The Greater

OMENTUM
Anatomy, Physiology, Pathology, Surgery
With an Historical Survey

Editors
D. Liebermann-Meffert and Harvey White
Consulting Editor for Section of Surgery
E. Vaubel

With a Foreword by Sir Alan Parks

With 262 Figures, Some in Color

Springer-Verlag Berlin Heidelberg GmbH

ISBN 978-3-662-02376-1 ISBN 978-3-662-02374-7 (eBook)
DOI 10.1007/978-3-662-02374-7

Library of Congress Cataloging in Publication Data

Main entry under title: The Greater omentum. Bibliography: p. 1. Omentum - Surgery.
2. Omentum. I. Liebermann-Meffert, D. (Dorothea), 1936--. II. White, Harvey, 1938- .
Ill. Vaubel, E. (Ekkehard) [DNLM: 1. Omentum. WI 575 G786) RD548.G73
1983 617'.558 82-19495
This work is subject to copyright. All rights are reserved, whether the whole or part
of the material is concerned, specifically those of translation , reprinting, re-use of illus-
trations, broadcasting, reproduction by photocopying machine or similar means, and
storage in data banks. Under § 54 of the German Copyright Law where copies are
made for other than private use a fee is payable to "Verwertungsgesellschaft Wort",
Munich.
© by Springer-Verlag Berlin Heidelberg 1983
Originally published by Springer-Verlag Berlin Heidelberg New York in 1983
The use of registered names, trademarks, etc. in this publication does not imply, even
in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
Reproduction of figures: Gustav Dreher GmbH , Stuttgart

2124/3130-543210
In honor of
Martin Allg6wer's
65 th birthday
Foreword

Since RUTHERFORD MORISON left us with the concept of the

Omentum being the 'abdominal policeman', clinicians have
tacitly assumed that they know sufficient about the structure
and function of this organ. However interest in the omentum
and its relationship to clinical surgery has recently been develop-
ing. This book examines all aspects with special reference to
surgery and should provide a welcome impetus in research and
clinical practice.
The editors and contributors have produced a book which is
comprehensive and well illustrated and contains detailed refer-
ences to the important original sources - so essential in a work
of this nature. It is written for those who wish to share the
delight of acquiring knowledge - even about a comparatively
humble organ - as well as for practical surgeons. Both will
find ample information to arouse their interest and expand their
surgical horizons in exciting ways of which they will almost
certainly not have dreamt.
I welcome a book of this calibre on a subject which deserves
our increasing interest. I delight in the fact that it is dedicated
to my friend and colleague MARTIN ALLGOWER.

ALAN PARKS
President
Royal College of Surgeons of England

While this book was in press, Sir ALAN PARKS died. The editors
would like to pay tribute to a great and compassionate surgeon
with an enquiring and inventive mind. They are very grateful
for his interest in their subject and for his generosity in allowing
his name to be associated with the book.
Preface

Late in 1976 DOROTHEA LIEBERMANN-MEFFERT and I realized

that there was a clear requirement for a small book on the
uses of the omentum in the practice of surgery with a special
emphasis on the surgical techniques of transposition and trans-
plantation. When we started to plan a small and modest manual
we identified a need far greater than our original concept and
the book became more ambitious. We decided that it was impor-
tant that a comprehensive book should be written. However,
our aim was first and foremost the production of a book for
surgeons which would help to establish the techniques more
widely. Although omental surgery is undertaken in numerous
centres - and notably by IAN KIRICUTA in Rumania and HARRY
GOLDSMITH in USA - its application is somewhat neglected.
During the next two and a half years a number of sections
including the historical appendix and sections on embryology,
anatomy and pelvic surgery were nearly completed. However,
a new stimulus was required and we saw a need for others
with experience different from our own to be associated with
a book which was more comprehensive than our original con-
cept. We therefore asked EKKEHARD VAUBEL to become consult-
ing editor and in addition invited a number of experts to contrib-
ute to the book. They have greatly enriched our original endeav-
our and without their experience and contributions the book
would have lacked many essential aspects and we are deeply
grateful to them.
The original idea was born during a conference at which Profes-
sor MARTIN ALLGOWER was President. Many of the contributors
and DOROTHEA LIEBERMANN-MEFFERT, with her remarkable edi-
torial skills and industry, work in his internationally acclaimed
department. It seemed appropriate therefore to dedicate the
book to this great and stimulating surgeon. We hope that our
attempt to re-examine an apparently pedestrian subject and ap-
proach it with a new stimulus and from new angles will be
a fitting tribute to him on his sixty-fifth birthday. This has
been a book of international cooperation which is one aspect
of surgery close to his heart. Although the omentum is not
his field of special interest, I hope that he will realize that one
of the signs of greatness is that personal enthusiasms can provide
a stimulus beyond ones own endeavour. It is in this spirit that

IX
we offer the book as a tribute to a remarkable surgeon and
director of research.
In addition to recording a personal debt to DOROTHEA LIEBER-
MANN-MEFFERT who has tirelessly undertaken so many of the
tasks required in writing a book with editors and contributors
in different countries, I would like to record our gratitude to
our families for their understanding and support. We owe a
special debt to Mrs. TH. DEIGMOLLER, Mrs. D. GROSSHANS and
Mr. R. BRECH of the Springer-Verlag, Heidelberg, for their help,
encouragement and patience over three years and to their artist
Mr. KEN FINCH, Heidelberg, for his careful and clear dia-
grams.
It is impossible to acknowledge all those who have given such
willing help but we would especially thank our secretaries and
particularly Miss ELISABETH SCHEURER, Basel, who prepared the
typescript, Mr. PETER ARGAST and Mr. MARK KAUFMANN, Insti-
tut fur Pathologie, Basel for technical support in experiments
undertaken to clarify some anatomical questions which arose
while writing the book. We are indebted to Mr. DIETMAR HUND,
Mrs. ELEONORE HUND and Mrs. ESTHER GISIN, Photoabteilung
Kantonsspital, Basel, who photographed many of the figures
specifically for this book to Mrs. ADELE HERZFELD and the staff
of the Medizinische Bibliothek der UniversiHit, ZLF, Basel for
their help.
As we intend the book primarily for surgeons, it is inappropriate
that all sections should contain the same depth of detail. Our
aim is that they should have insight in areas which now require
their understanding because of the growing multidisciplinary
approach to problems. The use of the omentum in surgery with
newly developing techniques such as microvascular anastomoses
seems destined to increase. We hope that this book will serve
as a foundation to such developments.

HARVEY WHITE

x
Contents

Anatomy and Functional Anatomy

1 Anatomical Definitions, Composition, and Config-

uration 1

2 Topographical Relations 3
2.1 Relations in Man 3
2.2 Relations in Animals 5

3 Development and Appearance 13

3.1 Embryological Development 13
3.2 Structural Peculiarities in Childhood 20
3.3 Omentum in the Adult 23

4 Structures 26
4.1 Stroma 26
4.2 Tissue Constituents 28
4.3 Vessels and Innervation 30
4.4 Mesothelial Lining 41
4.5 Milky Spots (Lymphoreticular Organ) 46

References 57

Physiology and Functions

5 Distinctive Peculiarities of Omental Tissue 63

5.1 Movement......... 63
5.2 Adhesiveness and Cohesiveness 64
5.3 Hemostasis .... 65
5.4 Ability to Encapsulate . . . . 65
5.5 Capillary Ingrowth . . . . . 65
5.6 Absorption from the Peritoneal Cavity 66
5.7 Capillary Fluid Exchange in the Omentum: Physi-
ology and Pathophysiology . . . . . 67
5.8 Omental Fluid Transport and Dialysis . 84
5.9 Defense Mechanisms . . . . . . . . 90
5.9.1 Phagocytosis and Foreign Body Reaction 90
5.9.2 Immunological Concepts . . . . . . . 91

XI
5.10 Matrix for Tissue Grafts . . . . . . 92
5.10.1 Autotransplantations of Splenic Tissue 92
5.10.2 Tumor Implants in Experiments 96
References 96

Clinical Aspects
6 Clinical Signs and Methods of Assessment 103
6.1 Examination and Investigation .... 103
6.2 Radiographic Manifestation . . . . 105
6.3 Ultrasonography and Computed Tomography 106
6.4 Endoscopic Procedures 107
6.5 Laparotomy 109
References . . . . . . 109

Pathological Conditions, Specific Investigations,

and Therapy
7 Diseases of the Omentum . . . . . . . . . . 111
7 .1 Congenital Abnormalities and Pediatric Diseases 111
7.2 Injuries of the Omentum 118
7.3 Hernias.................. 120
7.4 Adhesions................. 126
7.5 Omentitis, Inflammatory Reactions, and Parasites 129
7.6 Torsion and Infarction 142
7.7 Tumors 147
7.7.1 Pathology 147
7.7.1.1 Benign Tumors 147
7.7.1.2 Cysts . . . . 154
7.7.1.3 Malignant Primary Tumors 156
7.7.1.4 Tumor Metastases 159
7.7.2 Symptoms, Signs, Clinical Diagnosis and Therapy 161
7.7.2.1 Benign Tumors . . . . . 161
7.7.2.2 Cysts . . . . . . . . . 163
7.7.2.3 Malignant Primary Tumors 165
7.7.2.4 Tumor Deposits .... 167
7.8 Rare Tumor-like Changes 169
References . . . . . . . 175

Experimental Basis for Reconstructive Surgery Using

the Omentum
8 Experiments of Clinical Value ..... 187
8.1 Vascular Ingrowth and Graft Incorporation 187

XII
8.2 Revascularization and Drainage 189
8.2.1 Revascularization and Edema Absorption of the
Brain and Spinal Cord 189
8.2.2 Revascularization (Ischemic Heart and Ureter) 197
8.2.3 Drainage (Hydrocephalus) 198
8.3 Protection 199
8.3.1 Coverage of Defects 199
8.4 Reconstruction 200
8.4.1 Antral Patch Esophagoplasty Using an Intact
Omental Pedicle 200
8.4.2 Rectal Valve Substitution Using the Intact Pyloric
Valve Based on an Omental Pedicle 200
8.4.3 Island Skin Flaps and Island Composite Flaps Em-
ploying the Omentum 204
8.5 Body Surface Heterotransplant and Biological
Dressing 205

References 207

Protective and Reconstructive Surgery with the Omentum

in Man
9 Surgical Principles and Techniques 211
9.1 General Aspects . . . . . . . 211
9.1.1 Indications and Contraindications 211
9.1.2 Assessment and Preparation for Surgery 214
9.1.3 Access to the Omentum . . . . . . . 217
9.1.4 Repair of the Defect . . . . . . . . . 221
9.1.5 Postoperative Care, Sequelae, and Follow-up 223
9.2 Particular Surgical Procedures . . . . . . 224
9.2.1 Surgical Principles and Techniques: Omentopexy,
Omental Mobilization, and Transposition 224
9.2.1.1 Intra-abdominal Transposition . . . . 230
Omentoportoduodenopexy for Drainage 237
Omentopexy for Ascites 240
Omental Cuff for Cardiopexy . . . . 241
Protection of Intestinal Defects 242
Urogenital Organs and Pelvic Surgery 243
Urinary Tract Reconstruction 247
Pelvis . . . . . . . . . . . . . . 251
Urogenital and Intra-abdominal Fistulae 259
Vascular Protection in Reconstructive Arterial Sur-
gery ........... 266
9.2.1.2 Extra-abdominal Transposition 272
Intrathoracic Transposition 272

XIII
 Transposition to the Cranium and Extremities 278
Lymphatic Relief . . . . 283
9.2.1.3 Exteriorized Transposition 284
Chest, Neck, and Axilla 284
Abdominal Wall 294
Extremities ..... 295
Histopathology of the Exteriorized Omentum 299
9.2.2 Free Omental Transfer with Microvascular Anas-
tomosis 302
9.2.3 Free Omental Grafts 307
9.3 Limitations of Omental Transposition and
Transfer . . . . . . . 308
Color Plate of Chapter 9 309

References 321

Historical Review
10 History ........ ... . 331
10.1 Historical Glance at the Terminology 331
10.2 Historical Survey . . . . . . . . . 333
10.2.1 The Classical Period and Ideas of Anatomy, Func-
tion, and Surgery . . . . . . . . . . . . . . 333
10.2.2 Tradition in the Middle Ages . . . . . . . . . 335
10.2.3 Observation and Experience in the Renaissance 337
10.2.4 Modern Trends . 340
10.2.5 The Scientific Age 345
10.3 Plastic Surgery 349

References . . 351

Subject Index . . . . . . . . . . . . . . . . . . . 356

XIV
Contributors

RUDOLF AUSFELD, Dr.

Departement fur Chirurgie, Urologische Klinik
Universitats-Klinik, Kantonsspital,
SpitalstraBe 21,4031 Basel, Switzerland

JURG BRENNWALD, Dr.

Departement fUr Chirurgie, Abt. fUr Microchirurgie
U niversitats-Klinik, Kantonsspital
SpitalstraBe 21, 4031 Basel, Switzerland

ALDO COLOMBI, Priv.-Doz., Dr.

Departement fur Innere Medizin, Dialyse-Zentrum
Kantonsspital, 6004 Luzern, Switzerland

HANS JOACHIM DITTLER, Dr.

Chirurgische Klinik und Poliklinik rechts der Isar der Technischen Universitat
Ismaninger-Str. 22, 8000 Munchen 80, Federal Republic of Germany

RJAM VAN DONGEN, Prof. Dr.

Academisch Ziekenhuis bij de Universiteit van Amsterdam
Eerste Helmersstraat 104, 1054 EG Amsterdam, The Netherlands

MICHAEL DURIG, Dr.

Departement fUr Chirurgie, Universitats-Klinik, Kantonsspital
SpitalstraBe 21,4031 Basel, Switzerland

BERNHARD ENDRICH, Dr.

Institut fUr experimentelle Chirurgie, Universitat Heidelberg
1m Neuenheimer Feld 347,6900 Heidelberg 1, Federal Republic of Germany

FRITZ GLOOR, Prof. Dr.

Institut fur Pathologie
Kantonsspital, 9006 St. Gallen, Switzerland

HARRY GOLDSMITH, M.D.

Hitchcock Clinic Dartmouth Medical School
Hanover, New Hampshire 03755, USA

ULRICH GROSS, Prof. Dr.

Klinikum Steglitz der FU Berlin, Institut fUr Pathologie
Hindenburgdamm 30, 1000 Berlin 45, Federal Republic of Germany

FRITHJOF HAMMERSEN, Prof. Dr.

Anatomisches Institut Technische Universitat Munchen
BiedersteinerstraBe 29, 8000 Munchen 40, Federal Republic of Germany

xv
FELIX HARDER, Priv.-Doz., Dr.
Departement fUr Chirurgie, U niversitats-Klinik, Kantonsspital
Spitalstra13e 21, 4031 Basel, Switzerland

PHILIPP HEITZ, Prof., Dr.

lnstitut fur Pathologie, U niversitats-Klinik, Kantonsspital
Schonbeinstra13e 40, 4031 Basel, Switzerland

ANN LIEBERMANN, cando med.

U ni versi tii t F rei burg
Nelkenweg 4, 7800 Freiburg, Federal Republic of Germany

DOROTHEA LIEBERMANN-MEFFERT, Priv.-Doz., Dr.

Departement fur Chirurgie, U niversitiits-Klinik, Kantonsspital
Spitalstra13e 21, 4031 Basel, Switzerland

KONRAD MESSMER, Prof. Dr.

Institut fur experimentelle Chirurgie, Universitat Heidelberg
1m Neuenheimer Feld 347, 6900 Heidelberg 1, Federal Republic of Germany

URS NEFF, Dr.

Departement fur Chirurgie, U niversitiits-Klinik, Kantonsspital
Spitalstra13e 21, 4031 Basel, Switzerland

MARIE-LuISE PORTMANN, Dr. phil.

Bibliothek fur Medizingeschichte
Klingelbergstra13e 23, 4056 Basel, Switzerland

THOMAS RUEDI, Priv.-Doz., Dr., Chefarzt

Kantonsspital, 7000 Chur, Switzerland

VOLKER SCHUMPELlCK, Priv.-Doz., Dr.

Univ.-Krankenhaus Eppendorf, Departement fur Chirurgie
Martinistra13e 52, 2000 Hamburg 20, Federal Republic of Germany

GEORG STALDER, Prof. Dr.

Departement fur Innere Medizin, Abt. Gastroenterologie
Universitiits-Klinik, Kantonsspital
Petersgraben 4, 4031 Basel, Switzerland

EARL STEWARD, M.D.

Dartmouth Medical School
Hanover, New Hampshire 03755, USA

HEINZ TILLMANNS, Dr., Chefarzt

Gyniikologische Klinik am Marien-Hospital
Nassauer Stra13c 1,4700 Hamm, Federal Republic of Germany

PETER TONDELLI, Priv.-Doz., Dr.

Departement fur Chirurgie, U niversitiits-Klinik, Kantonsspital
Spitalstra13e 21, 4031 Basel, Switzerland

JOACHIM TORHORST, Prof. Dr.

Institut fur Pathologie, Universitiits-Klinik, Kantonsspital
Schon beinstraf3e 40, 4031 Basel, Switzerland

XVI
ULRICH TROEHLER, Priv.-Doz., Dr. med. et phil.
Bibliothek und Institut fur Medizingeschichte, Universitat
Klingelbergstral3e 23, 4031 Basel, Switzerland

EKKEHARD V AUBEL, Prof. Dr.

Chirurgische Universitatsklinik, Abt. Allgemeinchirurgie und Traumatologie
Klinikum Steglitz der FU Berlin
Hindenburgdamm 30, 1000 Berlin 45, Federal Republic of Germany

JOCHEN WALDSCHMIDT, Prof. Dr.

Chirurgische Universitatsklinik, Abt. Kinderchirurgie
Klinikum Steglitz der FU Berlin
Hindenburgdamm 30, 1000 Berlin 45, Federal Republic of Germany

HARVEY WHITE, M.A., D.M., MCh (Oxon), FRCS (Eng)

Royal Marsden Hospital
Fulham Road, London SW3 611, Great Britain

FRANTICEC ZAK, Priv.-Doz., Dr.

Toxikologische Pathologie 1040/A04 Ciba-Geigy
Postfach, 4002 Basel, Switzerland

XVII
Acknowledgments

Advisor for Section of Surgery

G. Rutishauser, Prof Dr.
Departement fUr Chirurgie, Urologische Klinik, Kantonsspital
Spitalstr. 21, 4031 Basel, Switzerland

We are grateful to the following for suggestions, information, short contribu-

tions, and ad vice:

R. ACHINGER, Dr., 1. Toomes, Dr.

St.-Antoni us-Hospital
Akademisches Lehrkrankenhaus Abt. Hand- und plast. Chirurgie
5180 Eschweiler, Federal Republic of Germany

PH. G. ARNOLD, M.D.

Plastic and Reconstructive Surgery, Mayo Clinic
Rochester, Minnesota 55901, USA

H. CESNIK, Prof. Dr.

III. Chirurgische Abteilung, Landeskrankenhaus
Rosenberggurtel 12, 8010 Graz, Austria

URSULA L. FAlX-SCHADE, Dr.

Diakonie, Plastische Abteilung
4000 Dusseldorf 31, Federal Republic of Germany

H. FISCHER, Prof. t
Max-Planck-Institut fUr Immunbiologie
Stiibeweg 51, 7800 Freiburg, Federal Republic of Germany

M. HOLUB, Prof.
Institute for clinical and experimental Medicine
Czechoslovak Academy of Science CSA V
Praha, Czechoslovakia

1.B. HUGH, Dr.

St. Vincent's Medical Centre,
376 Victoria Street, Darlinghurst 2010, Australia

F.G. INGLIS, M.D., F.R.C.S. (C)

Professor and Head Department of Surgery, University of Saskatchewan,
University Hospital
Saskatoon/Canada, S7N OXO

XVIII
S. JUSKIEWENSKI, Prof.
Universite Paul Sabatier Faculte de Medecine Toulouse Rangueil
Laboratoire d'anatomie appliquee 133
Route de Narbonne, 31077 Toulouse Cedex, France

PATEL J, M.D.,
Department of Surgery, Rochester General Hospital, University
Portland Av., Rochester Ny 14621

C.A. PISSIOTIS, M.D., Prof.

Department of Surgery University of Athens
2, Iasiou Street, Athens/Greece

G.A. SCHLOSSER, Priv.-Doz., Dr.

Universitatskrankenhaus Eppendorf, Chirurgische Klinik
MartinistraBe 52, 2000 Hamburg 20, Federal Republic of Germany

W. WESTENDORF, Prof. Dr.

Agyptologisches Seminar der Universitat
PrinzenstraBe 21,3400 Gottingen, Federal Republic of Germany

B.W. ZWEIFACH, DM, Prof.

University of California, San Diego, Department of applied mechanics and
engineering sciences Bioengineering, M-005,
La Jolla, CA 92093, USA

Technical Assistance

SUSANNE VOSMEER-JENZER, med. Laborantin

Department fUr Chirurgie, Kantonsspital
SpitalstraBe 21, 4031 Basel, Switzerland

MARTIN LIEBERMANN, Stud. med. dent.

7800 Freiburg, Federal Republic of Germany

HORST KIECHLE, Stud. ing.

7800 Freiburg, Federal Republic of Germany

XIX
 Anatomy and Functional Anatomy

1 Anatomical Definitions, Composition, and Configuration

D. LIEBERMANN-MEFFERT

The greater omentum is the free hanging mesenteric tissue apron

in the peritoneal cavity, arising from the stomach and covering
the intestines (Fig. 1). The lesser omentum is the membrane be-
tween the lesser curvature of the stomach and the liver hilum.
Though both structures have the same name they differ in shape,
morphology, development, and functional behavior. In this
book by "omentum" we understand the greater omentum.

Composition The omentum is composed of a trabecular connective tissue

framework which carries (Fig. 2):
Arteries, veins, and lymphatics
Transparent thin membranes between the trabeculae containing
tissue-free interstices, i.e. holes
Fat tissue, connective tissue cells, and cellular aggregations
called "milky spots"
Mesothelial lining on both surfaces with a single layer of flat
cells which are interrupted over the milky spots

Configuration The macroscopic aspect of the omentum depends on the species,

the age of the individual, nutrition, and the state of stimulation,
eg., pathological conditions. In man and animals the omentum
of the embryo, neonate, and infant is poor in fatty substance;
age increases the fat content.

.... Fig. 1. The greater omentum in its natural position in man. Anatomical
waxwork 1789, Collection of the Josephinum, Vienna. (Photograph: R. NE-
DOROST, Vienna, 1980, courtesy of Prof. E. VAUBEL)

1
Fig. 2. Main tissue texture
and constituents of the
omentum
Lesser omentum

Stomach

t i ssue
meshes

Trabecu la
conta i n ing
Artery
{ vei n --+-11+-
ArteriOles
Term inal
0
lymphatics

Venules
Milky
s pot

lymphat ic

2
 2 Topographical Relations
D. LIEBERMANN-MEFFERT

2.1 Relations in Man (Fig. 3 a, b)

Location The omentum usually extends over a large area. Arising from
the greater curvature of the stomach it crosses the transverse
colon and descends in front of the abdominal viscera, occasion-
ally down to the symphysis. Its right upper edge faces the liver,
and on its left is the spleen; its anterior surface faces the parietal
peritoneum, i.e., the abdominal wall, and its posterior surface
passes over the viscera. The omental portion between the stom-
ach and colon is called the gastrocolic ligament, and the portion
below the colon is the" apron. "
Under pathological conditions, for example, if the stomach or
the transverse colon are prolapsed or markedly distended, the
omentum will extend further toward the pelvis. Axial rotation
of the stomach will also effect its relations (see Sect. 7.1). In
severe meteorism or colonic distension, and in the presence of
intra-abdominal exudates, the omentum may be coiled up, lying
in the upper abdomen. If the abdomen contains large quantities
of fluid it may even lie on the anterior surface of the liver.
Attachments to the The origin of the right omental edge varies; it may arise from
Viscera the duodenum and ascending colon or it may hang down merely
from the pyloric area. On the left side, an extension of the
gastrocolic omentum may lie over the anterior surface of the
stomach, or over the upper part of the spleen [19]. The omentum
is attached to various organs (for details see [9, 10D. Such at-
tachments of peritoneal tissue are called ligaments.

Spleen. The omentum forms the ligament between the spleen

and stomach and attaches the spleen to the dorsal abdominal
wall. This fine membraneous ligament is frequently given off
to the lower part of the spleen just below the hilum; another
membrane forms the phrenocolic ligament, upon which the
spleen is incompletely fixed.
Gallbladder. The right edge of the gastrocolic ligament, particu-
larly when it exceeds the pylorus, forms a mesentery for the
gallbladder. This ligament may be very broad in children and
may extend from the cystic duct to the anterior portion of the
fundus of the gallbladder [82].
Transverse Colon. Epiploic appendices in many individuals form
the anti mesenteric surface of the transverse colon; they are

3
Fig. 3 a, b. Diagram
showing peritoneal reflec-
tions and topographical re-
lations of the omentum a
in the sagittal section and b
transverse section
4
------~-=---J----+------------- Uver
Lesser omentum _____---l----I!L/f..____--:~rTl==fI
---,fI-I.------;L----/-----___ Omental bursa
-""""#-,..~-+--=~----_f------------ Stomach
Gastrocolic + ..,=- ....-----/----------- Pancreas
ligament _ __ _ _-4-#-*
P====:::~I
Transverse colon -----_jHl--#--\--'.._
..J.J..~=-+----_jl__---------- Duodenum
Apron of
greater oment um --------I~4\_ --\I'll-'------'\,------\---_______ Mesentery
Peri toneum,________+-\\
Abdominal cavity,________-ll-~~-- -1r-++l--\-- --Rectum
Urinary bladcIer-----=-----\---=,--""c--__
Liver Antenor Stomach
u~.r;;....l,---- Omentum
.......-M/n--+- GastrospleniC
ligament
Cava I vel n ----HMI --"--:-~-=-~F)- ..... -I- -"I\J.-I.- Omental bursa
Aorta \.-11'(- ---/,11---1-- Pancreas
- oH- ---M4L,I--- - KIdn ey
-=-4:f.--/-_ _ _ Spteen
b R Posterior L
 located in the area where the posterior surface of the omentum
becomes attached to the colon. Both may appear as a homoge-
neous mass of fatty tissue, but there are criteria by which the
structures can be distinguished [76]:
The omentum has a more granular surface pattern
The epiploic appendices have a smoother surface
The embryological attachment of the omentum can be recog-
nized as fusion line of fibrous tissue.

Omental Bursa Head of the Pancreas. The portion of the omentum which comes
(Lesser Sac) off the greater curvature of the gastric antrum fuses to the ante-
rior surface of the head of the pancreas [1, 17].

Dorsal to the gastrocolic ligament and the stomach lies the cavi-
ty called the" omental bursa," which communicates with the
main peritoneal cavity through the epiploic foramen of
Winslow. In relation to the total abdominal volume the omental
bursa represents a potentially large cavity with various exten-
sions (recesses) into the subphrenic area above and into the
greater omentum below [37]:
The subphrenic (superior) recess is the most voluminous of the
spaces and extends between the caudate lobe of the liver and
the diaphragm.
The lineal recess lies between the spleen and stomach.
The inferior recess includes all the remaining lower part in the
area of the transverse colon, the gastrocolic ligament, and the
vault between the main epiploic vessels [49].
Occasionally an incomplete caudal recess exists in the left
portion of the apron, confirming BoucHET's [11] description.
Saccular protrusions independent of the main recesses may also
be found, but we, as well as others [9, 11, 37, 49, 89], have
seldom observed large recesses extending to the caudal edges of
the apron producing the two double layers of mesentery as usu-
ally shown in anatomical textbooks.

2.2 Relations in Animals

Incidence Phylogenetic Distribution of the Omentum. Low vertebrates such

as fish, amphibia, reptiles, frogs, and birds have no omentum,
with the exception of the giant salamander and the chicken
embryo, where it is rudimentary [46]. Mammalia have an
omental apron along the greater curvature of the stomach; it
is small in low Mammalia, and large in predatory and domesti-
cated animals such as the dog and cat in which it envelops
all the intestinal loops [33, 44, 46, 75].

5
Attachments No attachment to any part of the viscera occurs in low Mamma-
lia, rodents, hoofed animals, and carnivores. Fusion to the colon
beginning at the right colonic flexure is found progressively in
marsupials and half monkeys [46]. In monkeys and men the
omentum is fused to the entire transverse colon. The spleen
is located in the tissue of the left edge of the omentum in all
laboratory animals and is not fixed to any other part of the
abdominal wall. Occasionally additional spleens are found.

Omental Bursa All vertebrates have a bursa behind the liver and stomach, which
is differently shaped in each species [46]. The omental apron
is patent in rodents, and the cat and dog: it forms a sac of
two sheets with mesothelial surfaces, the outer facing the perito-
neal cavity, the inner the bursa.

Similarities Between Description of the gross and cellular morphology in the text
Omenta of Man is generally applicable to all omenta [33]. The human omentum
and Animals and the animal omentum have the same texture, mesothelial
lining, and cellular content [8, 89] in the milky spots, which
are discrete opaque nodules [77] in the transparent tissue. How-
ever, the human omentum has not yet been studied in great
depth. Most information on the tissue and its function is avail-
able from studies of laboratory rodents. Ultrastructure investi-
gations have been performed in the mouse and rat [6, 14, 28,
39], and there seems to be little variation.
Comparative Pig (Fig. 4). The omentum covers the entire intestines and con-
Architecture of sists of a trabecular framework which contains a small amount
Omenta in Laboratory of adipose tissue along the vessels and thin mesothelial mem-
Animals branes between them.

Fig. 4. Pig omentum.

(DITTLER)

6
Fig. Sa. Omentum of an
adult female German shep-
herd dog. b Trabeculae in
the adult dog omentum.
Detail of a. (LIEBERMANN)

Adult Dog (Fig. 5 a). The very large omentum covers the entire
intestines; it is built up of a net-like framework of connective
tissue trabeculae (Fig. 5 b) containing a great number of richly
anastomosing fine blood vessels which are continuous with
paired arteries and veins pasing centrally in the trabeculae [72,
75]. In radiograms of the spread-out omentum the trabeculae
appear as a system of multiple communicating arcades [72].
A varying amount of adipose tissue is found alongside the
vessels. In the meshes between the trabeculae, thin connective
tissue membranes are interposed and are often perforated.
Meshes and trabeculae are in the same plane [75].

7
Fig. 6. Omentum of a male
dog puppy 4 weeks before
term. (LIEBERMANN)

Dog Puppy (Fig. 6). The omentum consists mainly of a delicate

tissue membrane containing several vascular arcades. Yellow-
white nodules alongside the vessels correspond to milky spots ;
these are numerous.

Cat (Fig. 7). The omentum in cats is large and its texture is
similar to that of the dog, although there are less blood vessels.

Rabbit (Fig. 8). The omentum is a, very delicate, fragile mem-

brane of transparent tissue containing some vessels of tree-like
arrangement in the periphery. Except for paired arterioles and
venules and in the areas of adipose tissue, the microscopically
visible blood vessels do not cross over each other [50], and
meshes and trabeculae are in the same plane [77].

Guinea Pig. In situ the large omentum is uniformly coiled up

in the upper abdomen. It is a delicate membrane with only
a few vessels surrounded by a small amount of fatty tissue
(Fig. 9).

