sutures are placed near
the edge of the prosthesis; the two
ends of a nonabsorbable stitch are
passed through a fold. (From Chev-
rel and Flament [13], with permissi-
on from Elsevier)
⊡ Fig. 64.4. Each limb of the suture
is passed through the abdominal
wall separately, but through the
same buttonhole stab wound.
(From Chevrel and Flament [13],
with permission from Elsevier)
 490 Chapter 64 · In Support of Standard Procedure in Abdominal Hernia Repair
neous stitch. The passage of each end of the stitch
through the muscle must be separated by at least
1.5 cm. If they are closer, the muscle fibers may be
cut by the knot, which may cause small lateral re-
currences. The surgeon stands on the opposite side
of the stitches he or she is placing. Doing so, he or
she has a better view of the retromuscular space,
and the tailoring of the prosthesis is easier and
64 more precise. The transfixing sutures are placed
clockwise along each semilinear line (Spiegel line)
and at each extremity of the laparotomy. Twelve
stitches are usually enough, but in cases of huge
incisional hernia, up to 21 stitches may be used.
The stitches are knotted on one side and then on
the other side of the laparotomy.
The tailoring of the prosthesis is important:
The sutures must be placed under tension. This
fixation procedure allows recuperation of lateral
muscle function because the physiological tension
lost by midline detachment of the muscle is rees-
tablished (remember Wylie!).
In epigastric incisional hernias, the upper part
of the prosthesis is placed between the rectus abdo-
minis anteriorly and the ribs and internal oblique
posteriorly. If there is a loss of substance due to
retraction of the very short muscular fibers in this
location, the prosthesis may be fixed by a stitch
going around the rib on each side. The surgeon
must be careful not to pass the stitch through the
cartilage; that may cause postoperative pain. The
surgeon must also be attentive to cover the »fatty
triangle« described by Conze et al. [17].
At the end of the procedure, we trim the ex-
cess prosthetic tissue. Two close suction drains
are placed in contact with the prosthesis. Closure
of the musculoaponeurotic layer in front of the
prosthesis is always possible, thanks to the tension
of the prosthesis. Two drains are placed beneath
the skin. Dermolipectomy in the case of obese
patients, as already mentioned, may be done for a
much better cosmetic result.
Postoperative Care
During the early postoperative period, respiratory
physiotherapy resumes as soon as possible. Aspira-
tion drains are monitored and are usually removed
on the 3rd or 4th postoperative day. Antithrom-
boembolism measures must be used.
Results
In a recent series of 693 nonabsorbable prosthetic
repairs [18], the postoperative course was unevent-
ful in 96.4% of the patients. Five patients died
during the postoperative course, one from infec-
tion. Other deaths were from cardiac or respira-
tory causes. Superficial infection occurred in eight
cases (1.2%). Deep infection occurred in nine pa-
tients, one being lethal, but in only one case did we
have to remove the mesh.
The long-term results were evaluated by careful
follow-up. We observed 42 recurrences (6.7%),
which were often small lateral recurrences. Thirty
of them were successfully treated, leading to a final
good result of 98%.
Discussion
Naturally, this technique, although in our minds
the best, cannot be applied to all cases; other sites
of prosthetic implantation may be chosen on an
anatomical basis.
Intraperitoneal positioning of the prosthesis is
easy, and some published studies report good re-
sults [19]. However, we do not believe that intra-
peritoneal implantation has any advantages, ex-
cept rapidity. Of course, the peritoneum rapidly
envelops the prosthesis and offers a good defense
against infection without hematoma formation,
but adhesions of the bowel loops to the prosthesis
are frequent, thereby hindering intestinal transit
and rendering reintervention dangerous. We have
observed 17 cases of intraluminal migration of in-
traperitoneal prosthesis, and similar cases have
been reported in the literature [20]. When possi-
ble, interpositioning of the omentum between the
viscera and the prosthesis, as advocated by Rives et
al. in 1973 [3], can provide protection against these
complications.
Laparoscopic placement of a prosthesis is a
variant of intraperitoneal placement. We think this
technique may be used for small hernias but that
Chapter 64 · In Support of Standard Procedure in Abdominal Hernia Repair
it is ineffective for large hernias because the pros-
thesis cannot be placed under good tension due to
the pneumoperitoneum. This technique may be
dangerous because dissection of the intrasaccular
adhesions is difficult and may lead to bowel fistu-
las. Finally, laparoscopic treatment cannot give a
good cosmetic result because it does not treat the
problem of excess skin.
Premuscular positioning of the prosthesis is an-
other option [21]. This technique consists of clos-
ing the midline by reflected flaps of the interior
layer of the rectus sheath, this suture being rein-
forced by a large premuscular prosthesis, usually
Prolene. The problem with this technique is the
necessity of lifting a huge cutaneous flap, which
may lead to long-lasting seromas.
Conclusion
We can say that the standard retromuscular prefas-
cial prosthesis can be applied in about 80% of the
cases we are confronted with. But an abdominal
wall surgeon must know other techniques to fix
the 20% of cases in which a retromuscular prosthe-
sis cannot be used.
References
1. Bauer JJ, Harris MT, Gorfine SR et al.: Rives-Stoppa proce-
dure for repair of large incisional hernias: experience with
57 patients. Hernia 6:120–123, 2002
2. Kingsnorth A: The management of incisional hernia. Ann
R Coll Surg Engl 88:252–260, 2006
3. Rives J, Lardennois B, Pire JC et al.: Les grandes éventra-
tions. Importance du »volet abdominal« et des troubles
respiratoires qui lui sont secondaires. Chirurgie 99:547–
563,1973
4. Rives J, Pire JC, Flament JB et al.: Traitement des éventra-
tions. In: Encyclopédie medico-chirurgicale. Techniques
chirurgicales–appareil digestif. Elsevier, Paris, 1977
5. Flament JB, Rives J, Palot JP et al.: Major incisional hernia.
In: Chevrel JP (ed) Hernias and surgery of the abdominal
wall. Springer, Paris, 1997, pp 128–158
6. Wantz GE: Incisional hernioplasty with Mersilene. Surgery
172:129–137, 1991
7. Stoppa R, Moungar F, Verhaeghe P: Traitement chirur-
gical des éventrations médianes sus ombilicales. J Chir
129:335–343, 1992
8. Miedema B: Repair techniques for major incisional her-
nias. Am J Chir 187:148–152, 2004
491 64
9. Pourcher G, Deguelte S, Diaz Cives A et al.: Giant incisional
hernias: a new criteria for evaluation and treatment. Her-
nia [submitted]
10. Wylie G: Ventral hernia caused by laparotomy. Am J Obs-
tet 20:53, 1887
11. Flament JB, Avisse C, Palot JP et al.: Trophic ulcers in giant
incisional hernias–pathogenesis and treatment. A report
of 33 cases. Hernia 1:71–76, 1997
12. Flament JB: Retro rectus approach to ventral hernia repair.
Oper Tech Gen Surg 6:165–178, 2004
13. Chevrel JP, Flament JB: Traitement des éventrations de la
paroi abdominale. In: Encyclopédie medico-chirurgicale.
Editions techniques. Techniques chirurgicales–appareil
digestif. Elsevier, Paris, pp 40–165, 1995
14. Flament JB, Palot JP: Prosthetic of massive abdominal
ventral hernia. In: Fitzgibbons RJ, Greenburg AG (eds)
Nyhus and Condon’s hernia (5th edn). Lippincott, Phila-
delphia, 2002, pp. 341–365
15. Flament JB: Funktionelle anatomie der bauchwand. Der
Chirurg 5:401–407, 2006
16. Amid PK: Classification of biomaterials and their related
complications in abdominal wall hernia surgery. Hernia
1:15–21, 1997
17. Conze J, Prescher A, Klinger U, Saklak M, Shumpelick V:
Pitfalls in retro-muscular mesh repair for incisional hernia:
the importance of the «fatty triangle.» Hernia 8:255–259,
2004
18. Flament JB, Palot JP, Lubrano D et al.: Retromuskuläre
netplastik: Erfahrungen aus Frankreich. Chirurg 73:1053–
1058, 2002
19. Arnaud JP, Cervi C, Tuech JJ et al.: Surgical treatment of
post operative incisional hernias by intra-peritoneal inser-
tion of a Dacron mesh. Hernia 1:97–99, 1997
20. Flament JB, Avisse C, Palot JP et al.: Complications in in-
cisional hernia repairs by the placement of retromuscular
prostheses. Hernia 4:525–529 (suppl 1), 2000
21. Chevrel JP: Traitement des grandes éventrations média-
nes par plastie en paletot et prothèse. Nouv Presse Med
8:695–696, 1979
 65