8
Fig. 7. Omentum of an
adult female cat. St, stom-
ach. The spleen (S) can be
seen mobile on the left
omental edge. (LIEBER-
MANN)
Rat and Mouse. The omentum of both these rodents is small
and most often coiled behind the stomach. In spread prepara-
tions it appears as a transparent, sac-like structure. Its fat depos-
its are mainly peripheral, and large areas seem to be avascular
(Fig. 10a, b).
9
Fig. 8. Omentum of an
adult female rabbit. Many
milky spots can be seen in
the membraneous portion
(arrows). S, spleen. (LIE-
BERMANN)

10
Fig. 9. Omentum of an
adult male guinea pig.
S, spleen. (LIEBERMANN)

11
Fig. 10. a Fresh dissection
specimen of an adult male
white rat with stomach,
omentum, and small bowel.
b Fresh dissection specimen
of omentum and stomach
of an adult male Swiss
mouse. (LIEBERMANN)

12
 3 Development and Appearance
D. LIEBERMANN-MEFFERT

3.1 Embryological Development

Introduction The classical concept of the development of the omentum was

that the stomach rotated and a long dorsal mesentery containing
the spleen and pancreas became folded to form a dependent
large inferior recess known as the lesser sac [65, 69]. Subsequent
fusion of the two layers was thought to produce the greater
omentum. Attachment to the transverse colon in the 4th month
of gestation has been described as taking place progressively
from the hepatic toward the splenic flexure in man [95, 96].
Although there have been arguments against this theory [38,
46, 47, 58, 96] and although SWAEN in 1896 [93] and BROMAN
[12, 13], described the lesser sac as forming independently, the
classical concept of rotation and fold formation still holds in
most of the modern embryological textbooks.
Recent work on embryology of the stomach has shown that
its definitive shape and position are due to asymmetrical growth
of the gastric wall and irregular enlargement of the lesser sac.
No evidence has been found for any organ rotation along im-
aginary axes in the upper abdomen [16, 54, 55, 66], and the
greater omentum is thought to develop as an independent struc-
ture in close relation to the spleen and not as a "fold" of the
dorsal mesogastrium [54, 57, 87].
Omental Bursa In very young embryos the intestinal organs are located in or
on the surface of a bulky mesenchymal tissue mass which is
connected to the tissue of the spine (Fig. 11). SWAEN [93] and
BROMAN [12] observed that in the 2- to 5-mm CR embryo clefts
appeared within this mass, enlarged subsequently in various di-
rections, and formed irregular narrow spaces by coalescence.
These spaces were called "recesses." Growth of the pneuma-
toenteric recess toward the left and dorsal to the stomach re-
sulted in the formation of the primitive lesser sac, which is the
omental bursa proper. Fusion with an enlargement of the" he-
patoenteric" and "pancreaticoenteric" recesses isolated the in-
testinal organs more or less completely from the mesenchymal
mass. The retaining tissue connexions thus became attenuated
and are the primitive ligaments.
KANAGASUNTHERAM [43, see 36] recently confirmed these obser-
vations. He also described that in the early stage of gestation,
i.e., up to a 9- to 10-mm CR embryo, no portion of the primitive
lesser sac connected with the general abdominal cavity. This

13
Fig. 11 a-c. Transverse
B
section (8 J.lm) of a human
embryo, 9 mm long,
showing the origin of the
spleen (arrowed in circle),
to which the primitive DU
omentum is closely related.
a is at about 30 times mag- VM
nification and band care HER
details of the region from
which the omentum will
develop. Sp, tissue of prim-
itive spleen and omentum;
'illll=St
~ Li
St, stomach; DM, dorsal
mesenteric root (mesenchy-
mal mass), which is directly OM
continuous with the dorsal
mesentery of the intestine; Pe
VM, ventral mesentery
(lesser omentum);
HER, hepatoenteric recess;
DU, duodenum; B, bowel
in umbilical coelom;
Pe, peritoneal cavity;
Li, liver, right lobe.
(LIEBERMANN)

14
Fig. 12a-d. Transverse
St -----''''fi;I
section (S ~m) through a
human embryo, CR length
27.S mm, showing the
extent of the hepatoenteric
recess (arrowed) at different
levels of the embryo. a The
most cranial section at the
site where the recess ap-
peared to separate the
spleen from the stomach
wall. Note the bulgy
omentum at a lower level c
and d. St, stomach;
OM, omentum; Sp, spleen;
Pe, peritoneal cavity;
DM, dorsal mesogastrium.
For detail see text.
(LIEBERMANN)

OM

dorsal R L

15
Fig. 13. Transverse section
of a human enbryo, CR
length 27.8 mm. Same
embryo as in Fig. 12 at
another section level. Note
the bulgy omentum, the at-
tenuated dorsal mesogas-
trium (short arrows), and
the blood vessels in the
omentum (OM arrowed).
For details see text.
St, greater gastric
curvature;
Pa, pancreas.
(LIEBERMANN)
Spleen and Its
Ligaments
16
was also true in the 8.5-mm CR embryo (Fig. 11 a-c), which
was the smallest in my study of 137 human fetuses.
In the 15- to 30-mm CR embryo the lesser sac was found to
be continuous with the peritoneal cavity via the enlarging hepa-
toenteric recess. At this stage the lesser sac was still narrow
(Figs. 12a- d, 13) and, when compared with later stages of devel-
opment, completely occluded in places [see also 43], with the
result that considerable mesenchymal connexions existed be-
tween the dorsal surface of the stomach and the mesenchymal
mass as in earlier stages.
In the 35- to 50-mm CR embryo the main lesser sac establishes
continuity with the general abdominal cavity through a common
orifice the" foramen of Winslow" [43]. The lesser sac now in-
creases in size and extends between the tissue of the stomach
wall and its mesenchymal surface where no cavity previously
existed, thus separating the spleen from the stomach (Fig. 14),
a process which progresses from right to left, involving first
the caudal region of the spleen.
HAMILTON'S Textbook of Embryology [36] describes that the
spleen appears in embryos of about 10 mm CR length (ca. 6th
week of gestation) as a localized condensation of mesenchymal
Fig. 14. Transverse section
(811m) of a human
embryo, CR length
37.7 mm. Note the small
clefts which appear in the
omental tissue below the
spleen (arrowed, for de-
scription see text).
Sp, spleen; St, stomach.
(LIEBERMANN)
Greater Omentum
cells in the dorsal mesogastrium. I found a similar aggregation
of cells with elongated nuclei (Fig. 11) located within the surface
of the gastric wall [56, 57]. It has been shown in a consecutive
series of embryos that the spleen, the greater omentum, and
the gastric fundus develop from this region [56]. Focal areas
of hematopoiesis are present in the primitive splenic tissue while
still attached to the stomach in the 40- to 50-mm embryo. Subse-
quently a cleft appears which separates the spleen from the stom-
ach, and many small clefts convert the mass of adjacent omental
tissue into the thin gastrolinealligament (Figs. 12a~d, 13,14).
In the serial sections of the 8.5- and 9-mm CR embryo it was
impossible to discern the primitive omentum by tissue cell cri-
teria. However, in the 15- to 30-mm CR stage there was a tissue
area with differently arranged cells between the spleen and stom-
ach wall, and there was a bulky mass in the region below the
spleen, the "omental fringe" containing vessels which course
down in front of the greater gastric curvature (Fig. 13). Al-
though the enlarging lesser sac usually fuses with spaces in the
omental fringe there were a few embryos which lacked this con-
neXIOn.
Macroscopically the minute fringe of the omentum first becomes
visible in the 20- to 30-mm CR embryo (Fig. 15a). From the
stage of 40 mm CR on it is possible to inject material via the
foramen of Winslow into the lesser sac. By this method the
omental insertions and the spaces in the omentum are easy to
determine. Up to 90 mm CR the omentum is freely floating
in the abdominal cavity. The various pocket-like spaces with
17
Fig. 15a-c. Macroscopical
figure of a a human
embryo, CR length
22.1 mm, with bowel still
in the umbilical coelom,
and b a human embryo,
CR length 35 mm. The in-
testines are returned to the
abdominal cavity and the
omentum (arrowed) is
freely floating over the
transverse colon (tc)
SI, stomach; c is the same
embryo from lateral. The
pancreas (Pa) and the mes-
enteric root Dm, which is
independent of the
omentum (arrowed), can be
seen. The spleen (Sp) con-
tains a few hematopoietic
foci (TA) (see text). (LIE-
BERMANN)

Fig. 16

Fig. 16. The finger-shaped

recesses can be seen in the
human embryo with CR
length of 105 mm (lateral
view). The omentum was
stil\ not attached to the co-
lon (c) in this embryo (see
text), SI, stomach;
Sp. spleen (LIEBERMANN)
finger-shaped protrusions (Fig. 16) within the omentum are
mostly connected with each other and with the proper lesser
sac behind the stomach through openings in the tissue below
the spleen and in the region of the duodenum (Fig. 17 a-c).
There is no evidence that any attachment occurs before the
60-mm CR stage. The first event of "secondary" attachment

18
 a, b
Fig. 17 a--c. Specimens of
three embryos, CR length
80-110 mm, in which the
omentum was filled via the
omental bursa in situ to
demonstrate the extent of
the omental recesses (see
text). (LIEBERMANN)

which I noticed was that of the dorsal mesogastrium with the

posterior body wall; this took place between the 60- and 100-mm
CR stages, progressing from the head of the pancreas toward
the splenic hilum (Fig. 18). Between 80 and 120 mm CR the
omentum slightly increased in length. In my series fusion of
the omentum with the colon took place at this stage first III

19
Fig. 18. Specimen with
lifted omentum in a human
embryo, CR length
116 mm, showing its at-
tachment to the right and
left colonic flexures (see
text). The hole between the
greater gastric curvature
and transverse colon was
made in this case to deter-
mine the border of the
omental bursa. (LIEBER-
MANN)
Histology
Premature Newborn
20
the region of the hepatic flexure, second in the region of the
spleen, and last in the middle portion of the transverse colon
(Fig. 18). This is similar to LOCKWOOD'S observation [58] but
disagrees with TOLDT'S description [96].
When fixation with the transverse colon was complete in the
150-mm CR fetus, the omentum showed very little increase in
length in the following months of gestation. Injection of material
frequently showed a cavity in the bulky omental portion below
the spleen while the right portion almost always remained small
and patent. This corresponds to the observations of BOUCHET
[9, 10], who often found a persistent left gastrocolic recess in
the adult.
The histology of the omentum was studied in the fetus, newborn,
and infant by SEIFERT in 1923 [89], MARCHAND in 1925 [60],
and BORISOV in 1964 [8]. These data will not be reviewed because
this subject of cellular development needs reinvestigation with
modern techniques.
3.2 Structural Peculiarities in Childhood
J. WALDSCHMIDT
The omentum is attached to the transverse colon along the tenia
omentalis and does not reach the colonic flexures, ending as
a short folded fringe just below the colon. It is a fatless thin
membrane in which the specific vascular pattern (see Sect. 4.3.2)
can be seen (Fig. 19).
Fig. 19. The rudimentary
omentum in a premature
infant

Mature Newborn The omentum extends a little beyond the transverse colon, usu-
ally covering a quarter of the small bowel, but still does not
reach the colonic flexures (Figs. 20, 21 a, b). The inferior recessus
of the omental bursa is open. Macroscopically there is a specific
vascular pattern, but no fatty tissue or lymphatic nodes can
be seen in the transparent membrane. I have not observed acces-
sory spleens in the omentum at this age.

Fig. 20. The omentum in a

neonate. The omental
apron is very short but
covers some of the loops of
the small intestine. It con-
tinues to develop with in-
creasing age, and the fat
content also increases
along the vessels

Three to Four Months The omentum extends distal to the transverse colon, covering
two-thirds of the small bowel. It contains a small amount of
fatty tissue alongside the vessels; the various fat islands do not
join but fat is accumulated at the site of vessel branching.

21
One to Five Years Most of the intestines are covered by the omentum, which now
also extends beyond the colonic flexures. It is often attached
to the ascending colon and occasionally also to the descending
colon. The fat deposits form large confluent plaques, which
follow the vessels. The transparent mesh structures can be seen
clearly. Small nodes macroscopically similar to lymph nodes
are occasionally observed (Fig. 21 c).

Five to Ten Years Depending on its length and degree of fat the omentum now
resembles that of the adult. A special feature of this age is the
low distal insertion of the omentum on the ascending colon.
It may reach the cecum, producing kinking of the terminal il-
eum, associated with abdominal symptoms. This distal omental
insertion should not be confused with other membranous condi-
tions in the ileocecal region (Sect. 7.1, Figs. 71, 72). A series
of clinical photographs illustrating omental growth from birth
to 11 years is shown in Fig. 21 a-d.

22
.... Fig. 21 a-d. Clinical photo-
graphs illustrating omental
development in children.
Note that the deposition of
fat starts close to the stom-
ach along the vascular
arcades. a 7 days;
b 10 weeks; c 31/ 2 years;
d 11 years.
(WALDSCHMIDT)
3.3 Omentum in the Adult
D. LIEBERMANN-MEFFERT
All variations between a fat laden and lean omentum occur
(Figs. 22, 23). The relationship appears to be much more closely
dependent upon the weight rather than the age and sex of the
subject. The variations in the shape are also marked. The vascu-
lar pattern is discussed in Chap. 4.3, and its wide range of varia-
tions is shown.

Size in Man Very short omenta 7 cm in length [86, 89] and comparatively
long ones of 70 cm [23, 81, 89] have been observed, but accord-
ing to DAS [17, 18] and our measurements, its length usually
ranges between 14 and 36 cm and its width between 20 and
46 cm. Men have slightly larger omenta than women. The
omental volume depends upon the body weight of the individual
[17], which may be judged to some extent when planning
omental transposition. However, preoperative assessment is lim-
ited in accuracy as some individuals have unexpected sizes at
laparotomy.

Omental Size in Some The sizes of the omenta of the most common laboratory animals
Laboratory Animals are given in Table 1.

Table 1. Size of spread-out omenta of my series of different adult laboratory

animals. Length and width were measured according to DAs's description
[17]

Species Number Length Width Body Position

n (em) (cm) weight
(kg)

Dog 4 39.7 ± 7.0 34.8 ± 5.0 23.2 ± 1.2 Symphysis

Cat 32 24.8±6.5 19.5±4.1 26.0±6.5 Symphysis
Rabbit 12 7.6±4.2 10.9±3.2 2.8±0.8 Upper abdomen
Guinea pig 20 6.8 ± 1.3 8.0 ± 1.8 0.8 ± 0.6 Behind stomach
Rat 10 2.8±0.3 5.2±2.1 0.3±0.4 Behind stomach
Mouse (C 3 H) 11 2.2±0.2 2.6±0.2 0.03±0.03 Behind stomach

23
 Fig. 23. Magnified view of
an human omentum
showing fatty appendages.
(LIEBERMANN)

00II Fig. 22a, b. Adult

omentum. a Necropsy
specimen of a 36-year-old
woman with a lean
omentum, in which the
vessels and small deposi-
tion of fat are reminiscent
of lace. b 69-year-old male
subject with heavy deposi-
tion of fat in bilobed
omentum. (LIEBERMANN)

25
 4 Structures
D. LIEBERMANN-MEFFERT

4.1 Stroma

The omentum is composed of:

Loose Fibrous Connective Tissue Framework. This carries the

vessels, the fat pads, which contain the fatty tissue alongside
the vessels (Figs. 2, 24a- c), and cellular elements. Close to the
fat pads or in the membraneous portions of the omentum fre-
quently lie small ovoid structures of opaque appearance (Fig. 8)
which are called "milky spots" ([77], see Sects. 4.5, 5.7). No
connective fiber meshes are apparent within these structures [14,
15].

Thin Lace-like Membraneous and Transparent Network. The

membraneous parts are located between the fat pads as shown
in Fig. 24 a-c. The collagen and elastic fibers of this part are
so arranged that numerous meshes or openings are formed, with

Fig.24a

26
Fig. 24 a--c. Series of
human omenta with vary-
ing fat content. Note fat
pads alongside the vessels.
The membraneous network
between the fat pads con-
tains different amounts of
fat tissue. Formaldehyde-
fixed human specimens
from necropsies. a and b
have the same magnifica-
tion. (LIEBERMANN)

27
Fig.25a
6 10 12

/·- -14

4 12

diameters ranging from less than 1 to 60 !lm. In some areas

there is only a narrow isthmus separating the meshes while in
other places much larger expanse lies between them [28, 39].

4.2 Tissue Constituents (Fig. 25 a, b)

Texture Collagen, elastic and reticular fibers form the texture of the
wide meshes, which are connected by microfibrils. Through the
meshes pass blood vessels, lymph vessels, and nerve fibers.

Cells As in loose areolar connective tissues there are commonly fixed

cells (fibroblasts, fibrocytes, fat cells, pericytes) and motile cells
(histiocytes, monocytes, plasma cells, lymphocytes, eosinophilic
granulocytes, mast cells) in the network. Most numerous are
fat cells. The fat cells of the omentum belong to the white
adipose tissue. They lie directly beneath the peritoneal mesothe-
lium, with which they are connected by a few microfibrils. The
intercellular substance will not be discussed here.

28
Fig. 25a, b. Texture and
cells of loose areolar con-
nective tissue. Semische-
matical representation of a
sectional and b three-di-
mensional view. 1, fibro-
blast and fibrocyte;
2, histiocyte; 3, plasma
cell; 4, monocyte; 5, lym-
phocyte; 6, eosinophilic
granulocyte; 7, mast cell;
8, blood vessel; 9, pericyte;
10, collagen fiber; 11, mi-
crofibrils; 12, elastic fiber;
13, reticular fiber;
14, nerve fiber; 15, lymph
vessel; 16, adipose cell.
(KRSTIC [48])

29
 4.3 Vessels and Innervation
Arterial Blood Supply (Figs. 26-28)

Introduction The first account of omental vascularization which we found

was in THEODORIC'S writings in 1267 [94]. The traditional picture
of widely open gastroepiploic and epiploic arterial arcades dates
back to the work of RUYSCH in 1702 [83], HALLER [35], and
BARKOW [4]. This concept, although drawn from single observa-
tions, still holds and serves as the basis for using the omentum
on a vascular pedicle in reconstructive surgery [1, 17, 45].
However, in 1916, following arteriographic studies on a larger
series, DESCOMPS [20] doubted that there were wide arterial
arcades in man. Subsequent examinations and our own series
demonstrated the wide range of varieties and the impossibility
of predicting any standard pattern of vascularization [9, 10,
22, 53].
Assessment In our experience direct observations of the omentum [1, 26,
of Vascular 49, 89] do not reliably demonstrate the vascularization because
Architecture of the large amount of fat tissue surrounding the vessels and
the small vascular diameter at the periphery. Fat cannot be
satisfactorily removed, for example, in post mortem specimens
and connective tissue cords may also be mistaken for vascular
cords. Angiography performed in vivo [53] or postmortem even
shows small vessels and permits measurement of the vascular
diameters. In 16 human cadavers we introduced a catheter in
situ through the aorta, which had been clamped below the origin
of the celiac trunk. Contrast medium (barium gelatine) was in-
jected (Fig. 26), and exposures of the specimen gave a clear
picture even of delicate vessels (Fig. 27 a-e).
The micro vascularization has been studied by means of intravi-
tal microscopy and is described in Sect. 5.7. The ultrastructural
basis of the capillary permeability has been examined with per-
oxidase as a tracer [39].
Arterial Distribution Blood supply of the omentum is provided by the right and left
gastroepiploic arteries (Fig. 28 a, b). Both arteries are derived
from the celiac trunk, pass tortuously along the greater gastric
curvature, and decrease progressively in diameter while giving
off branches to the stomach and omentum (Fig. 27). Gastric
branches were about 3 times more numerous (20.9 + 4.8 SD)
than epiploic branches (7.9 ±2.1 SD) in our series of 16 subjects.
This is similar to DESCOMPS'S [20] and EL-EISHI'S description
[24]. We occasionally found small epiploic arteries rising from
the ascending gastric or even the proper gastric wall vessels
which cross the main gastroepiploic artery.

30
Fig. 26. Arterial distribu-
tion in the human
omentum after postmortem
intra-aortal injection of a
barium-gelatine mixture in
situ. Wide epiploic vessels
and dorsally crossing left
epiploic artery are seen.
(ARGAST, KAUFMANN,
ZYSSET, BOSSARD,
LIEBERMANN)

The individual and local distance of the gastroepiploic artery

from the stomach (Fig. 28 b) was very variable and ranged from
0.3 to 4cm (mean 2.0cm±0.54SD) in our series. The right
gastroepiploic artery is larger and considerably longer
(25-31 cm) than the left (14-21 cm). Both arteries connected
in 11 of our 16 specimens. This was 10-15 cm left of the midline
of the greater gastric curvature (Figs. 27 a-d, 28 b). The total
length of the anastomosing gastroepiploic vessels was 46 cm
(+ 5.7 SD). However, the vascular diameter at the anastomosing
point was usually very small (Fig. 27 a-d). In our series 5 of
16 subjects had no connection at all (Fig. 27e, 0. We found

31
Fig. 27 a-f. Series of post-
mortem arteriograms
showing the great variation
of arterial distribution. The
cut off tree-like arterial
stumps behind the gastric
fundus are the splenic ar-
teries. f is a detail from e
showing an incomplete gas-
troepiploic arcade (arrow).
The exposure factors for
the arteriograms were
50 kv, 200 mAs, and 0.25 s.
Structurix D4 Agfa-
Gevaert films were used.
(ARGAST, KAUFMANN,
BOSSARD, LIEBERMANN)

32
Fig.27b

33
Fig. 27c,d

34
Fig. 27e,f

35
 no other sources supplying the omental apron. Small branches
descending from the pancreatic artery have been described anas-
tomosing with omental vessels [1]. In our series and in that
of BOUCHET and of DESCOMPS [9, 20] this connection could not
be found nor was there any relationship to the vessels of the
colon and mesocolon or the fatty epiploic appendages. The vas-
cular supply to these epiploic appendages of the colon which
may underlie the omentum derives from the middle colic artery
through vessels which enter the colic surface of the appendages
[71, 76].
The epiploic arteries can be divided into those originating from
the right gastroepiploic artery and those from the left gastro-
epiploic artery. All these epiploic arteries are individually dis-
tributed and vary in length and caliber (Fig. 28 b). Five to 13
(7 ± 2 SD) are found on the right, and usually one is found
from the left gastroepiploic artery (Figs. 27, 28). While the right
epiploic artery seldom branches in the center of the omentum,
the left epiploic artery gives off numerous small vessels to supply
to omental margin below the spleen, which thereby becomes
the area of the omentum with the best blood supply.
The right epiploic arteries descend mostly at right angles and
bifurcate close to the marginal part of the omentum. Some are
united through many small anastomoses (Fig. 27 a-e). In half
of our series the left epiploic artery coursed downward posterior-
ly close to the omental margin below the spleen (Fig. 28a). In
the other eight it traversed the omentum obliquely at a varying
distance from the stomach and behind the right epiploic arteries,
giving off epiploic arteries posteriorly. Occasionally there were
anastomoses with the right epiploic arteries (Fig. 27 a, c).
The omental margin was supplied by numerous capillaries which
may have minute anastomoses; the traditional epiploic arcade
[4] is rare and was found only in 1 to 16 subjects forming very
small anastomoses (Fig. 27 e).

Milky Spot Vessels At the lateral branches of the epiploic arteries and at their termi-
nal branches numerous microvascular structures of characteris-
tically constant architecture have been described (Fig. 29), [8,
50, 75, 77, 101]. They are similar in men and animals. The
vascular network may be densely packed with various cells of
the reticular system and fat cells (see Sect. 4.5). The basic vessel
geometry and its function is described in Sect. 5.7. The outstand-
ing feature is that the vascular walls have many fenestrations
and that because of the discontinuous mesothelial lining above
the spots the glomus-like vascular structures are exposed to the
peritoneal cavity (Sect 4.4).

36
Fig. 28. a Nomenclature,
origin, and individual dis-
tribution of the omental
arteries. The gastroepiploic
arcades were incomplete in
5 of 16 specimens. b The
mean size of the anastomo-
sis which is most often
smallest is shown in this
figure. Barium gelatine was
injected at high pressure in
postmortem specimens.
The diameter, therefore, is
greater than that measured
in vivo when the omentum
is transferred microsurgi-
cally (Sect. 9.2.3)
Aorta--------------------~ --\------------ Spleen
Celiac axis -------------::=~rv_ ~---T-'rt<;:----'----J'c---------S pie n i c artery
Gastroduodenal-----,I---==~ \+--~---"r--- Left gastroepiploic
artery artery
Right gastro - --=:~~",=d,­
epiploic artery IV.-'--~Tt------j-- Site of anastomosis
Gastr i c bran c hes --~-----If-----\-\,--J
If-'..----\---Left epiploic artery
Rig ht -------------;1------,,,(1
ep iploic -------+------'--------f,
arter i es -------+-------------+l-----------j
Marginal ______+ ______.¢'_
bifurcation
~~&_-+--------3.5 ± 0.3
3.3 ± 0.3 ----------7'''-- \1-"~'_\_-----2.2 ± 0.4
)\-----'\-------1. 4 ± 04
05 ±02 --------=-~~=*'r_-V
'=1t-----/--0.7±0.2 (n=11)
1.5±0.3 ----\--~ 1l-----l----·--1.6± 0.4
2.4 ± 0.6 ----------+---H------1t----'
"'-----\,-----0.3 ± 0.1
0.4 ± 0.3 ------1-------1~---~II_----1t__\
-----\-\----1.4 ± 0,4
1.0 ± 0.5 -------/-----'------11
1------0,9 ±0,3
-+___________ < 0,3
0.3± 0,0 3 ---------"--c------;___~
<0,3 -------
37
Fig. 29. Vascular network
showing the arteriovenous
structures of the milky spot
system and vascular shunt
in the rabbit omentum. In-
dian ink injection (DITTLER)

Venous Drainage (Fig. 30)

Clear accounts of the venous drainage in the human are given

by DESCOMPS and by BOUCHET [10, 20]. The normal venous
drainage parallels the arteries and empties into the portal sys-
tem. Usually there is only one accompanying vein of greater
caliber for each artery in the apron [89]. The gastroepiploic
vein increases in diameter after receiving branches from the
stomach and omentum. We found the gastroepiploic vein lying
distal to the artery and 1-4 cm from the greater gastric curva-
ture. The veins'arising from the anterior and posterior gastric
surface usually encircle the gastroepiploic artery at the same
level from both sides before entering the gastroepiploic vein.
According to NETTER [71] the gastroepiploic vein empties into
the superior mesenteric vein in 83% of subjects, just before en-
tering the portal vein. Sometimes it joins the first part of the
splenic portal vein.

Lymphatic Drainage of the Omentum (Fig. 31)

Introduction As early as 1747 ALBRECHT VON HALLER [35] and later RANVIER
[77] and ECCLES [23] postulated lymphatic drainage of the
omentum. However, no evidence was presented to support this

38
Fig. 30. Venous drainage
Inferior vena cava - - - - - t -

Portal vem -----~.....

Gastr i c vem S - - ----,.--=7:Rr'I:---"

Inferior me-
Spl en ic vein - - - -/- ----tt::-fJA\_ r~--------s".,"="~'_t_­ sent eric vem
Ri ght 9ast~o­ Leoft gastro-
ep fplolc vem ---=::.....,::,>tt-~~~""
epiploi c ve in
5 u per i or me-- - - / --».,df-18'=t+
senter ic vein
II--+-""'"----t-- Left epiplOIC
vein

RI ght - - - - - - t - - \ \
eplplolc - - - - / - - - - f f
ve ins ---~---fL__JI

hypotheses [61, 74, 89] until 1933 when BECHER and FISCHER
[5] and ZSCHAU [100] first visualized the complex lymphatic
drainage of the omentum using specific uptake techniques.
The extensive omental lymphatic network has been subsequently
shown after intravital injection of soluble proteins or other
agents into the tissue and the omental margin which were taken
up by the contiguous microscopic channels [21, 29, 74, 90, 91,
102] or into a cannulated lymph vessel [42, 72, 102]. The descrip-
tion of the lymphatic system in man [8, 21, 74, 90] is close
to that in animals. In animals of different species the perfusion
and dynamics of drainage have been followed under the micro-
scope ([41, 102] Sect. 5.7).
RANIVER [77] believed that the "milky spots" he discovered
were lymph nodes but SEIFERT [89], demonstrated the difference
between both structures (Sect. 4.5, see Table 2).

Lymphatics The terminal lymphatics (Figs. 31, 32) form a delicate irregular
interconnecting arrangement with parts bulging to form a
bizarre pattern and shape of flattened tubes [8, 72, 74, 102].
Some of the saccular terminal lymphatics are located within
the vascular system of the milky spots; "embedded" in the
cellular aggregations of the milky spot they are also exposed
to the abdominal cavity because of the gaps in the mesothelial
lining (Fig. 32).

39
Fig. 31. Lymphatic drain- Thoracic duct- - - - - - - - - ; ' \
age
u-;+ - - - - Spleen
Celiac lymph nod es --r-----"'''''<tH'-jIoo;;;~:rL_l,...
Left gastroepiploic
nodes
Pyloric lymph nodes----'v"~"
----.:'7'7~--+--- Stomach
Right gastroepiplo i c -r--:7<--~~~:::;'<---:::;;;;;;~
node

l } - - + - - - - Valve

~_--\,-- Lymphatic in
posterior layer

Terminallympha- <f--l..----II
tics in the apron

The lymphatic net is irregularly distributed, its full extent being

difficult to gauge even in thin tissues, but it is much more exten-
sive as demonstrated by the dye uptake data [72]. At a vessel
diameter of 40-50 /lm the terminal lymphatics converge to form
collecting channels [72, 102]. These have a more prominent wall
and are provided with valves [29, 74] spread at intervals of
400-1500/lm [102]. Such a valve consists of a conus, bulb, and
two thin valve leaflets (Fig. 32, see also Sect. 5.7), and causes
a local bulge of the lumen up to double its diameter [72, 102].
Lymphatics join these collecting channels in their progress in
a proximal direction, but the caliber of the channels increases
surprisingly little. Most of these connecting vessels course ex-
centrically in the trabeculae parallel but at a small distance to
the blood vessels [29, 72, 74]. Drainage of the peritoneal cavity
may largely bypass the system through the celiac lymph nodes
to the thoracic duct. There are two main routes of lymphatic
drainage in the omentum (Fig. 31):
To the right toward the subpyloric nodes
To the left toward the splenic nodes
In the proximal parts of the omental apron lymphatics commu-
nicate with lymphatics which drain the stomach and pass along
the greater gastric curvature [72, 85].

Lymph Nodes Lymph nodes seem to be lacking or are at least very infrequent
in the omental apron, in the gastrocolic ligament, and along
the greater curvature [85]. There was none visible in 16 human
omenta examined by us in detail.

40
Fig. 32. Semischematic
diagram of terminal lym-
phatics. The saccular struc-
tures are located within the
vascular network of the
milky spots. Note the close
relationship to the Iym-
phoreticular elements, e.g. ,
macrophages and the expo-
sure to the abdominal cavi-
ty by mesothelial gaps (for
legend and details see
Sect. 4.4 and 5.7 and
Figs. 39, 51)

Innervation

The only information available on the innervation of the

omentum is that of SEIFERT in 1923 [89]. He described nerve
fibers for the omental vessels, but was unable to demonstrate
any innervation of the omental tissue, thus explaining the appar-
ent lack of sensory perception.

4.4 Mesothelial Lining

Main Framework of
Loose Connective
Tissue
The cells which cover serous membranes are called mesothelial
cells (Fig. 33; see also Sect. 4.5). The mesothelial surface lining
of the omentum in general resembles ordinary mesentery and
consists of a continuous layer of single, flat pavement cells.
CARR [14] showed that the intercellular junctions at this location

41
Fig. 33. Electron micro-
scopic image (TEM) of a
mesothelial cell shown
semischematically. The
apical surface bears micro-
villi (Mu), the number of
which changes with differ-
ent abdominal conditions.
The basement membrane
(Bm) is thin and is missing
above the milky spots. The
large number of vesicles
(V) indicates that active
fluid exchange takes place
between the mesothelial
cell and serous fluid of the
cavities. The microvilli
would facilitate this
process by increasing the
surface area available for
exchange of soluble sub-
stances. Mesothelial cells
may be capable of taking
up particulate materials.
(With slight alteration
from LENTZ [52])

are tight (desmosomes), with no space between the plasma mem-

branes (Fig. 34a, b). The cells occasionally have long and un-
evenly distributed microvilli on the free surface (Figs. 33, 34a,
Fig. 39 [14, 59]). The basal side is lined by a basement membrane
(basal lamina, Figs. 33, 34), which was sometimes in apparent
continuity with the content of the vesicles of the mesothelial
cells [14]. In the mouse there is little basement membrane be-
neath the mesothelial cells as seen in Fig. 34 b compared, for
example, with the rabbit [3]. The basement membrane is a coat
containing filamentous material [52]. It parallels the basal plas-
ma membrane of the cell and provides a thin barrier against
passive diffusion (see Sect. 5.6). Omental mesothelial cells com-
monly have a thin basement membrane (Bm, Fig. 33), which,
however, is completely lacking above the milky spot.

Lace-like Membrane The surface mesothelium of the lace-like network is thrown up

in folds and is very thin (Fig. 34 [14]). This part is composed
of two layers of mesothelial cells which enclose a small connec-
tive tissue space [1-2 )..lm (mouse)]. This space contains collagen

42
Fig. 34a, b. Thin-foldad
mesothelium from the lace-
like omental portion in
transmission electron mi-
croscopy (TEM, a) The
mesothelial cell nucleus (N)
is long and indented. Note
the numerous micropinocy-
totic vesicles (arrowed), the
desmosomes which bind
adjoining mesothelial cells
(D), and the microvilli
(Mv). F, fibroblast. Some
collagen lies between the
mesothelial cells
( x 15,000). Immediately
below them is, in a few
places, an indefinite base-
ment membrane. This is
shown in b (Bm), which is a a
detail from a. (Courtesy
of CARR [14], Saskatoon,
Canada)

\Mv

and a few reticular cells [27]. The mesothelial cells are plate-like
and thin and are joined by desmosomes; the cytoplasm is very
tenuous, having a depth of only 20-40 Ilm in places [14, 27,
28]. In some places the body of a single cell constitutes the
entire width of the tissue, and the same mesothelial cell takes
part in the formation of both sides of the omentum, bridging
over from one side to the other (Fig. 35, [14]). The only other
cells to be seen are a few scattered macrophages within the
collagen layer or sticking to the mesothelial surface. Due to
the presence of such a cell lying within the tissue or the presence
of a mesothelial cell nucleus, the whole tissue ranges between
only 0.1 Ilm [39] and 6 Ilm [28] in thickness. Along both surfaces

43
Fig. 35. The TEM section
through the omentum
shows the way in which
one mesothelial cell may
bridge across from one side
of the omentum to the
other. The nucleus is nar-
rowed at the point
arrowed, where it extends
into the area of tenous cy-
toplasm. D, desmosomes
(CARR [14]), x 10,000
Milky Spot Area
Gaps in the Omental
Mesothelium
44
of the cell are vesicles and microvilli extending into the abdomi-
nal cavity ([14, 39] Fig. 33, 39, Sect. 4.5.).
MADISON et al. [59] found that the density of microvilli on the
surface of cultured omental mesothelial cells can be greatly
altered by various stimuli. Increase and decrease of its surface
potential thus provides the cell with an effective regulating func-
tion. Studies by FEDORKO and HIRSCH [27] have shown that
certain macromolecules and small particles are transported by
vesicles across the mesothelial cells of the omentum.
Mesothelial cells in the area of the milky spot differ morphologi-
cally from those in other omental regions because they have
less and smaller microvilli [59] and almost no basement mem-
brane [14, 39].
VON RECKLINGHAUSEN in 1862 and 1863 [78, 79] described
"organic pores" in the diaphragmatic peritoneum, but I found
no indication in his publications that he also exmained omental
mesothelium or termed the pores" stomata," as is often quoted.
That there is a discontinuity in the mesothelial layer above the
omental milky spots has been described by MUSCATELLO 1895
[70] and MAXIMOW 1927 [64]. This observation has been sup-
ported by recent work (Fig. 39 [6, 14, 28, 39, 68, 73]). Circular
openings were found, leaving spaces of 1 ~m up to 10 ~m diame-
Fig. 36a, b. Scanning elec-
tron microscopic (SEM)
study of the rat omentum.
a Low-power view of inter-
cellular gaps between me-
sothelial cells covering
omental milky spots. Con-
nective tissue fibers are rec-
ognizable under the gap
labeled with a double
arrow. Smaller intercellular
gaps are also seen, and one
of them is labeled with a
single arrow. x 1,900
b High-power view of two
gaps. A lymphocyte is
passing through the right
gap, and connective tissue
fibers and an unidentifiable
cell are present under the
left gap. (MIRONOV [68])
x 9,500

ter between the mesothelial cells [6, 68, 73]. These spaces
(Fig. 36) lead down into the center of the milky spot [6]; they
were termed differently by the various examiners as: gaps,
crypts, stoma, or stomata.
The lack of surface mesothelium and the deep gaps expose the
underlying vessels and the cells of the milky spots to the surface
(Figs. 37, 39). Milky spot macrophages, lymphocytes, and the
other cells, therefore, have easy and ready access to the peritone-
al cavity and are found to emigrate and re-enter the milky spot
[7, 39, 73].

45
Fig. 37. Survey TEM
picture of the surface of a
milky spot, showing an en-
trance to a crypt (arrowed).
Cells marked M a are mac-
rophages in the depths of
the milky spot. C, covering
cells of superficial macro-
phages; L, lymphocytes.
(CARR [14]) x 6,000

4.5 Milky Spots (Lymphoreticular Organ)

D. LIEBERMANN-MEFFERT, H. WHITE, and A. LIEBERMANN

Introduction In 1874 RANVIER [77] observed opaque spots in the omentum

of rabbits which he called taches laiteuses. He ascribed their
arteriovenous picture and the resemblance of the cells found
in these structures (Fig. 38) to those known in lymph nodes.
RANVIER [77], therefore, assigned the nodules to the lymphatic
system. He thought that the omentum had the function of a
"vaste [huge] ganglion lymphatic" and that the peritoneal cavi-
ty was the "lymphatic sinus." This view has long been accepted
[29, 30, 70, 80). Although MILIAN [67] had already recorded
numerous phagocytic elements in the spots, it was SEIFERT in
1920 [88] who first distinguished milky spots from lymph nodes,
assigning them to the RES (Table 2).
CARR [14] correctly proposed calling the spot" lymphoreticular
organ." Recently it has been shown that these structures play
an important role in fluid exchange (see Sect. 5.7) and defence
mechanisms (Sect. 5.9).

Table 2. Their anatomical differences are as follows

Structure Lymph node Milky spot

Sinus architecture +
Germ center +
Glomus-like capillary system +
Capsule +

46
Fig. 38. Milky spots from
RANVIER'S publication in
1874 [77]

Fig. 39. Semischematical

diagram illustrating the
structures and cellular
composition of an acti-
vated milky spot. Struc-
tures and cells are out of
scale. The actual diameters
are given at the top left
and in Figs. 39, 51. The
terminal lymphatics within
the spot and its character-
istic vascular system (see
Sect. 5.7) with arteriove-
Fig. 38
nous communications
(which are patent in the
normal steady state while
Vessel ~ = 25 fUT1
the glomus-like arterial net Cell - - - - - < I '" 25fW1
is collapsed) and fenestrae
in the capillary wall are
Meso hellol cell---+
shown in Fig. 51. The fen-
estrae (endothelial pores)
are also greatly out of scale Arten a Ie ----f-.+HI----1iif-
in the diagram Fig. 51 be-
cause they are actually Venule
500-800 A in diameter.
Within the spot and on its
surface (Figs. 41, 42) Iym- -m-A:H-.f.::-- FI bro bios
phoreticular cells are
crowded, being in close
contact with the vessels
and lymphatics. "Gaps" in
the mesothelium Termmal
-H-,,",*-- Iymphohc
allow a free communica-
tion between the milky
spot constituents and the
peritoneal cavity. Stimula-
tion mobilizes tissue fixed
macrophages; they trans-
form into migrating cell el-
ements which obtain mi- -'¥-<>'1-- Fat cell
crovilli. These, as shown in
the figure (Mv), appear
first on the cell surface to-
ward the peritoneal cavity.
Both tissue-fixed and free
macrophages engulf parti-
culate matter and act as
phagocytes ig.39

47
Morphological Milky spots are provided with (Fig. 39):
Definition Permanent glomus-like pattern of vascular structures
A specific cellular population
A specialized mesothelial surface
Mesothelial cells and reticulum cells form the stroma of the
spot. These cells can be morphologically distinguished by their
cellular constituents [7, 14]. The cellular composition is found
to change with the age of the individual and the intra-abdominal
condition [7, 39, 88]. The morphological characteristics of these
structures in the human do not differ essentially from those
in laboratory animals [8, 14, 25, 28, 50, 60, 63, 64, 88].

Functional Definition Milky spots are organs specialized for defense against damaging
foreign bodies: Because of their specific cellular content the
milky spots are said to be the immediate source of free macro-
phages of the peritoneal cavity [6, 14,28,68], which are involved
m:
Phagocytosis of foreign material
Selective storage of many agents: dyes, particulate matter, and
bacteria
Production of antibodies
These functions make the omentum responsible for the surface
cleanliness of the abdominal cavity [31,34,97].

Location The milky spots occur throughout the greater omentum on both
surfaces of the free apron and in the gastrocolic ligament; the
spots are concentrated mostly along the omental vessels and
at points of division of arterioles and venules [8]. They lie at
the periphery of loose connective tissue and directly beneath
the peritoneum [2, 14, 28, 39, 50).

Identification The ovoid-, round- or irregular-shaped opaque spots are readily

visible in the omentum of fetuses and the newborn. They are
yellow-white in color; in adults the large fat deposits make them
difficult to distinguish. SEIFERT [88] observed milky spots in
the thin connective tissue meshes, with an appearance similar
to that of small fatty nodules. Milky spots are shown in Fig. 8.

Dimensions Their size has a wide individual range between macroscopical

and microscopical dimensions. Milky spots are recorded to be
larger in man, ranging between 3.5 and 0.5 mm 2 [8], than in
animals, where they range from 3 mm 2 to less than 100 11m2
[28, 77].

Incidence and The omentum of all species contains numerous milky spots [8,
Characteristics 39, 50, 77, 88]; they appear and disappear with different abdom-

48
Fig. 40. Life cycle of a fetal + neonatal adult
milky spot (for further
details see text) inactive irritation repair active

Primary Fatty • Secondary

milky spot organ .. milky spot

r""""F-jb-r-os-j-s"'1 ~
inal conditions [7, 14, 40, 51, 63]), and their number varies
between individuals. Milky spots, characterized by the typical
glomus-like vascularized structures, develop in the middle of
intrauterine life [8]. Related to their cellular population three
different types of spots have been distinguished ([88], Fig. 40):

Primary Milky Spots. These only occur in fetuses and infants

[50, 75, 88]. They contain crowded undifferentiated mesenchy-
mal cells, a few fibroblasts with long branching intercellular
processes, and almost no fat cells [8, 75, 88].

Inactive Milky Spots. In the sixth prenatal month the number

of mesenchymal elements in the spots decreases, being progres-
sively replaced by fat cells [63, 89]. This transforms the spot
into a fatty organ, preserving its vascular net and a few mesen-
chymal cells. The fat cells possibly carry a potential for cellular
proliferation and may transform into active macrophages [14,
50, 63, 88].

Active Secondary Milky Spots. Any intra-abdominal irritation

~ mechanical injury, chemical agents, particulate matter, or mi-
croorganisms ~ causes the involution of the organs and reverts
them to active" secondary" milky spots [88]. The spot increases
in size [7, 88, 97], fat disappears, and numerous phagocytic
elements appear [31]. Certainly active milky spots are present
also in the normal steady state (Figs. 41 a, b, 42).

The transformation from the inactive to the active milky spot

is gradual and all stages may be observed in the same omental
area [89]. The change into an active spot is reversible. Repeated
stimulation and transformation (Fig. 40) finally lead to calcifica-
tion of the milky spots, fibrosis, degeneration of their ca pillaries,
and involution, which seems to be more common in old age
[30].

49
Fig. 41 a-c. a Ultrathin
section of a milky spot of
mouse omentum (normal
steady state) showing a
framework of reticulum
cells (R), lining mesothelial
cells (Me), and capillary
endothelial cells (En) popu-
lated with lymphocytes (L)
and macro phages (Ma).
Blood vessels (Bv) and ca-
pillaries (C) run through
the milky spot. (BEELEN
[6]). b Milky spot of a rat
omentum (normal steady
state) showing a cluster of
plasma cells (Pc). (BEELEN,
[6]).

a
1,0 JJ fT1

50
Fig.41c A portion of a
milky spot in the rat
omentum after induction
of acute inflammation with
NBCS, showing three dif-
ferent PA patterns in three
types of macrophages. 1,
Resident macrophage with
reaction product in nuclear
envelope (N£) and in
RER; 2 Exudate resident
macrophage with reaction
product in the nuclear en-
velope (N£) and in the
RER and in the lysosomal
granules (G); 3 Exudate
macrophage with reaction
product only in the lysoso-
mal granules (G). (BEELEN
et al. [7]) x 3,500

Fig. 42a-d. Surface topog-

raphy of a milky spot in
scanning electron micro-
graphs. Many macrophages
(Ma) , lymphocytes (L), and
mast cells are found a on
the surface of the milky
spot and d in mesothelial
gaps [6,14, 73, 98]. Macro-
phages in this location
show a great variation in
shape between rounded
and extremely flattened
cells (a and c). Lympho-
cytes have a wide range in
shape and density of
microvilli (b and d) .
Macrophages and
lymphocytes may be
clustered together band
processes can be seen
which may come into such
intimate contact with each
other that the junction is
barely visible or
interdigitate. a x 1,584;
b x 3,420; c x 3,780;
d x 9,225 (ORENSTEIN and
SHEL TON [73])

51
Fig. 43. Mesenchymal cell.
1, cell processes; 2, mito-
chondria; 3, granular
endoplasmic reticulum;
4, Golgi apparatus;
5, nucleus. [48]
Cellular Constituents
of an Active Milky
Spot
The Cells of the
Milky Spot
52
The active milky spot contains numerous lymphoreticular ele-
ments which are located within the spot and on its surface
(Figs. 39, 41 a, b, 42a, b). The most numerous cells are macro-
phages and lymphocytes. Less frequent are dentritic macro-
phages and plasma cells. Many periadventitial cells are also seen
close to the capillaries; occasional undifferentiated mesenchymal
cells, fibroblasts, and other cellular elements are present [14,
28,39,98,99). Neutrophils occur only under pathological condi-
tions such as inflammatory response following migration from
the blood vessels [89].
General Organization of Cells (TEM Image)
All cells have basic similarities:
A Limiting Plasma Membrane. The membrane may bear micro-
villi. These are slender processes on cells which are endowed
with absorptive function, such as on mesothelial cells. Fluid,
molecules, and other substances are taken up and transported
in pinocytotic vesicles (see Sect. 5.7).
Fig. 44. Macrophage. 1, 2,
lysosomes; 3, 4, phagocytic
vacuoles ; 5, microvilli;
6, round-shaped processes;
7, cytoplasmic folds;
8, pinocytic vesicles.
x 10,000 [48]

Cell Organelles Embedded in the Cytoplasm. Cell organelles are

the endoplasmic reticulum, Golgi apparatus, ribosomes, and mi-
tochondria. These are involved, for example, in peptide and
protein synthesis, concentration of substances, storage, and
transport.

Occasional Inclusions. Inclusions are secretory granules, lipid

droplets, and granules.
These structures are illustrated in Figs. 43 and 44. For details
see LENTZ [52] and KRSTIC [48].

Cell Types Found in Milky Spots (Fig. 39). The cells of the milky
spot differ in shape but also in type, number, and organization
of the organelles, which is the basis for the identification of
the various cell types in the spot:

1. Fibroblasts and Fibrocytes. These are fixed cells in the loose

areolar connective tissue and are described and shown in
Fig. 39.

2. Reticular Cells. These cells are fixed tissue cells which may
transform into macrophages under certain circumstances
(for details see [14, 92]).

53
 3. Mesenchymal Cells. These are relatively fixed immature and
very active elements in the connective tissue and in the milky
spot. They are connected to each other by many processes
and contain a small number of organelles and mitochondria,
a granular endoplasmic reticulum, and a Golgi apparatus.
Mesenchymal cells may leave the cell group to serve as the
origin for other tissues or organs (Fig. 43 [48]).

4. Histiocytes (Macrophages). Histiocytes are fixed tissue cells

but may become motile and phagocytic. They are 10-20 !lm
in diameter and take up particulate matter and fluid. On
their surface they carry many irregular microvilli and round-
shaped processes. Lysosomes, phagocytic vacuoles, cyto-
plasmic folds, and numerous pinocytotic vesicles are present
(Fig. 44, [48]).

5. Lymphocytes. These are migrating cells in the loose connec-

tive tissue and are very frequent in the milky spot. They
range between 5 and 9 !lm in diameter and are the smallest
cells of the spot. The two types of lymphocytes, T - and
B-Iymphocytes, cannot be distinguished morphologically.
Under certain conditions B cells are found to transform
into antibody-producing plasma cells [34].

6. Plasma Cells. The chromatin of these cells is so arranged

that it gives a cartwheel appearance to the nucleus. The
cell has an extensive rough surface endoplasmic reticulum
which synthesizes antibody (immunoglobulins) and trans-
ports it to the Golgi complex, from where it migrates in
large vesicles to the cell surface in a process of reverse pino-
cytosis [34].

7. Mast Cells. These migrate in the loose connective tissue

of the mesentery and omentum, and their greatest concen-
tration per unit area has been found in the omental milky
spots [98, 99]. They are up to 20 !lm in diameter and contain
numerous granules. A few microvilli, folds, and in vagina-
tions are found on their surface. Mast cells playa role in
regulating the lipid metabolism.

8. Eosinophilic Leukocytes. Eosinophils may migrate in the tis-

sues or settle in the milky spot. They have a diameter of
about 12 !lm, a few villi or pseudopodia on their surface,
and many membrane-bound granules. Eosinophils become
more numerous in allergic conditions and have been shown
to phagocytose antigen-antibody complexes.

54
 9. Polymorphonuclear Leukocytes. These are active cells in the
early stage of inflammation and are found on the mesotheli-
um in the region of the milky spot after having migrated
through the capillary walls. They play an important role
in the defense of the body by removing foreign substances.
From actively migrating cells protrude pseudopodia (cyto-
plasmic extensions), which contain a few glycogen granules
but almost no organelles.

10. White Adipose Tissue. Fat cells are large and spherical.
Mature cells have a large central lipid droplet surrounded
by a thin peripheral rim of cytoplasm, which gives the cell
its signet-ring appearance. The nucleus is compressed to a
crescent shape and has a peripheral position. Mitochondria
having a dense matrix, cristae extending across the organ-
elles, a few short cisternae of rough-surfaced endoplasmic
reticulum, an inconspicuous Golgi apparatus, and some free
ribosomes are present; pinocytotic invaginations are
common at the cell surface.
Fat tissue is a very active tissue; assimilation and mobiliza-
tion of lipids is controlled by hormonal and nervous factors
[52]. According to HODEL [39] the fat cells of the tiny
omental fat pads are filled with one single fat droplet, which
reaches diameters of 100 /-lm in well-fed animals, while in
starved animals many of these cells are depleted of fat, with
large reductions of the size of the fat droplet, and with
a different state of cytoplasmatic action.

Concept of Activation Cellular Response Intra-abdominal stimulation by foreign bodies

of Milky Spots leads to an acute inflammatory response [2, 32]. This occurs
with:
Increase of cells in the milky spots and mobilization of histio-
cytes [6].
Decrease of fat cells; this means retransformation of the" inac-
tive" fatty milky spot nodules into "active" secondary milky
spots [25, 88] and occurance of milky spots on the omental
surface.
Fixed mesenchymal cells mobilize from the enlarged milky spots
[2, 88], begin to migrate toward the surface of the omentum,
and are transformed into active phagocytes or macrophages [2].
These collect beneath the serosal surface and engulf the material
which enters through and between the mesothelial cells [2].
Loaded phagocytes return to the milky spots.
Some foreign material remains encapsulated in the milky spots
for ever [89]. Malignant cells and bacteria reaching the milky
spot may increase in number and change the spot into a mctasta-

55
 sis or - in the case of myobacteria - into a "tubercle" [88].
A small amount of particulate matter enters the omentum via
direct surface transmission [2, 59] during the first hour of in-
flammatory response; this has been shown by intraperitoneal-
deposited 239pUO particles [84].

Immune Response. Milky spots are by no means preformed

structures, but are extremely dynamic formations [7] which
come and go in the course of specific immune reaction and
provide an hypothesis linking cellular changes with response
of the immune system [31, 40]. This hypothesis should be re-
membered in the interpretation of the cellular changes in the
milky spots.
FISCHER and co-workers [31, 34, 40, 62] were able to show the
development of milky spots in different phases microcinemato-
graphically after intraperitoneal injection of foreign material.
With this technique, which was combined with methods of im-
munofluorescence and thymidine incorporation, FISCHER'S
group described antibody formation in the milky spots of mice.
Using horse-radish peroxidase as a tracer, HODEL [39] was able
to demonstrate that the foreign antigen migrated from the ab-
dominal cavity into the omental tissue through the wide gaps
overlying the milky spots or throught the larger mesothelial
junctions and became engulfed by dentritic macrophages.
MATTHES et al. [62] showed how the T- and B-Iymphocytes mi-
grated through the omental tissue toward the antigen-containing
macrophage at an increased velocity. The lymphocytes appeared
to recognize the foreign material at or on macrophages which
had already phagocytized. The lymphocytes then stopped their
migration and were transformed into immunoblasts. Those cells
in close contact with macrophages divided and appeared to dif-
ferentiate into antibody-secreting plasma cells 5 days after im-
munization [34]. FISCHER and co-workers [31, 34, 40, 62] found
that at that time the milky spots consisted mainly of specific
antibody-forming plasma cells. In the center of such plasma
cell accumulations dentritic macrophages were always present.
The maximal serum titers following antigen stimulation were
found by WALKER and ROGERS [97] to coincide exactly with
those on the 5th day, on which HAJDU et al. [34] observed the
greatest number of mature plasma cells.
Repeated immunization caused large confluent milky spots
which, as well as plasma cells and macrophages, contained a
marked number of mast cells. Both CARR [14, 15] and HOLUB
[40] postulated that omental mesenchymal cells are pluripoten-
tial, e.g., capable of differentiating in different directions pro-
vided that there is an appropriate stimulus.

56
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61
Physiology and Functions

5 Distinctive Peculiarities of Omental Tissue

M. DURIG and A. LIEBERMANN

The function of the omentum has long been the subject of much
speculation. This is reported in the historical section (Sect. 10.2).
Detailed investigation in more recent years has shown that under
pathological conditions [33] the omentum is endowed with very
distinct capacities.
These are:
Plasticity
Adhesive and cohesive properties to traumatized and inflamed
surfaces
Hemostasis
Capillary ingrowth and neovascularization
Absorption of fluid and molecular substances from the peritone-
al cavity
Phagocytosis of particulate matter and foreign body reaction
All procedures which use the greater omentum for plastic or
reconstructive surgery depend on these basic capabilities.

5.1 Movement
H. WHITE and A. LIEBERMANN

The omentum has been known since classical times to be impor-

tant in combating abdominal infection and has been observed
to be associated with and even wall off sites of intraperitoneal
sepsis. Active migration to these areas was postulated by CORNIL
and CARNOT [26] and MILIAN [86]. Although HEUSNER [59]
spoke out strongly against active migration, the theory persisted
[14, 112, 114]. MORISON [87] used the term" abdominal police-
man, " which caught the imagination and perpetuated the theory
of an active role. However, experiments established beyond
doubt that the movements of the omentum were passive and
resulted from movements of the animal, bowel, and diaphragm
[2, 32, 43, 44, 112, 113, 133]. The ingenious theory of SCHUTZ
[116] that straightening and distention of hyperemic vessels in
the omentum alters its shape and distribution within the peri to-

63
 neal cavity and the theory of positive chemotaxis had to be
discussed in the light of a more scientific approach with metal
markers [2] and direct observations through abdominal
windows [44].

5.2 Adhesiveness and Cohesiveness

A. LIEBERMANN and M. DURIG

Etiological Factors Adhesions develop after [35, 89]

1. Mechanical trauma to serosal surfaces such as rubbing with
gauze or thermal injury by hot laparotomy packs
2. Tissue ischemia
Traumatic organ injury causes vascular lesions, leading to
tissue anoxia and venous obstruction [9, 35]
Ischemia is considered to be a potent stimulus for the devel-
opment of adhesions
Reperitonealization of peritoneal defects causes tissue tension
and ischemia, favoring adhesion formation [35]
3. Foreign material of various kinds including: glove powder,
gauze lint and tampons, suture material, some drugs and
substances used intraoperatively, and absorbable hemostatics
4. Intra-abdominal infections
5. Motility of intestines
Reduced or suppressed peristalsis of the gut lengthens the
time of omental contact with the other organs; this favors
the development of adhesions

Pathology Mechanical injury to serosal membranes causes an immediate

exudation of albumin, globulin, and fibrinogen. The raw surface
activates fibrinogen to become fibrin, and a fibrinous network
develops within 10 min, and is fully developed after 2 h [89,
90]. After 3 h the injured surface adheres to the adjacent tissue
[14, 35, 46, 114]. The exudative phase is followed by organiza-
tion of the fibrinous adhesions and ingrowth of capillaries and
fibroblasts (Table 7, Sect. 8.1)).
WJERESZINSKI'S [142] studies showed that omental adhesions de-
velop much more rapidly than adhesions between other abdomi-
nal viscera. Even detached from the blood supply and freely
transferred, omental tissue retains this characteristic. After
4 days new blood vessels have already developed their own en-
dothelium. At this time the fat content of the fatty cells has
disappeared, and there is an increase of fibrous and angioplastic
elements. After 21 days the free transplant is completely con-
nected with the recipient organ [82, 127]. In contrast to the

64
adhesions formed by intact omental tissue, free omental grafts
detached from their circulation will shrink.

5.3 Hemostasis
M. DURIG

The omentum appears to have the ability of reducing hemor-

rhage from injuries, for example, to the liver and spleen. It
has been shown that though the hemorrhage was profuse and
beyond control by pressure, application of the omentum caused
almost immediate hemostasis [12, 14, 16, 46, 58, 80, 123, 127].
Omental extracts have the same hemostatic effect, as shown
in experiments [29]. This may be due to the ability of the
omentum to accelerate prothrombin activation and the rapid
change from fibrinogen to fibrin found in the presence of
omental tissue.

5.4 Ability to Encapsulate

M. DURIG and A. LIEBERMANN

Experiments of DE RENZI and BOERI [107] showed that the

omentum was able to encapsulate infarcted organs. This was
demonstrated with the spleen of dogs deprived of their blood
supply. After 10 days the whole organ was surrounded by
omentum showing capillary ingrowth. Two and a half months
later the splenic tissue had changed into a fibrous mass, without
effecting the viability of the animals. Animals, however, in which
the omentum had been resected before the ligature of the splenic
vessels died from toxemia.
PIRONE (cited by RUBIN [114]) and WILKIE [140] reproduced
these findings in rabbits and also showed histologically that
polymorphonuclear leukocytes and mesothelial cells from the
omentum entered the infarcted organ. This proliferation paral-
leled the ingrowth of capillaries and finally caused complete
transformation of the splenic tissue into scar tissue. The same
has been observed with foreign organs [107, 114].

5.5 Capillary Ingrowth

A. LIEBERMANN and H. WHITE

The vascular connection between the omentum and damaged

liver was investigated by BOLJARSKI [12] in rabbits, dogs, and
cats. A firm adhesion formation developed between the

65
 omentum and underlying tissue between 14 and 24 h later and
capillary ingrowth after 3 or 4 days. Similar connections were
demonstrated in a number of tissues including pleura, bronchus,
and esophagus by THOMPSON et al. [127] and later in the wall
of the stomach and ileum by M YLLARNIEMI [90].
The same process has been observed in devascularized kidneys
[99]. After splitting the kidneys the parenchymal surface was
covered with omentum and the whole organ also wrapped in
omentum. Two months later the renal artery was divided and
the kidney on the opposite side removed. The animals survived,
and at autopsy there was a good blood supply to the remaining
kidney through the omental vessels. Years later, in a similar
study, ELISKA [34] confirmed an arterial supply by the omentum
after decapsulation of kidney in order to exclude collaterals.
The potential of the omentum to form vascular adhesions has
also been shown with ischemic myocardium and brain (see
Sect. 8 [20, 75]).
Even when deprived of its blood supply and transferred as a
free graft the omentum maintains an angiogenic property. This
has been demonstrated in the anterior chamber of the eye in
the rabbit [130]. However, many tissues are known to have
this property, which is not specific to the omentum but probably
results from a diffusable angiogenic factor released from
ischemic tissue.
Vessels from free omental grafts have been shown to penetrate
the wall of the aorta, in addition to the heart and pericardium
[129, 131]. However, the clinical benefit of these connections
must be questioned [101], for the free graft by stimulating the
outgrowth of capillaries from heart muscle would, at least ini-
tially, reduce the available myocardial circulation.

5.6 Absorption from the Peritoneal Cavity

A. LIEBERMANN, M. DURIG, and H. WHITE
The absorption of fluid, dissolved particulate matter, and molec-
ular substances from the peritoneal cavity takes place rapidly
and effectively. This has been examined by many investigators,
who confirmed RECKLINGHAUSEN'S [106] observation that fluid
was mainly absorbed by the lymphatics in the serosa of the
tendinuous diaphragm [21, 28, 121].
That the omentum was involved in the absorption from the
abdominal cavity was first observed by MAFFUCCI in 1882 (cited
in [88]). In 1895 MUSCATELLO [88] found that some indigo
carmine injected into the peritoneal cavity of rabbits and dogs
was taken up by the omentum via" lymphatics. " This was later
confirmed by CUNNINGHAM [28] and BAILLIF [7].

66
 WILKIE [140] found that resection of the omentum reduced ab-
sorption of both particulate matter and fluid. He was able to
quantitate the reduction in the absorption of saline solutions
injected into the peritoneal cavity. After resection of the
omentum in cats the amount absorbed fell by one-third. The
ability to absorb particulate material was demonstrated by ex-
periments undertaken in cats by WALKER [133]. After injection
of charcoal powder into the peritoneal cavity he found that
it was "spotlessly" clean by 48 h and the material could be
identified in the omentum.
Absorption via lymphatics, however, when compared with the
absorption via omental blood vessels in experimental animals
was low (Sect. 8.3). If these results can be extrapolated to man,
omental transposition for lymphedema is unlikely to be of great
benefit despite the fact that lymphatic anastomoses can be de-
monstrated (see Sect. 8.3).

5.7 Capillary Fluid Exchange in the Omentum:

Physiology and Pathophysiology
B. ENDRICH, F. HAMMERSEN, and K. MESSMER

Introduction Since the greater omentum appears to be one of the essential

areas of fluid exchange in the abdominal cavity, it seems neces-
sary to review today's understanding of microcirculatory anato-
my, hemodynamics, and fluid exchange of the omentum.
In laboratory animals, large areas of the omentum consist of
thin translucent tissue with a redundant microcirculatory sys-
tem. Due to this unique feature - tissue transparency and vascu-
lar redundancy - the omentum of the dog, cat, rabbit, and rat
has widely been used as an experimental model, particularly
for studies of the terminal vascular bed. In fact, for more than
4 decades, this structure has served and still serves as one of
the "classical" models in microvascular research [37, 67, 100,
109, 125,144-147].

Techniques of Prepara- After anesthesia, the omentum is exteriorized through a small

tion and Observation midline abdominal incision just below the sternum, whereafter
the animal is placed on its side. The omentum is draped over
a small, heated platform of the microscope stage and the edges
of the omental tissue are held down by small wedges of moist-
ened cotton [144, 146].
Special care should be taken:
1. To irrigate the tissue continuously with Ringer's (or any other
isotonic) solution

67
Fig. 45. Characteristic rep-
resentation of the venous
side of the microcirculation
in the rabbit omentum. A
collecting venule (II) is seen
at the right margin. x 210.
(ENDRICH)

2. Not to stretch or compress the preparation

3. To ensure a constant, physiological temperature of the ani-
mal as well that of the irrigation fluid
4. To adjust the temperature of the heated platform to the given
temperature
With these precautions, omental blood flow becomes stable in
less than 5-10 min upon completing the preparation, with little
changes during the first 2 h of exposure [67, 146, 147]. If the
upper layer of the omentum is removed using microsurgical
instruments, resolution and microscopic image can be improved;
the preparation might last longer because of the lower light
intensity necessary for transillumination (Fig. 45). To define the
adequacy of the preparation, the following criteria are used:
No sticking of leukocytes in collecting venules
No capillary or venular stasis
No petechial bleeding (Fig. 46a, b) [143, 145, 147]
As a "functional" test, the response of arterioles to topically
applied epinephrine has been suggested [138]. Other criteria of
microvascular integrity can be established by comparison of rel-
ative sizes of arterioles and venules (relation of diameters = 1 : 3),
rapidity of blood flow, and intermittent circulation through ca-
pillaries [138, 143].
Since the versatility of intravital microscopy has been greatly
augmented by adaptation of closed circuit television to micro-
vascular research [64, 66] (for further details see [68]), ZWEIFACH
et al. [67, 68, 109, 125, 146, 147] provided precise diameter,
red blood cell velocity, and pressure maps of the visceral micro-
circulation of mammals.

68
Fig. 46a, b. A preparation
of the rabbit omentum
considered to be inade-
quate for microvascular
studies. Such a preparation
is characterized by adher-
ence and sticking of leuko-
cytes to the vascular en-
dothelium and by extrava-
sation of blood cells pri-
marily at branching points.
x 160. (END RICH)
Structure
and Function of the
Microvasculature
, .
a ~ • b
Microvascular Arrangement and Anatomy of the Omentum
The microvascular beds of the omentum consist of rather large,
abundant networks (Fig. 47, see Sect. 4 anatomy). In general,
a 80- to 100-)lm feeding artery traverses the omentum accompa-
nied by one or two muscular venules with diameters almost
double that of the feeding artery. These feeding arteries branch
continuously until vessels of 25-30 )lm in diameter are formed.
They provide inflow vessels to a network of true capillaries,
which in the rabbit omentum may consist of as many as
50-100 individual capillaries [67,146]. The terms used to classify
the microvascular bed are: artery, arteriole, precapillary, capil-
lary, postcapillary, and collecting venule [143, 145].
Arterioles refer to 20- to 40-)lm vessels coated by a single layer
of smooth muscle cells. By contrast, small arteries reveal a
thicker wall (approximately 10 )lm) and are wider (50-100 )lm).
The branching arterioles give off long ramifications of almost
capillary dimension defined as "terminal arterioles" because
they represent the last 200-300)lm of these vessels. Further-
more, the term "precapillary" refers to those muscular vessels
from which the majority of capillaries originates [145]. The latter
represent simple endothelial tubes covered by a basal lamina
(basement membrane) on their exterior surface and encircled
by processes of pericytes [53, 96].
The venous circulation begins where capillaries join each other
to form larger, confluent vessels. These wider capillaries
(10-15 )lm, postcapillaries) empty into thicker-walled, collecting
69
Fig. 47. The microvascular
bed of the rabbit
omentum. Small vessels are
usually embedded in vary-
ing amounts of fat cells. A
network of true capillaries
can be seen in the middle
of the picture. x 80 approx
(courtesy of Prof. B.W.
ZWEIFACH)

nonmuscular venules which interconnect to form 40- to 60-llm

muscular venules [143, 145]. Vessel diameters, vessel length, and
vascular centerline blood cell velocities are summarized in Ta-
ble 2. Microvascular pressure measurements have also been per-
formed by mea ns of tiny micropipettes (1- to 2-llm tips) and
by the electrical servo-nulling device [139]. Such pressures can
be recorded continously for up to 60 min in vessels of down
to 7 11m in diameter [68, 145].
As a result, today's classification of microcirculatory channels
within the omentum is based not only on microscopic observa-
tions and qualitative descriptions but on quantitative data based
on ZWEIFACH'S pioneering work.

Lymphatic While structural and functional changes of arterioles, capillaries,

Microcirculation and collecting venules were already well known, for a long time
very little information on the terminal or initial lymphatics was
available [18].

Structure of the Terminal Lymphatics. If lymphatic capillaries

of the splanchnic viscera are filled directly with dye-colored solu-
tion from micropipettes [148] (Fig. 48), they appear to originate
in two ways :
1. As blind endothelial sacculations about 40- 60 11m wide
(Fig. 32)
2. As a network of endothelial channels 20-30 11m in diameter
[18, 78, 148]

70
Fig. 48. Visualization of
lymphatic endothelial sac-
culations after injection of
dye. These blind endings
were seen within a milky
spot of the rabbit
omentum. x 200 approx
(courtesy of Prof. B.W.
ZWEIFACH [148])

At the level of light microscopy, the endothelial wall is extremely

thin with no obvious discontinuities [148]. The terminal lym-
phatics are lined with endothelium occasionally supported by
traces of basement membrane-like material. By confluence of
several terminal lymphatics, effluent-collecting lymphatics are
formed, which have relatively thick walls (2-3 /lm) and charac-
teristic irregularly spaced valves [148]. These channels become
progressively lined with other elements such as connective tissue
fibers and smooth muscle cells [13, 148]. Electron microscopy
has revealed distinguishing features between these and blood
capillaries. They are represented by the wider, irregular lumina
of terminal lymphatics, the absence of a continuous basal
lamina, the occurrence of occasionally open endothelial junc-
tions, and the presence of fine" anchoring filaments' apparently
attached to the abluminal lymphatic endothelial plasmalemma.
These filaments (diameter 4-11 nm), morphologically similar to
micro fibrils (see Figs. 25, 39) extend throughout the adjoining
interstitium between the collagen bundles in which they are
firmly embedded [18, 78].
This structural interrelationship between the lymphatic endothe-
lium and the surrounding connective tissue provides a means
of keeping the lumen of the lymphatic capillaries open and of
connecting the lymphatics firmly to the surrounding tissue. An
increase of interstitial fluid with a consecutive separation of
collagen and elastic fibers to accommodate this increased fluid
volume will produce tension on the collagen bundles which,

71
 in addition, will also pull along the anchoring filaments. This
mechanism causes both widening of the lymphatic lumina and
production of open interendothelial junctions by separating
loosely overlapping endothelial cells. The latter process may
be facilitated by the incompleteness of the basal lamina, and
will finally provide oneway open passages for fluid and particu-
late matter from the interstitium into the initial lymphatics, with
the endothelial cells operating like a "swing valve" [78].
It should, however, be emphasized that the majority of the initial
lymphatics do not contain any fluid over a prolonged period
of time and, therefore, they exist in a collapsed state which
renders these vessels almost indiscernible from their surround-
ings. The pressure required to open these channels, however,
is low.

Function of the Lymphatic Microcirculation

Pressure Measurements. Using sharp micro pipettes, ZWEIFACH

and PRATHER [148] were able to puncture terminal lymphatics,
and to measure simultaneously pressures in these channels and
adjacent precapillaries and venules in the mesentery and
omentum. The pressures in the terminal lymphatics varied from
0.6 to 2.5 cm H 2 0 [148] (Fig. 49), and the values fluctuated
in the range of 3-4 cm H 2 0 over a period of 15 min. With
an increase of only 3-4 cm H 2 0, fluid began to move from
the terminal lymphatic as long as a pressure gradient existed
[148].
Additional experiments with two micropipettes placed in an up-
stream and downstream direction of vessels showed that pres-
sure differences of 1.0 cm H 2 0 were sufficiently high to open
and close the valves (Fig. 50). Larger lymphatic vessels of the
mesentery (150-300/Jm) undergo spontaneous contractions
every 2-6 s. Species differences might exist because lymphatic
vasomotion has not been observed in the mesentery of cats and
rabbits but was reported in guinea pigs, rats, and mice [148].
Spontaneous contractions were shown to induce variations of
lymph pressure from -0.5 to 12 cm H 2 0. This phenomenon
might reflect a myogenic behavior because the change in vascu-
lar diameter was preceded by the slow increase in pressure. Sub-
sequently, the vessel wall contracted and the luminal pressure
increased further within a very few seconds by 2-3 cm H 2 0
[148].
As soon as the downstream valves are open, a steep fall of
pressure occurs. Respiratory cycles and peristaltic movement
of the intestine will change lymphatic pressure and aid in build-