In Support of Individualized Procedures

in Abdominal Wall Hernia Repair
M. Miserez, E. Peeters, F. Penninckx
 494 Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
Introduction
This paper describes our algorithm for a tailored
approach to patients with abdominal wall hernias,
excluding inguinal hernias. We believe that, even
more than in inguinal hernia repair, an individu-
alised approach is most appropriate for an optimal
outcome.
Abdominal wall hernias include both ventral
and incisional hernias. A ventral hernia is a pri-
mary abdominal wall hernia (e.g. epigastric, um-
65 bilical, Spigelian). Any hernia developing at the site
of a previous incision is referred to as an incisional
hernia. Many different factors (patient, hernia, sur-
geon, economic) play a role in the choice of the
most appropriate surgical procedure for ventral
or incisional hernia repair. Patient factors include
risk factors for hernia development or hernia re-
currence (⊡ Table 65.1), details on previous hernia
repair with respect to the plane of previous mesh
implantations, symptoms at the time of presen-
tation (e.g. incarceration), and the importance of
aesthetic aspects to the patient (e.g. postoperative
bulge). Hernia factors include the size of the defect
and hernia sac, the location of the defect (e.g. paras-
tomal), and the presence of additional muscle dia-
stasis or bulging around the defect. Surgeon fac-
tors imply that the surgeon should ideally have
both open and laparoscopic expertise. Economic
aspects refer to the cost of the new generation
of meshes (including specially designed intraab-
dominal meshes with antiadhesive properties and
»megaporous« meshes with larger pores and mostly
lower weight or density than the classical macropo-
rous meshes) and the hospital costs associated with,
for example, the use of a laparoscopic procedure
(laparoscopic equipment, disposable materials).
Classification and Definition
In the absence of an ideal ventral/incisional her-
nia classification and taking into account differ-
ent hernia details (e.g. defect location, diameter
and surface area, patient habitus, risk factors), the
Chevrel classification based on the location and
width (transverse diameter) of the hernia defect
currently offers the simplest, easiest system for
⊡ Table 65.1. Risk factors for hernia recurrence
 Obesity
 Smoking
 Diabetes
 Immunodeficiency (including cirrhosis, malnutrition,
etc.)
 Chronic cough
 Prostatic hypertrophy
 Constipation
 History of abdominal aortic aneurysm
tailoring the approach to the individual patient [1].
Type 1 hernias (width <5 cm) can be described as
small, type 2 hernias (width 5–10 cm) as medium,
type 3 hernias (width 10–15 cm) as large, and type 4
hernias (width >15 cm) as giant [2]. The latter are
sometimes accompanied by a loss of domain in the
abdominal cavity. Hernia width is more important
than hernia length because the possibility for ap-
proximation of the lateral edges of the hernia defect
depends on this hernia width. Moreover, hernia
width is often correlated with the length and thus
with the overall hernia surface area. In determin-
ing the hernia defect size in incisional hernia, the
size of additional defects (e.g. Swiss-cheese defects)
or eventual weaknesses or bulging over the entire
previous incision need to be taken into account
when calculating the final defect size. Of course,
the preoperative hernia diameter needs to be veri-
fied intraoperatively, and the surgical strategy may
need to be modified as a result of this.
When a mesh is used for hernia repair in the
ventral abdominal wall, it can be placed anterior to
the abdominal wall muscles (onlay), between the
fascia edges (inlay or interposition), or posterior
to the abdominal wall muscles [sublay if extrap-
eritoneal and underlay or intraperitoneal onlay
mesh (IPOM) technique if intraperitoneal]. (See
⊡ Fig. 65.1). Most authors agree that the current
gold standard in open mesh repair is the sublay
extraperitoneal repair popularised by Rives [3] and
Stoppa [4]. The main disadvantage of this tech-
nique is the extensive retromuscular dissection
necessary for implanting the prosthesis, which can
lead to postoperative wound complications such as
hematoma and seroma formation.
Therefore, open onlay mesh repair, initially pop-
ularised by Chevrel [5], has been recently promoted
Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
again [6] and could be especially useful in locations
where the retromuscular plane is more difficult
to dissect (e.g. semilunar line, subcostal). Although
easier than the sublay approach, it has not gained
widespread acceptance because of the less physi-
ological localisation of the mesh, in which a high
intraabdominal pressure might push the mesh away
from the fascia and could ultimately lead to early
recurrence, especially in cases of inadequate fixation
and/or overlap of the defect. Moreover, the exten-
sive subcutaneous dissection might result in subcu-
taneous seroma formation and wound dehiscence.
Because of the immediate contact of the subcutis
with a large surface of foreign body material, mesh
infection is also more likely to develop [2]. High-
level evidence in the literature, however, is limited,
and only a randomised controlled trial (RCT) with
onlay vs. sublay mesh positioning as a variable will
be able to solve this pertinent question.
On the other hand, because of the absence of
any overlap between mesh and healthy tissue, and
thus a high risk for hernia recurrence, inlay repair
should be abandoned.
In both open onlay and sublay mesh repair,
special attention should be paid to closing the ante-
rior fascia by adapting the abdominal wall muscles
and anterior rectus sheath on the midline. This
reconstruction of the abdominal wall is especially
495 65
⊡ Fig. 65.1. Terminology of
mesh location for ventral/incisi-
onal hernia repair
important in large and giant hernias to avoid early
mesh migration (leading to an early hernia recur-
rence) or later bulging of the mesh with a bad
aesthetic result and abnormal functioning of the
abdominal wall muscles during respiration. In this
case, the sutured fascia acts as an extra buttress, and
a faster mesh ingrowth due to better contact with
host tissue can be expected. This is referred to as
mesh augmentation. In cases in which the fascia
cannot be closed completely, the mesh is used (par-
tially) as a bridge between the fascia edges (»mesh
bridging«; ⊡ Figs. 65.1 and 65.2). Whether closure of
the posterior rectus sheath (above the arcuate line
of Douglas) before sublay mesh implantation is an
important factor in preventing postoperative bulg-
ing/herniation remains unclear. We prefer to close
this posterior rectus sheath as much as possible in
order to create a barrier between the (polypropyl-
ene) mesh and the viscera and also to restore the
original anatomical planes as much as possible.
Very Small Ventral or Incisional Hernias
(≤2 cm Maximum Diameter)
The data in the literature on the value of primary
suture repair in small ventral or incisional hernias
are very limited. Two RCTs are available. The
 496 Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
65
⊡ Fig. 65.2. Anatomical de-
monstration of mesh augmenta-
tion techniques and inlay mesh
positioning
first trial compared the long-term recurrence rate
of a continuous suture repair (polypropylene) vs.
sublay polypropylene mesh repair in 181 midline
incisional hernia patients (diameter ≤6 cm) [7]. A
subanalysis of small incisional hernias (hernia sur-
face area ≤10 cm2) showed a significantly increased
10-year cumulative recurrence rate of 67% vs. 17%
for the suture repair patients (p=0.003). The overall
long-term complication rate (small and larger her-
nias), which was available for 126 patients with an
average follow-up of 8 years, showed no significant
difference (8% for suture repair vs. 17% for mesh
repair; p=0.17). However, six patients in the mesh
group developed a fistula between the mesh and
the skin (n=3), a mesh infection (n=1), or an en-
terocutaneous fistula (n=2). Further details on the
association between hernia defect and complica-
tion rate are not available. The authors concluded
that suture repair should be abandoned.
Another RCT compared the long-term recur-
rence rate (mean follow-up 64 months) after suture
repair (interrupted nonresorbable suture) vs. sub-
lay mesh repair (polypropylene mesh or plug) in
primary umbilical hernia patients [8]. Here, too,
the recurrence rate was significantly increased in
the suture repair patients (11% vs. 1%; p=0.0015).
A subanalysis showed a recurrence rate of 10%
(suture) vs. 0% (mesh) in the very small hernias
(≤3 cm) and a recurrence rate of 13% (suture)
vs. 3% (mesh) in the larger hernias (>3 cm) [9].
Complications in the overall group did not differ.
Also in this paper, no data are given with respect
to body mass index (BMI) or other risk factors for
hernia recurrence.
Thus, although the recurrence rate in the
small hernias is clearly in favour of mesh repair in
both trials, it is not entirely clear that both groups
were comparable concerning risk factors for de-
veloping a recurrent hernia. Moreover, it is not
certain whether the data for these small hernias
with a diameter of around 3 cm (surface area of
10 cm2= diameter of 3.6 cm, provided the defect
is circular) are valid for even smaller hernias
with a maximum diameter the size of a finger
(1.5–2 cm), this being the majority of umbilical
hernias. Therefore, also taking into account the
chronic risk of mesh-related complications [10],
in the absence of any risk factors and without
muscle diastasis around the defect, we suggest
a suture repair for very small ventral (umbili-
cal, epigastric, Spigelian) or incisional hernias
(e.g. trocar site hernias).
Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
After all of the avascular weakened scar tissue
is excised, the suture repair should preferably be
performed with a one-layer nonabsorbable mono-
filament suture of size 0 or 1, or slowly resorbable
polydioxanone. Transverse adaptation of the fascial
edges without a »vest-over-pants« Mayo technique
[11] is suggested.
Small and Medium-Size Ventral/
Incisional Hernias (2–10 cm Maximum
Hernia Width)
For these hernias we suggest an open sublay or
laparoscopic IPOM mesh repair. In a retrospective
analysis of 175 consecutive patients with open sub-
lay repair and average hernia size between 8.5 cm
and 10.6 cm, anterior fascial closure was associ-
ated with a decreased risk for prosthetic infection
(2% vs. 26%; p<0.01). The recurrence risk after
a follow-up period of 20 months was not shown
to be statistically different, although recurrence
rates were increased by almost threefold in the
nonclosure group (16%) vs. the closure group (6%;
p=0.10) [12]. With adequate mobilisation of the
skin and subcutis laterally, anterior fascial closure
is almost always possible in these hernias during
open sublay repair. When a small gap remains, the
medial edges of the anterior rectus sheath can be
fixed onto the mesh, or a small polyglactin mesh
can be used as an additional inlay mesh to avoid
lateral retraction of these edges.
Laparoscopic mesh repair has the main advan-
tages of decreased wound complications, especially
in obese patients, and a shortened hospital stay
[13]. On the other hand, a laparoscopic repair in-
volves the use of a more expensive intraabdominal
antiadhesive mesh, and both postoperative acute
and prolonged pain may be higher after a laparo-
scopic procedure. All of these parameters should
be taken into account when calculating cost-effec-
tiveness. Recurrence rates in the midterm seem to
be comparable with those for open repair. How-
ever, from the available randomised trials so far,
it is very difficult to draw any final conclusions
because of the low patient numbers and the het-
erogeneity of inclusion criteria, definitions of post-
operative outcome parameters, and duration and
497 65
methods of follow-up. To answer these questions,
a large RCT was initiated both in Europe and the
United States. It seems that the trial in the United
States, comparing open onlay repair and laparo-
scopic repair, was prematurely stopped because of
an unacceptable number of wound complications
in the open group [14]. The European LAPSIS
trial, running under the auspices of the European
Hernia Society, currently includes more than 200
patients and compares not only open sublay re-
pair vs. laparoscopic repair but also, in every arm,
the use of a biological mesh (Surgisis Gold) vs. a
nonresorbable prosthesis. Inclusion criteria are pa-
tients with a BMI <40 and a primary or incisional
hernia with a maximum diameter of 4–10 cm. All
eligible patients in our department have been pro-
posed to enter the trial. The primary end point is
a composite end point of major complications at
3 years (hernia recurrence and/or mesh infection
and/or reoperation related to the previous hernia
repair) [15].
For all patients with a very small hernia who do
not undergo suture repair and for all other patients
with a maximum hernia width of 10 cm that do
not fulfil the inclusion criteria for the LAPSIS trial,
either a laparoscopic or an open sublay mesh re-
pair can be offered. In the absence of further high-
level evidence-based data, we propose laparoscopic
repair to the patient, especially in cases of BMI