72
Fig. 49. Representative
tracings of pressures in the
terminal lymphatic net- seconds
work. This map was recon- , i i , I I

structed from several rats

mesentery preparations be-
cause the entire network is 10
rarely seen in one prepara- ~ ------ -----
tion. (ZWEIFACH and
o cmH 20
PC=2
PRATHER [148])

seconds
Iii ii i

f~fV\f\v
a cmH 20
-----------
, s~~O~dSi

~~~\i\j\ ----------
.... ....
........
...
,
to
.... ....

Valves
cmH:10 I
I
I
I
I
/
I
I
seconds I
~ J
J
I

~ ----------------
Collecting lymphatic
channel (200 fLm )

Fig. 50a, b. Valve leaflets

within a lymph vessel.
Note the difference in lu-
minal diameter between the
arteriole (left side), the
lymph vessel, and the
venule located to the right.
x 190 appro x (courtesy of
Prof. B.W. ZWEIFACH
[148])
a b

73
 ing up a pressure gradient sufficiently high for a slow movement
of lymphatic fluid.

Movement of Cells. It is, however, not only fluid that is moved

into the lymphatic system but also cells. Studying the rat mesen-
tery as an experimental model by means of intravital microsco-
py, TV monitoring, and subsequent electron microscopy, cellu-
lar components were identified in lymphatic vessels [108]. These
preparations, however, are subject to effects of exposure outside
the abdominal cavity as well as surgical microtrauma, resulting
in a varying degree of inflammatory reaction and vasodilatation.
Small particles, about 3 J.lm in diameter and cells, average size
5 J.lm, probably lymphocytes, were seen to proceed slowly to-
ward larger vessels with a velocity of about 1 J.lm/min, which
changed temporarily so that these corpuscles would move sever-
al microns within 10-15 s [108].
The omental lymphatics transport soluble material and particu-
late matter into the celiac lymph nodes. Fluids and substances
possibly adsorbed by proteins, such as metabolites or possibly
bacterial toxins [100], are carried away by this mechanism. The
data obtained so far indicate a remarkable similarity in morpho-
logical features and microcirculatory function of the omental
and the mesenteric lymphatic system between different animal
species and man.

Milky Spots

Prior to any discussion of capillary fluid exchange within the

omentum, the milky spots (taches laiteuses [104]) deserve a
separate description because their capillary network differs
quantitatively from the rest of the omentum, and it appears
to be more readily accessible to macromolecules because of the
discontinuous mesothelial cover (See Sect. 4.5).

Microvascular Pattern Studies in laboratory animals have demonstrated that the

of the Milky Spots pattern of milky spot vessel geometry in the omentum of dog
[8, 77], rabbit [67, 146, 147], cat [109], and rodents [68] is very
similar to man [39, 76]. It is composed of arterioles from which
parallel capillaries and capillary loops originate that merge into
venules (Fig. 51). In addition, the feeding arteriole is connected
via shorter AV communications to the venous system [13, 67,
77, 146]. This pattern allows distribution of blood flow as de-
manded; when the shunts are closed, the blood streams along
the capillaries of milky spots which are arranged in a glomus-like

74
Fig. 51. Semischematic rep-
resentation of the micro-
vascular module of a milky
spot. The blood capillaries
show close spatial interre-
lationships with terminal
(initial) lymphatics which
might facilitate the transfer
Feeding arteriole 25)1m - - - - - f l-I--lt<f-+
of blood cells into the lym-
Precapillary 20 I'm
phatic system
Capillary 6 - 13/1m
-t'dI--h-- Lymphatic vessel

Venule 24/1m

);~fL'ijrtttj~;p- Collecting
venules 13--30 Jim

capillaries

pattern. One precapillary feeds numerous capillaries; there

might be as many as 82 vessels when the milky spot is 0.43 mm 2 ,
and 220 vessels when it is 0.73 mm 2 [13, 67, 146, 147]. These
capillaries are closely adjacent to each other, have relatively
wide lumina and empty into one or several veins. The vascular
diameters within the milky spots were equal in the fixed speci-
mens of dogs [77] and in in vivo preparations of rabbits [146,
147].
When comparing the microvascular pattern of the milky spots
with those found in the thin parts both of human omental
meshes and the tissue close to arteries and arterioles, one finds
that these microvessels may also form glomus-like networks
which are due to the small fat lobules they enmesh [8] (Fig. 52).
Capillary pressures and flows were found to be pulsatile
throughout the microvasculature both in the milky spots and

75
Fig. 52. The microvascular
bed of the rat omentum
(dark -field transill umina-
tion). A complete mapping
of the glomus-like micro-
vascular networks can be
obtained by constructing a
photomontage [49, 51]. As
seen in the right lower and
upper edge, a precapillary
(P) is approaching the ter-
minal network while two
collecting venules (V),
located in the lower right
corner and the upper left
edge, are draining this mi-
crovascular module. Fibro-
sis (F) and an inactive
milky spot (MS) can be
seen in the middle of the
picture. The capillaries
have relatively wide
lumina. (Pictures taken
with the Wild Photomac-
roscope M400, Leitz,
Wetzlar, FRG)
x 140 approx

the rest of the rabbit omentum. Periodic fluctuations due to

the cardiac cycle were more pronounced at the arterial end of
the system; those due to respiration mainly appeared at the
venous side [68].
As a consequence, the function of the microvascular network
in milky spots might be considered identical when one looks
at the capillary alignment in other regions of the omentum.
In fact, quantitative studies of microcirculatory function in the
rabbit omentum strongly suggest that all vessels except for the
feeding arteriole and collecting venule represent vessels with a
potential exchange function [63, 68, 146, 147].

Morphology Electron microscopy of the omentum has revealed that its capil-
laries display numerous circular holes in their endothelia (fenes-
trae) which are bridged by a thin membrane (diaphragm)
(Fig. 53).
HODEL [60] demonstrated in rats and mice that parts of the
greater omentum are morphologically different from the mesen-
tery, because mesothelial gaps and fenestrated capillaries were
found in the milky spots facilitating exchange of fluid and parti-

76
Fig. 53. Semi schematic
drawing of a fenestrated
cappilary endothelium. The
capillary is surrounded by
the basement membrane
Fen, fenestrae. (LENTZ [79])

Fig. 54. Schematic repre- culate material between the blood stream, surrounding tissue,
sentation of the pathways and the peritoneal cavity. Moreover, it has been demonstrated
of transport across the cap-
illary endothelium: that probe molecules of different molecular sizes, e.g., horse-
1, transport by means of radish peroxidase and ferritin [22, 24, 71, 122], penetrate rapidly
small vesicles which are from the peritoneal cavity into the omental capillaries (Fig. 54).
generated by invagination In addition, the structural organization of the microvasculature
of and subsequent detach-
ment from the cell mem- within the milky spots suggests a facilitated direct transfer of
branes; 2, fusion of small lymphocyte-like cells or parts of them via endothelial gaps into
vesicles and formation of the circulation. This view is strongly substantiated by the fact
"channels"; 3, vesicular
transport of material into
an intercellular cleft by-
passing its occluding 1 2 3 4 5 6
macula (*); 4, free diffu-
7
sion; 5, interendothelial
transport pathway (" small
I
pore"); 6, combination of
4 and 5; 7, transport
through diaphragms of en-
dothelial fenestrae. (HAM-
MERSEN [52])

77
that excision of the omentum significantly retards the absorption
of particulate material in rodents [60, 114].
Macrophages and also mesothelial cells pick up a great amount
of debris (see Sects. 4, 5.8). The mesothelial cells overlying the
milky spot lack a basement membrane, appear contracted, and
form a discontinuous layer equipped with actually open as well
as "potentially" open junctions [40]. These mesothelial gaps
on top of milky spots indicate that the cells of the milky spots
are readily accessible for absorbed material from the peritoneal
cavity, which then is phagocytosed [60].
Since the intercellular gaps appear to be functional, i.e., tran-
sient structures, additional pathways must be available to trans-
port fluids and macromolecular substances from the peritoneal
cavity into the milky spots. When comparing mesothelial with
endothelial cells, a number of structural similarities suggest more
or less identical transport mechanisms through these cellular
linings. First of all, both types of cells originate from the same
source, i.e., the mesoderm, and both display a great number
of cytoplasmic vesicles which serve as a carrier system for fluids
and macromolecules [23, 40, 96]. In addition, the mesothelial
junctions appear to be less tightly sealed by intercellular adhe-
sive devices and in this respect they resemble those junctions
found at the venous segments of blood capillaries (for further
details see Sect. 4).
In summary, these morphological findings, in particular the ex-
istence of discontinuous mesothelial cells interspersed with mac-
rophages on the milky spot's surface [67, 104], are indicative
of specialized regions with regard to the movement of cellular
elements. The production of an exudate might be a mechanism
by which the omentum collects particulate matter to be phagocy-
tosed in situ or to be propelled into underlying tissue via intercel-
lular gaps to be ingested by macrophages or transferred into
the lymphatics [40, 60].

Capillary Fluid Exchange of the Omentum

In STARLING'S classical concept of capillary fluid exchange, two

compartments were distinguished, namely the intravascular and
the interstitial spaces [124]. This was based on the assumption
that lymph constitutes a negligible portion of total exchange
between blood and tissue [68]. The balance of fluid between
the intravascular and interstitial compartments is achieved by
the permanent interaction of hydrostatic and colloid osmotic
forces and by permeability characteristics of the interface be-
tween blood and tissue, namely the capillary wall. Blood enters
these exchange vessels at a relatively high pressure and leaves
the microcirculation at a much lower pressure [68]. Transport
of fluid is maintained by two mechanisms: a convective transfer
of blood through the capillaries, and a radial transfer through
the tissue by a diffusive or percolative motion of blood ultrafil-
trate [17, 27, 68, 71, 85, 97, 146]. Capillary fluid exchange,
however, is not only regulated by these two flow patterns -
the convective or intravascular, and the diffusive or extravascu-
lar - but also on the basis of concentration gradients in line
with molecular size, lipid solubility, and a restriction imposed
by the capillary wall properties [23, 53, 55, 71, 96, 122, 141].
Until recently, analyses of fluid exchange have primarily consid-
ered the interaction of intravascular pressure and plasma colloid
osmotic pressure while neglecting extravascular factors. Howev-
er, since GUYTON [50] began to present data of a negative inter-
stitial tissue pressure, attention was more and more focused
on physicochemical features of the interstitial ground substance.
It has become evident that any analysis of fluid motion must
include not only the properties of the interstitial gel surrounding
blood capillaries, but also blood and lymphatic capillary mor-
phology [18, 53, 68, 78].
Different techniques have been employed to characterize the
exchange of fluid between the blood and interstitium. At the
macroscopic level, exchange has been studied within the organ
as a whole with different parameters deduced from the gain
or loss of weight (or volume) of the organ or as a function
of disturbances in arteriovenous hydrostatic pressure differences
relative to flow [27, 55, 68, 97]. A second approach has been
to study individual elements of a capillary network by intravital
microscopy, and to characterize capillary fluid exchange, based
on substantial sampling of data [63, 68, 76, 85, 146].
The measurement of permeability of single capillaries, i.e., the
rate at which fluid passes the capillary barrier under the influ-
ence of hydrostatic pressures and osmotic gradients, was pio-
neered by LANDIS with his micro-occlusion technique [76].
Briefly, a selected capillary is occluded by compressing its ve-
nous end with a glass micropipette until the blood flow stops.
Any subsequent movement of a single red cell (Fig. 55) trapped
in the occluded blood vessel can be considered to be the result
of fluid exchange from the capillary lumen into the surrounding
tissue or vice versa [68]. In this event, red cells move with the
velocity of the fluid which they displace and thus can be used
as markers. The distance between two red cells becomes a
measure of loss or gain of fluid [68, 76], which can be quantita-
tively analyzed. ZWEIFACH and INTAGLIETTA [146] used the same

79
Fig. 55. Technique of oc-
cluding minute vessels by
means of a fine needle. [36]

technique in conjunction with photomicrographic techniques,

enabling accurate data to be obtained on the motion of single
red blood cells. They demonstrated in rats, rabbits, and cats
that more than 85% of the capillaries showed outward motion
of fluid, i.e., filtration. In the rest of the omental capillaries,
red blood cells remained stationary after occlusion. Only in a
very few capillaries could cell motion actually be interpreted
as fluid absorption [146]. Similar results were reported by
BROWN and LANDIS [17], studying the effect of local cooling
on capillary permeability of the frog mesentery. They demon-
strated fluid absorption to occur as frequently as filtration only
at a temperature ranging between - 2° and + 2° C. SVANES et al.
[125], however, found no significant change of capillary perme-
ability in mammals when temperatures were reduced from 37°
to 20° C. It should, however, be noted that under physiological

Table 3. Summary of in vivo data on vascular diameter and length, blood

cell velocity (as measured along the center line of a given blood vessel), and
microvascular pressures available from the omenta of different species. Data
derived from [37, 63, 64, 65, 67, 68, 109, 147]

Diameter (~m) Rabbit 18-43 8.0-11.4 30-53

Cat 18-40 10 21-78
Rata 21-38 8.0-13.0 18-26
Length (~m) Rabbit 125-380 56-217 84-180
Cat 380 150 350
Blood cell velocity (mm/s) Rabbit 0.77-2.74 0.72-1.32 0.72-3.31
Rata 0.50-1.40 0.20-0.80 0.40-1.05
Pressure (cm H 2 O) Rabbit 38-55 25-38 21-29
Cat 33 21.5 15
Rata 34-48 20

a From ENDRICH and INTAGLIETTA, unpublished data.

80
Fig. 56. Graphical repre-
sentation of fluid exchange
in the omentum as ana- > til
a::U/
lyzed by direct in vivo mi- <{a::
.... => COLLOID
croscopy. It should be ::!~ OSMOTIC
~ ~ VENOUS
noted that the capillary Uo>.
O--L-_ _ __ _ _ __ _ _ __ ATMOSPHERIC
pressure exceeds the colloid
osmotic pressure through- FLOWS
out the microcirculation.
This will result in fluid fil-
tration throughout the
entire microvascular net-
BLOOD
CAPILLARY } OB CONVECTIVE

work while excess fluid is ENDOTHELIUM }

carried away by the lym-
UL TRAFILTRATION
phatic system. INTAGLIETTA
and ZWEIFACH [67]
}111~i~;;;~il OE PERCOLATIVE

~
INTERSTITIUM
DIFFUSIVE
ENDOTHELlUMl
& FENESTRAEJ
LYMPHATIC } OL CONVECTIVE
CAPI LLARY

EFFECTIVE
COLLOID OSMOTIC & HYDROSTATIC

O~------------- ATMOSPHERIC

conditions of 37° C, fluid absorption by postcapillaries and col-

lecting venules has almost never been observed [63, 68, 146].
In view of the hydrostatic pressures summarized in Table 3 and
the fact that vasomotor activity in the omentum is almost com-
pletely absent after anesthetizing the animal [63, 68], a "modi-
fied" representation of capillary fluid exchange within the
splanchnic viscera has been introduced by INTAGLIETTA and
ZWEIFACH [68] (Fig. 56]. In the omentum, capillary blood pres-
sure exceeds the effective colloid osmotic pressure throughout
the microvascular network. The resulting lymph flow consists
of both the plasma ultrafiltrate from the arterial capillary and
the hydrodynamic bulk passage of plasma at the venous site.
Furthermore, quantitative data from the splanchnic viscera have
clearly demonstrated the existence of a permeability gradient
[55, 68, 146].
By comparing the amount of fluid loss during a micro-occlusion
on the arterial side of a capillary with the fluid loss on the
venous side of the same capillary, the apparent difference in
fluid transfer was thought to result from a difference in local
"fluid transfer properties" because the intra/extravascular
"driving force" was lower at the venous side, with the colloid

81
 osmotic pressure almost unchanged [68]. Permeability to water-
soluble material as well as a gradient of hydrodynamic conduc-
tivity in postcapillaries and collecting venules can therefore be
attributed to differences in capillary morphology [55, 68].
To explain the exact mechanism of transfer across the endothe-
lium, great interest has been focused on the structural equivalent
of the "small" and "large" pore system of the capillary wall.
It was generally accepted that small pores were located within
the inter-endothelial clefts [53, 54, 71,-96, 141]. Using electron
dense tracers, evidence has accumulated that plasmalemmal ve-
sicles (mean inner diameter 50 nm) serve as a carrier system
for large molecules and therefore represent the likely structural
equivalent of the large pore system [53,54,96,122]. In addition,
plasmalemmal vesicles were also believed to playa role in the
transport of water and solutes [96, 122].
It should, however, be emphasized that until now experimental
evidence has only been obtained to support the transport of
macromolecules because electron-dense tracers such as ferritin,
dextran, and others were exclusively located within these vesi-
cles, for which a transit time of 1-5 s has been calculated (for
Ref. see [53]). Whether this transport system worked by means
of freely moving vesicles, fusing vesicular chains, or true transen-
dothelial channels [45, 96, 122] remains, however, to be eluci-
dated.
Typical visceral capillaries have only a few endothelial vesicles
but are equipped, instead, with large numbers of endothelial
fenestrae. From a dimensional point of view, these fenestrae
(diameter: 40-60 nm, Fig. 56) fit closely to the postulated large
pores but they may also form at least part of the small pore
population.
Most recently, PALADE et al. [96] introduced the concept of the
existence of transendothelial channels in continuous type capil-
laries. Since these channels are additionally eq uipped with size-
limiting structures and are assumed to be water filled, they fulfill
two prerequisites in representing the structural correlate of the
small pore system. According to this hypothesis, the equivalent
of the large pores should be represented by those few channels
which lack any size-limiting structures (diaphragms and stric-
tures). A majority of investigators, however, still believes that
endothelial clefts are equivalent to small pores, as originally
introduced by KARNOVSKY [71]. Therefore, it is still appropriate
to identify large pores with a vesicular carrier system, whereas
small pores are still related to leaky parts of interendothelial
junctions [53,54,71,141].
The endothelia of post-capillaries and collecting venules, howev-
er, should be considered seperately because they represent spe-

82
cialized microvascular segments. Their endothelial junctions al-
ready appear more permeable under normal conditions, and
they are primary targets for the action of mediators of inflam-
mation like histamine, bradykinin, and others [3, 4, 23, 54, 83].
The increased permeability rate of these segments will ultimately
result in a gradient of vascular permeability [55, 68, 85, 146],
which is, at least in part,· due to the existence of endothelial
fenestrae as well as poorly differentiated junctional complexes
between endothelial cells [96, 122]. This feature might also
explain the easy separation of endothelial cells along these seg-
ments after topical application of histamine and similar agents
[3, 54, 83]. Consequently, large inter-endothelial gaps are
formed through which all the blood constituents can possibly
escape almost unimpeded. Blood cells will be barred by the
basement membrane for a very limited time interval before they
pass into the interstitium [54].

Conclusions

The omentum consists of a microcirculatory system in which

diameters, blood cell velocities, and pressures have been mea-
sured directly in mammals. As a result, the quantitative relation-
ship between different exchange fluxes has been established in
the omentum. Ongoing studies on the effects of exposure, micro-
surgical injury, and chemical composition of irrigation fluids
suggest that even under so-called normal conditions a varying
degree of inflammatory and vasodilatory response is always
present [63]. These artifacts might cause higher permeabilities,
augment the rate of fluid filtration through a concomitant in-
crease of permeability, and slightly increase local capillary pres-
sures [63, 68]. Consequently, the exchange flows derived from
microvascular data are probably higher than those which really
exist. It would appear that in the omentum under steady state
conditions most of the fluid passing the capillary barrier
becomes lymph, particularly in view of the fact that even with
an abnormally increased permeability (due to experimental con-
ditions), the amount of fluid transferred is of the same magni-
tude as the lymph flow, thus leaving a very small margin for
additional flux to be reabsorbed [68].
In the omentum, absorption can occur only in those regions
of microvascular venous endothelium where" leaks" permit the
equilibrium of arterial ultrafiltrate and venous leakage of macro-
molecules. Based on direct measurements of pressure and ex-
change in the microcirculation of the omentum, this seems un-

83
 likely, because (a) capillary hydrostatic pressures are con-
sistently higher than corresponding colloid osmotic pressures,
and (b) absorption is rarely observed in the omentum when
studied with the microocclusion technique [68]. Moreover, it
is worth considering that, if a presumed system of large pores
at the venous microcirculation permits outward motion of plas-
ma, the colloid osmotic pressure in free interstitial fluid will
balance the intravascular protein concentration to some extent,
thus neutralizing a source of absorptive" suction" in the neigh-
borhood of" leaks" [68].
From these considerations it can be concluded that the fluid
originating from the omental microcirculation does not return
directly into the blood stream but most likely enters terminal
lymphatics. This transport could also be accomplished by cyto-
plasmic vesicles, which may operate in the absence of a convec-
tive fluid exchange between vascular and interstitial compart-
ments. For the omentum, it seems likely that protein will be
exchanged to a varying degree throughout the entire terminal
vascular bed, particularly if pinocytosis contributes significantly
to protein carriage. In our opinion, the evidence of vesicular
transport as a primary source of tissue and lymph protein is
far from conclusive because it is still very difficult to analyze
a dynamic and time-dependent process by electron microscopy.

5.8 Omental Fluid Transport and Dialysis

A. COLOMB!

The omentum has a surface of about 1,500 cm 2 in the adult.

According to ESPERANCA and COLLINS [38] the omentum repre-
sents 2.7% of the peritoneum in infants compared with 15.2%
in an adult of 60 kg body weight. Although there are some
differences in the histological structures of blood vessels and
lymphatics, the peritoneal transport mechanisms of the
omentum correspond roughly to those of the whole peritoneal
membrane [48]. Omental transport represents therefore some
10%-15% of whole peritoneal transport.
Diffusion due to concentration gradients between blood and
dialysate and convective transport accompanying ultrafiltration
form the mechanism by which solute movement takes place
across this semipermeable membrane. Only a small portion of
the 1,200 ml of splanchnic blood flow enters the peritoneal capil-
lary network. NOLPH and SORKIN [92] found a peritoneal blood
flow of less than 120 ml/min; this would be 10% of the total
splanchnic volume, and represents three times the maximum
urea clearance.

84
Fig. 57. Resistances (R) to
the solute movement be-
tween capillary lumen and
peritoneal cavity. R i , stag-
nant column of blood;
R 2 , endothelium; R 3 , endo-
thelial basement membrane
of the capillary; R 4 , inter-
stitial tissue; R 5' meso-
thelial basement mem-
brane ; R 6 , mesothelial cell
layer; R 7 , stagnant dialy-
sate film within the perito-
neal cavity

The reasons for this comparatively low urea clearance despite

the small molecular weight of urea (60 daltons) result largely
from different diffusion resistances between the capillary lumen
and peritoneal cavity [25]. These different resistances are shown
in Fig. 57. The mesothelial gaps of up to 500 A seem to represent
a much smaller resistance to solute transfer than the intercellular
endothelial channels [48, 91, 105, 136].
Besides peritoneal blood flow and permeability the dialysate
flow is the third factor in the determination of peritoneal clear-
ance. During 5 decades of clinical peritoneal dialysis numerous
investigators have tried to increase the efficiency of this treat-
ment by increasing the only variable factor, the dialysate flow.
The introduction of hemodialysis between 1940 and 1950 with
its much higher small molecule clearances initiated these efforts,
which ended up in 1978 with the description of the so-called
semicontinuous peritoneal dialysis by DI PAOLO et al. [30] . By
means of a single needle system they reached a dialysate turn-
over of 10 liters/h. However urea clearance remained lower than
30% of the values obtained by hemodialysis.
The ingenious idea of POPOVICH et al. [102] in 1978 brought
a turning point in clinical peritoneal dialysis by extending dialy-
sis time from 30 to 168 h/week using continuous ambulatory
peritoneal dialysis. For clinical purposes peritoneal permeability
can be measured by means of the peritoneal clearance:

C=AxV
P

where A is the outflow concentration, V the outflow volume,

and P the plasma concentration. For a dialysate flow of 2 liters/
h, urea clearance is 21 ml/min, creatinine clearance is 13 ml/min,

85
Table 4. Comparison of dialysis systems (weekly clearances in liters)

Clearance Mol.wt. Human Hemo- Hemo- IPD CAPD

of (daltons) kidney dialysis filtration (2 I/h) (8 I/d)
168 h/wk 15 h/2k 9 h/wk 30 h/wk 168 h/wk

Urea 60 1,008 125 54 38 56

Creatinine 113 1,200 99 58 23 50
Vitamin B12 1,355 15 30 7 45
Inulin 5,200 1,200 4 63 9 28
Ultrafiltrate 1,200 2-6 60 4-5 5-16

IPD, intermittent peritoneal dialysis; CAPD, continuous ambulatory peritone-

al dialysis.

and inulin clearance is 5 ml/min. In order to compare the effi-

ciency of different dialysis systems it is more convenient to use
the weekly clearance in liters (Table 4).
As can be expected, the peritoneal clearance depends on the
molecular weight and on the radius of the hydrated ion. For
practical reasons nephrologists speak about" small molecules"
(SM) when molecular weight is less than 350 daltons, about
"middle molecules" (MM) when it is between 350 and
2,000 daltons, and about "large molecules" when it exceeds
2,000 daltons. Celophane membranes used for hemodialysis
have smaller middle molecule clearances than the modern cellu-
lose acetate or polyacrylonitril membranes. Natural membranes
such as the glomerular membrane and the peritoneum have a
still higher MM clearance. The human kidney is capable of
an inulin clearance (5,200 daltons), reaching that of creatinine
with a molecular weight of 113 daltons (Table 4). The higher
MM clearance of CAPD compared with hemodialysis is of
special interest because uremic toxins are supposed to be of
the middle molecular weight range [6]. Furthermore it is impor-
tant to remember that due to the" solvent drag effect" trans-
membranous MM transport approaches SM transport when
convective solute movement is an important factor [57]. Convec-
tive transport is more important with CAPO than with hemodia-
lysis. The weekly ultrafiltration rate for the human kidney is
1200 liters, for hemofiltration 60 liters, for CAPO 5-16 liters,
and for hemodialysis 2-6 liters.
In contrast to the glomerular system the peritoneum is perme-
able even for large molecules such as proteins. This results in
daily protein loss of 8.8 ±0.5 g [11] with peritoneal dialysis;
with peritonitis daily dialysate outJlow may contain up to 30 g
protein, two-thirds of which are albumins [11].
Peritoneal ultrafiltration is partly due to the blood pressure in
the arterial side of the capillaries and to a much greater extent
Fig. 58. Changes of dialy-
sate glucose (+ ~~ +) and
mg%
,,
urea (x ~~ x) concentra-
tions and corresponding al-
1500 \
,,
terations in the osmolality \,
of dialysis fluid (.-.) ,,
due to glucose (+-+)
\,
and to urea ( x - x ).
D To , total dialysate osmo-
1300 ,,
,,
lality; DGO' dialysate glu-
,,
cose osmolality; Duo, dia-
lysate urea osmolality; DG , ,,
dialysate glucose concen- ,,
tration; Du , dialysate urea
1100
,
,
concentration +,
"'" mosmli
'\,
900 ,, 360
, 340
" Oro 320
• _ _ e --~'~---.--------------~
\
,, • 300
,,
700
, 280
260
'\
\., ..., 240
......, 220
500 " "" ... 200
" 180
" DG
" ...... 160
.........
140
300 120
100
80
Du 60
100
/:=:~-:,:--:-:D~~=~=--=-=-::-=-=-..- _-_-_-_-: ~~
",," )(--)( Duo
2 4 8h
Dwell time

to the osmotic gradient between dialysate fluid and blood. Glu-

cose up to now has proved best as an osmotic agent although
rapid absorption from the dialysate is a major disadvantage
both in the osmotic capacity of the dialysis fluid and in patients
metabolism. Usually peritoneal dialysis solutions have an osmo-
lality of 347-512 mosm/liter. Since glucose absorption from the
dialysate occurs simultaneously with the water shift into the
peritoneal cavity, the osmolality of dialysis fluid decreases rather
rapidly. This osmolality decrease is only partly compensated
by the transfer of urea into the dialysis solution (Fig. 58). There-
fore ultrafiltration decreases with increasing dwell time in the
peritoneal cavity.

87
Fig. 59. Peritoneal ultrafil-
tration at different dwell +400
times in patients with
(0--0) and without
( + -- + ) peritonitis. +300 -

+200

-300

-400 Dwell time

Peritoneal pharmacokinetics are of increasing interest. The

solutes have molecular weights of between 200 and 800 daltons
and have different protein-binding characteristics. Some infor-
mation on the peritoneal permeability of poisons and drugs
is summarized in the "Giftindex-Liste II" by SEYFFART [120].
On peritoneal absorption, however, there is little information
concerning mainly antibiotics and insulin [47, 115].
Injury and inflammation of the peritoneum alter its transport
characteristics significantly. Inflammation of the peritoneal
mesothelium results in a decreased ultrafiltration capacity [137].
The reason for this is an increased glucose absorption (Fig. 59).
KNAPOWSKI et al. [74] found an increased diffusion for electro-
lytes in isolated patches of rat peritoneum injured by abrasion
of the mesothelium. This increased diffusion occurs in both di-
rections.

Complications of Surgeons usually perform open peritoneal lavage or place the

Dialysis Due to the catheters into the abdomen under sight by a small laparotomy
Omentum incision. However, most physicians are used to blind catheter
insertion and may be faced with some omental complications.
With both the stylet catheter (WESTIN-ROBERTS) and the long-
term silastic catheter, the omentum is at risk. While introducing
the catheter the tip may become entangled in the omentum,
especially if there are adhesions and if the stylet has not been
drawn back sufficiently to allow the catheter to be flexible

88
Fig. 60. Entangled stylet
catheter in the omentum
(WESTIN-RoBERTS)

(Fig. 60). Pain occurs and will not allow the catheter tip to
be moved forward into the pelvic gutter. Another complication
is the interposition of the catheter between the omentum and
the anterior abdominal wall. In this situation the dialysate enters
the peritoneal cavity rapidly but will not drain because outflow
obstruction increases with increasing intra-abdominal pressure.
The silastic Tenckhoff catheter can usually be placed in the
pelvic gutter. However, the omentum can reach the upper perfo-
ration holes and may occlude them (Fig. 61); sometimes organ-
izing thrombus may encase the catheter and cause total obstruc-
tion. In order to avoid these complications omental resection
prior to catheter implanation has been recommended [19]. Re-
section will, however, diminish the peritoneal surface and might
give rise to peritoneal adhesions at the resection site. With mod-
ern implantation techniques this is usually unnecessary.

Fig. 61. Ob. trllction of the

catheter ( to. ( ' K IIO!''') " .
scquela of int rposition bc-
t\ een the mentum and
abdominal \ all

89
 5.9 Defense Mechanisms
5.9.1 Phagocytosis and Foreign Body Reaction

A. LIEBERMANN and H. WHITE

MAFFUCCI in 1882 (cited in [88]) and MUSCATELLO in 1898 [88]

gave first accounts of phagocytosis and foreign body reaction
by the omentum. Their studie and many subsequent ones
showed that the omentum is able to absorb intraperitoneally
injected substances. Various foreign bodies have been admin-
istered, such as

1. Dyes [7, 32, 56, 86, 112, 117]

2. Chemicals [26, 32, 56, 60]
3. Foreign bodies
Particulate matter [44, 56, 140]
Suspended material [7, 112]
4. Tissue particles of organs [44, 86, 112]
5. Bacteria [31, 32, 86, 111, 118]

This omental absorption has been most impressively shown after

intraperitoneal administration of suspended charcoal [140].
With an intact omentum most charcoal particles were taken
up by the omentum and found alongside the omental vessels
after a few hours. If, however, the omentum was removed before
injection, the charcoal particles were scattered around in the
abdominal cavity and on the surface of the adjacent organs.
If larger "particles" such as sterile glass splinters or cotton
wool were injected, the foreign material became attached to
the omental surface regardless of its size and with no sign of
peritonitis. If particle size exceeded the omental absorption ca-
pacity it became completely encapsulated by tissue pouches
[107].
Living organisms such as Staphylococcus aureus and Mycobac-
terium tuherculosis are treated in a similar way by the omentum
as dead material when they are injected into the peritoneal cavi-
ty. Omentectomized animals showed an increase and an intense
accumulation of bacteria in the peritoneal fluid, with a reduced
survival rate of the animals. In controls with the intact omentum
the bacterial content in the peritoneal fluid became less and
most bacteria were found to be attached to the omental surface
or engulfed by phagocytes [41]. The uptaken material was usual-
ly disaggregated. Residuals of the foreign material may be stored
in vacuoles of the phagocyte or extruded. Mortality was low
in these animals.

90
 5.9.2 Immunological Concepts

The above experiments and surgical experience shows that

omentectomy lowers the resistance to abdominal infections.
PORTIS in 1924 [103] was one of the first to outline the role
of the omentum in antibody production. He described" a most
marked phagocytosis which could be accelerated by previous
intraperitoneal immunization, and which [in this opinion] oc-
curred in the cells comprising the milky spot." He, therefore,
assumed that the omentum was able to produce antibodies.
OAKLEY [94], ROBERTS [110], and WALKER and co-workers [133,
134, 135] supported the idea of potential antibody production
by the omentum. They found in tissue suspensions that intrave-
nous injection of an antigen increased the antibody titers in
liver, spleen, and lymph nodes, but very little in the omentum.
Intraperitoneal injection, however, provoked greatest antibody
titers in omental tissue. Further support for active participation
of the omentum in immune response was given by WALKER
[133, 134]: animals intraperitoneally grafted with an omentum

Fig. 62. The tissue of the

mouse omentum is com-
posed of collagen fibers.
fibroblasts, macro phages,
and mesothelial cells. After
i.p. stimulation with anti-
gen many lymphoid cells
occur (arrowed) which arc
transformed into antibody-
containing plasma cells
(HAJDU [51]). Rasterelec-
tron microscopy. x 1700
[from HOLUB 61]

91
Fig. 63. a Neoformation of
lymphatic cell areas
10 days after immuniza-
tion. x 160 b The same
area with immunofluores-
cent IgG localization.
(courtesy of M. HOLUB,
Prague) x 160

from previous i.p. immunized animal gave a secondary immune

response upon challenge with this antigen.
By improved techniques [5, 69, 70, 73, 126] it could be estab-
lished on the cellular level that the antibodies were produced
in plasma cells of milky spots [43, 62, 70, 72, 84]. Plasma cells
derive from lymphoid cells (Fig. 62) and become much more
numerous after antigenic stimulation ([43] Fig. 63). The
omentum has been regarded as the immune factory of the abdo-
men by FISCHER [42].

5.10 Matrix for Tissue Grafts

5.10.1 Autotransplantations of Splenic Tissue
M. DURIG and F. HARDER

A serious risk of splenectomy is the increased postoperative

incidence of bacterial sepsis, known as the" overwhelming post-
splenectomy infection, OPSI." This complication is associated
with the extremely high mortality rate of 50%-80% and affects
infants and young children [93, 132]. Because of the immune
function of the spleen, the susceptibility to infections has been
attributed to "postsplenectomy" immune deficiency [15, 98,
132]. Preservation of the traumatized splenic tissue is therefore
advocated, particularly for children. Because of its proximity,
nature, and similar embryological origin [81], the omentum is
a suitable recipient organ for splenic tissue grafts if a damaged
spleen cannot be safely preserved by coagulation, fibrin glue,
splenorrhaphy, arterial ligation, or segmental resection [1, 95,
98, 119, 132]. Dislodged splenic particles will implant and
become functional in the mesenteric surfaces (see Sect. 7.8.1).
This phenomenon is known as splenosis.

92
Indications Autotransplantations of splenic tissue may be considered after
severe traumatic splenic rupture, splenectomy following acciden-
tal damage at operation, or splenectomy at the time of pancrea-
tectomy for benign disease.

Contraindications Autotransplantation is (or may possibly be) contraindicated in

the presence of: idiopathic thrombocytopenic purpura, hemo-
lytic disorders related to the spleen coexisting severe intra-ab-
dominal infections and splenic diseases such as mononucleosis
and occationally Hodgkin's disease.

Laboratory Findings Characteristic findings are : depressed IgM levels, increase of

After Complete vacuolized erythrocytes (" pitted-red cells "), increase of Howel-
Splenectomy Jolly bodies, and decrease of TUFTSIN (phagocytosis-promoting
pep tides) produced by the spleen [132]. Patients with accessory
spleens or splenosis do not show these changes (Sect. 7.8.1).

Operative Technique Preparation ofthe Implant. We implanted with success (Table 5)

thin splenic slices about 3 mm in width ([98] Fig. 64), splenic
fragments weighing between 100 and 1,000 mg, and homoge-

Fig. 64. Splenic slices trans-

planted to the greater
omentum

93
Fig. 65. Splenic tissue being
inserted into the omental
recessus (courtesy of Dr.
K. AIGNER, Allgemeinchir-
urgie, U niversitatsklinik,
Giessen, West Germany)

nized splenic tissue [1, 119]. It appears to be important to have

a large surface area and ideally more than one-third of the spleen
should be implanted. In one of our 21 patients an abscess of
one omental pouch occurred but there was no loss of trans-
planted tissue, and its function remained.

Localization of the Splenic Implant. Splenic tissue is implanted:

(a) between the leaves of the omental recesses (Fig. 65, [1]).
- This technique is especially used in children; (b) into an
omental pouch. After placing the homogenized or preferably
sliced splenic tissue onto the widely spread-out omental surface
a pouch is formed by folding over the omentum and suturing