>35–40, on the condition that he or she be willing
to cover the additional cost for the intraabdomi-
nal prosthesis since these costs are currently not
covered by the social security system in Belgium.
In a specific subgroup of these patients, we try to
avoid the use of an intraabdominal prosthesis by
using an endoscopic totally preperitoneal repair,
as in laparoscopic totally extraperitoneal (TEP)
inguinal hernia repair [16]. Good candidates for
this technique are patients with a lateral incisional
hernia (e.g. postappendectomy) or a hernia that is
localised subxiphoidally, suprapubically, or close
to other bony edges (iliac spine, costal margin). In
many cases, direct contact between the mesh and
the bowel can be avoided, and a simple polypro-
pylene mesh is used.
Ideally, anterior fascial closure and mesh aug-
mentation should also be aimed at during a lap-
aroscopic procedure, not to decrease the risk for
 498 Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
prosthetic infection as in open repair but mainly to
decrease the risk for early mesh migration or late
bulging of the mesh. We believe this is especially
true for the large and giant hernias, but it is exactly
in this group of patients that this is most difficult to
accomplish due to excessive tension on the tissues,
even after decreasing the intraabdominal pressure
of the pneumoperitoneum. Chelala et al. described
excellent results (low incidence of seroma forma-
tion and chronic pain, low recurrence rate) in a
large group of patients with systematic laparo-
65 scopic closure of the defect (although no closure
was performed in 4.5% of cases), but it is not clear
how many patients actually had a large defect
[17]. Whether this closure really needs to be done
in small and medium-size hernias remains to be
shown [18].
In all cases, exploration of the complete scar
is warranted, and additional hernias or bulging or
diastases over a previous incision need to be ad-
dressed and treated as the original hernia. In the
absence of any weaknesses, we use a tailored ap-
proach based on different parameters to determine
the need for coverage of the whole incision in a
patient with an incisional hernia [19].
Large Ventral/Incisional Hernias
(10–15 cm Maximum Hernia Width)
Although a laparoscopic approach is feasible [20,
21], we feel that a low chance for recurrence, to-
gether with an optimal functional and aesthetic
result, can be obtained only by an open sublay
repair with excision of redundant, often thinned
compromised skin and a maximal attempt at ana-
tomical reconstruction of the abdominal wall. In
addition, (laparoscopic) adhesiolysis can be very
cumbersome in large and giant hernias, and the
mortality rate in cases of unrecognised enterotomy
can be as high as 7.7% [22].
In most smaller hernias during open repair,
the anterior fascia can readily be approximated
on the midline, but in these larger hernias, ad-
ditional relaxing incisions may be necessary to
obtain this goal. Apart from decreasing the risk
for prosthetic infection, this adaptation is mainly
important in large and giant hernias, as men-
tioned before. The most radical relaxing incision
technique is the component separation technique
(CST) described by Ramirez et al. in 1990 [23].
Another possibility is multiple small relaxing in-
cisions bilaterally on the anterior rectus sheath
according to Clotteau and Premont [24] or one
single relaxing incision on each anterior rectus
sheath two-thirds from the midline according
to Gibson [25], with or without turndown of the
anterior rectus sheath according to Welti and Eu-
del [26]. If, however, a large defect remains at the
level of the anterior fascia (mesh bridging), most
authors also agree that a so-called megaporous
mesh should preferably be avoided to decrease
the risk for early or late bulging of this type of
soft, (too) elastic prosthesis.
Giant Ventral/Incisional Hernias
(>15 cm Maximum Hernia Width)
This group of patients present with the most chal-
lenging hernias. For the same reasons as discussed
above, we believe laparoscopic repair is not indi-
cated. In the case of loss of domain in the abdomi-
nal cavity, a preoperative pneumoperitoneum [27]
and optimal preparation of the patient (e.g. weight
loss, respiratory physiotherapy, bowel preparation)
may be necessary. Especially in this patient group,
in whom anterior fascial closure is important for
an acceptable functional and aesthetic result, this
closure is at the same time the most challenging,
due to retraction of the fascial edges laterally, and
CST is necessary in the majority of cases.
Skin coverage with a well-vascularised skin
and subcuticular flap without undue tension is
extremely important in this group to avoid wound
dehiscence or superficial wound infection, which
might be the start of a real disaster, with mesh
infection and fascia disintegration. Therefore, all
compromised skin tissue of bad quality needs to
be excised at the end of the procedure. An exten-
sive lateral dissection together with adequate sub-
cutaneous drainage and avoidance of dead space
on the midline are key points to preserve skin
integrity at the incision during the postoperative
course. To do this, a multidisciplinary approach
involving the plastic surgeon to create an autolo-
Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
gous skin (plus fascia) flap is necessary in a subset
of these patients.
Due to a small part of the rectus muscle that
remains, it is nearly always necessary to open the
semilunar line to develop a nice extraperitoneal
plane (beneath the transversus abdominis muscle)
for mesh implantation; even then, it is almost im-
possible to close the posterior rectus sheath as a bar-
rier between the mesh and the viscera, so a specially
designed mesh with antiadhesive properties will
be needed. Whether a simple and cheap polygla-
ctin mesh acts as an equally effective antiadhesive
barrier between polypropylene and the viscera re-
mains controversial [28, 29]. In addition, Petersen
et al. showed that extraperitoneal mesh implanta-
tion might even further compromise anterior fascial
closure, in contrast to intraperitoneal mesh implan-
tation [12]. Taking all of these findings together,
a more straightforward intraperitoneal (underlay)
mesh implantation without extraperitoneal dissec-
tion might be a better option in these patients [30],
despite the inherent risks of a more extensive adhe-
siolysis. A third option is an onlay mesh technique
in combination with CST, as was done in 18% of the
⊡ Fig. 65.3. Algorithm for determining surgical strategy as a function of hernia width in ventral/incisional hernia repair (CST
component separation technique)
499 65
patient population reported on by Kingsnorth et al.
[6]. In such cases, it is possible to overlap the relax-
ing incisions with the same mesh, extending far lat-
erally and thereby reducing the risk for abdominal
wall bulging or even abdominal wall rupture [31].
Conclusion
The algorithm in ⊡ Fig. 65.3 summarises our cur-
rent approach based on the maximum hernia
width. Of course, this algorithm is only a rough
guide to quickly determine the best approach. Pre-
operative patient details (including the skin condi-
tion, such as thinning or ulceration) and intraop-
erative hernia characteristics (especially in cases
of unexpected multiple hernia orifices at different
locations) will influence the surgical strategy in the
individual patient. Therefore, we strongly believe
that the abdominal wall surgeon should master
both laparoscopic and different open procedures
in order to use them in a tailored way in the in-
dividual patient who presents with a ventral or
incisional abdominal wall hernia.
 500 Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
References
1. Chevrel JP, Rath AM (2000) Classification of incisional
hernias of the abdominal wall. Hernia 4:7–11
2. Korenkov M, Paul A, Sauerland S, Neugebauer E, Arndt
M, Chevrel JP, Corcione F, Fingerhut A, Flament JB, Kux
M, Matzinger A, Myrvold HE, Rath AM, Simmermacher RK
(2001) Classification and surgical treatment of incisional
hernia. Results of an experts’ meeting. Langenbecks Arch
Surg 386:65–73
3. Rives J, Lardennois B, Pire JC, Hibon J (1973) Les grandes
éventations. Importance du « volet abdominal » et des
65 troubles respiratoires qui luis sont secondaires. Chirurgie
99:547–563
4. Stoppa R, Petit J, Abourachid H, Henry X, Duclaye C, Mon-
chaux G, Hillebrant JP (1973) Original procedure of groin
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tulle prosthesis by subperitoneal median approach. Chi-
rurgie 99:119–123
5. Chevrel JP, Rath AM (1997) The use of fibrin glues in the
surgical treatment of incisional hernias. Hernia 1:9–14
6. Kingsnorth AN, Shahid MK, Valliattu AJ, Hadden RA, Porter
CS (2008) Open onlay mesh repair for major abdominal
wall hernias with selective use of components separation
and fibrin sealant. World J Surg 32:26–30
7. Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaasdonk
EG, Jeekel J (2004) Long-term follow-up of a randomized
controlled trial of suture versus mesh repair of incisional
hernia. Ann Surg 240:578–583
8. Arroyo A, Garcia P, Perez F, Andreu J, Candela F, Cal-
pena R (2001) Randomized clinical trial comparing suture
and mesh repair of umbilical hernia in adults. Br J Surg
88:1321–1323
9. Perez F, Arroyo A (2002) Authors’ reply. Br J Surg 89:628
10. Costa D, Tomas A, Lacueva J, de Asis Perez F, Oliver I, Ar-
royo A, Sanchez A, Andreu J, Gallego JA, Calpena R (2004)
Late enterocutaneous fistula as a complication after um-
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11. Mayo WJ (1901) An operation for the radical cure of umbi-
lical hernia. Ann Surg 34:276–280
12. Petersen S, Henke G, Zimmerman L, Aumann G, Hellmich
G, Ludwig K (2004) Ventral rectus fascia closure on top of
mesh hernia repair in the sublay technique. Plast Reconstr
Surg 114:1754–1760
13. Sajid MS, Bokhari SA, Mallick AS, Cheek E, Baig MK (2009)
Laparoscopic versus open repair of incisional/ventral her-
nia: a meta-analysis. Am J Surg 197:64–72
14. Itani KM, Neumayer L, Reda D, Kim L, Anthony T (2004)
Repair of ventral incisional hernia: the design of a rando-
mized trial to compare open and laparoscopic surgical
techniques. Am J Surg 188:22S–29S
15. Sauerland S, Miserez M, Grass G, Stützer H, Neugebauer E
(2004) LAPSIS: a randomised controlled multicentre trial
of laparoscopic versus open ventral hernia repair using a
classical versus a collagen mesh (Surgisis Gold). Langen-
becks Arch Surg 389:429
16. Miserez M, Penninckx F (2002) Endoscopic totally preperi-
toneal ventral hernia repair. Surg Endosc 16:1207–1213
17. Chelala E, Thoma M, Tatete B, Lemye AC, Dessily M, Alle
JL (2007) The suturing concept for laparoscopic mesh
fixation in ventral and incisional hernia repair: mid-term
analysis of 400 cases. Surg Endosc 21:391–395
18. Agarwal BB, Agarwal S, Gupta MK, Mishra A, Mahajan
KC (2008) Laparoscopic ventral hernia meshplasty with
»double-breasted« fascial closure of hernial defect: a
new technique. J Laparoendosc Adv Surg Tech A 18:222–
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19. Miserez M, Tomczyk K, Penninckx F (2007) The local patch.
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nia: prevention and treatment. Springer, Heidelberg, pp
226–232
20. Kirshtein B, Lantsberg L, Avinoach E, Bayme M, Mizrahi
S (2002) Laparoscopic repair of large incisional hernias.
Surg Endosc 16:1717–1719
21. Ferrari GC, Miranda A, Sansonna F, Magistro C, Di Lernia
S, Maggioni D, Franzetti M, Pugliese R (2008) Laparoscopic
management of incisional hernias > or = 15 cm in diame-
ter. Hernia 12:571–576
22. LeBlanc KA, Elieson MJ, Corder JM 3rd (2007) Entero-
tomy and mortality rates of laparoscopic incisional and
ventral hernia repair: a review of the literature. JSLS
11:408–414
23. Ramirez OM, Ruas E, Dellon AL (1990) »Components sepa-
ration« method for closure of abdominal-wall defects: an
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24. Clotteau J, Prémont M (1979) Treatment of severe me-
dian abdominal cicatricial eventrations by an aponeurotic
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25. Gibson CL (1920) Operation for cure of large incisional
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26. Welti H, Eudel F (1941) Un procédé de cure radicale des
éventrations postopératoires par auto-étalement des mu-
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leur gaine. Mem Acad Chir 12:791–798
27. Goni Moreno IG (1947) Chronic eventrations and large
hernias. Surgery 22:945–948
28. Jenkins SD, Klamer TW, Parteka JJ, Condon RE (1983) A
comparison of prosthetic materials used to repair abdo-
minal wall defects. Surgery 94:392–398
29. de Vries Reilingh TS, van Goor H, Koppe MJ, Bodegom
ME, Hendriks T, Bleichrodt RP (2007) Interposition of
polyglactin mesh does not prevent adhesion formation
between viscera and polypropylene mesh. J Surg Res
140:27–30
30. Bernard C, Polliand C, Mutelica L, Champault G (2007)
Repair of giant incisional abdominal wall hernias using
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31. de Vries Reilingh TS, Bleichrodt RP (2007) [Reply to letter
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Chapter 65 · In Support of Individualized Procedures in Abdominal Wall Hernia Repair
501 65
Discussion