it to itself (Fig. 66). This technique is mostly used in adults.

Fig. 66. Completed omental

pouch containing splenic
tissue

94
Postoperative The postoperative complications are similar to those of a lapa-
Complications rotomy and are largely dependent on associated injuries. Specific
complications caused by the splenic implant have not been re-
ported yet. Should intra-abdominal infection occur, a graft ab-
scess in the omental pouch may be a possibility. One of our
21 patients showed such a splenic necrosis (Table 5).

Table 5. Replantation of autologous splenic tissue in

21 patients treated in the Surgical Department of the
University Hospital, Basel, using different types of
splenic graft. In all 16 patients examined scintigraphi-
cally 3 months after translantation ingrowth of the
replant was shown. In one patient * an abscess of
one omental pouch occurred. However, there was no
loss or impairment of transplanted tissue and its func-
tion in the other pouches as shown on scintigram

Type of replant No of patients Ingrowth

Slices 4 4
Fragments 7 4
Homogenized 10 8*

Follow-up After successful tissue implantation IgM levels, appearance of

erythrocytes, Howel-lolly bodies, and Tuftsin values return to
normal within 20 weeks. The presence of active splenic tissue
can be shown qualitatively and quantitatively on scintigrams
within 3 months of transplantation (Fig. 67). Living and histo-
logical normal splenic tissue after previous implantation was
also found when re-Iaparotomy became necessary for other rea-
sons in one of our patients. PATHEL and co-workers had similar
results in a follow up of 30 patients (Personal communication
1982, lAMA in press). He described initial degeneration of the
splenic transplant in the omental pouch followed by complete
regeneration to "normal splenic tissue" at 5 weeks [98 b].

Fig. 67. Scintigraph of

splenic tissue (arrows) in
omental pouch 3 months
after transplantation
(DuRIe;)

95
 5.10.2 Tumor Implants in Experiments

D. LIEBERMANN-MEFFERT

The omentum has been used to study tumor genesis [10] and
the migration of tumor cells after i.p. inoculation [49, 128].
TOBAI et al. [128] found that the milky spots after i.p. injection
of sarcoma cells enlarged by the increased number of macro-
phages. Two to five days later the milky spots were occupied
by tumor nodules. The mode of how tumor cells became en-
closed in endothelial cells oflymphatic vessels, e.g., intravascular
migration is shown. Sites of the peritoneum without milky spots
were not affected [49, 128]. GREEN and WILLIAMS [49] presented
evidence of a close relationship between inflammatory responses
and tumor cell attachment to the omental milky spots.

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 Clinical Aspects

6 Clinical Signs and Methods of Assessment

G. STALDER

6.1 Examination and Investigation

Clinical Picture The clinical diagnosis of omental disease is difficult because

and Examination there are no organ-specific signs. It is usually not possible to
distinguish clinically between the rarer omental diseases and
disease processes originating from other sites. Radiology, ultra-
sonography, and computed tomography are frequently unhelp-
ful. Definite diagnosis can be made only by direct observations
and biopsy during laparoscopy or exploratory laparotomy.

Patients with omental disease present with various signs and

symptoms and can be divided clinically into three main groups:
(a) mass lesions, (b) acute vascular lesions, and (c) inflammatory
processes.

Symptoms and Signs Mass lesions of the omentum are most frequently caused by
with Mass Lesions solid tumors and cysts, and metastatic malignant tumors, e.g.,
gastrointestinal or ovarian carcinomas. Small tumors or cysts
are asymptomatic and may be found incidentally at laparotomy.
Larger lesions present with abdominal distention and vague ab-
dominal pain. Malignant tumors may lead to weight loss.

Solid tumors of the omentum (Sect. 7.7) can occur at any age.
The patient usually observes a distention of the abdomen and
may sometimes feel a palpable mass. Abdominal pain with or
without radiation to the back or flank may be present but an
undefined sense of heaviness is more frequent [9]. Benign tumors
can remain symptomless and of the same size for years. A rapid
increase of size and the occurrence of symptoms should always
raise suspicion of hemorrhage or malignancy. With malignant
omental tumors weight loss, general malaise, and weakness arc
found. In metastatic omental tumors occurring with intra-ah-
dominal malignancies such as ovarian or gastrointestinal carci-
noma, the symptoms from the primary site of the tumor may
predominate.

10.3
 The findings on clinical examination are dependent on the size
of the tumor, the ability of the patient to relax the abdominal
musculature, and the obesity of the abdominal wall. If omental
tumors are palpable, their localization is most frequently in the
right upper or right lower quadrant. The palpable mass is firm,
round, mobile, and sometimes nodular. Ascites is present in
50% of malignant tumors. Distant metastases are rare in prima-
ry malignant tumors of the omentum [4].

Cysts of the omentum are grouped according to their clinical

presentation. Diagnostic features are mainly functions of size,
localization, and presence or absence of complications such as
hemorrhage, infection, torsion, or rupture of the cysts.
Omental cysts are most commonly found in childhood
(Sect. 7.7.2), and the differential diagnosis is enteric duplication,
enteric cysts, mesenteric cysts, or cysts of the pancreas [7]. In
adults, trauma to the abdomen may cause the formation of
a cyst. A rare cause is echinococcal infection. It may be difficult
to differentiate omental cysts from ascites, ovarian and pancre-
atic cysts, or pseudocysts. The accepted classification is as
follows [1]:
1. Incidental cysts found at operation or autopsy without pre-
vious symptoms. These cysts are usually small and filled with
clear fluid. About 40% of cysts are diagnosed in this way [10].
2. Symptomatic cysts present as an acute abdomen. The preop-
erative diagnosis is acute appendicitis in most cases. The
pathological conditions underlying the acute symptomatol-
ogy are hemorrhage, inflammation, torsion, rupture, or small
bowel obstructions. About 20% of the cases with omental
cysts are in this group [10].
3. Asymptomatic cysts with the physical signs of an abdominal
distention. Occasionally intermittent or constant pain,
nausea, or vomiting may occur. A mobile non-tender firm
smooth mass is found on clinical examination, leading to
elective surgery. This is found in 40% of patients with cysts [10].

Symptoms and Signs Vascular lesions can be secondary to omental torsion in patients
with Vascular Lesions with pre-existing factors such as adhesions, emboli, or degenera-
tive vacular disease and trauma (Sect. 7.6). Although there
might be rare cases where torsion seems to be spontaneously
reversible with episodes of periodic abdominal pain, torsion and
infarction of the omentum usually lead to an acute abdomen
with sharp pain in the right upper or more frequently in the
right lower quadrant. The preoperative diagnosis in these pa-
tients is usually acute cholecystitis or acute appendicitis. At op-
eration in about half of the patients frank gangrene of the

104
 omentum will be found and torsion with venous congestion
without infarction in the rest of the patients. Recurrent torsion
after operation has not been reported.

Symptoms and Signs Inflammatory lesions of the omentum may occur secondary to
with Inflammatory inflammation of the peritoneum. Peritonitis leads to adhesions
Lesions of the omentum around the inflammatory process as in acute
cholecystitis, acute appendicitis, or acute diverticulitis. It can
also be seen in acute pancreatitis or pelvic inflammatory dis-
eases. The adhesions persist most often after healing of the in-
flammation and the omentum will remain fixed.
Tuberculous peritonitis can be the cause of massive adhesions.
Frank small bowel obstruction caused by omental adhesions
can occur but it seems very rare. Vague symptoms such as ab-
dominal cramps, colic, nausea, and tenderness may result from
adhesions, and care must be taken not to subject the patients
to unnecessary and potentially harmful operations. The
omentum can be involved in parasitic diseases, and in countries
with a high prevalence of parasitic infections this is an important
differential diagnosis (Sect. 7.5) in all cases with inflammation.

6.2 Radiographic Manifestation

Conventional Plain abdominal films, barium examinations of the upper and

Radiographic lower gastrointestinal tract, urography, and abdominal angiog-
Procedures raphy are the conventional radiographic procedures available
for further investigation of a suspected intraperitoneal disease
process. On plain abdominal films only nonspecific changes can
be seen in the presence of omental disease, including an elevated
diaphragm, homogenous soft tissue shadows in the middle or
lower abdomen displacing bowel gas, and possibly calcifications
in cases with omentitis or an echinoccocal cyst [10].
Lateral view plain films usually show the mass lying anteriorly
to the bowel gas. With barium contrast studies it is shown that
the intraperitoneal mass is extrinsic to the gastrointestinal tract
[3]. The typical findings include a smooth indentation of the
stomach from the greater curvature side with superior and poste-
rior displacement of this organ to the right. Small bowel loops
arc equally displaced and arranged around the mass. The com-
pression of the large bowel by the mass may lead to incomplete
filling of the ascending and transverse colon on barium enema.
The transverse colon is orten displaced to inferior and posterior
or anterior parts of the abdomen [4].
The intestinal transit time remains normal except in patients

105
 with large omental tumors and cysts where bowel loops become
completely obstructed by compression from the outside [10].
Malignant tumors may ultimately infiltrate parts of the gastroin-
testinal tract.
Large omental tumors and cysts can displace a kidney or ureter.
Compression of the urinary bladder or ureter may sometimes
lead to unilateral hydro-ureter and hydronephrosis [10]. In typi-
cal cases the ureter is obstructed at the level of the sacral prom-
ontory [5].

Angiography Visualization of omental vessels is common in selective celiac

and mesenteric angiography, and sometimes an unsuspected
omental lesion is found incidentally by this method. Cysts may
lead to a widening of the gastroduodenal artery and displace-
ment of omental branches. Tumors may lead to hypertrophy,
tortuosity, and stretching of omental vessels [2]. The main indi-
cation for selective abdominal angiography is the preoperative
evaluation of patients with omental disease.

6.3 Ultrasonography and Computed Tomography

Ultrasonography Ultrasonography (US) and computed tomography (CT) are the

and Computed most accurate noninvasive investigations for confirmation of
Tomography a suspected omental mass lesion on clinical grounds. Both me-
thods, allow easy discrimination between a solid tumor and a
cyst [7]. The exact determination of the antero-posterior extent
and localization of the lesion and the outlining of its size can
be carried out accurately by US or CT [8).
The location of the omentum anterior to the small bowel and
colon makes it possible to differentiate omental lesions from
mesenteric masses, cysts of the pancreas, ovarian cysts, and gas-
trointestinal duplications by US and CT [6]. Omental masses
can be clearly separated from the liver and spleen by these meth-
ods. CT is superior for showing the precise relationship of the
omental mass to the bowel.
Limitations of both methods are that smaller tumors and cysts
under 1 cm diameter are missed, that metastases adjacent to
the primary tumor cannot be resolved from the primary tumor,
and that it is not possible to differentiate between benign and
malignant tumors and between tumors and inflammatory
"pseudotumors" [6].
The clear demonstration and localization of cysts by US and
CT allow direct puncture and aspiration of cyst contents. Cyto-
toxic substances can be instilled directly for treatment of malig-

106
 nant cysts. The guided puncture of solid tumors makes possible
the aspiration of material for cytological examination. Finally,
US and CT are excellent tools in following the changes in size
of malignant tumors under medical treatment.

6.4 Endoscopic Procedures

Laparoscopy Laparoscopy is very useful for the diagnosis of omental disease

since the omentum can be well visualized by this method and
biopsies can easily be taken. Under normal conditions the
omentum lies on top of the bowel loops. Its fat content is depen-
dent on the nutritonal state of the patient. In the absence of
adhesions the omentum can be moved by shifting the patient
to one or the other side or mechanically by the laparoscope
itself or by an ancillary probe.
In the acute abdomen caused by inflammation the omentum
is concentrated on the site of the inflammatory process and
can therefore give an indication of the origin of the disease
process, as in acute cholecystitis for example. The following
omental lesions can be diagnosed by laparoscopy:

Adhesions are usually caused by previous abdominal surgery

or by localized or generalized inflammatory processes in the
past. Thin, poorly vascularized sail-like adhesions can be cut
with small scissors inserted through the laparoscope. Adhesions
may lead to complications when undertaking laparoscopy and
obstruct the vision to parts of the abdominal cavity. The pres-
ence of adhesions is not an absolute contraindication for lapar-
oscopy, but the site of insertion of the Verres needle for air
insufflation and of the laparoscope have to be chosen carefully.

Partial or total infarction of the omentum is a rare cause of

acute abdomen. On laparoscopy the infarcted part of the
omentum is edematous with blue-red discoloration and promi-
nent vessels and sometimes with hemorrhagic ascites. In infarc-
tions secondary to torsion the cause can sometimes be seen.

In acute pancreatitis ascites with a high content of pancreatic

enzymes and fat necrosis can be found by laparoscopy. In fat
necrosis small yellow and white elevated spots, sometimes with
a red halo, are seen on the surl~lce of the intestinal loops, the
mesentery, and the omentum (Fig. 68).

The macroscopic appearance of the omentum in omentitis

depends on the stage of the disease process. Initially it presents
with edema, hyperemia, and ascites, followed by thickening and

107
Fig. 68. Yellow-white ele-
vated spot fat necrosis on
the omental surface in
acute pancreatitis (Iaparos-
copy. STALDER)

adhesions. It can be difficult to differentiate between inflamma-

tory processes of the omentum and tumors by macroscopic in-
spection.
In tuberculosis the omentum is affected together with the perito-
neum by nodular inflammatory changes, ascites, and adhesions.
The infection can spread through direct contact from the tuber-
culous organ as in lymph node tuberculosis of the ileocecal
region or from a tuberculous salpinx.
In omentitis laparoscopy is of special diagnostic value because
it is possible to take direct biopsies of the inflammatory masses
and it is easy to collect ascites for smears and bacterial cultures.

Tumors and Cysts. The differentiation between primary and sec-

ondary omental tumors is difficult by macroscopic inspection
alone although in cases with secondary involvement the
omentum is often closely attached to the primary tumor as with
carcinoma of the stomach, uterus, gallbladder, or colon. Tumors
affecting the omentum near its insertion can cause massive con-
gestion distal to the tumor.
When a cyst of unknown origin is seen biopsy and puncture
are not recommended because of the danger of disseminating
echinococcal disease to the peritoneal cavity. In this situation
laparoscopy should be followed by laparotomy.

Gastrointestinal and Endoscopic examination of the stomach, colon, or urinary tract

Urological Endoscopy may give valuable information on the nature of an omental

lOR
 mass, and it may show secondary involvement of these organs
by malignant omental tumors. Malignant processes of the upper
GI tract, colon, or urinary bladder can be seen and biopsies
are easily taken.
Endoscopy is generally less valuable than contrast media radiol-
ogy in demonstrating displacements and compression of adja-
cent hollow organs by omental mass lesions.

6.5 Laparotomy

Assessment and Operation and postoperative care follow the rules of abdominal
Surgical Techniques surgery and are the same as described in Sect. 9.2. Surgical treat-
ment of processes involving the omentum is often required in:
Primary omental diseases, for example:
Some congenital malformations
Injuries of the omentum and herniation
Acquired conditions, inflammation, and parasites
Torsion, infarction, and adhesions
Tumors and cysts
Associated omental pathology, for example:
Cancer of the stomach, pancreas, and transverse colon
Disease of the transverse colon
Ovarian carcinoma

References

1. ADLER GG (1967) Zur Chirurgie der Omentumzysten. Zbl Chir

92: 145-149
2. DEUTSCH V, AOAR R, MOZES M (1971) Angiography of the greater
omentum. Am 1 Roentgenol 113: 174-180
3. HALLER 10, SCHNEIDER M, KASSNER EG. SLOVIS TL. PERL LJ (1978) Sono-
graphic evaluation of mesenteric and omental masses in children. Am
1 Roentgenol 130: 269-274
4. HUCK MAN MS. FISHER MS (1974) Roentgenographic signs of tumors of
the greater omentum. Cancer 33: 1526-1530
5.1ACOBSSON B, MELLGREN G. REUTERSKIC)LJ) G (1976) Angiography of
omental cysts in a child. Acta Radiol [Diagn] 17: 573-576
6. LEVITT RG, SAUEL SS. STANLEY Rl (1978) Detection of neoplastic involve-
ment of the mesentery and omentum by computed tomography. Am .I
Roentgenol 131 : 835-838
7. MITTELSTAEDT C (1975) Ultrasonic diagnosis of omental cysts. Radiology
117:673-676
8. SANDERS RC (1975) B-scan ultrasound in the management of abdominal
masses in children. lAMA 231 :81-83
9. STOUT AP, HENDRY .I, PURDIE FJ (1963) Primary solid tumors of the
great omentum. Cancer 16:231 245
to. WALKER AR. PUTNAM TC (1973) Omental. mesenteric. and retroperitoneal
cysts: a clinical study of 33 new cases. Ann Surg 178: 1.\ 19

109
 Pathological Conditions, Specific
Investigations, and Therapy

7 Diseases of the Omentum

7.1 Congenital Abnormalities and Pediatric Diseases
J. WALDSCHMIDT

7.1.1 Pathology

Introduction. Malformations of the omentum are rare. Hypoplasia, dysplasia,

hyperplasia, duplication of the omentum, and an abnormal at-
tachment to the colon have been described. Failures in intrauter-
ine bowel rotation, bowel atresia, omphalocele, or large dia-
phragmatic defects are mostly associated with hypoplasia of
the omentum or abnormal attachments (JUSKIEWENSKI, personal
commincation, 1981).

Agenesis and Aplasia Agenesis and aplasia of the omentum together with agenesis
of the Omentum of the ligaments, spleen, and vascular pedicle have not been
satisfactorily documented as all references in the literature [30.
167,230] are unsupported by personal observations.

Aplasia of the Embryologically these ligaments develop from the same tissue
Splenic Ligaments source as the omentum. The absence of the phrenicolienal liga-
ment is a frequent secondary finding and has no clinical rele-
vance. Extreme splenic mobility may lead to torsion of the
greater omentum and spleen ([14, 22. 69, 112]. WALDSCHMIDT.
personal cases, see also Sect. 7.6).

Hypoplasia of the In gastroschisis, which is a congenital paraumbilical defect of

Gastrocolic Ligament the abdominal wall, the omentum is present as a rudimentary
and Omental Apron fringe (Fig. 69) along the greater curvature of the stomach ([100]
WALDSCHMIDT. personal cases). Although small it always enve-
lops the gastroepiploic vessels. and the spleen and pancreas are
present. Gastroschisis is combined with nonrotation and malro-
tation of the gut or atresia of parts of the boweL in which
failure of omental development or its absence is also a common
observation (JUSKIEWENSKI [198]. personal communication.
1981). The cause of omental deficiency in these malformations
is unknown. Secondary intrauterine damage of the omentum

111
Fig. 69. Rudimentary
fringe of the omentum
along the greater curvature
in a neonate with gas-
troschisis defect. (Courtesy
of Prof. JUSKIEWENSKI,
Toulouse)

may follow strangulation and ischemia, lack of support by the

mesocolon, and" anarchistic" development (JUSKIEWENSKI, per-
sonal communication, 1981) or a missing stimulus for growth
may playa part (Sect. 3). SCHIEFFERDECKER [194] reported on
a very short omental apron (0.5-2.0 cm long) in a 50-year old
man in whom the gastrocolic ligament was normal.

Pathological Transverse Colon. In coloptosis the gastrocolic ligament is often

Attachments abnormally long and the omental apron correspondingly short.
Gastrocolic separation, in which the caudal omental margin is
attached to the transverse colon without simultaneous malrota-
tion of the gut, is rare (150 cases in the literature). WALDSCHMIDT
et al. [247] found this anomaly associated with diaphragmatic
defects or omphalocele 3 times in 10 years (ca. 3,000 opera-
tions). The stomach and transverse colon were connected by
a broad mesenteric sheath (Fig. 70), which may have contained
omental tissue and was lying entirely in the thoracic hernial
sac. The omental apron was missing.

Ascending Colon. In children the omentum may be attached

to the ascending colon and may even reach the cecum (Figs. 71 a,
72 a). This must be distinguished from the pericolic membrane

112
Fig. 70. Gastrocolic separa-
tion

Fig. 71a-c. Diagrams illus-

trating a Attachment of the
omentum to the cecum.
b Pericolic membrane of
Jackson. c Common
ventral ileocecal mesentery

113
Fig. 72 a--c. Clinical photo-
graphs illustrating a At-
tachment of the omentum
to the cecum. b Precolic
membrane of Jackson.
c Common ventral
ileocecal mesentery.
(WALDSCHMIDT)

of Jackson (Figs. 71 b, 72b), which represents a remnant of

the ventral mesocolon [151]. The other abnormality from which
these two malformations must be distinguished is that of a
common ventral ileocecal mesentery (Figs. 71 c, 72c) with a
mobile cecum ([95, 157, 208, 210, 211] JUSKIEWENSKI, personal
communication, 1981).

Deficient Attachments Atresia of the transverse and of the sigmoid colon is rare with
Colon only 30 cases reported, and in these no reference is made to
the greater omentum. WALDSCHMIDT observed one case of

114
Fig. 73. Atresia of the
transverse colon with fail-
ure of the omental attach-
ment

atresia of the transverse colon in which the omental apron was

long and floating freely in the abdominal cavity (Fig. 73). The
defect was corrected by anastomosing the ascending and de-
scending colon and suturing the omentum to the dorsal surface
of the newly formed transverse colon. In one neonate with
atresia of the sigmoid colon WALDSCHMIDT found the omental
apron was not attached to the apparently normal transverse
colon.

Malrotation of the Intestine (Fig. 74a-c). If in malrotation of

the intestine the omentum is present, it may be floating freely
(malrotation II, retroposition of the colon); attachments may
be limited to one flexure (malrotation I and II, nonrotation),
or may be present only in the right half of the colon (nonrota-
tion, malrotation I) so that it is attached only to the cecum
and the ascending colon.

Defects in Small defects in the omentum are frequent and occur spontane-
the Omentum ously or after trauma (Sect. 7.2) in all regions (Fig. 75). Often
. the defects are discovered by chance at laparotomy or laparos-
copy, and unless prolapse of bowel occurs through them, they
have no special or clinical significance. Although spontaneous
resolution occurs, strangulation and gangrene may be a poten-
tial danger (Sect. 7.3). Large defects in the gastrocolic ligament
and internal herniation with displacement of the intestine into
the omental bursa may occur, as found by WALDSCHMIDT in
three neonates.

115
Fig. 74a-c. Malrotation of
the intestine. a Freely
floating omentum.
b Omentum fixed to the
small bowel and sigmoid
colon. Ladd's membrane
can be seen attaching the
cecum to the lateral ab-
dominal wall. c Omentum
attached to the mobile as-
cending colon and small
bowel

7.1.2 Symptoms, Signs, and Diagnosis

Special investigations of malformations of the gut, preparation

for surgery, and postoperative care will be found in the books
of pediatric surgery. Pathological attachment, especially that
to the cecum, may cause recurrent abdominal pain; if strangula-
tion of the cecum occurs, nausea, vomiting, tachycardia, and
palor are some of the first symptoms and signs. The symptoms
of splenic torsion are characteristic: sudden, occasionally inter-
mittent abdominal pain is followed by vomiting and the signs
of an acute abdomen. Most often the spleen can be palpated

116
Fig. 75. Congenital defect
in the omentum.
(W ALDSCHMIDT)

as a mobile tumor. Transomental prolapse is usually accompa-

nied by recurrent abdominal pain followed by the signs of an
acute abdomen if bowel strangulation occurs.

7.1.3 Treatment

Congenital bowel abnormalities are treated surgically according

to the principles of pediatric surgery, and preservation of the
omentum is of secondary importance.

117
Recurrent Splenic The recommended treatment for splenic torsion is splenectomy
Torsion whatever the cause [14, 69]. However, because of the potential
danger of an overwhelming fulminant septicemia (see Sect. 5.10),
splenectomy should be avoided if possible during the first
4 years of life [69, 162]. The free flap-like portion of the
omentum is sutured to the left lateral abdominal wall and the
diaphragm. In this way a bearing surface for the spleen is pre-
pared and the splenic flexure of the colon becomes fixed. Care
must be taken that the lower pole of the spleen is positioned
deeply in the new funnel-shaped recess. Subsequent autotrans-
plantation of splenic tissue is the method of choice.

Pathological Attach- Detachment of the adhesions poses no surgical problems. Care-

ment to the Cecum ful hemostatis is necessary.

Coloptosis Surgery is not usually indicated but in patients with significant

symptoms the gastrocolic ligament is drawn tight, the right
flexure of the colon is sutured to the lateral abdominal wall
using OMBREDANNE'S technique, and the taenia omentalis of the
transverse colon is sutured to the ventral abdominal wall or
greater gastric curvature.

Gastric Volvulus with Primary and secondary torsion of the stomach must be distin-
and without guished. Primary gastric torsion is not associated with other
Herniation into the malformation. The stomach is rotated on its longitudinal or
Omental Bursa its transverse axis. The gastrocolic ligament is drawn tight and
the site of omental insertion at the taenia omentalis is sutured
to the ventral abdominal wall.
In secondary torsion, these maneuvers are not generally suffi-
cient because the volvulus is a sequel or concomitant anomaly
of other malformations. Treatment of the cause of the torsion,
for example, the herniation into the bursa, the large dolichosig-
moid, or the diaphragmatic hernia is required.

Defects in the Congenital and traumatic defects in the omentum are closed,
Omentum taking care of the epiploic vessels and hemostasis.

7.2 Injuries of the Omentum

H. WHITE, D. LIEBERMANN-MEFFERT, J. WALDSCHMIDT,
and H. TILLMANNS

Closed Blunt Blunt abdominal trauma is not uncommon in everyday life.

Abdominal Injuries An early account of omental laceration is given by CUTLER in
1859 [45]. Omental injury may not be recognized as a clinical

118
Fig. 76. Defect in the
greater omentum following
a blunt injury in a 9-year-
old girl (WALDSCHMIDT)

entity unless the trauma is severe [222]. The circumstances giving

rise to blunt injury are increasing with high velocity impact
in passengers wearing seatbelts in cars. In addition to hemato-
mas, tears may occur and have been described in both children
and adults (Fig. 76 [28]). Symptoms and signs of an acute abdo-
men will occur with such injuries. Occasionally the bowel may
become incarcerated in an omental tear, and this demands lapa-
rotomy [28].

Open Abdominal At laparotomy the omentum is at risk from handling and dissec-
Injuries tion, mainly because omental adhesions are very frequent. He-
matomas may occur, but direct vision and access allow the
surgeon to overcome such problems. Diagnostic upper abdomi-
nal and gynecological laparoscopy and laparoscopic tubal liga-
tions may cause damage [9], including tears, hemorrhage, and
surgical emphysema. As direct vision and access in laparoscopy
are limited, the extent of the injury may not be recognized and
therefore inadequately treated. Continued clinical monitoring
of girth and bowel sounds as well blood pressure and pulse
measurements are therefore important in assessing the patient.
Penetrating injuries by sharp objects such as knives, peritoneal
lavage, and dialysis (see Sect. 5.8) may cause omental injury
or even herniation along the track of entry. Infants who receive
intrauterine transfusions may have a risk of intra uterine damage
and herniation of the omentum [125]. There is also a report
of a glass splinter entering the peritoneal cavity [183] and of

119
 an intrauterine contraceptive device [187] encysted in the
omentum. Laparotomy is mandatory after penetrating abdomi-
nal injury.
Surgical techniques are similar to those discussed in Sect. 9.1.

7.3 Hernias
H. WHITE and J . WALDSCHMIDT

Introduction. Omental prolapse following abdominal injury led

to the first surgical operations on the omentum. Treatment was
confined for centuries to the resection of the protruded
omentum or, exceptionally, to its replacement (Sect. 10.2). Early
accounts of the omentum being present in inguinal hernia date
back to PARE; unless the omentum was incarcerated and had
to be dissected to avoid lethal peritonitis [180], there was no
surgical progress until the turn of the century. The first clear
description of the omentum occurring in inguinal hernia, its
incarceration, and the modern ideas of surgical repair were given
by OBERST in 1882 [164] and ECCLES in 1894 [52]. Incarcerated
omentum in an internal, mesenteric hernia was first described
by TREVES [240]. NYHUS and co-workers [160] recently gave
detailed accounts of the various types of hernia and their treat-
ment, including a comprehensive review of the available litera-
ture.

7.3.1 Pathology

Congenital Hernias A number of congenital hernias and defects occur, the most
in Neonates and common being diaphragmatic, exomphalos, gastroschisis, and
Children inguinal. Even in the congenital diaphragmatic hernias, which
may be major defects such as the absence of the hemidiaphragm
associated with hypoplasia of the lungs or more minor ones
such as herniation through the foramina of Bochdaleck, Mor-
gagni, or the para-esophageal opening (Fig. 77) the omentum
plays little part [185]. The omentum is small and even vestigial
in neonates, and although it may be found in association with
the stomach or transverse colon its presence appears incidental
rather than having an effect on the pathogenesis or clinical
picture (Sect. 7.1). A rare congenital herniation of the omentum
into the pericardium through a pericardioperitoneal communi-
cation has been described [79, 184].
Although viscera are found in inquinal hernias in over 30%
of all infants under 3 months old, a prolapse of the omentum
into a hernial sac is extremely rare. Presumably the growth of

120
Fig. 77. Locations of con- S,te of Morgognl hernlC!
genital weakness of the
diaphragm and the most
common site for traumatic
laceration (TA)

SlIe 0 esophageal -+_-I--f-E=-_ __ ~"i,';;,

hIatus hernlC

Fig. 78. Visceral and Age 0 -3 months 3-12 months 1,-5 years 6- 11, years
omental hernias in children

vIS cera
i Omoo"m I O
/~
3'3'10

.J.,.V;U0.'.'.
29"10
J1
:crJ:·: 0".
~
0'/.

8m"%
7°'0
180

umber
of cases
R IL
273 11,5
R LI
61 35
R I l
311 205
R IL
141 102

the omentum (Sect. 3) accounts for its presence in hernial sacs

in older children (Fig. 78). Embryologically the left inguinal ca-
nal usually closes earlier than that on the right and this will
to some extent account for the predominance of right-sided
hernias with both visceral and omental prolapse.

Internal Hernias
Acquired internal hernias may occasionally occur at the perito-
neal reflections (e.g., paraduodenal fossae). These usually
contain the small bowel but the omentum may sometimes be
included. Herniation into the lesser sac, although rare [115],
may occur through the Foramen of Winslow, lesser and greater
omentum, transverse mesocolon [19, 227], and supravesical
fossa [105]. The incidence cannot be accurately assessed but
about 1,000 cases have been reported in the last 50 years [92].
Transomental strangulations may be spontaneous [40] or asso-
ciated with straining and an increase in intra-abdominal pressure
[114]; trauma is often described preceding herniation. The
omentum may also be present in the sac of an hiatal hernia

121
Fig. 79. Transomental
strangulation of the ileum
through an omental defect.
Eleven-year-old male.
(W ALDSCHMIDT)

([57, 149, 158] Fig. 80). Incarcerated omentum in an internal,

e.g., mesenteric hernia, may occur, but intestines are more com-
monly found [63, 141, 142].

Transomental Strangu- Transomental strangulation is rare in adults; it appears to be

lation of the Bowel more frequent in the elderly [19, 118, 142]. In children only
three cases have been found in the literature ([94] Fig. 79).
Omento-omental strangulation has not been observed in infancy
[114].
Post-traumatic internal hernias through the lesser and greater
omentum as well as the transverse mesocolon [227] have been
described. However, one of the most important sites of hernia-
tion which is now becoming important after trauma is the dia-
phragm (Fig. 80). Originally this occurred following penetrating
injuries such as gunshot wounds but now particularly follows
road traffic accidents as a result of the blunt injuries which
can be sustained. Three phases have been described; the initial
or post-traumatic phase, the latent or interval phase, and the
late or obstructive phase. One of the earliest descriptions of
this clinical picture was by AMBROISE PARE in 1564 [168]:
"A captain received a gunshot wound, the ball entering at
the end of the sternum near the ensiform cartilage, passing
through the muscular part of the diaphragm and emerging

122
 b

c
a
Right Hiatal Peri- Let Trans-
cord ial costal
n=37 n =17 n=454 n=25
(6.9%) (0) (3.20J0) (85.3 0J0) (4.6 0J0)

Fig. 80. a Location of trau- between the fifth and sixth true ribs on the left side. The
matic diaphragmatic lacer- wound healed externally (end 0.[ initial phase) but he continued
ations (TA) in 533 ruptures
reviewed from the litera- to have a stomach disorder like a sort of colic so he could
ture [247]. Most are caused eat only sparingly. Eight months later (end 0.[ latent phase)
by blunt accidents (67,4%) he developed severe colic-like pain in the epigastrium and
and only 0.3% occur spon-
taneously. band c show
died (end of obstructive phase). At autopsy, in the thorax was
the two types of hiatal found a large part of the colon filled with air; it had entered
hernia containing the through a hole only large enough to admit the tip of the
omentum in the hernial sac little finger made through the diaphragm by the wound".
After blunt trauma a similar picture can be observed. The period
between the original trauma and subsequent diaphragmatic her-
niation may be several years [32, 132]; the high mortality of
20%-35% reviewed by WALDSCHMIDT et al. [247] may relate
to failure of recognition of herniation and incarceration; the
results of immediate repair of acute diaphragmatic hernias have
been reported as good [51, 133].
Though the bowel more commonly herniates into the pleural
cavity following diaphragmatic injury, strangulated omentum
has been reported [181, 217]. Help in distinguishing herniated
omentum from other intrathoracic tissue can be obtained by
computed tomography [188].
Iatrogenic internal herniation after surgery may occur either as
an early or a late complication. The omentum may be involved

123
Fig. 81. Inguinal hernia
containing the omentum in
the hernial sac. (Courtesy
of Prof. VAUBEL, Berlin;
from VON DE BOURGERY,
Traite complet de ('anato-
mie de ('homme, 1840)

in hernias especially after surgery of the diaphragm and gastro-

esophageal junction and the raising of a colostomy when the
lateral space has been inadequately closed.
External Hernias Acquired external hernias almost invariably occur at sites of
congenital weakness, for example, at the femoral canal. Previous
surgery of the abdominal wall may also lead to weakness or
distortion at sites such as the obturator canal or lumbar triangle.
The omentum may well be the most common organ in epigastric
hernia [140] and in the true umbilical hernias of childhood,
but figures of the incidence are difficult to obtain as most resolve
spontaneously [160]. Inguinal hernias in the adult commonly
contain the omentum (Fig.St), and it has repeatedly been re-
corded that hernias containing the omentum are less tender on
palpation [52, 164].
In small and incarcerated hernias it is difficult to be clinically
certain whether bowel, omentum, or both are present (see also
[52]). The importance of distinguishing this does not affect man-
agement significantly. It is often possible to be more certain
whether larger hernias with wide necks contain the bowel or
not. Auscultation and palpation in these patients may influence
the decision of whether surgery is advisable in cases where ob-
struction is progressing to strangulation.

124
 Although the sites where external omental hernias develop may
be related to some congenital weakness at, for example, the
femoral canal, previous surgery of the abdominal wall may lead
to weakness or distortion at sites such as the obturator canal
or lumbar triangle. Occasionally the omentum has been ob-
served to occlude hernial necks in children and adults by adhe-
sions preventing the bowel prolapsing into the hernial sac.
Traumatic Herniation. A sudden rise in the intra-abdominal
pressure following injury may lead to the development of a
hernia at a site of congenital weakness or a scar.
Iatrogenic external omental prolapse may follow almost any sur-
gical procedure on the abdomen but is less common after mus-
cle-splitting than muscle-cutting incisions. Omentum presenting
at the suture line of a laparotomy incision often accompanies
a dehiscence of the deep layers of the wound. If the deep layers
dehisce after the skin has healed, an incisional hernia which
may contain bowel and omentum develops.

Open Hernias Traumatic open prolapse of the omentum often follows a pene-
trating abdominal injury and has been described since classical
times [71]. There is also a report of omental herniation through
the abdominal wall of a newborn infant after intrauterine ex-
change transfusions [125].

7.3.2 Symptoms, Signs, and Diagnosis

Post-traumatic diaphragmatic hernia may cause cardiorespira-

tory disturbances, shock symptoms, and gastrointestinal compli-
cations, even after a prolonged interval [247]. The symptoms
and signs of internal and external herniation with the omentum
in the sac clearly depend to a large extent on the site of hernia-
tion. Ileus and a developing picture of intestinal obstruction
in both young and old is described [94, 232].

7.3.3 Treatment

Treatment should be along established principles, reducing the

omentum together with the hernia and repairing the defect. Dif-
ficulty in reducing the omentum may be experienced if there
are adhesions to the sac. These occur after episodes of inflamma-
tion which may follow subacute obstruction, untreated incarcer-

125
 ation, and the trauma produced by an unsatisfactory truss. In
these cases where the omentum is damaged or strangulated it
is necessary to resect and not return devitalized tissue to the
peritoneal cavity.
Wound dehiscence clearly req uires repair. Although autoampu-
tation or surgical ligation was practised in cases where the
omentum presented following injury, exploration is now manda-
tory. Herniation into diaphragmatic defects also requires sur-
gery with either transthoracic or transabdominal access.

7.4 Adhesions
H. WHITE and H. TILL MANNS

7.4.1 Pathology

Introduction. Any trauma to, or inflammation of, an abdominal

organ, and most foreign bodies which enter the abdominal cavi-
ty, result in peritoneal adhesions (Sect. 5.2). Adhesions, there-
fore, are common after laparotomy and may obstruct the access
to the peritoneal cavity if re-exploration is required. Early ac-
counts of omental adhesions date back to JOBERT DE LAM BALLE
[97], HENNECKE [85], and ECCLES [52]. They observed that the
omentum mounts a mechanical barrier against infection by its
inflammatory adherence to the viscera, sealing off a focus of
bacterial invasion and converting the potential source of wide-
spread peritonitis into a focal abscess. Recently ELLIS [58] and
MYLLARNIEMI et al. [154, 155] studied the adhesion-inducing
mechanisms of the omentum in detail (for review see Sect. 5.2).

Congenital Adhesions A number of congenital peritoneal adhesions and folds are pres-
ent in neonates. These are variable and may be found between
the parietal and visceral peritoneum, between organs and the
peritoneum, and on occasion may form pouches, e.g., paraduo-
denal fossae. Normally the omentum is quite distinct from these
congenital peritoneal adhesions and folds (Sect. 7.1). However,
in malrotation of the bowel and gastroschisis the greater
omentum, although small (Sect. 7.1), may become involved in
the defect and form abnormal attachments by developmental
adhesions. This occurs most commonly at the hepatic and
splenic flexures (Sect. 7.1).

Post-traumatic Surgery is perhaps the most common cause of adhesions. In

Abdominal re-exploration of the abdominal cavity, whatever the disease
Adhesions process, adhesions were found most frequently in the area of

126
 laparotomy scars, followed by those close to the visceral scar.
The number and extent of previous operations increased the
amount of omental adhesions encountered [154]. Completely
"aseptic and atraumatic conditions" caused less abundant adhe-
sions, which disappeared spontaneously [154].
After handling and retraction, the omentum may adhere to areas
of blunt trauma, to sites of anastomosis, or to sites of other
definitive surgical procedures. Mass ligatures or injury on the
omentum itself will lead to an area of ischemic necorosis and
predispose to adhesion formation. Another well-documented
factor in adhesion formation is the talc and other dusting
powder which can be transmitted from surgeons gloves. There
is also evidence that adhesions form at sites of ischemia within
the peritoneal cavity or of the omentum itself [58].

Inflammatory Infection, however, leads to an inflammatory response and after

Abdominal the chance arrival of the omentum at the site of infection, adhe-
Adhesions sions usually develop. The advent of the omentum helps to
contain the infection but may result in the formation of perma-
nent adhesions. Adhesion formation is a very rapid process fol-
lowing injury and inflammation (see Sect. 5.2 [154, 155]. The
concept is that injury - both direct and transmitted - induces
an inflammatory response and a fibrinous exudate, and fibrous
adhesions develop within a few hours [58]. Some fibrous adhe-
sions become organized with an ingrowth of many capillaries
while others remain as a fibrous avascular scar. The character
of adhesions varies, and they may be soft and filmy, vascular,
or fibrous. Adhesions to the abdominal wall or viscera are found
to cover large areas or form small fibrous cords.

Splenic Flexure Trac- This syndrome has been first described by MAcHELLA et a1. in
tion Syndrome 1952 [128]. Discomfort or pain in the left upper abdominal
quadrant (often referred to as the precardial area, left flank,
or lateral thoracic area) left shoulder, and arm may be caused
by gaseous distension of the splenic flexure and partial bowel
obstruction due to abdominal adhesions [137]. Diagnosis of the
adhesions is difficult because physical and radiological findings
are not characteristic. Diagnostic criteria are the history of previ-
ous abdominal surgery, increased discomfort after a heavy meaL
and increased pain with colic distension resulting from feces.

Adhesions to Pelvic The gynecologist is frequently confronted with the question of

Organs whether lower abdominal pain is caused by adhesions. Acute,
chronic, or recurrent localized or diffuse lower abdominal pain.
intestinal spasms, back pain, dismenorrhea. painful sexual inter-
course, adnexalgia, abdominal pain during pregnancy. and pri-

127
 mary or secondary sterility all may be caused by omental adhe-
sions to pelvic organs [67, 129, 213, 241]. Sometimes the adhe-
sions are well vascularized enough to become the main blood
supply to pelvic cysts and uterine myomata. The history of pre-
vious operations, or gynecological diseases such as pelvic inflam-
matory disease, may help with the diagnosis when physical find-
ings are not characteristic.

7.4.2 Symptoms, Signs, and Diagnosis

Clinical Picture. Non strangulating or incomplete omental adhe-

sions usually show no clinical symptoms. Some adhesions, how-
ever, lead to intermittent or chronic pain. Occasionally bowel
obstruction with pain, vomiting, constipation, and abdominal
distension may be caused by fibrous omental cords.

7.4.3 Treatment

If omental adhesions are found by chance at laparotomy they

should only be divided if it is judged that complications might
subsequently occur, unless division is required to provide access
to the desired site. When laparotomy is undertaken for an acute
abdominal emergency and it is found that the cause is adhesions,
the omentum is mobilized as delicately as possible and the
vessels ligated individually with absorbable ligatures to minimize
the further formation of adhesions. Care has to be taken in
the presence of newly developed adhesions because the underly-
ing organ may be perforated. Dissection of the adhesions and
partial omentectomy usually relieve the symptoms of the splenic
flexure traction syndrom. The indications for surgery should
be critically judged. In gynecological operations laparotomy is
preferable to the vaginal approach if extensive adhesions are
expected. The technique of adhesiolysis is described above, but
the access to the pelvic organs may be even more difficult. Al-
though omental adhesions can complicate vaginal gynecological
operations, they are often less significant because the adhesions
are located above the uterus.

DanKer Point Laparoscopy following previous abdominal sur-

gery or peritonitis can be dangerous as the omentum may be
adherent to the anterior abdominal wall or organs and be at
risk of laceration with the insertion of the instrument (see
Sect. 7.2). In addition to laceration and the possible develop-
ment of further adhesions or damage to neighboring organs,
hemorrhage is the main danger.

12H
 7.5 Omentitis, Inflammatory Reactions, and Parasites
U. GROSS

7.5.1 Pathology

Definition The term" omentitis" is used to distinguish the inflammatory

process involving the greater omentum from epiploitis, which
also includes the inflammation of the lesser omentum and the
appendices epiploicae [27]. Although often occurring with a gen-
eralized or localized peritonitis of the visceral or parietal perito-
neum [52, 261], omentitis gives a separate clinical picture [26,
27, 56, 178, 255].
Classification Historically omentitis was classified according to its appearance
[193] into" plastica simplex, plastica adhaesiva, or plastica pur-
ulenta," or according to its etiology [166] into spontaneous,
post-operative, or post-traumatic forms. For clinical purposes
the latter classification is sufficient and further subdivisions
[166] are of no practical value [255].
Spontaneous omentitis occurs with:
Bacterial infection due to chronic appendicitis, pelvic inflamma-
tory disease, cholecystitis, and pancreatitis [56, 166]
Infection due to foreign material (fish bones, needles, splinters
of wood, coproliths) following intestinal or uterine perforation
[8,56,161,166,244]
Compression and incarceration in a hernial sac [52, 189]
Torsion and infarction of the omentum (see Sect. 7.6)
Parasites
Specific changes of the omentum, for example, in the presence
of tuberculosis [52, 209, 249], Boeck's disease, syphillis, and
gonorrhea [27, 52]
Yersinia (WALDSCHMIDT, personal case, 1980) and actinomyco-
sis [147]
Postoperative Omentitis. The operations which precede omentitis
are most frequently herniotomy, appendectomy [166. 176]. cho-
lecystectomy, and gynecological operations [17, 161]. The most
common predisposing factors are suture material, fibers from
swabs and talc [88, 219], X-ray contrast medium [135. 136],
other foreign bodies [44], and residual feces [27,56. 166,155].
Post-traumatic Form. Trauma of the omentum, hematoma, and
iatrogenic foreign bodies may cause omentitis [17, 51. 56].
Frequency About one hundred cases. six of whom were children (W ALD-
SCHMIDT, personal cases) have been reported in the literature
since the first account was given by PIPELET and POUTEAU [180].

119

Macroscopic
Picture
Idiopathic Omentitis
Fig. 82. Postoperative
omentitis. Greater
omentum dissected 59 days
after gastric resection for
gastric ulcer without perfo-
ration (male 49 years). The
omentum changed into a
firm plate-like mass with a
puckered surface. (GROSS)
5 em
130
However, a higher incidence of omentitis can be assumed [166],
because only the cases with clinical symptoms are actually re-
corded and also omentitis is clinically difficult to identify [17,
176].
The macroscopic appearance varies in the different forms and
stages of omentitis; it may involve the entire omentum or only
part of it and often produces adhesions.
Postoperative omentitis is five times more common than the
spontaneous form [27]. Initially hyperemia, tissue thickening,
and ascites are observed. Later, nodular or disk-shaped firm
swellings are found in the inflamed omentum. This gives the
surface a rough and uneven appearance (Figs. 82, 83), and in
the late stages gray-red granite-like hemorrhages, puckering, and
rolling of the omentum may occur [27, 52, 56]. Islands of fatty
tissue which seem to be normal are scattered in the changed
areas (Fig. 84a). When the omentum walls off pus it becomes
thickened and vascular. In the early stages it is edematous, and
later firmly adherent [150].
The histological picture shows variably developed granulation
and scar tissue arranged in a laminar or reticular pattern [75]
(Fig. 84 b). It is more densely interspersed with leukocytes, lym-
phocytes, plasma cells, histiocytes, and fibroblasts (Fig. 85 a, b).
Fig. 83. Nodular surface
partly caused by string-
shaped or confluent adhe-
sions between fatty lobules
following the organization
of the exudate. Same case
as Fig. 82. x 4 (GROSS)

The localization of cellular infiltration is predominantly perivas-

cular [26,27,56, 161, 166]. Absorbent fatty xanthous histiocytes
and xanthous granulations are observed in the marginal area
of necrosis of the fatty tissue [166, 255] as well as giant cells
[27, 56]. NYLANDER [161] has observed eosinophilic leukocytes
at this site but does not explain their significance. WINTER [255]
describes tubular abscesses surrounded by cell girdles made up
of epithelioid cells, fatty histiocytes, multinuclear giant cells with
vacuoles, phagocytized leukocytes, drops of oil, and nonspecific
arteritis.
In the early stage of inflammation, exudation of fibrinogen,
formation of fibrin, and migration of cells - primarily leukocytes
and macrophages - occurs. Eventually this becomes organized
and leads to the nodular swelling mentioned in the macroscopic
appearance of omentitis.

Nodular Mesothelial In two infants, seven children, and four adults, ROSA! and
Hyperplasia in DEHNER [189] found tumor-like reactive proliferative changes,
Hernial Sacs which were restricted to some prolapsed omental areas. ROSAI
et al. compared them with squamous metaplasia of the peritone-
um. Histologically they are solid nodules with typical mesothe-
lial cells, abundant mitoses, polynuclear cells, and so-called strap
cells.

Nodular Panniculitis In various lipoid dystrophies, the omentum may become in-
(Lipoid Dystrophies) volved. Abnormal fat collections may be seen in children with

131
a

132
 Fig. 85. a Progressive fi-
broplasia and focal round
cell and leukocytic inflam-
matory infiltration of the
omentum . x 100 b Chronic
fibroblastic and granulat-
ing omentitis; focally de-
generated fatty tissue
(arrow). Same case as
Fig. 82. H & E, x 100
(GROSS)

~ Fig. 84a, b. Macroscopic

section with coarse or fine
reticular fibrosis between
some larger and almost
normal fatty nodules.
Small round indentations
in the fatty tissue at the
site of oil cysts (arrows).
Histological section. HE
x 6; a and b are the same
case as shown in Fig. 82
(GROSS)
nodular nonsuppurative panniculitis [86]. Mesenteric panniculi-
tis or systemic nodular panniculitis may also involve the
omentum [87, 220, 225, 242] and is regarded as a variant of
Christian-Weber disease. Women seem to be somewhat more
frequently affected than men, the ratio being 1.8: 1 and the aver-
age age 53 years (7-82 years, [50]). According to STEINBERG
[225], irregular nodular manifestations can also be observed
in other organs. The microscopic features are similar to those
described above. The pathogenesis is unknown.

133
 Fat Necrosis of the Omentum in Pancreatitis
P. HEITZ

Fat Necrosis Pancreatitis is classified [192] into: acute and relapsing acute
pancreatitis; and chronic relapsing and chronic pancreatitis.
Incidence. The disease is rare in children; the mean age of all
patients is about 55 years [73].
Clinical Picture. (See Sect. 6 and [49].) Should laparoscopy or
laparotomy be undertaken, conspicuous lesions are found,
especially in the acute necrosing form of the disease, but not
in its early phase, e.g., in acute interstitial edematous pancreati-
tis.
Pathology. Macroscopically the predominant finding is fat ne-
crosis, e.g., yellow-white and chalky foci which may be scattered
all over the omentum and the mesentery of the intestine. In
addition, the peritoneal cavity contains a slightly turbid, brown
tinged fluid with globules of oil. In later stages of the disease
this fluid may become infected and produce suppurative periton-
itis. Histologically acute fat necrosis consists of foci of shadowy
outlines of adipose cell membranes filled with pink, granular,
opaque precipitate. This is most probably fatty acid released
from triglycerides by pancreatic lipase. The fatty acids subse-
quently combine with calcium; this is called saponification and
forms white-chalky calcified foci. The leukocytic reaction to the
fat necrosis is only moderate (Fig. 86).
The lesions are characteristic for acute necrosing pancreatitis,
but are not pathognomonic because they may occur after duode-
nal perforation or traumatic injuries of adipose tissue. In general
there are no omental lesions found in chronic pancreatitis.

Fig. 86. Acute necrotizing

pancreatitis. Necrosis of
adipose tissue precipitate
and beginning of saponifi-
cation. Leukocytic reaction
(riKht). H & E, x 130
(HEITZ)

134
 Tuberculous Omentitis
U. GROSS

Tuberculosis The frequency of reported tuberculous omentitis ranges between

3% [107], 29% [47], and 53% [23]. Younger women accounted
for nearly three-quarters (72%) of the 182 cases reported from
India [216] and 32 cases (65%) from Iran [23]. However, men
predominated in a study from England (60%, [107]).
Tuberculous omentitis is a local manifestation of an abdominal
tuberculosis and largely observed in the neighborhood of af-
fected abdominal organs [167]. It develops by spread of tubercu-
lous foci or, for example, the intestine in the ileocecal region
or salpinx. Transmission may be by direct spread or via lym-
phatics. Hematogenous tuberculous omentitis without involv-
ment of abdominal organs and the peritoneum is rare.
Numerous disseminated and/or confluent caseous tubercular
foci are described in both layers of the greater omentum and
in adhesions in the neighborhood [64, 167]. The exudation may
be serofibrinous or suppurative. It forms the basis for adhesions
and agglutination in the organization of the exudate, during
which the omentum can be transformed into a firm, elongated,
plate-like mass in the upper abdomen [52]. Occasionally the
omentum shrinks, and adhesions between loops of bowel almost
obliterate the peritoneal cavity (plastic peritonitis). Macroscopic
and microscopic changes in the omentum after intraperitoneal
injection of mycobacteria have been described by SEIFERT [207].

Parasitic Diseases
F.ZAK

The omentum has properties which tend to limit the spread

of infection. It is able to wrap itself around sites of inflammation
and wall off foci of infection. The omental vessels show an
inflammatory response and leak protein. The reaction persists
for a longer period than in other peritoneal vessels [250]. Parasit-
ic infestations are always accompanied by a more or less marked
granulomatous tissue reaction; this is characterized by the for-
mation of focal nodules composed predominantly of mononu-
clear-type cells and granulation tissue with peripheral fibrosis.
Dead parasites and their eggs and/or larvae, which are too large
to be ingested by phagocytes, become surrounded by macro-
phages which fuse to form large multinucleate giant cells. In-
volvement of the omentum has rarely been described and then
only in some parasitic diseases.

135
Fig. 87. a Initial circumoval
granuloma in the omentum
showing an egg of Schisto-
soma mansoni (with promi-
nent lateral spine) in the
center. H & E, x 250
b Advanced "healing"
circumoval granulomas in
the omentum with rem-
nants of egg capsules (1)
and with giant-cell forma-
tion (2). H & E, x 100
(ZAK)

Trematodes In schistosomiasis (bilharziasis), due to massive infection with

Schistosoma (S. mansoni or S. japonicum), pairs of male and
female adult worms (10-25 mm) may occasionally be found in
the veins of the omentum during surgery or autopsy. Sometimes
numerous ectopic miliary nodules showing the histological ap-
pearance of egg granulomas (pseudotuberc1es) are seen in severe
infection (Fig. 87 a, b), especially with S. mansoni and S. japoni-
cum [20, 53, 221], and occasionally S. haematobium [24]. Rarely
large (1-4 em) pseudotumors, "bilharziomas," may develop in
the omentum. These are localized masses of fibrous inflammato-
ry tissue usually containing many eggs, and are probably caused
by a reaction to the eggs produced by one or more pairs of
worms in a single site; altered host reactivity may also be a
factor [20].
In paragonimiasis, abdominal infestation is much less common
than in the lungs. Free adult worms have been noted in the
abdominal cavity with an associated fibrinous exudate contain-
ing ova and eosinophils. Abscesses due to the presence of adult
worms have also been seen in the omentum [53]. Granulomatous
inflammation of the omentum may occasionally be provoked
by other types of trematode which are known to migrate to
ectopic sites [15]. BEAVER et al. [15] found numerous small

136
Fig. 88. Hydatid cysts in
the omentum. Scoleces (1)
of Echinococcus granulosus
in the broad capsule (2) are
attached to the germinal
layer by a short stalk (3).
H & E, x 250 (ZAK)

granulomata containing trematode eggs in the omentum of a

19-year-old man in Honduras, which were identified as those
of Achillurbainia recondita, a trematode parasite of the opossum.

Cestodes The occurrence of single or multiple hydatid cysts of variable

size (up to 10 cm) in the omentum (Fig. 88) has been described
[7, 10,41, 77]. Infection by larval tapeworms of the genus Echin-
ococcus has been a serious problem, especially in some sheep-
raising regions. The unusual localization of hydatid cysts in
the omentum may create serious diagnostic and therapeutic dif-
ficulties. During surgery, cysts containing viable scoleces should
be sterilized before drainage or extirpation to prevent spread
and anaphylaxis [20].
Sparganosis refers to infection by a sparganum or second stage
plerocercoid larva of certain pseudophyllidean tapeworms. The
majority of infections in man are caused by larvae of Spirometra
mansonoides; the adult tapeworms live in the intestines of dogs
and cats. In severe infections, cystic nodules containing viable
spargana and surrounded by granulation tissue with circumfer-
ential eosinophilia, or small abscesses, may also be found in
the omentum [20, 221]. Diagnosis depends upon gross and mi-
croscopic identification of the sparganum.

Nematodes Eosinophilic [159, 233] or granulomatous [16, 191, 197, 233]

omentitis has been described in women with ectopic extra-intes-
tinal enterobiasis (Fig. 89). It is generally accepted that adult

137
Fig. 89. Ova of E. l'ermicu-
laris within the suppurative
area of the omentum.
H & E, x 320 (Courtesy of
Prs. INGLIS and MURPHY,
Dept. of Surgery Universi-
ty Hospital Saskatoon,
Canada)

worms of Enterobius vermicularis may wander from the perine-

um into the female genital tract and thence into the peritoneal
cavity [16, 233]. Suppurative, eosinophilic, or granulomatous
inflammation may arise around both degenerating adult worms
and chitinous material from the ova in the peritoneum,
especially the omentum [20, 191, 233,235, 244]. Exceptionally,
similar inflammatory lesions were described in a male patient
with perforated appendicitis [21, 197). Minute necrotic lesions
surrounded by a variety of inflammatory cells including many
eosinophils and fewer giant cells were noted in the omentum
in toxocariasis (visceral larva migrans) [221, 257]. These micro-
scopic lesions usually heal leaving very small scars. Migration
of some other nematode larvae may ocassionally evoke similar
histological changes, namely those of Ascaris lumbricoides [53],
Necator american us [53], Strongyloides stercoralis [20, 31, 96],
Ascaris suis [53], Ankylostoma caninum [53], Oesophagostoma
[78, 221], and Anisakis [20, 259]. Serial or step sections, howev-
er, may be required to find the parasite. Granulomatous omenti-
tis around Ascaris lumbricoides eggs has been observed following
perforation of suppurative cholangitis in ascariasis [20, 42].

Filarial Nematodes In Bancroftian and Malayan filariasis, degenerating dead adult

worms produce a spectrum of inflammatory changes from acute
suppuration to chronic granulomatous reaction and fibrosis.
These changes may obstruct lymphatic vessels and cause lym-
phangitis, lymphatic varices, chylous cysts, and lymphedema
[20, 36]. These conditions may occasionally occur in the
omentum [20].

138
Pentastomids Granulomatous peritonitis and omentitis were observed around
encysted degenerating pentastomid larvae [20]. Adult worms in-
habit the respiratory tract of reptiles and the nasal passages
of some mammals. Man may infect himself through contamin-
ated water or vegetables, and then serve as the intermediate
host.

Protozoa In the algid type of fatal acute falciparum malaria, congestion

with capillary stasis and hemorrhages may be noted in the
omentum. Microscopically, congested capillaries and small veins
were seen to contain many parasitized erythrocytes [53, 130,
221]. Malarial parasites may also be found lying free in the
blood vessels together with masses of malarial pigment (hemo-
zoin) [20]. The omentum is usually involved in diffuse amebic
peritonitis, which is a serious complication of perforated colonic
amebic ulcers or of amebic liver abscesses [5, 221].
In the subacute form of African sleeping sickness caused by
Trypanosoma rhodesiense, effusions in the pleural, pericardial,
and peritoneal cavities are common [53], and may contain try-
panosomes, lymphocytes, and mesothelial cells [20]. The
omentum shows congestion and edema but only minimal lym-
phocytic inflammatory infiltration [106]. In visceralleishmania-
sis (kala-azar), the causative protozoan parasite (Leishmania
donovani) shows a predilection for the reticuloendothelial sys-
tem. It may also be found in massive numbers in the cytoplasm
of histiocytes and proliferating reticuloendothelial elements in
the omentum and enlarged omental lymph nodes respectively
[53, 221].

Fungi and The omentum is usually involved in the relatively rare condition
Actinomycetes of abdominal actinomycosis [37]; trauma, inflammation or im-
munosuppression may be responsible for the infection [147].
The condition presents as a chronic suppurative process with
characteristic" sulphur" granules and very marked fibrosis. At
histopathological examination typical actinomycotic colonies
are obvious. Isolated intra-abdominal actinomycosis confined
to the greater omentum has also been described [138, 147].

7.5.2 Symptoms, Signs, and Diagnosis

V. SCHUMPELICK

Although it is often asymptomatic, omentitis may cause abdomi-

nal symptoms. This is on account of the extent of the inflamma-
tory process [27, 261] or of adhesions. Spontaneous pam or

139
 pain on pressure has been reported as well as nausea, vomiting,
wind, and constipation. In late stages of all forms of omentitis,
in tuberculous omentitis and in children with Christian-Weber
disease [86], intermittent or continuous pyrexia has been ob-
served.
Occasionally the thickened omentum can be palpated as a
mobile abdominal mass, and a protuberant abdomen with no
subcutaneous fat may be found in children with abdominal
omental fat collections or with Christian-Weber disease [86].
Parasitic diseases of the omentum may produce excessive adhe-
sion formation and signs of a subacute or acute abdomen. In
actinomycosis, serosanguineous ascites [138] or purulent effu-
sion [147] may be present. Omental echinoccoccus infestation
is rare and if present may be combined with parasitic invasion
of other organs, e.g., liver, lung (personal communications from
WALDSCHMIDT, 1980, and PISOITIS, 1980). In postoperative
omentitis an interval from several weeks to some years may
occur between operation and the development of symptoms [27].
Differential Diagnosis. Primary and secondary benign and malig-
nant tumors of the omentum (Sect. 7.7), intestinal tumors, and
tumors of retroperitoneal tissue must be considered [204].

Assessment Clinical. Careful examination of the abdomen is required in

an attempt to differentiate between omentitis which presents
as a superficial and freely mobile tumor and retroperitoneal
tumors, which are more deeply tethered and appear fixed [204].
Palpation in the knee-elbow position is of value, especially in
children (see Sect. 7.7).

Laboratory. Occasionally the ESR (erythrocyte sedimentation

rate) is increased. However, apart from nonspecific inflammato-
ry changes there are no special histological features. Tentative
diagnosis is verified by parasitological examination of the blood
and feces as well as of any tissue which can be obtained. In
malaria parasites are found in the blood, and actinomycosis
may cause extreme anemia [138]. Diagnosis of actinomycosis
becomes apparent from microscopy of the omental tumor
masses rather than from cultures of pus [147]. In schistosomiasis
sigmoidoscopy or cystoscopy may be important, and eggs are
sometimes found in the feces or urine.

Radiography
Gc>nc>ral Ahdominal Vic>w. Occasionally soft tissue shadows and
calcification may be found in chronic forms. Gastrointestinal
transit time is normal; only in the late stages does any anatomi-
calor functional change occur.

140
 Angiography. This is of value only in a few cases [39, 135].
Computed Tomography and Sonography (see Sect. 6.4) and Inva-
sive Investigations (Sect. 6.5). These may help with the diagnosis,
especially if biopsy is undertaken.

7.5.3 Therapy

Conservative Antipyretics, anti-inflammmatory agents, and antibiotics are

Treatment often effective in treating omentitis. Chemotherpy is required
in tuberculous omentitis [23, 47, 107] and penicillin alone or
with excision of diseased areas in actinomycosis [147].

Operative Treatment Indications for Surgery. Surgery is required if omentitis leads

to symptoms of an acute abdomen, for example, complicated by:
- Hemorrhage
- Peritonitis
- Fistula formation (external, intestinal, or urinary)
- Local abscess formation
- Displacement and obstruction of the bowel [27, 176]
Further indications are some parasitic infestations:
- Larger schistosomal pseudotumors (bilharzioma)
- Isolated abscess formation in paragonimiasis
- Echinococcus cysts
- Omental nodules in sparganosis
- Omental actinomycotic nodules
- Amebic peritonitis after bowel or liver perforation
However, surgery should not be undertaken unless it is clear
that resolution of the omentitis is not taking place.
Preparation for Surgery (Sect. 9.1)
Anesthesia. Combined intratracheal anesthesia with a good re-
laxation is req uired (Sect. 9.1).
Positioning. Supine position

Surgical Technique
Exposure and Resection. Midline incision in adults and trans-
verse upper abdominal incision in children give the best access
to the omentum. The abdominal cavity is explored to exclude
inflammatory foci such as appendicitis, adnexitis, cholecystitis
and diverticulitis, tumors, or other causes of bowel obstruction.
The affected areas are widely resected, taking care of the blood
supply to the residual omentum [201]. Adhesions must be de-
tached.

14 t
 Hydatid cysts need special care. Cysts containing viable scoleces
should be sterilized before extirpation to prevent anaphylaxis
[20]. Multiple echinococcus cysts [10] or actinomycosis [147]
usually require omentectomy, which is performed either along
the teniae omentalis of the transverse colon - or, if the gastro-
colic ligament is involved - along the greater gastric curvature
(for technique see Sect. 9.1,9.2). Lavage and drainage are usual-
ly required.

Results and Prognosis The risks of postoperative complications increase with septice-
mia, fistula, or hemorrhage, and postoperative peritonitis may
be a potential danger. If complications are not present and if
the affected areas can be removed completely, the results of
surgery are good and recurrence of omentitis is rare [27, 166,
255, 261].

7.6 Torsion and Infarction

P. TONDELLI

7.6.1 Pathology

Introduction. OBERST [164] gave the first clear account of

omental torsion in 1882 (Sect. 10.2), and an account of infarc-
tion of a twisted omentum was given by EITEL in 1899 [54].
In 1932 JOHNSON described omental infarction without torsion
[98]. These first observations were followed by numerous case
reports and successive reviews of the literature (infarction with
torsion: [2,11,12,29,68,76,127,131,172,223,238]; infarction
without torsion: [48, 62, 68, 175, 199, 200, 214, 258].
Most of the hypotheses concerning pathogenesis of this rare
condition were largely speculative and copied from earlier publi-
cations. In the literature dealing with infarction and torsion
of the omentum, despite the many reports, there is a poverty
of facts and little progress in knowledge over the last 100 years.
Usually omental infarction with and without torsion leads to
an acute abdomen, which demands laparotomy. If the surgeon
does not find the more common causes of an acute abdomen
such as appendicitis or cholecystitis, the possibility of omental
infarction must be considered to explain the clinical picture.

Classification and Epidemiology. There are two types of infarc-

tion:
1. Omental infarction with torsion:
Primary torsion, which is rare

142
 Secondary torsion, which is found with hernias, adhesions,
cysts, and tumors of the omentum
2. Omental infarction without torsion:
Primary infarction
Secondary infarction, which is found with hernias

1. Omental Infarction with Torsion

Primary Torsion Primary omental torsion is unipolar and similar to a bowel
volvulus (Fig. 90a). The edge of the omentum is not fixed but
freely mobile.

Incidence. In 1981 BASSON et a1. [12] reviewed 223 well-docu-

mented cases of primary omental torsion to which they added
five of their own. Primary omental torsion was most often found
between the ages of 30 and 40 years. The sex ratio of men to
women was 3: 2.

Pathogenesis. The causes of primary omental torsion are un-

known. As early as 1906 P A YR [172] worked experimentally
on omental torsion. Although his observations on cadavers are
of historical value they are scarcely more satisfying than the
speculative attempts of other authors to explain the cause of
the condition. LEITNER et a1. [119] reviewed the various hypothe-
ses in 1952; the following factors were suggested as predisposing
to omental torsion:
Anatomical variations such as long" linguiform." or bipartate
omentum
Irregular fat distribution in the omentum in adiposity
Abnormal arrangement of the omental blood vessels
The cause of torsion was attributed to "abdominal trauma,"
for example, a blow, a cough and compression, a sudden change
in position of the body, or hyperperistalsis of the bowel together
with passive omental movement.

Secondary Torsion Secondary torsion is bipolar (Fig. 90 b). The free omental edge
is fixed. having a second point of rotation, for example. in a
hernia, or resulting from an adhesion or an omental tumor.

Incidence. Although case reports are rare in the literature this

type of torsion may occur much more frequently than primary
or unipolar torsion. The rarity of reports may be explained
by the fact that omental torsion is recorded only as a secondary
finding in abdominal operations.
The youngest child reported with secondary omental torsion
was 4 months old [169]. WALDSCHMIDT et al. [247] operated on

143
144
<0lIl Fig. 90. a Primary omental
torsion. b Types of second-
ary omental torsion.
c Secondary torsion of the
omentum and spleen in
nonrotation and failure of
omental attachment.
d Omental infarction with-
out torsion
Primary Infarction
Fig. 91 a, b. Age and sex
distribution of children
with primary omental
torsion (a), and primary
omental infarction (b), re-
viewed by WALDSCHMIDT
a 9-day-old male with secondary torsion occurring together with
omphalocele, nonrotation of the bowel, and freely floating
omentum (see Sect. 7.1): the spleen was located at the edge of
the omentum (Fig. 90c), and torsion may have occurred intra-
uterinely because both omentum and spleen were already necrot-
ic. WALDSCHMIDT et al. [24 7] found reports on 16 children in
the literature; their age and sex distribution are shown in
Fig. 91 a.
2. Omental Infarction Without Torsion
Primary infarction usually involves a limited area (Fig. 90d),
and in contrast to the secondary infarction no recognizable
cause can be found.
Incidence. Primary omental infarction is rare and only about
100 cases have been reported to date. Among these, WALD-
SCHMIDT et al. [247] found 20 children, to whom he added one
of his own, a 9-year-old male (Fig. 91 b).
Pathogenesis. The pathogenesis of primary omental infarction,
which in turn is called idiopathic, is unknown and gives rise
7
n = 16
.•••...
5
'"
.a
E
:;)
z 3 ...
2 4 6 8 10 12 14
 to numerous hypotheses. These have been reviewed by SCHNUR
et a1. [199] in 1972; predisposing factors were thought to be:
Vascular, and hematological diseases such as Burger's disease
and polycythemia
Localized hemorrhage and thrombosis due to traction on a very
fatty omentum or abdominal compression
All these theories are, however, unconfirmed, as are the unsup-
ported anatomical attempts to explain the disease by embryolog-
ical abnormalities.

Secondary Infarction Like torsion, incarceration in a hernia leads to omental infarc-

tion of the so-called secondary type due to throttled blood circu-
lation.

Sequelae and Pathomorphology. Localized or generalized micro-

circulatory disorders after torsion or other causes may lead to
omental necrosis with hemorrhagic exudation and aseptic peri-
tonitis. Smaller foci of omental necrosis may become organized
and replaced by scar tissue (see Sect. 7.5) while larger necrosis
probably leads to abscess formation [2, 11, 76, 199].

7.6.2 Symptoms, Signs, and Diagnosis

Laboratory findings are not characteristic. Symptoms and signs

are similar in primary and secondary torsion and infarction,
and there is no difference between adults and children [247].
Abdominal pain and most often localized pain on pressure or
localized peritonealism is found. In omental torsion an intra-
abdominal mass has been palpated in one-third of the patients
[131]. The picture of an acute abdomen requires laparotomy.
For unknown reasons omental infarction, including primary in-
farction with and without torsion, occurs predominantly in the
right half of the omentum; most frequently, therefore, appendi-
citis or cholecystitis are suspected preoperatively. In the
223 cases reviewed by BASSON and JONES 1981 [12] the preopera-
tive diagnosis in 166 patients (74(~)) was appendicitis and in
57 (26%) was cholecystitis; occasionally ulcer perforations were
suspected preoperatively.
If the surgeon cannot find the expected cause of an acute abdo-
men during laparotomy, and other pathology is excluded, and
if hemorrhagic exudate is present, one should consider the rare
possibility of omental infarction and search for this condition.

146
7.6.3 Therapy

The treatment of an omental infarction with and without torsion

requires resection of the necrotic areas in the omentum. Remain-
ing infarcted tissue can lead to abscess formation. Simple resolu-
tion of the torsion is dangerous and should not be performed
because the omentum may subsequently become necrotic due
to the damage to the blood vessels. Omental resection may be
combined with appendectomy.

7.7 Tumors
F. GLOOR and J. TORHORST

7.7.1 Pathology
7.7.1.1 Benign Tumors

Introduction and Definition. Primary tumors of the omentum

arise from the normal histological structures of the greater
omentum. Accordingly there are tumors of fatty tissue, of con-
nective tissue with a possibility of bone and cartilage metaplasia,
of nerve tissue, of vessels (endothelium, pericytes, smooth mus-
cle), of peritoneal lining (mesothelium) and of the "milky
spots. " The latter consist of accumulations of non-differentiated
mesenchymal cells, histiocytes, lymphocytes, and to a lesser
extent also plasma cells and mast cells. These are effector cells
of the defense mechanisms of the omentum. For that reason,
the cellular composition of .. milky spots" varies ([34, 167] this
book, Sect. 4). The primary tumors of the omentum belong to
the multiform group of soft tissue tumors (Table 6. WHO [59]
1969, AFIP 1980). So far, approximately 250 soft tissue tumors
of the omentum have been described.

Incidence. The frequency of benign soft tissue tumors of the

greater omentum is unknown because there have been no sys-
tematic studies. The tumors seen intraoperatively are most often
found by chance because small tumors cause no clinical symp-
toms (see Sect. 7.7.2). The reported incidence. therefore. depends
upon the frequency of the various abdominal operations and
upon the systematic manner with which the omentum is
searched for tumors [249].
In the material examined in the Institute of Pathology in St.
Gallen, comprising surgical specimens from a predominantly
rural area with approximately 450.000 inhabitants. live benign

147
 Table 6. Histological classification of soft tissue tumors and cysts (modified
for tumors which may occur in the omentum. From histological classification
of soft tissue tumors. Armed Forces Institut of Pathology, Washington DC,
1980)

Tumors Benign Malignant

Tumors and tumor- 1. Fibroma 1. Fibrosarcoma

like lesions of 2. Nodular faciitis
fibrous tissue 3. Myxoma
4. Fibromatosis
II Tumors of fibro- 1. Fibrous histio- 1. Malignant fibrous
histiocytic tissue cytoma histiocytoma
III Tumors of adipose 1. Lipoma 1. Liposarcoma
tissue 2. Angiolipoma
3. Lipoblastoma
4. Angiomyolipoma
5. Myelolipoma
IV Tumors of smooth 1. Leiomyoma 1 Leiomyosarcoma
muscle tissue 2. Angiomyoma 2. Epitheloid
3 Epitheloid leiomyosarcoma
leiomyoma
(Leiomyoblastoma)
V Tumors of striated 1. Adult rhabdomyoma 1. Rhabdomyosar-
muscle tissue 2. Fetal rhabdomyoma coma
VI Tumors of blood 1. Hemangioma 1. Hemangioendo-
vessels 2. Hemangiopericytoma theliosarcoma
3. Angiomyoma 2. Malignant hem-
angiopericytoma
VII Tumors of lymph 1. Lymphangioma
vessels 2. Lymphangiomyoma
VIII Tumors of meso- 1. Localized meso- 1 Diffuse meso-
thelial tissue thelioma thelioma
IX Tumors of bone- 1. Chondroma 1. Extraskeletal
and cartilage- 2. Osteoma chondrosarcoma
-forming tissue 2. Extraskeletal
osteosarcoma
X Tumors of peri- l. Neurinoma 1. Malignant neuri-