Kurzer: Dr. Flament, have you ever seen a hernia

that you thought was inoperable, that you couldn’t
operate on?
Flament: Yes. There are some people—old patients,
with fistula and a short life expectancy; in these
cases we do not operate. But in young patients
with loss of domain, we perform a progressive
pneumoperitoneum; we could always reintegrate
all of the abdominal cavity. And in very rare cases
we perform a resection, for example, a left hemi-
colectomy to close the abdominal wall.
Deysine: A comment on the small hernias below
2 cm, which are most common. My experience
at the VA Hospital doing these little hernias with
conventional suture repair was a recurrence rate
of 100%. The motion of the abdominal wall when
the patient stands up is so strong that it will break
it. Since I began using small pieces of mesh, some-
times the tip of a plug, just to obliterate those little
holes, the recurrences went away.
Schumpelick: Maybe this should be studied in a
trial. I also believe that small trocar hernias can be
done by stitches with good results.
 66

In Support of Standard Procedure

in Hiatal Hernia Repair
P. K. Chowbey, T. Mittal, V. Soni, R. Khullar, A. Sharma, M. Baijal, A. Dey
 504 Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
Introduction
Laparoscopic esophageal surgery has gained pop-
ularity due to the unprecedented view it allows of
esophageal hiatal hernias and the ease of access to
the surgical site offered by the minimal-access ap-
proach. Numerous series have demonstrated the
safety and efficacy of approaching gastroesopha-
geal reflux disease (GERD) and hiatal hernia
repair laparoscopically [1, 2]. Despite increasing
experience with laparoscopic hiatal hernia repair,
authors continue to report recurrence rates of
up to 43% with sutured cruroplasty [3, 4]. This
66 compares laparoscopic hiatal hernia repair poorly
with open repair, as it is well documented that
open hiatal hernia repair with the addition of
Stamm gastrostomy is associated with very low
recurrence rates [5, 6]. Additionally, intrathoracic
wrap migration rates of up to 26% have been re-
ported for patients undergoing laparoscopic fun-
doplication with primary sutured hiatal hernia
repair [7].
Some possible patient-related and procedure-
related mechanisms for recurrence include inap-
propriate patient activity immediately after sur-
gery, inadequate excision of the sac, inadequate
mobilization of the esophagus, inadequate crural
closure secondary to widely spaced crura sutured
under tension, and postoperative rupture of the
cruroplasty due to continuous excursion of the
diaphragm.
Several technical details have been considered
to minimize these high recurrence rates, including
excision of the sac with complete detachment of
the sac from the hiatus and mediastinum, adequate
mobilization of the esophagus with a minimum
of 3 cm of intraabdominal esophagus, and the use
of mesh cruroplasty in patients with large hiatal
hernias. The purpose of using prosthetic materials
is to achieve a tension-free hiatal repair. The mesh
may be used to close the gap between two widely
spaced crura or to reinforce a suture cruroplasty.
There has been debate regarding the type, size,
and shape of mesh and the technique of mesh
placement; these are matters of future research in
this field.
The aim of the present study was to evaluate
the effect of mesh reinforcement in laparoscopic
hiatal hernia repair on recurrence rate and side ef-
fects during long-term follow-up.
Materials and Methods
Patients
A total of 430 patients (165 men and 265 women)
underwent laparoscopic hiatal hernia repair be-
tween January 1994 and December 2007 at Sir
Ganga Ram Hospital, Delhi, India. Their mean age
was 42.4 years (range 25–72 years). In the period
between 1994 and 2002, suture cruroplasty was
performed for most of the patients with hiatal her-
nias, except for those with a very wide hiatal defect
in whom the crura could not be brought together
with sutures. In those patients, mesh cruroplasty
was performed. After 2002, crural repair was re-
inforced by using a mesh for hiatal hernias (>5 cm
hernial defect) as routine practice.
Preoperative Investigation
Preoperative evaluation included a chest X-ray,
upper gastrointestinal endoscopy, and barium
swallow for all patients. Manometry and 24-h pH
monitoring were not routinely performed. Fluoro-
scopic evaluation provided a reasonable measure
of esophageal motility. The presence or absence
of dysphagia was considered another reasonably
sound predictor of whether the patient would tol-
erate full fundoplication. An antireflux procedure
was performed in most circumstances.
Indications for Surgery
Sliding hernia: All symptomatic patients
Paraesophageal hernia: Even asymptomatic pa-
tients were operated on to avoid the potential risk
of life-threatening complications such as incar-
ceration, volvulus, perforation, and bleeding.
Exclusion criteria: Patients with symptoms of
GERD without hiatal hernia
Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
Surgical Technique
Our aims of surgery are as follows:
▬ Reduction of contents
▬ Excision of the sac
▬ At a minimum, a 3-cm intraabdominal length
of esophagus
▬ Division of the short gastric vessels to mobi-
lize the gastric fundus
▬ Tension-free sutured crural repair in a hiatus
<5 cm wide
▬ Prosthetic repair of the crural gap in a hiatus
>5 cm wide
▬ A short, floppy 360° wrap
Anesthesia
The procedure is performed under general anes-
thesia with endotracheal intubation.
Position
The patient is placed in reverse Trendelenburg
position with the knees slightly flexed. The sur-
geon stands between the patient’s legs. The camera
assistant is positioned to the right of the patient
and the assistant surgeon to the left of the patient
(⊡ Fig. 66.1).
505 66
Ports
The camera port (10 mm or 5 mm) is made above
the umbilicus, one-third of the distance between
the umbilicus and the epigastrium toward the left
of the midline. Additional ports, three 5-mm and
one 10-mm, are placed as shown in ⊡ Fig. 66.2. The
5-mm port in the epigastrium is used to retract the
left lobe of the liver using a Nathanson liver retrac-
tor (our preferred method). In some cases we also
use a fan retractor for retraction of the liver. The
5-mm port in the right midclavicular line and the
10-mm port in the left midclavicular line are the
surgeon’s left-hand and right-hand working ports,
respectively.
Reduction of Contents
With the use of atraumatic bowel graspers, the
stomach is grasped and retracted, and the contents
from the hernial sac are then reduced (⊡ Fig. 66.3).
Excision of Sac
A right diaphragmatic crus is identified after di-
viding the gastrohepatic ligament (⊡ Fig. 66.4), pre-
serving the hepatic branch of the vagus in most
cases. Ultrasonic coagulating shears (UltraCision;
Ethicon Endo-Surgery, Cincinnati, OH, USA) are
⊡ Fig. 66.1. Operating theater
layout
 506 Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
66
⊡ Fig. 66.2. Port positions
⊡ Fig. 66.3. Stomach being reduced from mediastinum using
bowel grasper
used to divide the peritoneum at the anterolateral
edge of the hiatus. The natural tissue plane that
exists between the peritoneal and pleural layers of
the hernial sac is developed, and the sac is sepa-
rated completely. Once the complete dissection of
the sac has been performed, the sac is excised close
to its attachment to the gastroesophageal junction
and removed so that it does not interfere with sub-
sequent repair.
⊡ Fig. 66.4. Gastrohepatic ligament being divided to visualize
the right crus
Esophagus Mobilization
Circumferential esophageal mobilization is done
using ultrasonic shears so as to have a minimum of
3 cm of intraabdominal esophagus around which
the fundal wrap is created. In our experience, it has
been possible to mobilize the esophagus to achieve
an intraabdominal length of 3 cm in all cases, and
we have not felt the need to perform an esophageal
lengthening procedure.
Division of Short Gastric Vessels
The short gastric vessels are divided to mobilize the
gastric fundus, using ultrasonic coagulating shears,
until the left crus is identified (⊡ Fig. 66.5). This
helps us in creating loose, floppy fundoplication.
Cruroplasty
The retroesophageal window is enlarged, and then
the esophagus is retracted to the patient’s left with
a sling made with a Penrose drain or umbilical
tape. The size of the hiatus is then assessed in the
anterior–posterior plane (⊡ Fig. 66.6).
If the size of the hiatus is <5 cm, a primary
posterior suture cruroplasty is performed using
two or three intracorporeal sutures (2-0 Ethibond;
Ethicon, Somerville, NJ, USA) for crural approxi-
mation. Sutures are tied loosely so as not to stran-
gulate the muscle fibers. A sufficient gap is left
between the crura by visual impression to allow
Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
⊡ Fig. 66.5. Greater curvature of the stomach being mobilized
by dividing the short gastric vessels using ultrasonic coagu-
lating shears
⊡ Fig. 66.6. The size of the hiatus is assessed in the anterior–
posterior plane
passage for a food bolus and thereby prevent dys-
phagia. We prefer to err on the side of a wider hia-
tus in place of tight closure. Tight closure may lead
to intractable dysphagia, which might not respond
to any other measure and may need reexploration
and removal of sutures.
If the size of the hiatus is >5 cm, a mesh repair
is performed either to reinforce a sutured repair
or to bridge the gap between the widely spaced
crura.
Before placing the mesh we prefer to approxi-
mate the crura posteriorly as much as can be
achieved without tension. In our initial practice,
we used polypropylene mesh (Prolene; Ethicon).
507 66
⊡ Fig. 66.7. 2–0 Ethibond suture being used to fix the crural
soft mesh near the right crus
⊡ Fig. 66.8. Gastrogastric suture with 2–0 Ethibond for fundal
wrap
There has been concern about using polypropylene
mesh because it causes dense fibrosis, so later we
started using lightweight meshes, UltraPro (Ethi-
con) and CruraSoft (Bard, Murray Hill, NJ, USA).
The CruraSoft is a V-shaped mesh that conforms
to the hiatal anatomy. The mesh is fixed using 2-0
Ethibond (Ethicon) sutures (⊡ Fig. 66.7), with its
margins overlapping the crural margin by 2–3 cm.
The gastric fundus is wrapped around the
lower esophagus to create a tension-free wrap.
Two gastrogastric seromuscular sutures are placed,
which include a seromuscular bite on the esopha-
geal wall to ensure correct positioning of the fun-
doplication and prevent slippage (⊡ Fig. 66.8). We
 508 Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
routinely perform Nissen 360° fundoplication in
most patients, but in patients with a history of dys-
phagia, detected motility disorder, and age >65, we
perform partial fundoplication.
Postoperative Management
Postoperatively, patients are kept on a liquid diet
on the1st postoperative day and gradually started
on a soft diet, progressing to a normal diet as tol-
erated. They are advised to chew their food well
and not to take large bites. All tablets are given in
66 a crushed form. We do not routinely recommend
a Gastrografin study before starting a diet for the
patient.
Follow-up evaluations took place at 7 days,
3 months, and 1 year after surgery. A barium swal-
low was performed at 3 months and 1 year after
surgery. Endoscopy was suggested for routine fol-
low-up but was refused by most of our patients in