pheral nerves (schwannoma) noma (neurogenic
2. Neurofibroma sarcoma)
2. Peripheral neuro-
blastoma
3. Clear cell
sarcoma
XI Tumors of the pluri- 1. Mesenchymoma 1. Malignant
potential mesenchyme mesenchymoma
XII Teratoma 1. Differentiated 1. Undifferentiated
teratoma teratoma

14~
Table 7. Primary omental tumors from two centers
in Switzerland

Benign 1 Fibroma 0
2 Lipoma • • 0
3 Leiomyoma 0
4
5
Hemangioma
Lymphangioma
•
•
• • 0
6 Mesothelioma
7 Chondroma •
8
9
Dermoid cyst
Hemangiopericytoma
•
0

Malignant 1 Diffuse mesothelioma •

The tumors shown are the findings of the Department
of Pathology, University of Basel (.) 1963-1977
(390,000 specimens of surgical pathology material)
and of the Institute of Pathology, St. Gallen (D)
1973-1979 (159,000 specimens of surgical pathology
material).

omental tumors were detected in 150,000 biopsies and surgical

specimens between 1973 and 1979. In the 390,000 biopsies of
the Institute of Pathology of Basel University (1963-1977) eight
benign soft tissue tumors of the omentum were found (Table 7).
STOUT et al. [229] state that from 1906 to 1961 in the Laboratory
of Surgical Pathology of Columbia University in New York
there were only 24 cases, of which 14 were benign and 10 malig-
nant.
Macroscopic and Histological Picture. Size and weight of
omental tumors vary considerably. Symptomatic tumors can
reach a weight of several kilograms. As a rule tumors are single
and distinctly demarcated. Multiple nodes of varying sizes are
found in cases of fibromatosis, leiomyomatosis peritonealis dis-
seminata, and lymphangiomatosis. Because of the difficulty of
radical operative removal these tumors tend to recur.
Classification. Histologically, corresponding to the origin of the
tissue, most of the primary omental tumors are mesenchymal
tumors from the large group of soft tissue tumors (Table 6).
Up to now, fibroma, lipoma, leiomyoma, myxoma, lymphangi-
oma, hemangioma, neuroma, and mesothelioma have been de-
scribed. Combinations of these types of tumors also occur.
Lymphangioma and leiomyoma seem particularly common in
the greater omentum. Larger tumors may show regressive chan-
ges in their center with necrosis, formation of cysts, and calcifi-
cations. The histological classification of benign tumors usually
offers no difficulty to the pathologist. Exceptions are the heman-
giopericytomas and the leiomyoblastomas. which are difficult
to classify into benign and malignant tumors.

149
 Age and Sex Distribution. Benign omental tumors occur in all
age groups [1, 229] ; WALDSCHMIDT refers to six children since
1963. There does not seem to be any sex preference.

Fibroma Of the four published fibromas, the size of only two is known
(17 x 15 x 9 cm, 5 x 2 x 2 cm), and data on age and sex in only
three cases (female 10,59 years; male 19 years).
A calcified fibroma in a 10-year-old male has been recently
found by WALDSCHMIDT. Histologically the tumors are rich in
collagenous fibers and may be calcified [55, 249]; in the 59-year-
old woman a multicentric tumor was present (Case from
St. Gallen).

Myxoma Both cases of myxoma known (male: 2, 33 years) were sympto-

matic because of their size (7 kg and 9,5 cm 0 respectively).
Histoligcally such tumors are characterized by elongated multi-
polar cells in a ground substance containing a great amount
of acid mucopolysaccharides [123, 229].

Fibromatosis There are no data available on the course of the disease in

the two patients with fibromatosis (female 42, male 71 years).
Histologically there is connective tissue containing many fibro-
blasts diffusely infiltrating the fatty tissue [229].

Lipoma Of the nine lipomas, age and sex are known in eight cases
(Female 3, 55, 56, 73 years; male 25, 25, 46, 53 years). The larg-
est tumor is 5 cm in diameter. Histoligcally the tumors are made
of mature fat cells and surrounded by a connective tissue capsule
[55, 80, 229], two cases are from Basel, one from St. Gallen).

Leiomyoma In this group of 12 cases with leiomyomas (female 4, 9, 23, 27,

45,47, 65 years; male 41, 42,52,65, 79 years), the size varies
between 4 mm and 20 cm in diameter (Fig. 92). Usually the
tumors are encapsulated by connective tissue. The large tumors
frequently show local regressive cystic changes. The histology
varies due to the different amounts of collagenous connective
tissue and the varying polymorphism of cells and nuclei in the
smooth muscle cells ([80, 124, 143, 229, 234] and one case from
St. Gallen). In women - particularly in cases of small tumors
- leiomyomatosis peritonealis disseminata must be differen-
tiated. This syndrome is interpreted as multicentric induction
of smooth muscle cell proliferation by the coelomic epithelium
(mesothelium) [103, 179].

Epitheloid Leiomyoma All four cases occurred in women. Age (49, 76 years) and size
(Leiomyoblastoma) (16,20 cm) are known in two cases. The tumors are encapsulated
and lobulated; on incision they are partly cystic with some areas

150
Fig. 92. Calcified leio-
myoma of the omentum in
a 52-year-old man. Inci-
dental finding on abdomi-
nal X-ray because of gas-
tric ulcer. Macroscopically
multilobular, hard, and
well-defined tumor
(to x 9 x 7 cm). (St. Gallen)

of necrosis. Histologically they are formed of large plump cells

with vesicular nuclei of varying polymorphism and ample cyto-
plasm [113]. The prognosis of such tumors in other locations
is dependent on the size, the number of mitoses, and the invasive
growth [116]. The differentiation of leiomyosarcomas on the
basis of morphological parameters is not always possible.

Hemangioma In our own cases, we found by chance an extensively hyalinated

hemagioma of the greater omentum (0 1 cm) in an 11-year-old
boy (Fig. 93). KOMI et al. [111] reported one case with intraperi-
toneal hemorrhage in a 6-year-old girl with Klippel-Trenaunay
syndrome, and DANZ et al. [46] described a malignant degenera-
tion of a hemangioma in a 49-year-old woman.

Hemangiopericytoma Four biologically benign hemangiopericytomas have been re-

ported (female 30, 50 years; male 63,92 years; 07, 8, 12, and
14 cm respectively). They are histoligically characterized by solid
cell groups surrounding proliferated blood vessels (Fig. 94). The
tumor cells are spindleshaped with eosinophilic or clear cyto-
plasm and regular oval nuclei. Each cell is surrounded by reticu-
lum fibers [229]. The biological behavior cannot be determined
with certainty from the histological pattern (see below: malig-
nant hemangiopericytoma [74, 229]).

Lymphangioma (See cysts of the omentum.)

Mesothelioma Two benign localized papillary mesotheliomas are known in

adults (female 41,61 years; 0 1.0, 5.5 cm respectively, [82], one
case Basel). Recently a mesothelioma involving the greater

151
Fig. 93. Hemangioma of
the omentum in an
ll-year-old boy. Incidental
finding at appendectomy.
Macroscopically firm, gray,
well-defined tumor (diame-
ter 1 cm). Histology : hya-
linized connective tissue
with multiple cavernous
vessels. (Basel) H & E x27

Fig. 94. Hemanigopericy-

toma in the omentum in a
50-year-old woman . Inci-
dental finding at hysterec-
tomy. A capillary coated
with pericytes is seen. (St.
Gallen) H & E, x 250

152
Fig. 95. Chondroma of the
omentum in a 30-year-old
black woman. Incidental
finding at laparotomy for
unexplained abdominal
pain. Macroscopically mul-
tiple firm gray-blue tumor
(diameter 1 cm). Histology :
multiple islands of cartilage
embedded in collagen
bundles. (Basel) H & E
x 15.5

omentum has been found by WALDSCHMIDT in a 3-year-old male.

Histoligcally, these tumors are composed of mesothelium-cov-
ered papillary connective tissue stalks containing tube-like glan-
dular formations.

Chondroma A 30-year-old black African woman with abdominal symptoms

of uncertain etiology was found to have multiple pea-sized hard
nodules in the greater omentum. The histological diagnosis of
one of these nodules was a polycyclically growing chondroma
(Fig. 95, case Basel). This is an isolated case in the literature.

Neurinoma and Only for one of the three known cases, were age, sex, and clinical
Neurofibroma findings published (female 5 years, tumor 0 8 em). The neurin-
oma (schwan noma) is characterized by partly intertwining
bundles of occasionally rhythmically arranged spindle cells with
oval nuclei surrounded by a fine net of collagen fibers. Large
tumors have localized areas of myxoid or fibrotic change. They
are not always well demarcated. In neurofibromas tumor cells
are separated from one another by varying quantities of collagen
[229, 249].

153
Teratoma About 20 teratomas are known. These probably originate from
sequestered parts of the ovary. Furthermore, an embryonic tis-
sue displacement or the development of a third ovary lying in
the omentum is discussed (literature in [91]). In addition, details
of three primary carcinoid tumors have been published [170,
249].

Tumors of Solitary extramedullary plasmacytoma and extramedullary mye-

Hematopoietic lopoiesis in the omentum are known in osteomyelofibrosis [104,
Tissue 173].

7.7.1.2 Cysts

Definition. By cysts we understand congenital or acquired

hollow spaces which do not communicate with an efferent duct
or the vascular system. True cysts are lined by endothelium
(mesothelium) or by epithelium, while false cysts (pseudocysts)
do not have such a lining.

Frequency and Age Distribution. Omental cysts are rare. In 1935

HORGAN compiled a table of 97 cases from the world literature
[89] and in 1964 OLIVER reported 150 cases, to which he added
three of his own [165]. Omental cysts are most frequently found
in childhood and young adults [89, 144, 165, 248]. LUCAYA
et al. [126] present a review of 36 omental cysts observed in
children and WALDSCHMIDT has tabulated from the literature
122 omental cysts in childhood (Fig. 96), to which he added
three of his own (female 8, 10 years; male 5 years). In adults
HORGAN [89] observed a more frequent occurrence among
females but WALDSCHMIDT found no sex difference in children.

30
Fig. 96. Age and sex distri- III
bution of 122 children with C
omental cysts. Reviewed by ~ 20
c
WALDSCHMIDT from the lit-
Cl.

"0
erature [13, 89, 165] and ....
E 10
Ili
three cases from W ALD-
SCHMIDT. Sixty-three of the Z
::I

122 children were female

56 were male, and in three
cases the sex was unre-
corded Age In years

154
Classification. According to the histological picture and the de-
velopmental mechanisms cysts can be classified into three
groups:

1. True Cysts Lined by Endothelium or Mesothelium. Most nu-

merous are the lymph cysts and lymphangiomas which are
occasionally interomental cysts following adhesions between
the omental peritoneal surfaces. The endothelium-lined cysts
are now generally classified with the lymphatic system [134,
156, 243]. Formerly an attempt was made to differentiate
between hematogenous and lymphogenous cysts [89]. Three
suggestions for the pathogenesis have been made:
- Developmental disturbance with abnormality in the lymphatic
system
- True benign tumor
- Drainage obstruction with secondary expansion of the lym-
phatic channels
A decision between these various possibilities on the basis
of the macroscopic and histological findings is not possible
in most cases.

2. True Cysts Lined by Epithelium. These are (a) dermoid cysts,

(b) cystic teratomas, and (c) urogenital cysts and intestinal
cysts. All are probably a result of tissue displacement [248].

3. Pseudocysts Devoid of Epithelium. Pseudocysts occur after

trauma and infection. They arise by liquefaction of adipo-
necroses, organization of hematoma, or bacterial inflamma-
tion with histiolysis. A typical picture is shown by the parasit-
ic pseudocysts, particularly the echinococcus cysts (see
Sect. 7.5).

Macroscopic and Histological Picture. Only the lymphogenous

cysts lined by endothelium will be described. The cysts can be
uni- or multilocular. They may be solitary or multiple (Fig. 97).
Their diameter ranges from a few millimeters up to 20 cm.
GANDHI et al. [72] described a 3.4 kg omental cyst in a 4-year-
old girl. The cysts generally contain serous fluid and more rarely
chyle or blood. The fact that the content of cysts is blood-stained
does not justify the diagnosis of a hemangioma, since there
can also be secondary bleeding into a lymph cyst [25].
Histologically cysts usually exhibit a very thin wall of connective
tissue and are lined on the inner surface by endothelium. Fre-
quently the endothelium is not detectable in some parts of the
wall because it has been destroyed secondarily by overdistension
of the cyst wall or inflammation. Occasionally hemosiderin de-

155
Fig. 97. Lymphangiomato-
sis of the omentum in a
52-year-old woman. Lapa-
rotomy for acute abdomi-
nal pain with torsion of
tumor. Symptom free
7 years after operation.
Macroscopically multiple
cysts in the omentum, en-
closed by connective tissue.
(St. Gallen)

, 2cm

posits or calcifications are found. In the case of thin-walled

lymph cysts no histological differentiation can be made between
primary abnormality and secondarily acquired expansion of the
lymphatic channels. The presence of a multichambered cyst with
endothelial lining and wide fibrous walls in which smooth mus-
cle cells and elastic fibers can be detected [13] permits the diag-
nosis of a lymphangioma or a hemangioma (Fig. 98).
Recurrence of a lymphangioma after surgical removal is rare
(one case in [248]). Malignant change in a lymphangioma of
the omentum has not as yet been observed and is unlikely.

7.7.1.3 Malignant Primary Tumors

Introduction and Definition. The majority of the malignant

omental tumors are metastases: WALSH and WILLIAMS [249] de-
scribed 2.9% primary tumors out of 272 malignant omental
tumors. In 15 years we detected one primary intraperitoneal me-
sothelioma and 334 omental metastases in our material at the
Institute of Pathology in Basel (see Sect. 7.7.1.4). In this case,
however, it was not certain whether its origin was actually in
the omentum.

Fibrosarcoma For 9 of 11 known cases, age and sex are published (female 24,
36,43,63 years; male 37,48,50,67,80 years). Prolonged follow-
up is known in only seven cases; in four of them, metastases
developed. These patients died 10 months to 7 years later. The
others were still living 4- 17 months after the operation, and
their subsequent fate is not known.
The size of the tumors varied between 15 and 30 cm. Macros-
copically the tumors were partly demarcated and partly invasive.

156
Fig. 98. Lymphangioma of
the omentum in a 20-year-
old woman. Incidental
finding at appendectomy.
Macroscopically there was
a sharply defined tumor in
the connective tissue sheath
(diameter 4 cm), with mul-
tiple cysts containing
yellow colloidal material
on section. Histology: mul-
tiple cysts lined with endo-
thelial cells embedded in
myxoid and hyaline con-
nective tissue. H & E x 16
(Basel)

Histologically the tumor tissue is either arranged in bands or

irregular islands. Collagenous and reticular connective tissue
are regionally very different even in the same tumor. Tumor
cell morphology varies from uniformly fusiform to bizarre poly-
morphic. Ultrastructurally, the cells show characteristics of
myofibroblasts [38, 99, 117, 122, 145. 249].

Fibrous So far, no such tumors occurring primarily in the omentum

Histiocytoma have been reported. This is probably due to the fact that the
morphological criteria were only recently defined. Some of the
previously unclassified sarcomas would now be classified as
malignant fibrous histiocytomas [55, 249,252]. Macroscopically
the respective tumors are multinodular, and usually well demar-
cated. Histologically, the great variability of the morphology
is characteristic; interlacing bundles of tumor cells are seen as
well as cartwheel cellular arrangements. Cytologically. cellular
and nuclear polymorphism is typical. As an indication of the
histocytic origin of the tumor, some of the cells store lipid drop-
lets or hemosiderin.

157
Liposarcoma The six known cases (female 60, unknown years; male 34, 47,
63, 65 years) are characterized by large (up to 10 kg) and some-
times multicentric tumors. Histopathologically, three cases show
the myxoid, one the round cell, and one the pleomorphic vari-
ant; the histological type of the sixth is not known. The various
morphological types of liposarcomas have been described by
EN ZINGER and WINSLOW [61]. Four cases have been followed
after diagnosis. Extensive metastases, e.g., local recurrence, were
described in two cases. Both died, one 2 days and the other
3 months postoperatively. The two others lived 3 and 6 months
postoperatively [84, 139, 146, 186, 229, 249].

Leiomyosarcoma For the four leiomyosarcomas (female 26, 29 years; male 38,
55 years) the maximal observation time was 18 months. In one
patient, who died 48 h after surgery, peritoneal metastases were
detected at autopsy. Two further patients died 36 hand
18 months after surgery. In one patient there was no follow-up
information available. Macroscopically, the tumors occurred
multicentrically and were well demarcated. Histologically, the
intertwining bundles of smooth muscles were characterized by
a long eosinophilic cytoplasm and varying content of collage-
nous connective tissue. The polymorphism of the cell nucleus
and the mitotic activity varies greatly. Prior to diagnosing a
primary leiomyosarcoma of the omentum, primary tumors of
the gastrointestinal tract or uterus must be excluded [38, 249].

Rhabdomyosarcoma The only case known occurred in a 53-year-old man. The prima-
ry tumor measured 8 cm. During the operation metastases were
found in the mesentery. The patient died about 6 weeks after
the operation. Histologically, there was no transverse striation
in the cytoplasm of this tumor [229].

Hemangio- The only case known was that of a 30-year-old woman. During
endotheliosarcoma the operation, apart from a large polycyclic and cystic omental
tumor, multiple peritoneal metastases were detected. No addi-
tional tumor spread was seen at autopsy 19 days later. The his-
tology was characterized by irregular, partly cavernous blood
vessels which were lined by highly atypical endothelial cells.
Solid tumor formation also occurred [101].

Malignant The three known cases (female 62 years; male 64, and unknown
Hemangio- years) died 110 years after the diagnosis with multiple metas-
pericytoma tases in the abdomen, lung, and brain. The primary tumors
weighed up to 2.5 kg, and were well demarcated. Histologically,
the tumor cells are arranged in solid, sometimes ring-shaped
formations around newly developed ramifications of sinusoidal

15X
 or capillary blood vessels. The single cell is surrounded by a
network of silver fibers. The tumor cells are uniform, round
to fusiform, with plenty of cytoplasm; the nuclei are oval and
regular [46, 60, 229].

Malignant (Difuse) Of the five documented cases involving the omentum (female 14,
Mesothelioma 65 years; male 3, 30, 32 years), three were found to have metas-
tases. In the female the differentiation of diffuse mesothelioma
from serous carcinoma of the ovary is not easy [102]. Macros-
copically, they were polycyclic, firm, and partly papillary
tumors. Histologically, there was a varying mixture of epithe-
lioid and connective tissue formation. Psammoma bodies may
occur [38, 55, 215, WALDSCHMIDT, personal communication,
1980). Etiologically, the exposure to asbestos may predispose
to the development of peritoneal mesotheliomas [212].

Extra-skeletal The only case described was that of a 54-year-old man who
Osteosarcoma died several months after diagnosis with peritoneal sarcomatosis
and abdominal lymph node metastases. The case is not a tera-
toma because no other tissue elements were present [245].

7.7.1.4 Tumor Metastases

Definition and Incidence. The majority of malignant omental

tumors are metastases. In the Institute of Pathology, Basel,
334 omental metastases have been documented in 15 years. The
most frequently observed primary tumors are cancer of ovary,
stomach, and colon (Fig. 99). Most omental deposits develop
as implants of tumor cells from peritoneal fluid. However, he-
matogenous, lymphatic, and transcoelomic spread also occur.

Macroscopic and Histological Picture. The macroscopic picture

varies from single minute gray foci to extensive adhesions or
tumor nodules. The omentum can become a thick indurated
sheet of tumor (Fig. 100). No conclusions can be drawn about
the primary tumor from the macroscopic spread, nor can defi-
nite conclusions about the primary tumor be drawn from histol-
ogy alone. Papillary growth and the formation of psammoma
bodies, for example, indicate an ovarian tumor (Fig. 101) but
may also be found in breast or thyroid cancer. Squamous metap-
lasia is a regular finding in endometrial adenocarcinoma, but
is also found in tumors of other sites such as the ovary and
pancreas.

159
Unknown
primary 76 10 Breast
tumor

Bil iary ducts 75 Stomach

27
+ pancreas

Co\on-
46 rectum
Ovary 94

6 Uterus

Fig. 99. Primary tumors in

334 cases of omental de-
posits. (Dept. of Patholo-
gy, University Basel,
1963-1977, surgical pathol-
ogy material)

Fig. 100. Omental metasta-

sis of a gastric cancer.
Macroscopic specimen.
( Basel)

160
Fig. 101. Omental metasta-
sis with psammona bodies
of an adenopapillary carci-
noma of the ovary in a
73-year-old woman. H & E,
x 150 CSt. Gallen)
Symptoms and Signs
Assessment
7.7.2 Symptoms, Signs, Clinical Diagnosis, and Therapy
V. SCHUMPELICK
7.7.2.1 Benign Tumors
Small omental tumors are usually discovered by chance during
laparotomy or autopsy. Usually there are no symptoms unless
the tumor reaches a certain size and displaces or compresses
bowel, stomach, or the urogenital tract. Frequently a giant ab-
dominal tumor is first noticed by the patient himself [254]. Com-
plications such as torsion of the pedicle, hemorrhage into the
tumor, or necrosis give rise to symptoms of an acute abdomen
[55, 117].
Clinical. The most important finding is a palpable lump which
is mobile. Superficial position, solid consistency, and lack of
fixation to the retroperitoneal tissue suggest an omental tumor.
Laboratory. Laboratory findings are not characteristic.
Radiography. The general abdominal view may show soft tissue
shadows, calcification, and displacement of viscera, suggesting
a space-occupying lesion. Truss pad effects, compression, or
displacement indicate an extraluminal site of the mass [90]. A
side view of the standing or hanging child is helpful for differen-
tiating between ascites, abdominal masses lying more posterior-
ly, and various malformations.
161
 Urography. Displacement or compression of the ureters may
be found in large omental tumors.

Angiography. Vessels with a curved course and a pathological

vascular pattern indicate the location and size of the tumor.

Computed Tomography (CT) and Sonography. These are the

most precise methods of noninvasive assessment [215, 224].
LEVITT et al. [120] examined 39 patients suspected of having
mesenteric or omental tumors. Twelve patients had negative
biopsies, and there were no false positive CT interpretations
in the group. However, 18 of the 27 patients with positive biop-
sies showed positive findings on CT scan.

Invasive Assessment Laparoscopy may confirm the diagnosis and operability by in-
spection and histological examination.

Differential Diagnosis Differential diagnosis includes the entire spectrum of intra-ab-

dominal space-occupying lesions. Among these are included
malformations of the intestine, choledochal cysts, ovarian cysts,
wandering spleen, and extraperitoneal tumors [203].

Therapy Conservative Treatment. If the diagnosis is established beyond

doubt as a benign tumor and the symptoms are not troublesome,
then in certain circumstances (e.g., age) surgical intervention
may not be justified.

Surgical Treatment. Small tumors without increase in size and

minimal or no symptoms need not be treated immediately. If
histological verification is impossible by laparoscopy or needle
biopsy, selective operation should be planned. In this way not
only is the histology confirmed but removal of the mass will
relieve the symptoms of compression and organ displacement.

Preparation for Surgery (See Sect. 9.1)

Anesthesia, Position, and Approach (see Sect. 9.1)

Surgical Techniques
Exposure (see Sect. 9.1).

Omentectomy. In benign tumors partial omentectomy is usually

sufficient. Care should be given to the blood supply of the resid-
ual omentum, no mass ligatures should be used, and careful
hemostasis undertaken. If excision requires bowel resection after
vascular impairment or through other damage, the general rules

162
 of bowel surgery are employed [201]. These principles hold in
ad ults and children.

Postoperative Care (see Sect. 9.1).

Prognosis The life expectancy with benign tumor is not reduced after com-
plete removal (see above). The recurrence rate is high in cases
of incomplete tumor resection [203].

7.7.2.2 Cysts

Symptoms and Signs The symptomatology of omental cysts varies. Small cysts are
usually discovered as chance findings at laparotomy and
autopsy. Subjective symptoms arise with growth of cysts, dis-
placement and obstruction of the lumen of bowel or stomach,
and painful protrusion of the abdominal wall. Complication
such as torsion of the pedicle, rupture, hemorrhage into the
cyst, or infection [10, 165, 169] occur with acute abdominal
symptoms. According to GLIVER [165], 15 of 150 cases compiled
from the literature showed the picture of an acute abdomen;
to these OLIVER added three of his own cases with acute symp-
toms. Rupture of a cyst is normally accompanied by bleeding
into the peritoneal cavity.

Assessment Clinical. Compared with other intra-abdominal tumors the

omental cyst is tense, lies in a superficial position, and is freely
mobile.

Laboratory. In echinococcus cysts CBR (Complement Binding

Reaction) is positive.

Radiography
General Ahdominal View. Soft tissue shadows, calcified patches
of echinococcus (old cysts), and mobile tumors may be distin-
guished.

Urography. Large cysts may cause displacement or compression

of the ureters.

Angiography is usually not necessary but an abnormal vascular

pattern of omental vessels can be demonstrated.

Computed TO/11ography alld SOl1ography [148]. These are the

best, non-invasive methods of diagnosing omental cysts.

163
 Invasive Assessment. Laparoscopy and laparotomy complement
each other [109]. Laparoscopy can achieve a diagnosis by in~
spection but with laparotomy excision of the cyst is possible.

Danger Points. Puncture of a cyst should not be performed either

at laparoscopy or at laparotomy because of the danger of dis~
semination of hydatid (see Sect. 7.5).

Differential Diagnosis Omentitis, omental, intestinaL and retroperitoneal tumors,

ascites [174], and cysts of the ovary, pancreas, spleen, and gall~
bladder must be considered. Complications may arise if the cysts
simulate acute appendicitis [3].

Therapy Conservative Treatment. Conservative treatment may be justified

if the cysts are asymptomatic.

Surgical Treatment. Depending on the symptoms and need to

establish the definitive diagnosis surgery can be planned. Imme~
diate operation is necessary with symptoms of intestinal obstruc~
tion and complications such as rupture, torsion of the pedicle,
hemorrhage, or infection. Relative indications of selective inter~
vention are small, asymptomatic cysts discovered by chance and
echinococcus cysts.

Anesthesia, Position, and Approach (see Sect. 9.1)

Preparation for Surgery (see Sect. 9.1)

Surgical Technique

Exposure and Resection. The access to the omentum is described

in Sect. 9.1. The cyst should be removed by dissection without
being opened. Scoleces of echinococcus cysts must be killed prior
to excision by installation of 40% glucose solution or formalin.
The wall of the cyst must be removed completely in order to
avoid regrowth by implantation. Marsupialization is reserved
only for emergencies with extensive infection or echinococcal
infestation [3]. The omentum should be checked for further
cysts, and care should be taken not to damage the residual
omentum, bowel, and mesenteric root. The defect in the
omentum is closed with absorbable sutures.

Results and Prognosis The results of operative treatment are good. Morbidity and mor-
tality are low. The risks are bleeding, bowel damage, infection,
and those due to anesthesia. The prognosis is good and recur-
rence is infrequent [248].

164
 7.7.2.3 Malignant Primary Tumors

Symptoms and Signs In the early stages of malignant tumor involvment symptoms
and signs are similar to benign tumors; in later stages the patient
may appear acutely ill with physical findings limited to the abdo-
men. The patient also may complain about dull ache in the
upper abdomen which radiates to the scapula [101]. In late
stages primary and secondary malignant tumors are often asso-
ciated with ascites.

Assessment Clinical. The abdomen may be diffusely tender and markedly

distended. The superficial position, solid consistency, and
mobile lump suggest an omental tumor. As metastases of un-
known primary tumors present as omental deposits, neoplasms
which are not located in the abdomen, for example, melanoma,
bronchocarcinoma and breast carcinoma, fibrosarcoma, and os-
teosarcoma should be considered [84].

Laboratory. Laboratory data are not characteristic. If metas-

tases of adenocarcinoma are suspected determination of CEA
is helpful.

Radiography. As in benign tumors, soft tissue shadows with

displacement of the gut can give the first indication [90]. Com-
pression or displacement of the ureters may be found in large
tumors of the omentum. Angiography may show an abdominal
course of vessels with a pathological pattern.

Computed Tomography (eT) and Sonograp/zy. These are the

most precise diagnostic methods (see Sect. 6.4) in the search
for metastases in the greater omentum. As screening methods
they cause least stress to the patient and can often be repeated
[224].

Endoscopy. If intestinal or urinary bladder wall involvement

is suspected assessment by preoperative endoscopy must be un-
dertaken.

Invasive Investigation. Laparoscopy with biopsy may confirm

the diagnosis.

Therapy Conservative Treatment. In advanced generalized malignant

tumor disease and local inoperability the attempt can be made
to treat the tumor with chemotherapy [190, 203, 239]. Similarly
palliative radiotherapy may be attempted.

165
 Surgical Treatment. Patients in good condition with operable
tumors of the omentum require surgery. In nonmetastatic, very
small, locally limited malignant tumors radical extirpation may
be achieved. However, with larger tumors, the possibility of
curative resection diminishes. Palliative measures even involving
colostomy may be required. The objectives of surgery are:
- Histological classification of the tumor
- Radical removal of the tumor
- Decompression of the stomach, intestine, mesenteric root, and
ureters
- Relief of complications such as bowel obstruction, hemor-
rhage, and tumor debris

Contraindications. Patients III a bad condition and with ad-

vanced local or widespread dissemination, invasion into the mes-
enteric root, and ascites should not undergo surgery.

Preparation for Surgery (see Sect. 9.1)

Anesthesia, Position, and Approach (see Sect. 9.1)

Surgical Techniques
Omentectomy. In small malignant primary tumors and omental
metastases, omentectomy with dissection along the transverse
colon preserving the gastrocolic ligament may be sufficient.
Large tumors require complete omentectomy (Sect. 9.2).
Extended Omentectomy. Tumor infiltration into the bowel wall
or lumen requires total omentectomy with removal of the
invaded bowel segment. Because the transverse colon is fre-
quently involved in the process, resection of the transverse colon
or eventually a hemicolectomy may be required.
Palliative Omentectomy. In generalized tumor disease, local
tumor reduction or palliative omentectomy can help symptoms,
and bowel obstruction can be treated by entero-enterostomy
or external stoma. The general rules of bowel surgery are applied
[201] during the operation.

Postoperative Care and Therapy (see Sect. 9.1)

Adjuvant chemotherapy may be attempted postoperatively III
malignant tumor [83, 190, 203, 239].
Adjuvant Radiotherapy. In the case of palliative tumor reduction
postoperative radiotherapy with fast electrons or neutrons
should be considered [215].

166
 Results and Prognosis. The operation risks depend upon the
general state of the patient, the extent of the intervention, and
the stage of the tumor. The necessity of opening the lumen
of the bowel, especially that of the colon more than doubles
mortality. Prognosis is very poor with malignant omental
tumors. Even after a radical removal of the tumor, a recurrence
rate of up to 80% and a rapid dissemination occurs. Preopera-
tive radiation, regional arterial perfusions, and adjuvant chemo-
therapy may improve survival [83, 139].

7.7.2.4 Tumor Deposits

Metastases of Ovarian Carcinoma
H. TILL MANNS

Pathology, Symptoms, In advanced ovarian carcinomas, metastases are frequently

and Signs found in the greater omentum. Since patients with ovarian carci-
nomas are usually late in presenting for treatment, omental me-
tastases are to be expected in 70% of cases [35, 182, 206]. Ac-
cording to the guidelines of FIGO [65], if there is tumor involve-
ment of the greater omentum, the carcinoma is classified as
stage III or IV and according to the TNM classification of the
UICC as stage T3.
Clinically the omentum often presents as a flat, solid, hardly
movable tumor in the mid-abdomen. It causes relatively little
discomfort, and at most a vague feeling of pressure or minor
discomfort.
Intra-operatively the tumor involvement of the omentum can
be seen ranging from individual, small, barely visible, or palp-
able metastatic nodules to solitary or confluent large tumors.
The omentum may become a rigid, board-like, and barely mov-
able tumor plate several centimeters thick. Due to transudation
from the dilated veins, the omentum that is infiltrated by carci-
noma is considered to be the main source of ascites.

Therapy According to current opinion, the plan of treatment for ad-

vanced ovarian carcinoma consists of the operative removal of
as much tumor tissue as possible. It is generally agreed that
resection of the greater omentum is recommended [35, 65, 108,
163, 182, 205, 206, 237]. Opinions diverge, however, concerning
prophylactic or obligatory omentectomy in early stages of
ovarian carcinoma if the omentum appears macroscopically to
be tumor ~ free at the time of operation. Advocates of omentec-
tomy believe that tumor spread and the development of ascites
can be delayed while opponents of the procedure fear that re-

167
 moval of the omentum as a protective organ will accelerate
tumor dissemination. There are no statistics available on the
significance of prophylactic omentectomy on survival time.

Surgical Procedure (Omentectomy in Ovarian Carcinoma). Es-

sentially, the procedure for resecting the omentum is simple.
The lower portion of the omentum is removed as far as the
transverse colon, leaving the upper portion intact. Isolated meta-
static nodules can, however, also be removed from the anterior
wall of the omental bursa. At its point of attachment to the
transverse colon, the omentum is divided. It is advisable to begin
the resection in the middle of the omentum and to continue
toward the flexures of the colon. It is not always possible to
follow the course of the omentum into the corners of the flexures
so that small portions remain. It is mandatory to sever the
omentum as close to the intestinal wall as possible. If the tumor
masses extend directly to the wall of the colon, the ligatures
tend to cut into the omentum, which leads to numerous minor
or even major hemorrhages. The hemorrhages stop spontane-
ously or after pressure is applied with a swab. If the tumor
has begun to infiltrate the intestinal wall, tumor tissue is inevita-
bly left behind. The decision to perform omentectomy at the
beginning or end of the operation must be based on the individ-
ual operative situation [35, 108, 205]. Occasionally, removal
of the omentum can represent the only possible palliative surgi-
cal method for treatment of ovarian carcinoma.

Metastases of Gastric Carcinoma

H. WHITE

Pathology The location, type, and size of gastric tumors all affect the
spread to the regional lymph nodes [93, 110, 231]. All types
of gastric cancer metastasize relatively early, invade the adjacent
structures, and disseminate into the mesentery and omentum,
which may be covered by numerous secondary carcinomatous
nodules or have changed into an indurated plate-like mass. In
this case ascites usually develops and is often hemorrhagic.
While tumors of the cardia and antrum of less than 2 cm are
found to have spread to regional nodes in only about 40%
of cases, tumors of the fundus and cardia of between 2 and
5 cm have lymph node metastases in some 80% of cases [231].
The lesser omentum, esophagogastric junction, splenic hilum,
and greater omentum are all anatomical sites of preferential
spread in view of their proximity. In attempted curative resec-
tion, therefore, these structures cannot be disregarded.

16X
Therapy Subtotal or total gastrectomy (see [93, 202, 236]), extended total
gastrectomy after McNEER, and radical clearance of the lym-
phatic fields of drainage [18], with outstanding results obtained
by the Japanese surgeons following extensive regional lymph
node dissection [110], have all improved the survival rate [93,
253].

Surgical Technique. In all attempts at curative resection and

even in early and small gastric cancers it is almost universally
recommended that the entire omentum is dissected from the
transverse colon and removed en bloc with the spleen, the malig-
nant gastric lesion, and the lesser omentum [18, 93, 110, 171,
202, 236, 253, 260].
In both subtotal and total gastrectomy it is recommended that
the dissection is started at the splenic flexure and continued
by sharp and blunt dissection toward the hepatic flexure (see
Sect. 9.2). The plane of dissection should split the plane of fusion
between the antrum and mesocolon so that the right gastroepip-
loic artery is clearly identified where it emerges at the inferior
border at the head of the pancreas. In case of inoperability
and palliative procedures simultaneous omentectomy may be
helpful if the omentum is involved in tumor growth.

7.8 Rare Tumor-like Changes

7.8.1 Tissue Deposits

D. LIEBERMANN-MEFFERT and F. GLOOR

Abnormal fat Abnormal fat collections in the omentum may occur in Chri-
Collections stian-Weber disease (non-suppurative panniculitis, see Sect. 7.5).
Lipodystrophy is characterized by inflammatory nodules in the
subcutaneous fat which leave shallow cutaneous depressions
after healing. HERNANDEZ et al.[86] found complete absence of
subcutaneous and mesenteric fat but an extremely fat omentum
in a 5-year-old girl. PETERMANN [177] operated on patients ad-
mitted for gastric ulcer disease in whom a extremely fatty
omentum had caused the gastric symptoms.

Splenosis Splenosis, first described by BUCHBINDER and LIPKOFF in 1939

[33], is the condition in which nodules of splenic tissue are
scattered throughout the omentum, on the serosal surfaces of
the viscera or mesentery subsequent to traumatic rupture of
the splenic capsule and seed of splenic pulp [43, 66, 226, 228,
251]. STEPHENSON et al. [226] reviewed 54 cases in which the

169
 implants were predominantly located on the omentum. As they
rarely cause symptoms splenic implants have no clinical signifi-
cance and are discovered by chance at surgery or autopsy
months or years after the trauma. Occasionally, however, sple-
nosis causes episodes of abdominal pain, and cord-like adhe-
sions with intestinal obstruction have been described [226].
The splenic nodules vary in number from a few to 400. Usually
they range in size from a few millimeters up to 3 cm, but nodes
of 7 cm diameter have also been descri bed [66]. They are covered
by a capsule in which small arteries penetrate. In section they
are dark red in color and resemble splenic tissue. Histologically
a plethoric splenic pulp is found with irregularly arranged lymph
follicles.
Splenic implants retain the ability to function ([66], see also
Sect. 5.10). ALBRECHT [4] and SCHILLING [195], who described
the first two cases in man, believed that splenic nodules represent