view of the invasiveness of the procedure. However,
it was done if the patient became symptomatic.
Surgical Outcome
Preoperative data were collected retrospectively.
Long-term follow-up assessment was prospectively
performed for 410 patients (95%) using a stan-
dardized questionnaire. Hiatal hernia recurrence
was assessed using barium swallow .The mean
follow-up period was 5.6 years (range 1–13 years).
Statistical Analysis
Statistical analysis was performed using, as appro-
priate, a chi-square test and Fisher’s exact test. A p-
value <0.05 was considered statistically significant.
Results
In 357 patients we repaired the hiatus with sutured
cruroplasty and in 73 patients with mesh cruro-
plasty (⊡ Fig. 66.9). Fifteen patients in the sutured
cruroplasty group and five patients in the mesh
cruroplasty group were lost to follow-up. There
was no conversion to open surgery.
Intraoperative Considerations
The intraoperative complication rate was 5.81%
(25 patients). Ten (2.32%) patients had a pleu-
ral tear, which was managed by positive pressure
ventilation during carbon dioxide desufflation to
ensure lung expansion. There were no postop-
erative sequelae. Ten (2.32%) patients had bleeding
from the short gastric vessels, which was managed
by the application of clips, and in five (1.16%) pa-
tients there was splenic capsule laceration, which
was managed by compression. No splenectomy
was required in any of our patients. In all patients,
an adequate intraabdominal length of esophagus
was achieved by mobilizing the esophagus. No
patient required a gastroplasty.
The postoperative morbidity was 2.7%
(12/430). Three (0.06%) of our patients developed
complete dysphagia (inability to swallow saliva).
All of these patients were managed conservatively
on intravenous fluids and cessation of all oral in-
take. Five (1.16%) patients developed atelectasis,
and four (0.9%) had pneumonia that responded
to intravenous antibiotics and chest physiotherapy.
There was no mortality. The mean duration of
hospitalization was 3.2 days (range 2–9 days).
Postoperatively, patients with suture cruro-
plasty had a dysphagia rate of 9.9% (34 patients
out of 342) compared with 14.7% (10/68) in the
mesh cruroplasty group at 3 months after sur-
gery (p=0.344). However, the dysphagia rate at the
1-year follow-up had improved in both groups and
was not significantly different between the groups
(3.8% vs. 4.4%; p=0.916). (See ⊡ Fig. 66.10.)
Radiologic follow-up evaluation showed a
hiatal hernia recurrence rate of 14.9% (51/342)
in patients with suture cruroplasty (⊡ Fig. 66.11).
Of these 51 patients, 12 were symptomatic. They
were initially managed medically; however, three
of these 12 patients required redo surgery. In all
three patients, we found a hiatal disruption with
intrathoracic migration of the fundal wrap.
During follow-up of mesh cruroplasty patients,
the recurrence rate was 5.8% (4/68; ⊡ Fig. 66.12)
Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
⊡ Fig. 66.9. Total number of patients undergoing hiatal hernia
repair with and without mesh
⊡ Fig. 66.10. Incidence of dysphagia in patients with suture
cruroplasty at 3 months and 1-year follow-up
compared with 14.9% in the suture cruroplasty
group (p=0.071). All of these patients had a small
sliding hernia on radiologic evaluation. These pa-
tients were asymptomatic and are being regularly
followed up. Most of these recurrences (three out
of four) were observed in the earlier patients.
Since 2005, there has been no recurrence during
follow-up.
No mesh-related complications were ob-
served.
509 66
⊡ Fig. 66.11. Recurrence rate in the suture cruroplasty group
⊡ Fig. 66.12. Recurrence rate in the mesh cruroplasty group
Discussion
The past 50 years have witnessed a paradigm shift
in the surgical repair of both inguinal and ventral
hernias. Several reports of randomized data show
a clear superiority of tension-free mesh hernia re-
pair for both inguinal and ventral hernias [8–10].
Creating a tension-free, primary sutured repair
of the diaphragmatic hiatus is difficult. It is a dy-
namic area due to diaphragmatic excursions with
 510 Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
constant motion, even at rest. Nevertheless, the
goal for repair of the hiatus should be to create a
tension-free repair. A high recurrence rate after
laparoscopic primary sutured cruroplasty, espe-
cially for large hiatal hernias [3, 4], suggests that
suture repair alone does not provide an optimal
tension-free repair. Our own experience demon-
strated a higher recurrence rate in patients with
sutured cruroplasty compared with those receiving
mesh cruroplasty (14.9% vs. 5.8%).
As with hernia repair in other parts of the body,
there is no consensus on the best prosthetic mate-
rial to use for the procedure. The most commonly
66 used mesh is polypropylene (Prolene; Ethicon)
[11–13]. Several different types of polytetrafluo-
roethylene (PTFE) and PTFE composite materials
have been used, including DualMesh (Gore, Flag-
staff, AZ, USA) [14] and a simple PTFE patch [15,
16]. Porcine small intestinal mucosa (Surgisis; Cook
Surgical, Bloomington, IN, USA), which provides
scaffolding for natural tissue ingrowth, is also used
[17]. In our initial 27 cases, we used Prolene mesh
because it is readily available, inexpensive, mal-
leable, and easy to handle. There has been concern
about the use of polypropylene mesh because it
causes dense fibrosis. As a result, we have started us-
ing lightweight, large-pore meshes–Ultrapro (Ethi-
con) and CruraSoft (Bard)–because they are tissue
friendly and known to cause less fibrosis.
The hiatal meshes are available in variable
shapes, including a V-shape, a U-shape, and a
⊡ Fig. 66.13. Techniques of mesh cruroplasty
completely circular mesh. There has been some
concern about the use of a circular mesh because
of its potential to cause circumferential fibrosis
around the esophagus, resulting in dysphagia. Our
preference is a V-shaped mesh (CruraSoft) for
closing the esophageal hiatus.
The technique for placing prosthetic materials
can be either posterior, anterior onlay, or interpo-
sitional when reapproximation of the hiatus is pos-
sible (⊡ Fig. 66.13). Most surgeons prefer primary
sutured repair of the hiatus followed by an onlay of
prosthetic materials posteriorly. The overall theme
remains that hiatal hernia repair should be made
as tension-free as possible, whether via an onlay
repair or an interpositional repair. Our preference
is to do an onlay repair for large hiatal hernias
(>5 cm).
The mesh is fixed at the hiatus using sutures,
tacks (not our choice), or, recently, fibrin sealant.
The topographic vicinity of the heart and other
major anatomical structures (liver, inferior vena
cava) and the fact that the diaphragm is very thin
in this area makes suturing technically difficult
and requires surgical expertise. An easier alterna-
tive is to apply tacks, but this has resulted in fatal
complications, including death by cardiac tampon-
ade [18]. The use of a fibrin sealant for mesh fixa-
tion was reported by Katkhouda et al. in an animal
experiment [19]. These authors were able to show
that fixation with fibrin sealant is mechanically
equivalent to stapler fixation. In a number of clini-
Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair
cal studies, both the efficiency of fibrin sealant and
also a reduction in postoperative complications
have been shown in inguinal hernia repair [20,
21]. The use of fibrin sealant is now also being
described for hiatal hernia repair. As protocol, we
prefer sutures for fixing the mesh but have on oc-
casion used fibrin sealant and found it to be a safe
and effective adhesive.
Higher rates of dysphagia have been reported
in patients with mesh cruroplasty [22, 23], and
there have been case reports of patients being
reoperated for mesh-induced fibrosis [24, 25]. In
most studies, the early results have shown a higher
rate of dysphagia in patients with mesh cruro-
plasty, but this rate became comparable at 1 year of
follow-up. In our study, the dysphagia rate was also
comparable at 1-year follow-up (3.8% vs. 4.3%).
Another major concern of using mesh at the
hiatus is erosion of the mesh into the esophagus or
stomach. Erosion of mesh is very rare and has been
reported only in case reports [26, 27]. In our expe-
rience, there were no mesh-related complications.
Summary
Reinforcement of the esophageal hiatus with a
prosthetic mesh has proven to be a safe and ef-
fective procedure to reduce postoperative hiatal
hernia recurrence. A few comparative studies of
laparoscopic hiatal closure with simple sutures ver-
sus mesh cruroplasty have shown that patients
with prosthetic hiatal closure have a lower rate
of hiatal hernia recurrence in comparison to pa-
tients with simple hiatal repair. However, some
patients with prosthetic hiatal closure suffer from
prolonged postoperative symptoms such as dys-
phagia. Fortunately, this resolves in most patients
without further treatment. A true complication
related to the use of prosthetic materials for hiatal
closure is rare.
Acknowledgments
I am thankful to Dr. Tarun Mittal and Dr. Ash-
ish Dey, my colleagues in the Minimal Access,
Metabolic & Bariatric Surgery Centre, for ac-
511 66
tively participating in the »pro standard pro-
cedure in hiatal hernia repair« project and in
preparing this article.
I am thankful to my colleagues Dr. Rajesh
Khullar, Dr. Anil Sharma, Dr. Vandana Soni, and
Dr. Manish Baijal for their invaluable assistance
in completing this project. I am grateful for their
constant and positive support in all the ongoing
projects and progress made in the Centre. I express
great appreciation to all my fellows and resident
doctors, Dr. Kshipra Dhawan and Dr. Neeraj Garg,
for their supportive help and efforts.
I sincerely thank Ms. Aenu Batra, Mr. Pankaj
Gupta, Ms. Shradha Verma, Mr. Satish Jha, and
Dhuruvendra Singh for their excellent secretarial
help and support.
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3. Hashemi M, Peters JH, Deemeester TR, Huprich JE, Quek
M, Hagen JA, Crookes PF, Theisen I, De Meester SR, Sillin
F, Bremner CG (2000) Laparoscopic repair of large type III
hiatal hernia: objective follow up reveals high recurrence
rate. J Am Coll Surg 190:553–561
4. Wiechmann RJ, Ferguson MK, Nauheim KS, McKesey P,
Hazelrigg SJ, Santucci TS, Macherey RS, Landreneau RJ
(2001) Laparoscopic management of giant paraesopha-
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5. Schauer PR, Ikramuddin S, McLaughlin RH, Graham TO,
Slivka A, Lee KK, Schraut WH, Luketich JD (1998) Compari-
son of laparoscopic versus open repair of paraesophageal
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6. Wichterman K, Geha AS, Cahow CE, Raue AE (1979) Para-
esophageal hiatus hernia with intrathoracic stomach and
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7. Granderath FA, Schweiger UM, Kamoiz T, Ashe KU, Point-
ner R (2006) Laparoscopic Nissen fundoplication with
prosthetic hiatal closure reduces postoperative intratho-
racic wrap herniation. Arch Surg 140:40–48
8. Burger JW, Luijendijk RW, Hop WC, Halm JA, Verdaasdonk
EG, Jeekel J (2004) Long-term follow up of a randomized
controlled trial of suture versus mesh repair of incisional
hernia. Ann Surg 240:578–585
9. Lichtenstein IL, Shulman AG, Amid PK, Montlior MM (1989)
The tension-free hernioplasty. Am J Surg 157:188–193
 512 Chapter 66 · In Support of Standard Procedure in Hiatal Hernia Repair

10. Vrijland WW, van den Tol MP, Luijendijk RW, Hop WC,
Busschback JJ, de Lange DC, van Geldere D, Rottier AB,
Vegt PA, IJzermans JN, Jeekel J (2002) Randomized clinical
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hernia. Br J Surg 89:293–297
11. Basso N, De Leo A, Genco A, Rosato P, Rea S, Spaziani
E, Primavera A (2000) 360° laparoscopic fundoplication
with tension-free hiatoplasty in the treatment of symp-
tomatic gastroesophageal reflux disease. Surg Endosc
14:164–169
12. Basso N, Rosato P, De Leo A, Genco A, Rea S, Neri Y (1999)
»Tension-free« hiatoplasty, gastrophrenic anchorage and
360° fundoplication in the laparoscopic treatment of pa-
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13. Hawasli A, Zonca S (1998) Laparoscopic repair of paraeso-
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26. Carlson MA, Condon RE, Ludwig KA (1998) Management
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27. Schauer PR, Ikramudin S, McLaughlin RH, Graham TO,
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66 phageal hiatal hernia. Am Surg 64:703–710

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24. Edelman DS (1995) Laparoscopic paraesophageal hernia
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Swanstrom LL, Hunter JG (1997) Complications of la-
 67

Strategy To Improve the Results?

In Support of Individualized
Procedures in Hiatal Hernia Repair
J. F. Kukleta
 514 Chapter 67 · Strategy To Improve the Results? In Support of Individualized Procedures in Hiatal Hernia Repair
Introduction
It has recently become evident that the durability of
crural repair determines not only the outcome qual-
ity of paraesophageal hernia (PEH) repairs but the
long-term success of antireflux procedures as well.
Because of the personal experience of individual
surgeons and surgical teams with the complexity of
hiatal repairs, several different techniques have been
proposed to correct this diaphragmatic disorder.
The results of the surgical treatment are far from be-
ing excellent solutions for all patients for all esopha-
geal and extraesophageal symptoms, but in general,
they promise good or satisfactory outcomes ap-
proximately 85–90% of the time. Since the introduc-
67 tion of laparoscopic techniques in hiatal repair, the
problematic cure has become even more complex,
partly due to the learning curve for everyone.
Several reviews of the available published data
on the hiatal environment [1–3] are quite repre-
sentative of the status quo: The procedures are not
standardized, and data with high levels of evidence
are lacking. There are too many controversies and
very little consensus.
The recurrence rate of a laparoscopic simple-
sutured PEH repair ranges from 0% to over 40%
[4]. The most important mechanism of failure of
antireflux procedures is, in 60–84% of cases, migra-
tion of the intrathoracic wrap [5, 6]. Both failures
are sequelae of insufficient closure or disruption of
the crural repair. Unlike in endoscopic repairs for
inguinofemoral or abdominal wall hernias, in which
the use of prosthetic meshes is a well-accepted part
of a successful tension-free repair concept, the use
of meshes in hiatal repairs is still under debate [3].
To improve the results of hiatal disorders, the
causes of failure must be analyzed, the predictors
taken into account, and the »pillars of the best
outcome« identified and reinforced. If the risk of
repair failure is anticipated, then individual adapta-
tion of the surgical technique can help prevent this
situation.
Concept
The objective of the following analysis of avail-
able published experiences is to highlight the con-
troversies, identify potential improvements of the
surgical technique, and reinforce the position of an
advocate of patient-related, individualized proce-
dures for hiatal hernia repair in order to improve
outcomes.
Material
For many years it was thought that reflux and all
its sequelae could be controlled by a tight wrap
to increase the lower esophageal sphincter pres-
sure and prevent the reflux [7]. A high incidence
of moderate to severe dysphagia and inability to
belch was the consequence. The formation of a
shorter and floppy fundoplication evolved as a
logical answer to a recognized inadvertent com-
plication. Today the successful control of reflux
is related to restoring adequate length of the ab-
dominal esophagus, bringing the gastroesophageal
junction back into the positive intraabdominal
pressure environment, creating a floppy full wrap
or partial wrap, and preventing intrathoracic wrap
migration by achieving a durable crural repair. The
partial wrap (Toupet [8]) was believed to be less
efficient in preventing the reflux but more reliable
in preventing dysphagia. Therefore, this technique
was recommended to be used in patients with ad-
ditional motility disorders of the distal esophagus.
Some of the above-mentioned beliefs could not be
confirmed in prospective controlled trials, which
brought up additional doubts about the correct-
ness of our pathophysiological understanding [9].
The successful application of prosthetic meshes
in the cure of groin and abdominal wall hernias
influenced the treatment of large hiatal hernias
of types II–IV [10]. Various mesh materials were
used to either reinforce the sutured crural repair or
to cover the large nonsutured defect in a tension-
free manner. The few sporadic reports on late
mesh-related complications [11–14], regardless of
the material used, raised an ongoing discussion on
risks and benefits, in which gut feelings and low
scientific evidence were used to try to convince
one another. The incidence of mesh-related com-
plications is obviously underreported. The major-
ity of existing studies are retrospective, and data of
higher levels of evidence are scarce.
Chapter 67 · Strategy To Improve the Results? In Support of Individualized Procedures
Analysis of the causes of recurrence contributes
to better understanding of the pathogenesis and
enables possible correction of the operative tech-
nique [15]. Among the factors predicting repair
failure, lack of surgical expertise is one of the most
important. Once again, it seems to be difficult to
differentiate whether the surgeon’s experience and
expertise or a successful therapeutic concept has a
more significant impact on outcome.
Arguments
Main Problem–Crural Repair Failure
Champion and McKernan [16] prospectively
measured hiatal diameters in 476 primary laparo-
scopic antireflux procedures. The smaller defects
(<4.5 cm) led to a recurrence rate of 0.9%. The
bigger ones (>5 cm) showed recurrence in 10.6%
of cases. The difference is highly significant: p<
0.000001. The size of the hiatus matters.
In 2001 Carlson and Frantzides [6] published
a review of 10,735 reported cases of minimally
invasive antireflux procedures. The most common
finding at redo operation for the failed repair was
an intrathoracic wrap herniation due to ruptured
crural closure [5, 6].
Mesh Reinforcement Reduces the
Recurrence Rate in Hiatal Repair
The literature review by Johnson et al. [2] on the
use of mesh in hiatal repair demonstrates a highly
significant reduction in recurrence rate in anti-
reflux and PEH procedures when mesh was used
either to reinforce the sutured repair or as a true
tension-free repair.
Champion and Rock [17] reduced their recur-
rence rate in laparoscopic sutured crural repair from
10.6% to 1.9% by employing a polypropylene mesh
to reinforce the sutured repair in 52 patients.
Frantzides et al. [18] presented a randomized
controlled study comparing laparoscopic sutured
cruroplasty and expanded-polytetrafluoroethyl-
ene-reinforced sutured cruroplasty. The recurrence
rate of 22% improved to 0% in mesh repair.
515 67
Basso et al. improved their recurrence rate of
9% of sutured crurorrhaphy to 0% when they rein-
forced their sutured crural repairs with a posterior
buttressing polypropylene mesh [19].
Granderath et al. [20] reviewed 42 studies re-
garding prosthetic hiatal closure. Mesh repairs
markedly reduced the recurrence rates both in
paraesophageal and antireflux surgery, with low
complication rates. The mesh material and its size
and shape are still controversial [20].
Risk of Mesh-Related Complications
Very few reports have been published on pros-
thetic complications such as erosion, stenosis, pen-
etrations, and migrations [11–14]. Although these
incidents are surely underreported, their numbers
are too small to justify a general reluctance to use
mesh in high-risk repairs. Even though the major-
ity of published results report no erosions, longer
follow-up is necessary because some complications
of a similar type (pledget erosion) may not appear
until after more than 6 years [21, 22]. To avoid
the lifelong risk of potential complications from
permanent prosthetic material, a new category of
reinforcing biomaterials has been proposed [23].
However, the role of the various acellular scaffolds
of human or porcine/ bovine origin is unclear and
their value still unpredictable.
Does the 360° Wrap Control Reflux
Better Than the Partial Wrap?
Strate et al. [9] randomized 100 Nissen and 100
Toupet procedures with and without preoperative
esophageal motility disorders. After 2 years, the
patients with Nissen fundoplication had a higher
incidence of dysphagia, but the Toupet repair con-
trolled the reflux equally or insignificantly better
than the Nissen repair. The patients’ preexisting
motility impairments did not correlate with the
postoperative complaints, so the authors declared
that tailoring antireflux procedures according to
esophageal motility is not indicated.
Wykypiel et al. [24] confirmed the equal ef-
ficiency of reflux control of Toupet compared with
 516 Chapter 67 · Strategy To Improve the Results? In Support of Individualized Procedures in Hiatal Hernia Repair
Nissen, besides restoring the preoperatively im-
paired bolus propagation after the Toupet proce-
dure. Both groups of researchers [9, 24] found the
Toupet procedure to be the better one, with fewer
side effects.
Why We Should Adapt the Surgical
Technique to the Individual Patient
1. Most patients with large paraesophageal
hernias are elderly. For many years, patients
may stay asymptomatic. Historically, treat-
ment was open surgical management of a
large diaphragmatic defect too invasive for an
67 older, minimally symptomatic patient who
frequently already had other comorbidities.
Because of rare but well-known and possibly
life-threatening complications [25], we contin-
ued to offer these patients a »prophylactic op-
eration« with a mortality of 0–5.4%. Accord-
ing to Stylopoulos et al. [26], the probability
of needing emergency surgery is only 1.16%
in the asymptomatic group. Therefore, only
symptomatic or progressively symptomatic
older patients should undergo elective surgery.
2. The incidence of failure of laparoscopic sim-
ple-sutured hiatal repair in patients with PEH
is known to be quite high. Especially in series
with systematic follow-up and consequent bar-
ium swallow examination, the recurrence rate
ranges from 0% to 42% [4]. Nevertheless, the
majority of patients are symptomatically im-
proved and do not require interventions, just
observation [27]. White et al. [27] conducted a
10-year follow-up of 31 patients who had had
laparoscopic repair of PEH. They found that
heartburn had improved from 54% to 12%,
chest pain from 36% to 9%, dysphagia from
30% to 3%, and regurgitation from 50% to
6%, despite the recurrence rate of 32%. Only a
small group needed reoperation.
3. The failure rate after fundoplication for reflux
disease after 5-year follow-up is 10–15% [28].
The most common failure pattern is intratho-
racic herniation of the intact wrap (61–84%)
due to disruption of the crural repair [5, 6,
29]. The reoperation rate of around 10% dem-
onstrates the necessity to technically improve
the durability of the cruroplasty.
4. Among the factors related to hiatal hernia
recurrence are technical reasons, anatomic
reasons (different hernia types I–IV, size of the
hiatus, condition of the crura), and patient-
related reasons, including obesity, chronic
obstructive pulmonary disease, constipation,
weight lifting, age, vomiting in the early post-
operative course, early physical activity, and
so on. Patients with these predisposing factors
should probably be primarily offered a mesh-
reinforced crural repair.
5. Mesh decreases the risk of recurrence in hiatal
repair [2, 17–19, 30, 31], but it carries the risk
of mesh-related complications. These are very
rare but may have disastrous consequences.
To eliminate this small but serious risk, sev-
eral surgeons promote the use of biomeshes,
namely porcine small intestine submucosa
[23].
Johnson et al. [2] reviewed the available lit-
erature and identified 19 studies reporting on
the use of mesh in hiatal repair (PEH, lap-
aroscopic fundoplication for reflux, or both).
There were 729 sutured repairs and 639 mesh
repairs with or without crura closure. After 20
months, there were fewer recurrences in the
mesh group: 1.8% vs. 10.7%. No erosion was
reported in this study or in series published by
Frantzides et al. [18], Basso et al. [19], Gryska
and Vernon [30], Granderath et al. [31], and
Champion and Rock [17].
The awareness of potential mesh-related late
sequelae in the dynamic hiatal area is certainly
important. Nevertheless, by respecting the
individual patient’s failure-risk profile, there
must be a place for primary mesh-reinforced
crural repair rather than waiting for a failure
and then using the mesh in a technically de-
manding redo repair later on. The lightweight,
megaporous, and oligofilament meshes have
demonstrated less chronic inflammatory reac-
tion and limited shrinkage in inguinal hernia
repair. With this prosthetic material there is a
justified expectation of good performance and
low risk in hiatal repair as well, but long-term
results are still lacking.
Chapter 67 · Strategy To Improve the Results? In Support of Individualized Procedures
⊡ Fig. 67.1. Small hiatal surface area
⊡ Fig. 67.2. Low tension on the suture line
6. The risk of failure of the crural repair is pre-
dominantly determined by the size of the
hiatus and the condition of the crura [32].
Measuring the hiatal surface area gives a ratio-
nal background for a tailored concept of hiatal
closure (⊡ Figs. 67.1–67.4).
Conclusions
▬ Solidity and durability of crural repair are key,
both for antireflux procedures as well as for
PEH repair.
▬ Patients with increased recurrence risk should
probably be offered a primary mesh-rein-
forced repair.
517 67
⊡ Fig. 67.3. Large hiatal surface area
⊡ Fig. 67.4. Higher risk of crural repair failure
▬ The recurrence risk depends strongly on the
size of the hiatus and the condition of the
crura. This justifies the simple sutured repair
in patients with small hiatal defects and mesh-
reinforced suture repair in patients with bigger
defects, weak crura, and/or additional elevated
risk factors.
▬ The traditional validation of Nissen vs. Toupet
wrap must be scrutinized or reconfirmed [9,
24, 33–35].
▬ The individualized approach to hiatal hernia
repair (tailored repair [32]) must reflect the
risk–benefit ratio of each individual patient,
based on the available evidence from long-
term follow-up if possible.
 518 Chapter 67 · Strategy To Improve the Results? In Support of Individualized Procedures in Hiatal Hernia Repair
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20. Granderath FA, Carlson MA, Champion JK, Szold A, Basso
N, Pointner R, Frantzides CT (2006) Prosthetic closure of
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21. Dally E, Falk GL (2004) Teflon pledget reinforced fundopli-
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23. Oelschlager BK, Barreca M, Chang L, Pellegrini CA (2003)
The use of small intestine submucosa in repair of paraeso-
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24. Wykypiel H, Hugl B, Gadenstaetter M, Bonatti H, Bodner J,
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phageal hernias: operation or observation? Ann Surg
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Long-term outcome is worse after laparoscopic than after
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29. Cadiere GB, Bruyns J, Himpens J, Vertruyen M (1996) Intra-
thoracic migration of the wrap after laparoscopic Nissen
fundoplication. Surg Endosc 10:187 (S43)
30. Gryska PV, Vernon JK (2005) Tension-free repair of hiatal
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Chapter 67 · Strategy To Improve the Results? In Support of Individualized Procedures
519 67
33. Spechler SJ, Lee E, Ahnen D, Goyal R, Hirano I, Ramirez F,
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 68

Questionnaire
 522 Chapter 68 · Questionnaire

1. How many hernias do you perform 4. Spermatic Cord

each year?
A. Do you believe that infertility (due to obstruc-
▬ Inguinal 6,175 tive azoospermia or ischaemic orchitis) is a
▬ Incisional 1,935 potential complication of inguinal hernia re-
▬ Hiatal 486 pair?
▬ Yes 85%
▬ No 15%
2. Percentage of Operations
Performed (%) B. Do you believe that the type of repair
(mesh vs. nonmesh) has an impact on the
▬ Inguinal integrity of the vas deferens and testicular
– Lichtenstein 35% function?
– Shouldice 13% ▬ Yes 62%
– TAPP 14% ▬ No 38%
– TEP 25%
– TIPP-Rives <1% C. Do you believe that the type of the mesh used
– Stoppa <1% (small porous mesh vs. large porous mesh) has
68 – Wantz <1% an impact on the integrity of the vas deferens
– Plug/PHS 8% and testicular function?
– Others 3% ▬ Yes 56%
▬ Hiatal ▬ No 44%
– With mesh 20%
– Without mesh 80% D. Is potential alteration of the spermatic cord
▬ Incisional a reason to tailor your approach in inguinal
– Sublay 51% hernia repair (i.e. young men, single tes-
– Onlay 3% ticle)?
– Inlay 4% ▬ Yes 74%
– IPOM 40% ▬ No 26%
– Others 2%

5. Infection
3. Type of Mesh Actually Used
A. Do you use single-shot antibiotic prophylaxis
Ingui- Inci- Hiatal in hernia surgery to prevent infections?
nal sional

Polypropylene 35% 21% 0 Inguinal hernia Incisional hernia Hiatal hernia

(i.e. Atrium, Marlex)
Yes 70% Yes 92% Yes 60%
Large porous polypro- 48% 33% 37%
No 30% No 8% No 40%
pylene (i.e. UltraPro)

Polyester (i.e. Mersilene) 10% 7% 0

B. Do you believe that the kind of mesh materi-
ePTFE (i.e. DualMesh) 5% 24% 8%
als (structure, polymer, kind of filament, pore
Biological mesh (i.e. 0 10% 42% size) has an impact on infection rate?
Surgisis)
▬ Yes 69%
Others 2% 5% 13% ▬ No 31%
Chapter 68 · Questionnaire
523 68
C. Do you implant permanent mesh materials C. Should a suspected injured nerve be saved or
(no biological meshes) in potentially contami- resected?
nated fields? ▬ Saved 4%
▬ Resected 96%
Hernia repair for incarcerated inguinal/
incisional hernias
D. How do you resect a nerve?
▬ Yes 90%
▬ No 10%
How? Ligate the Place end in
Hernia repair + elective cholecystectomy end? muscle?
▬ Yes 77%
Scissor 79% Yes 33% Yes 52%
▬ No 23%
Knife 7% No 67% No 48%
Hernia repair + iatrogenic small bowel
enterostomy Cautery 14%
▬ Yes 56%
▬ No 44%
E. Do you try to identify all three nerves during
Hernia repair + iatrogenic large bowel open inguinal hernia repair?
enterostomy ▬ Yes 40%
▬ Yes 21% ▬ No 60%
▬ No 79%

D. Do you think there is a place for an antibiotic- 7. Adhesion/Migration/Erosion

supplemented mesh in hernia repair to pre-
vent/treat infections? A. Do you believe in adhesions as a chronic in-
flammatory process?
In clean cases In contaminated In infected cases ▬ Yes 85%
cases ▬ No 15%
Yes 26% Yes 70% Yes 50%
B. Which factors are responsible for the develop-
No 74% No 30% No 50% ment of adhesions?
▬ Surgical technique (peritoneal
damage) 100%
▬ Kind of mesh material 96%
6. Chronic Pain ▬ Kind of fixation 93%
▬ Patient’s individual response 86%
A. Do you believe that patient-related factors (i.e.
age, gender, body mass index) are of major C. Which factors determine the adhesive potency
importance for the development of postopera- of a mesh material (multiple answers pos-
tive neuropathic pain? sible)?
▬ Yes 74% ▬ Polymer 79%
▬ No 26% ▬ Pore size 93%
▬ Kind of filaments (mono vs. multi) 79%
B. Do you believe that optimised (i.e. larger ▬ Kind of antiadhesive barrier 89%
pores, monofilaments) mesh materials are able
to decrease the overall amount of postopera- D. Have you ever seen complications following
tive neuropathic pain? hiatal hernia repair using a mesh material?
▬ Yes 78% ▬ Yes 52%
▬ No 22% ▬ No 48%
 524 Chapter 68 · Questionnaire

E. Is there a need for further mesh optimisation

for placement in the hiatal region?
▬ Yes 95%
▬ No 5%

68
 Subject Index
A B
Abdominal colposuspension 440
Abdominal stiffness 223
Abdominal wall compliance 347
Abdominal wall surface 144
Abdominopelvic pain 306
Acute inflammatory response 366
Acute laparotomy wound failure
402
Adhesion 345, 354, 346, 378, 385,
446
Afferent nociceptors 172
Allodynia 170, 180
Amnion-derived cells 402
Amniotic cell therapy 405
Antiadhesive barrier 348
Antibiotic prophylaxis 126
Antireflux procedure 504
Anxiety 164
Arcuate line 488
Aß-fiber 210
Augmentation 228
Autologous skin 498
Axon 178
Axonotmesis 178
Aδ-fiber 210
Bacterial colonization 395
Bacterial contamination 120
Bacterial resistance 126, 132
Band disconnection 430
Band erosion 430, 432
Band migration 432, 434, 435
Bariatric surgery 435
Bassini 464, 468
Bcl-2 (oncoprotein) 45
Bioacoustic effect 122
Biocompatibility 377
Biofilm 121
Biological tissue grafts 318
B-lymphocytes 306
Bridging 223, 228
Bulging 147
C Contaminated environment 144
Catecholamine-O-methyltrans-
ferase (COMT) 194
ß-catenin 306, 309, 311
Cefazolin 138
Cellular infiltration 108
Central nervous plasticity 181
Central neuroinflammation 171
C-fibers 210
Chemical barriers 357
Chronic groin sepsis 114, 116
Chronic inguinal pain 293
Chronic inguinodynia 290
Chronic pain 221, 222, 246, 257,
258, 266, 280, 294
Classification 120, 229, 494
C-myc 306, 309, 311
Collagen 172
Collagen coating 282, 389
Collagen deposition 368
Color doppler ultrasound (CDUS) 5
Complex regional pain syndromes
(CRPS) 170, 208
Component separation technique
143
Composite biomaterials 356, 394
Condensed PTFE (cPTFE) 355
Contaminated surgical field 104
Contamination 116
Cooper’s ligament 488
COX-2 309
Crural repair 517
526 Subject Index
Cyclooxygenase-2 306, 311
Cytokine growth factors 402
D Fistula formation 120, 121, 458
Deep infections 116
Degeneration 170
Depression 164, 195
Discomfort 223, 246
Double-crown technique 453
Drains 132
DualMesh 382, 397
DynaMesh IPOM 382
Dysejaculation 192
Dysesthesia 210
Dyspareunia 442
Dysphagia 511
E Gastric herniation 414
Early infections 80
Early wound failure 407
Effective porosity 378
Elasticity 236
Encapsulation 346
Enterotomy 335, 338
Entrapment 178, 180, 266, 294
Epineural fibrosis 179
Epineurectomy 179
Epineurium 178
Epineurotomy 179
ePTFE 44, 324, 356, 376, 382, 394
398
Erosion 434, 440, 442, 458
European guidelines 201, 476
Evidence-based medicine 480
Extensive scar tissue 223
F Hiatoplasty 425
Fascicles 178
Fatty triangle 490
Fibrin glue 357
Fibroblastic response 270
Fibroblasts 172, 311, 367
Fibrocollagenous ingrowth
378
Fixation 165, 258
Flap 499
Follicle-stimulating hormone (FSH)
58
Foreign body reaction 215, 423
Foreign body response 259
Foreign body sensation 276
Francis Usher 369
Fundoplication 506
G repair 405
Gastric banding 430
Gastric fundus 507
Gastroesophageal junction 506
Gastroesophageal reflux disease
(GERD) 504
Gastroplasty 508
Genetic factors 166
Genetic polymorphisms 194
Genetic variation 161
Genitofemoral nerves 178, 240
Genotype 194
Gentamicin 136
Global infection score (GIS) 482
Guidelines 478
Guillain-Barré syndrome 193
H 194
Haematogenous spread 116
Hernia recurrence 109, 336, 394
Hiatal hernia repair 416
Human acellular dermis (HADM)
104
Hyaluronic acid 388
Hyaluronic acid/carboxymethylcel-
lulose (HA/CMC) membranes
357
Hyaluronidase cream 357
Hyperalgesia 170
Hyperexcitability 170
Hyperpathic pain 180
I
Ideal mesh 373
Iliohypogastric nerve 178, 240, 289
Ilioinguinal nerve 178, 240
Impaired quality of collagen matrix
synthesis 402
Improved laparotomy wound
Incisional hernia 221, 325, 332,
402, 486
– Formation 407
– Model 403
– Repair 376
Individualized therapy 170
Indocyanine green (ICG) 31
Infection 87, 126
– of a prosthetic material 395
– Rate 447
Infertility 306
Inflammation 121
Inflammatory
– Cells 186, 367
– Pain 170
– Reaction 116, 441
– Response 223, 394, 446
Ingrowth maturation process
368
Inguinal Pain Questionnaire (IPQ)
Inguinodynia 287
Interfascicular neurolysis 179
International Association for the
Study of Pain (IASP) 209
Intragastric band migration 430
Intraneural blood flow 188
Intraperitoneal onlay mesh (IPOM)
82, 376, 446, 494

Subject Index
IPOM 324 Mayo technique 497
– Rabbit model 377 Mesh attachment 223
Mesh bowel intrusion 120
Mesh bridging 495
Mesh contraction 345, 346, 348
J Mesh cruroplasty 504, 510
Mesh explantation 293
Johnsen Score 23 Mesh infection 79, 119, 120, 336,
338, 447
Mesh inguinodynia 266
Mesh migration 423, 425, 458
K Mesh-related infections 98
Mesh removal 115, 166, 296
Keyhole technique 455 Mesh shrinkage 424
Ki67 23, 368, 383 Mesh surface 378, 386
Kugel repair 465 Mesh surgery in urogynecology
440
Microneurolysis 179
Midline tension 223
L Monocytes 383
Monofilament polypropylene (PP)
Laparoscopic fundoplication 414 98
Laparoscopic hiatal hernia repair Mononuclear round cells 311
504 MycroMesh (MM) 395, 397
Laparoscopic ventral hernia repair Myelin degeneration 258
82, 332, 366
Laparotomy wound breaking
strength 403
LAPSIS trial 497
N Paraesophageal hernia 414, 422,
Large-pore mesh 186, 376
Late infections 80 National database 476
Learning curve 465 Nerve damage 148
Lichtenstein 5, 14, 23, 52, 126, 252, Nerve division 243
464, 469 Nerve identification 239
Lightweight mesh 276, 376 Nerve injury 165
Lightweight polypropylene/ Nerve roots 178
carboxymethylcellulose 371 Nerve trauma 156
Linea alba 402 Neuralgia 253
Local anaesthesia 165 Neurapraxia 178
Luteinizing hormone (LH) 58 Neurectomy 166, 170, 241, 293,
294, 296
Neurofibromatosis 193
Neuroma 178
M Neuroma pain 180
Neuromodulation 178, 182
Macrophages 306, 309, 311, 383, Neuropathic-Pain 166, 170, 269,
396 288, 294, 466
Marlex 22, 30, 377 Neurotmesis 178
527
Neurotomy 181
Nissen Fundoplication 422, 515
Nitric oxide (NO) 58
Nociceptive stimulus 164, 170
Nociceptive system 164
Nonsteroidal anti-inflammatory
drugs 165
Notch-3 306, 309
O
Obstructive azoospermia 51
Onlay techniques 82, 222
Open onlay mesh 494
Orchialgia 240, 287
Orchitis 253
Overlap 356
P
Pain 166, 233, 252, 276
Pain level 236
Pain transmission 156
Pampiniform plexus 73
504, 514
Paraesthesia 223
Parastomal hernia 325, 446, 447,
452
Parietene composite 382
Parietex composite 382
Pathological regeneration 170
Patient safety in surgery 481
PCNA reaction 46
PDS (polydioxanone) 388
Peak systolic velocity (PSV) 5
Pelvic organ prolapse 440
Perfusion-related fluorescence
intensity (IC-CALC) 31
Perineurium 179
Peripheral surgical trauma 156
Peritoneal adhesions 306
Phenotype 194
Physical barriers 357
528 Subject Index
Physical fitness 195
Physical impairment 195
Physiotherapy 195
Planimetric analysis 386
Plug repair 301
Polyester 44
Polyglactin 910 mesh (PGM) 356
Polyneuropathy 170
Polypropylene 44, 126, 280, 355,
367, 377, 446
Polypropylene/expanded polytet-
rafluoroethylene (ePTFE) 367
Polypropylene mesh (PPM) , 355
Polytetrafluoroethylene 446
Polyvinylidene fluoride (PVDF) 22,
376, 382, 446
Pore size 223, 369, 376
Porosity 369
Postherniorrhaphy groin pain 164,
204, 279
Postherniorrhaphy inguinodynia
240
Postimplantation biomechanical
strength 398
Postoperative pain 234, 336
Postoperative sensory dysfunc-
tions 165
Pouch dilatation 430
Predictors of complications 252
Preoperative investigation 504
Preoperative pneumoperitoneum
486, 498
Prevention 136
Proceed 382
Prognostic factors 229
Prolene 14, 44
Proliferating cell nuclear antigen
45
Prophylactic antibiotics 84, 116
Prophylactic neurectomy 242
Prostheses 161
Prosthetic infection 497
Prosthetic mesh 486, 511
Prosthetic mesh infection 109
Prosthetic reinforcement 417
Pseudoneuroma 178
Psychosocial factors 194
PVDF 324
Q Sling procedure 440
Quality of life 258
Questionnaire 229
R 398
Randomized controlled trial (RCT)
468
Reactivation 195
Real-time adhesion formation 354
Recurrence rate 442, 452, 486
Recurrence rates after parastomal
hernia mesh repair 452
Reflex sympathetic dystrophy 208
Rehabilitation 195
Reherniation 149
Retroesophageal window 506
Retromuscular space 490
Retroperitoneal triple neurectomy
300
Revascularization 108
Risk factor 164, 494
Rives 486
S Surgical strategy 499
Sandwich technique 455
Scar plate 350
– Formation 224
Scar retraction 417
Scar tissue 270
Schwann cells 172
Self-assessment (SA) levels 156
Seroma 336
– Formation 98
Sexual dysfunction 192
SF-36 questionnaire 280
Shouldice 30, 464, 469
Shrinkage 383, 387, 441, 458
Single-peptide wound therapy
407
Skin necrosis 146, 147
Sliding hernia 504
Slippage 430, 507
Slipped nissen phenomenon
414
Small bowel obstruction 306
Small-pore meshes 186
Soft Tissue Patch (STP) 394, 397,
Sonographic resistive index (RI) 4
Spermatic cord 30, 270
Spermatogenesis 31
Spinal ganglion 181
Spiral tacks 234, 354
Standardisation 476
Standard procedure 472
Staphylococcus aureus 115, 136
Stem-cell-like multipotent cells
express 402
Stem cells 401, 402
3D stereography 347
s-testosterone 15
Stoppa 464
Stress urinary incontinence 440
sublay technique 222
Suburethral sling 440
Sudeck’s atrophy 208
Superficial infections 114
Surgical site infection (SSI) 98,
114, 106
Surgical trauma 161
Suture cruroplasty 504
Suture pull-out force 284
Suture repair 228
Sweat secretion test 218
Swedish Hernia Register (SHR) 201
T
Tailored approach 299, 472, 483,
494
Tailored concept 81
TAPP 203, 480
Targeted 170
Technical failure 471
 529
Subject Index

Tensile strength 397

Tensiometric measurements 404
TEP 5, 201, 203, 480
Testicular atrophy 4, 5
Testicular torsion 7
TGF-β 405
Thermography 24
TiMesh Light 382
Tissue incorporation 398
Tissue ingrowth 345, 346, 365, 376
Tissue–prosthesis overlap 339
Tissue response 394
Titanium-coated meshes 383
T-lymphocytes 306, 309, 311, 383
Toupet 514, 515
Toxicity 138
Trabucco 52
Triple neurectomy 181, 288
TUNEL 59
– Histochemistry 23

V
Vacuum-assisted closure (VAC)
therapy 122, 326
VAS 280
Vasography 14, 23
Von Willebrand factor 45, 46
Vypro II 14, 44

W
Wallerian degeneration 179, 215
Wantz 464
Watchful waiting 480
Wound breaking strength 405
Wound complication 336, 338
Wound infection 109, 136
– Rates 336
Wound oxygen levels 89
Wound tissue oxygenation 89
Wrap herniation 414, 416