accessory spleens.

Accessory Spleens Among 1,000 autopsies per year in the Institute of Pathology,
St. Gallen, about ten accessory spleens are found. Accessory
spleens have an appearance similar to splenosis, but in contrast
they are located in the omentum close to the splenic hilum or
tail of the pancreas and not on the mesentery, they are less
numerous (up to six), they possess a hilum, and the lymph folli-
cles show central arteries, e.g., they resemble miniature spleens.
Accessory spleens have no clinical significance.

7.8.2 Omental Pregnancy,

Endometriosis, and Decidual Noduls
H. TILLMANNS

Omental pregnancy is a special form of abdominal pregnancy

in which the omentum is either exclusively or predominantly
the site of implantation. Just as one must differentiate between
primary and secondary abdominal pregnancy, one must also
distinguish between primary and secondary omental pregnancy.
There are fundamental differences in the pathogenesis as well
as in the clinical course and appropriate treatment.

Primary Omental In primary omental pregnancy, implantation of the fetus occurs

Pregnancy directly in the greater omentum. In contrast to secondary
omental pregnancy, the embryo at the stage of implantation
is outside the uterus and Fallopian tube and becomes embedded
in the omentum. Pregnancy progresses here until the 3rd month.

170
 The course of this disorder is similar to tubal pregnancy. After
a brief period of amenorrhea, irregular uterine bleeding occurs.
Minor, subjective symptoms of pregnancy can be present. Sero-
logical tests for pregnancy can be temporarily positive. Atypical
pain develops in the lower abdomen. Due to the intra-abdominal
bleeding, the patients have a variable tendency to suffer from
circulatory distress and anemia. Finally - and certainly by the
3rd month of pregnancy - an acute, life-threatening clinical
picture develops with the symptoms of severe intra-abdominal
hemorrhage.
Laparotomy reveals an infarcted tumor located in the greater
omentum. It may be only the size of a plum and can bleed
to varying degrees. A large amount of old and fresh blood will
be found in the abdominal cavity. Except for an insignificant
enlargement and softening of the uterus, the genitalia are
normal. The tumor located in the omentum cannot be readily
recognized macroscopically as a pregnancy. Conclusive diagno-
sis is provided by histology.

Therapy. The surgical treatment consists of resection of the in-

volved portions of the omentum together with the ectopic preg-
nancy. Primary omental pregnancy is an extremely rare occur-
rence, and only a few cases are described in the literature [70,
81, 121, 153,246,256].

Secondary Omental In secondary omental pregnancy, development begins within

Pregnancy the uterus or Fallopian tube. The possible course of events is
that during the initial months of pregnancy an unnoticed
rupture of the uterus or Fallopian tube occurs or a tubal abor-
tion takes place. This event is hardly perceived by the patient
and overlooked by the physician. The pregnancy survives this
incident and consequently the chorion and/or the placenta con-
tinue to grow into the abdominal cavity and become embedded
in the serosa of the neighboring organs. Gradually they lose
their connection to the original site of implantation in the uterus,
the minor horn of the uterus, or Fallopian tube. If the secondary
implantation is located exclusively or predominantly in the
greater omentum, it is considered an omental pregnancy. A pre-
requisite for this disorder is that the omentum is immediately
adjacent to the uterus at the site of rupture and in tubal abortion
adjacent to the tubal orifice or connected by adhesions. As in
other abdominal pregnancies, the course of an omental pregnan-
cy exhibits few symptoms and is largely painless. There are,
however, some typical signs:
- Painful interval during early pregnancy
- Marked pain with fetal movements

171
 - Vague feeling of discomfort and minor bleeding at the end
of pregnancy
- Unchanging position and presentation of the fetus upon ex-
amination
- Easily palpable fetal parts as if directly beneath the skin
Anteroposterior and lateral X-rays and sonograms of the lower
abdomen provide very important diagnostic signs in advanced
abdominal pregnancy:
- Eccentric position of the fetus
- Usually a transverse presentation
- No shadow from the uterus around the fetus
- Unusual clarity of the fetal parts
- Maternal intestinal gas shadows cover the fetus
Further differential diagnosis is possible by filling the bladder
with air or contrast medium or by performing hysterosalpingo-
graphy and angiography.
Laparotomy is usually performed in early secondary abdominal
pregnancy because of the suspected diagnosis of a tumor of
the adnexa, myoma with a pedicle flap, or advanced tubal preg-
nany. In late abdominal pregnancy, laparotomy takes the form
of cesarean section due to misinterpretation of the findings by
the obstetrician - for example, after failure to induce labor in
a post-term pregnancy or premature separation of the placenta
- or also as the method of choice for a supposed abdominal
pregnancy. The diagnosis of an omental pregnancy may first
be made during the operation when the implantation site of
the placenta is exposed.

Surgical Procedure. In early omental pregnancy, an attempt can

be made cautiously to remove the placenta manually from the
omentum. If effective hemostasis is possible and omental defects
can be repaired satisfactorily, the omentum can be left in place.
This is easier after intrauterine death than with a living fetus.
Otherwise, the involved portion of the omentum must be re-
sected.
In advanced omental pregnancy, the procedure is basically the
same. However, due to the severely hypertrophied omental
vessels, massive hemorrhage is more frequently encountered
during separation of the placenta. In these cases, no attempt
should be made to preserve the omentum since gross injury
to the omentum is to be expected. It is not rare to find parts
of the placenta adhering to the walls of other neighboring organs
as well as the omentum, which can necessitate resection of por-
tions of the intestine and removal of the uterus and parts of
the adnexa. If sections of the placenta are in critical locations,

172
 e.g., in the region of the mesentery or the mesosigmoid, occa-
sionally parts of the placenta must be left in the abdominal
cavity to avoid life-threatening hemorrhage or necrosis in the
intestinal wall. They are spontaneously absorbed or can later
be removed after organization.
The operation in advanced abdominal pregnancy poses a large
risk for the mother. However, of all types of abdominal pregnan-
cies, secondary omental pregnancy has the best maternal prog-
nosis since the omentum can be readily exposed and easily re-
sected without complications and as such constitutes the most
favorable extrauterine implantation site for the placenta.

Endometriosis As far as we know, endometriosis of the omentum has only

been described once [218]. It was an insignificant secondary
finding in extragenital endometriosis.

Decidual In pregnancy or hormonal disorders, small nodules of decidual

Nodules cells can be found in the omental mesothelium as well as in
other places. They have no practical significance and histologi-
cally only rarely lead to difficulties with the differential diagnosis
[152].

7.8.3 Other Changes

G. A. SCHLOSSER

Portal Pathognomonic omental changes are observed in portal hyper-

Hypertension tension due to liver cirrhosis. Angiomatous vascular convolu-
tions are found (Fig. 102a), and thickened veins with an ex-
tremely narrowed vessel lumen can be seen (Fig. 102 b [196]).

Thalassemia Intercellular iron deposits can be found in omental tissue

(Fig. 103, [196]).

173
174
 Fig. 103. Iron deposits in
the greater omentum in
thalassemia. Berliner blue
reaction. x 250
(SCHLOSSER)
References
a Angiomatous
<III Fig. 102.
vascular convolutions in
the greater omentum in
portal hypertensions.
H & E, x 100 b Distinct fi-
brotic wall thickening and
obliteration of a vein in
portal hypertension.
H & E, x 100 (SCHLOSSER)
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lRS
 Experimental Basis
for Reconstructive Surgery
Using the Omentum

8 Experiments of Clinical Value

Introduction An experimental interest in the omentum in surgery arose in

1887. SENN [63] had the idea of overcoming the leakage of suture
lines by free omental grafts. Since then many conditions have
been reported in which omental grafts, plugs, patches, or sheets
and the omentum on its vascular pedicle have been used. These
clearly show its potential and limitations for surgical use.

Experimental Dogs, cats, pigs, rabbits, guinea pigs, rats, and mice have all
Animals been used in various experiments.

8.1 Vascular Ingrowth and Graft Incorporation

A. LIEBERMANN

General Aspects Pieces of omentum of varying size and thickness were removed
and attached to various organs of either the same or another
animal:

Recipient Sites To sites with intact serosa such as the stomach, pylorus, small
and large bowel, liver, spleen, kidney, urinary bladder, lung,
pleura, peritoneum, mesentery, aorta, and vena cava [6, 12, 19,
24, 52, 58, 64, 65, 66]
To similar sites with a damaged serosal surface [6, 12, 22, 59,
63, 68, 70, 73] or tightly wrapped to impair the blood supply
[18]
To similar sites but under septic conditions [8, 22, 54, 66]
To large, bleeding experimental defects of the liver and spleen,
cut surface of the lung and bronchial stump [5, 42, 54, 65,
66]
Esophageal and bowel anastomoses or experimental defects in
the stomach [25, 36, 44, 54, 65, 66]
In similar experiments omentum with a preserved vascular pedi-
cle was also used. The relationship between graft and host tissue
was examined macro- and microscopically at intervals. The

187
Table 8. Ingrowth of Omental Tissue. Events occurring during incorporation of the omental graft reviewed
and summarized from the almost identical records of various examiners [6, 19, 66, 68]. Predicled omentum
attaches in the same manner

Period of Time Macroscopic changes Histology

Attachment Up to 4 h The pliable graft lines the rece- No special features

Progress of pient surface; if held in place it
Ingrowth adheres after a few minutes
24 h The graft is attached lightly and
has a white rather than pink color
Firm union 48 h The graft adheres loosely; the fat
is white. When separated the adhe-
sive surface is granular
Neo- 3 ds The graft adheres more firmly;
vasculari- capillary oozing occurs upon sepa-
zation ration of the graft
1 wk The graft adheres firmly; separa-
tion is difficult. It is reduced in
thickness through fat reduction
and is gray
2 wks The graft can be separated only
by strong traction
Fat 3 wks The graft cannot be separated;
absorption Bleeding occurs freely on attempt-
ed separation. The fat is largely
absorbed and the omentum has
taken an appearance similar to the
host surface
12 wks The fat content is poor: the graft
is thin, almost identical to the host
surface, difficult to distinguish,
and occasionally identified only by
the suture material
Fibrotic 24 wks Complete absence of fat. Smooth
trans- surface or dense fibrosis
formation
Fibrin film between the graft and host,
coagulated fibrin in vessels. Hemorrhagic
inflammatory reaction, necrobiosis in
graft center, being less on its border
Fibroblasts occur at both sides of the in-
terphase. Less cell necrobiosis; host capil-
laries proliferate to anastomose with
omental vessels. Increase of histocytes and
macrophages
Many young blood spaces in the graft with
endothelialization and neoformation of
capillaries. Many fibroblasts and macro-
phages. Host mesothelium degenerates be-
neath the omentum
Fibrin layer between the graft and host.
Less necrotic areas, macrophages, and
giant cells. Resorption of fat in the graft.
Increase in fibroblastic and angioplastic
elements. The fat content in the adipose
cells close to the host and the mesothelial
lining below the graft is disappearing
Thin graft: Fat tissue is replaced by dense
angio- and fibroblastic tissue both invad-
ing the host
Thick graft: Some degenerative changes in
the fat tissue close to host, little change
in the periphery
Thin graft: Fibroblastic proliferation is far
advanced and most fat absorbed
Thick graft: Numerous fat cells are still
present
Thin xraft: Marked fat absorption and
reduced vascularization; mesothelial
lining of omentum is unchanged
Thick gUilt: Fibroblastic tissue
 stages during ingrowth are shown in Table 8, which summarizes
the observations of the various workers in this field: LOEWY
[54], FINTON and PEET [22], BRocQ et al. [8], BOTHE [6], THOMP-
SON and POLLOCK [66], VERNE et PEREL [68], and PETTET et al.
[58].
The size of the free graft was not important for ingrowth but
thick grafts have increased necrotic areas. Grafts remain viable
when stored on ice for 2 weeks [66] and may even be able to
be stored for a longer period.

8.2 Revascularization and Drainage

The rapid neo-formation of vascular connections between the

omentum and the neighboring tissue (see Sect. 5.5) and its fluid
absorption ability (see Sects. 5.6 and 5.7) stimulated interest in
using the omentum for revascularisation of badly vascularized
organs and drainage, for example, of ascites, hydrocephalus,
or lymphedema.

8.2.1 Revascularization and Edema Absorption of the Brain

and Spinal Cord
H. GOLDSMITH

Brain Introduction. The intact omentum has been used surgically by

our group for a variety of clinical conditions [10, 28, 30, 31
37]. These clinical usages stimulated experimental interest as
to whether the intact omentum could be transposed to the sur-
face of the brain and spinal cord with subsequent development
of vascular connections between the omentum and the underly-
ing neural tissue. It was felt that if omental transposition to
the brain were possible, it might offer the opportunity to add
a new source of blood to ischemic areas within the central
nervous system.

Surgical Technique. Revasculari::ation. The first attempt at using

the intact omentum for brain revascularization was reported
in 1973 using dogs as an experimental model [32]. The technique
involved extensive lengthening of the omentum, which was ac-
complished by removing the structure from the middle and distal
attachments to the greater curvature of the stomach. After the
omentum had been surgically lengthened, transverse incisions
were made along the chest, shoulder, and neck, which were
undermined and connected to form a subcutaneous tunnel

189
Fig. 104. a Placement of
the omentum in a subcuta-
neous tunnel along the
chest. The omentum will be
extended along the neck up
to the cranium. b, c
Omentum being mobilized
to cranial defect. (GOLD-
SMITH [32])

(Fig. 104a). At this point a U-shaped incision was made in the

temporoparietal area and a craniotomy performed. Following
this, the lengthened omentum was taken from the peritoneal
cavity at the upper end of the abdominal incision and placed
in the subcutaneous tunnel that extended to the cranial defect
(Fig. 104b, c). The omentum was then carefully laid upon the
brain and secured to the cut edge of the dura, followed by
closure of the overlying skin.
The above experimental procedure was found to be surgically
feasible, resulting in the formation of vascular connections be-
tween the omentum and the underlying brain. This was proven
grossly and histologically by injecting India ink through an
omental artery within the abdominal cavity, the material appear-
ing in blood vessels at the omental-cerebral interface and within
the brain tissue itself (Fig. 105).
After it had been observed that vascular anastomoses could
develop between the intact omentum and brain, the question
arose as to whether omental transposition might prevent cere-
bral infarction when performed prior to occlusion of the middle
cerebral artery (MeA). In order to answer this question, three

190
Fig. 105. Omental (0) and
cerebral (B) tissue con-
nected by blood vessels
filled with India ink.
Transparency was accom-
plished with methyl salicy-
late. x 3 (GOLDSMITH)

groups of dogs underwent total occlusion of their right MeA.

In Group I the MeA was simply ligated. In Group II the dogs
had their pedicled omentum placed on their brain simultaneous-
ly with MeA occlusion. In Group III the dogs had their
omentum placed upon their brain weeks to months prior to
occluding their MeA.
The results of this experiment showed that the gross and histo-
logical examination of the brain tissue from the dogs in Group I
(occlusion of the MeA) demonstrated a cerebral infarction rate
of 77%. Dogs in Group II (simultaneous placement of the

191
Fig. 106. Omentum (0)
placed on the lateral sur-
face of the frontoparietal
area 2 weeks prior to oc-
clusion of the middle cere-
bral artery in the dog. The
animal was killed 2 weeks
later, and no cerebral
infarct was noted. Heiden-
hain's stain, original mag-
nification x 2.5 (GOLD-
SMITH [33])

omentum with MeA occlusion) demonstrated a cerebral infarc-

tion rate of 80%. However gross and histological examination
of the brain slices of the dogs in Group III (occlusion of the
MeA weeks following omental transposition to the brain)
showed cerebral infarction in only 14% of the animals [33].
The infarcted areas of the animals in the study involved the
basal ganglion and surrounding areas and the internal capsule
and contiguous centrum ovale. Histological examination
showed necrosis, demyelinization, loss of ax ones, and prolifera-
tion of capillaries with hypertrophic walls. Also observed were
a large number of gitter cells within the cerebral infarcts, with
peripheral edema surrounding these locations.
The apparent ability of the intact omentum to prevent cerebral
infarction in the dog (Fig. 106) prompted further experimenta-
tion in the monkey [35]. In this study, 25 adult stump-tail
monkeys were studied. Three groups of monkeys were used as
controls; Group I had simple MeA occlusion, Group II had
their temporalis muscle laid directly upon the brain with subse-
quent occlusion of the MeA 4-6 weeks later, and Group III
had a 2 x 2 cm piece of free omentum placed on the brain with
MeA occlusion 4-6 weeks later. All the monkeys in these
groups (I, II, and III) developed a brain infarction and all,
except one, developed hemiparesis. In the experimental group
of monkeys, the omentum was placed on their brain 3-4 weeks
prior to MeA occlusion, with only two of the 13 monkeys devel-
oping a cerebral infarction with hemiparesis. (Fig. 107a, b) A

192
Fig. 107. a Angiogram in
the monkey, showing the
network of small omental
blood vessels overlying the
chest and shoulder (arrow).
b Subtraction angiogram of
the head of the monkey.
Arrow points to the
omental vessels at the
omental-cerebral interface
(GOLDSMITH)
comparison between the control and experimental animals in
this study showed that placing the intact omentum upon the
brain prior to MeA occlusion yielded a statistically significant
difference in preventing cerebral infarction (P < 0.002).
The favorable results of using the intact omentum to protect
the brains of dogs and monkeys raised the question as to wheth-
er omental transposition to the human brain might also be an
effective procedure (see Sect. 9.2.1.2).
193
Spinal Cord Introduction. The ability to add a new vascular supply to the
brain stimulated interest in determining whether mobilizing the
intact omentum to the spinal cord could also result in a new
form of additional vascularization to that organ.
Experimental evidence has shown that the spinal cord is adver-
sely influenced by a decreased blood flow to the spinal cord
following injury [16]. Ducker and Perot noted a progressive
fall in spinal cord blood flow at the site of injury with reduction
in the partial pressure of oxygen (P0 2 ) in the injured area [17].
Other physiological information of interest is that of Locke and
his associates, who showed that lactic acid concentration is in-
creased at the site of spinal cord injury [53]. It seemed reason-
able to believe that transposing the omentum to an injured spi-
nal cord would add a new source of blood directly to the cord.
Additionally, it was thought that the omentum would absorb
edema, which is widely recognized as being associated with spi-
nal cord trauma, by way of its network of lymphatic and venous
channels.

Experimental design and Surgical Technique. Initial experiments

in which the omentum was applied directly to the intact spinal
cord were done in our laboratory on dogs [34]. These animals
were subjected to a laminectomy at the level of the lower thor-
acic vertebrae. Following this procedure, the dura was opened
and the spinal cord exposed. The abdomen was then opened
and the omentum lengthened by removing it from its junction
with the spleen and from its middle and distal attachments to
the greater curvature of the stomach. The omentum was then
brought out through a separate incision located on the left later-
al abdominal wall, after which it was placed in a subcutaneous
tunnel and laid directly on the exposed spinal cord (Fig. 108).
Subsequent examination of the omental spinal cord area showed
that there was development of vascular connections between
the omentum, meninges, and spinal cord (Fig. 109).

Results. In order to determine how rapidly vascular connections

develop between the omentum and the spinal cord, animals were
killed after surgery at varying periods from hours to months.
It was unequivocally found that blood vessels developed be-
tween the spinal cord and omentum within 72 hrs after surgery,
an observation subsequently confirmed by investigators from
the Karolinska Institute in Sweden [51].
The experiments described above were performed on animals
with a normal spinal cord. The next experiment investigated
the effect the intact omentum would have when applied to an
injured spinal cord. The first attempt to answer this question

194
Fig. 108. Cross-sectio of
the omental-spinal cord in-
terface. (GOLDSMITH [34])

Fig. 109. Cross section of

the spinal cord with sur-
rounding omentum 72 h
posttransposition. Methyl
salicylate clearing of the
cord shows India ink with-
in the blood vessels of the
spinal cord (arrows).
(GOLDSMITH [34])

195
Fig. 110. India ink present
in the blood vessels at the
site of the spinal cord tran-
section. Note the blood
vessels growing longitudin-
ally through the transec-
tion site. Translucency was
accomplished using methyl
salicylate (GOLDSMITH)
196
involved a series of cats who underwent total transection of
their spinal cord in order to learn what effect the early applica-
tion of the omentum to the transection site would have in terms
of revascularization. It was found that the omentum caused
marked blood vessel proliferation at the point of transection,
with the ability of blood vessels to grow in a longitudinal fashion
through the area of spinal cord separation (Fig. 110).
After demonstrating that vascular channels developed between
the omentum and the spinal cord, and that blood vessels grew
between the ends of a transected cord, another series of experi-
ments were performed to see if the omentum might lessen the
autodestructive changes that normally occur within an injured
spinal cord. One of the most notable of these patho-biological
changes is that there is leakage of edema fluid through the endo-
thelial lining of the damaged blood vessels located in the area
of the trauma. The capacity of the spinal cord to reabsorb and/
or redistribute this edema fluid is limited because of the absence
of lymphatics within the central nervous system.
Extravasated edema fluid that accumulates within the interstitial
space within an injured spinal cord is rich in plasma proteins,
thus exerting a high osmotic pressure that attracts an ever in-
creasing amount of edema. As this interstitial fluid volume con-
tinues to expand, it begins to compress the uninjured capillaries
within and adjacent to the area of spinal cord injury. This pro-
gressively increasing interstitial fluid pressure eventually ob-
structs the lumen of the functioning capillaries within the area
of cord injury, thus causing ischemic necrosis with resulting
 complete transverse myelopathy. It seems reasonable to suspect
that any ability the omentum has in lessening severe injury with-
in the traumatized cord results from its ability to absorb edema
fluid.
In order to see if the omentum might aid in absorbing edema
at the surface of a traumatized spinal cord, a 420 gm/cm injury
was made using a standard weight-dropping technique [38]. La-
minectomy was performed on control cats, their dura being
opened with subsequent closure of the operative wound. These
control animals were compared with experimental animals
which had a laminectomy, their dura opened, followed by imme-
diate and delayed application of the intact omentum on their
injured spinal cord.

Results. Histological examination of spinal cord sections were

later evaluated as to the degree of spinal cord injury; the degree
of injury being based on criteria of edema, hemorrhage, axonal
swelling, neuronal death, and zonal necrosis. Differences were
noted in the lowering of the level of the injury in the experimen-
tal cats as compared with control animals. It was felt that this
favorable effect exerted by the omentum in decreasing the level
of injury in the experimental cats was due to the diminution
of edema formation within the spinal cord. Subsequent studies
[39] showed that the earlier the omentum was applied to the
injured spinal cord, the greater the likelihood of diminishing
the pathobiological events that routinely occur within the
injured structure.

8.2.2 Revascularization
M. DURIG

Ischemic Heart In order to form an effective collateral circulation in coronary

occlusion BECK and TYCHY [3] and O'SHAUGHNESSY [56] devel-
oped pericardial adhesions in dogs with the aid of the omentum.
O'SHAUGHNESSY in 1937 [56] and HUNTER in 1938 [45] per-
formed omentocardiopexy with some success in patients with
cardiac insufficiency.
Omentum on Vascular Pedicle. The pedicled omentum has been
attached experimentally in dogs to the myocardium and the
circumflex coronary artery ligated. Although the mortality rate
of the experimental animals was low, only a few anastomotic
vessels developed to supply the ischemic area. An increase of
collaterals was not observed [59]. Simultaneous implantation
of the gastroepiploic artery does not improve the circulation,

197
 and only a superficial revascularization of the myocardium
could be achieved [27, 47, 48, 56].

Free Omental Graft. In the hope of developing vascular connec-

tions, VINEBERG in 1962 [72] placed detached omental sheets be-
tween the pericardium and the myocardium to supply the
ischemic muscle. However, although there was some initial suc-
cess [69, 70, 71, 73], long-term results failed. First, due to its
distinctive characteristics the omentum took its blood supply
from the host tissue, which in this case was already ischemic
[59]. Secondly, extensive shrinkage of the omental tissue oc-
curred in all experiments even when anastomoses with larger
vessels took place. VINEBERG'S clinical attempts (1962-1975) to
revascularize the ischemic heart with the aid of the omentum
are now obsolete because of unsatisfactory long-term results
and the absence of angiographic proof of revascularization.

Ureter In cutaneous ureterostomy the denudation of the implanted ure-

ter and impairment of blood supply may cause fibrosis, which
finally leads to stenosis of the stoma. It has been speculated
that the revascularizing ability of the omentum may avoid
uretero-fibrosis. This has been examined in dogs in which the
ureter was deprived of its blood supply, wrapped in the
omentum, and placed in the retroperitoneum and skin [2]. Al-
though dye injection in the omental vessels proved revasculariza-
tion of the wall of the ureter, stenosis of the ureterostoma could
not be avoided using the omentum.

8.2.3 Drainage
M. DURIG

Hydrocephalus Because of the ability of the omentum to absorb fluid, attempts

have been made to drain the hydrocephalus via lumbo-omental
shunts using the vascular omental pedicle [50, 74]. As the dis-
tance to the brain was so long, Y ASARGIL and co-workers [78]
and Y ONEKA WA [79] transferred the detached omentum and
connected it micro surgically with the lingual artery and the ex-
ternal jugular vein. The omentum was laid directly on the cortex
between the dura and arachnoid. Dyes dissolved in hydrogen-
peroxide and isotopes attached to molecules of various sizes
including albumin in Ringer Solution were used to evaluate the
amount of absorption in the animal experiment. But no effective
drainage could be shown. The examiners observed formation
of a membrane at the site of omental implant which may have
been responsible for the impaired absorption. When the anasto-

198
 mosis became obliterated fatty degeneration of the graft and
necrosis occurred.
For drainage of internal hydrocephalus the lumbo-omental
shunt seems to promise more success. Following laminectomy
of L-l/L-2, the pedicled omentum was transposed to the dura
and arachnoid of the spinal cord. It could be shown with radio-
nucleotides and inulin that the omentum deviated 30% of the
cerebrospinal fluid which was found 3 hrs later in the portal
vem.
In a similar experiment in rats a six fold increase in uptake
of inulin by the omentum was shown when compared with con-
trols [74]. There was no leaks in either experiment. Whether
the size of the implant influences the absorption is still unknown.

8.3 Protection
M. DURIG

Intestinal Suture Lines The idea of protecting unsafe suture lines of the intestines by
the omentum to prevent leakage dates back to SENN in 1887
[63]. It has been observed that intestinal glands may invade
the protecting omentum [54, 75] and that a mucosal lining devel-
ops from the healthy bowel margin [19,67]. Subsequently many
workers have attempted to use the detached or pedicled
omentum for protection of intestinal anastomoses and defects
[4, 7].

Free Omental Graft. Pieces of omental tissue retained vitality

wherever they were attached [66], but this invariably also led
to intense adhesions with the adjacent organs [18, 54]. They
were no barrier against leakage [9, 64], and did not protect
underlying devascularized bowel segments from necrosis [13,
18, 55].

Omentum with Vascular Pedicle. While defects in the esophagus

can be successfully protected [27, 44, 77], recent studies have
shown that covering either small bowel or colonic anastomoses
with omentum has no influence on healing [9] and with large
defects there is a high mortality rate [43]. Vascularization of
the anastomotic area apparently did not improve in these experi-
ments, and surprisingly, there were more peri-anastomotic ab-
scesses when compared with the" unprotected" anastomoses.
Whether satisfactory incorporation of the omentum in the pres-
ence of infection occurs is still disputed [12, 22, 41, 42, 66],
and bowel stenosis is regarded as a frequent complication [13].
However, it was found that colonic anastomoses wrapped in

199
 the omentum were safer and superior to controls up to the
7th day as shown by studies of dehiscence with traction [55].
All workers conclude that although omental re-inforcement is
justified in any area of small bowel or colonic surgery, an advan-
tage is obtained using the pedicled omentum in esophageal and
rectal anastomoses [27, 44].

Peritoneal Defects The benefit of covering serosal and parenchymal defects [49]
with the omentum is supported by many experiments on the
lungs [66], liver [54], spleen [61], and pancreas [54]. All exa-
miners record a successful ingrowth of both free graft and pedi-
cled omentum while preserving its basic characteristics [49].

Urinary Bladder Successful covering of urinary bladder defects with the omentum
was first recorded by CORNIL in 1898 [11] and confirmed by
ENDERLEN [19] in experiments using dogs. The proof of omental
epithelialization with transitional epithelium and the appearance
of muscle structures which were connected with the urinary
bladder muscle have been described [40].

8.4 Reconstruction

8.4.1 Antral Patch Esophagoplasty Using an Intact

Omental Pedicle
D. LIEBERMANN-MEFFERT

Esophagoplasty It has been shown in animal experiments that esophageal anas-

tomoses at risk and large defects can be protected with the
pedicled omentum [29, 76]. PAPACHRISTOU and FORTNER [57]
and HUGH et al. [44] successfully used the gastric antral wall
based on the left gastroepiploic pedicle to cover defects in the
cervical esophagus, trachea, and pharynx (see Sect. 9.2.1.2).

8.4.2 Rectal Valve Substitution Using the Intact Pyloric

Valve Based on an Omental Pedicle
H. GOLDSMITH and E. STEWARD

Rectal Valve Introduction. The absence of a rectal valve, resulting from either
surgical removal or congenital absence, requires the perfor-
mance of a permanent colostomy. It has now been shown that
it is possible to mobilize the pyloric valve on an intact omental
pedicle to the anal region, in which position the transposed

200

Fig. 111. Technique for
mobilizing the pyloric valve
to the anal region
pyloric valve can function as a replacement for the excised rectal
valve [26].
Surgical Technique. A series of cats had their pyloric valves
removed from the normal position in the gastrointestinal tract
(Fig. 111). While the pyloric valve is being removed from intesti-
nal continuity, it is imperative that small blood vessels connect-
ing the pyloric valve to the gastroepiploic vascular arcade within
the omental apron are not disturbed. Also of great concern
when isolating the pyloric valve is to avoid injury to the common
bile duct, which lies along the inner curvature of the duodenum.
Following removal of the pyloric valve from its normal position,
gastrointestinal continuity is re-established by performing a
routine gastroduodenostomy.
The pyloric valve can be extensively mobilized by dividing the
omentum but preserving the intact gastroepiploic vessels within
the omental pedicle. After pyloric valve mobilization, an abdo-
minoperineal resection is performed, with a wide perineal ex-
cision being carried out in order to be certain of the removal
of the rectal sphincter mechanism.
201
Fig. 112. Healed pyloric
valve in the perianal region
9 weeks postoperatively.
Note valve-like configura-
tion of the pylorus at its
outlet which rresulted in
fecal continence (GOLD-
SMITH)

After abdominoperineal resection and mobilization of the

pyloric valve to the anal region has been performed, the proxi-
mal portion of the pyloric valve is anastomosed to the distal
end of the left colon. When performing this proximal anastomo-
sis, more tissue is taken on the cuff of the posterior portion
than on the anterior portion in order to create an angulation
at the colopyloric valve anastomosis. The distal end of the
pyloric valve is then sewn to the surrounding anal skin
(Fig. 112).

Results. The result of this experiment was to learn whether a

transposed pyloric valve could survive in the anal region and
to learn whether the mobilized pyloric valve could assume the
function of an excised rectal valve. It is known that a dog will
defecate indiscriminately in its cage even in the presence of an
intact rectal valve, as opposed to a cat, whose fastidiousness
usually results in the cat defecating only in a shoebox placed
in the animal's cage. It was considered that a cat with a trans-
posed pyloric valve was continent when the animal defecated
almost all the time in the receptable that had been placed in
its cage.
All pyloric valves which were transposed in the cat to the anal
region remained viable during the postoperative period, which
continued for 6-10 weeks after surgery until the animals were
killed. Of the nine cats which underwent pyloric valve transposi-
tion, four had complete anal continence; two other cats defe-
cated frequently in the box in their cages, but occasionally stool
was found outside this receptacle. It was of interest that these

202
last two cats were severely troubled with fecal impaction, requir-
ing weekly oil retention enemas, which were given under general
anesthesia (ketamine). It was felt that the persistence of fecal
impaction in these two cats may have led to their lack of com-
plete anal continence. The three other cats in the experiment
developed a postoperative perianal fistula, which caused com-
plete fecal incontinence. Since the fecal fistula arose from the
proximal suture line, which was proximal to the pyloric
sphincter, it was felt that the fecal fistula would never heal.
It must be remembered, however, that should this complication
occur in the human, one could expect to have direct access
to the fistula's opening for direct repair since it is well below
the level of the levator muscles, and also the valve could be
dilated in order to allow healing of the defect in the suture
line. There were two other cats in the study, which simply had
anal colostomies, and at no time did they ever show any form
of anal continence.
it was found that the pyloric valve can remain viable in an
area far removed from its normal position. It was also found
that anal continence could occur in cats which had been sub-
jected to an abdominoperineal resection followed by pyloric
valve transposition in order to replace the excised rectal valve.
Why the pyloric valve functions in this position remains un-
known. The blood supply remains intact in this operation, so
that nerve tissue which runs along with blood vessels would
also have to be considered to be intact. It is of interest to note,
however, that there remains uncertainty as to how the pyloric
valve functions in its normal position; this obviously would
be true in its ectopic position.
FISHER and COHEN in 1973 stated that the pyloric valve has
a high-pressure zone that relaxes gastric peristalsis, but which
contracts in response to endogenous duodenal stimuli, thus in-
fluencing reduction in duodenogastric reflux [23]. This phenom-
enon suggests that the pyloric valve acts as a true physiological
sphincter. However, KAYE et al. in 1976 failed to find a consis-
tent high-pressure pyloric zone [46]. If there is no high-pressure
pyloric zone, one would then have to suspect that the pyloric
valve acts at the gastric outlet by impeding gastric contents
being propelled into the duodenum by gastric peristalsis.
Perhaps this relative obstructive phenomenon explains how the
pyloric valve works in the anal region, with fecal material being
held back to the degree that there is distension above the pyloric
valve, with eventual hyperperistalsis resulting in a bowel move-
ment.
Although the physiological mechanisms of the transposed
pyloric valve to the anal region remain unsolved, it has been

203
Fig. 113. Transposed
pyloric valve in an autopsy
specimen demonstrating
the ability to mobilize the
structure in the human.
Note how the vasculature
is preserved between the
pyloric valve and gastro-
epiploic arcade in the
omental pedicle (GOLD-
SMITH)

shown by anatomical studies that it is technically feasible to

transpose the pyloric valve to the anal region in the human
(Fig. 113). Human experimentation will eventually prove the
practicality of replacing the rectal valve with a pyloric valve.

8.4.3 Island Skin Flaps and Island Composite Flaps

Employing the Omentum
D. LIEBERMANN-MEFFERT

Recently, EROL and SPIRA [20, 21] used the omentum as a carrier
material when developing large island graft flaps. In pigs they
grafted split or full thickness skin grafts onto the omentum
which they had transposed, spread out, and fixed to the abdomi-
nal wall. For protection of the graft they developed a special
inlay technique [20]. Subjacent muscles could be vascularized
with the omentum, and an "omental island myocutaneous flap"
could be thus obtained. The authors also made bone grafts such
as rib segment or tibia, brought the omentum out underneath
the abdominal skin, vascularized the bone by wrapping it in
the omental sheet, e.g., a tubed skin flap, and later transferred
the" omental composite osteocutaneous island flap" to any side
of the pig's body either on a lengthened omental vascular pedi-
cle, or transferred and connected it with microvascular anasto-
mosIs.

204
 Standard diagnostic assessment showed the vascularity of the
bone and the viability of the graft. New methods for neo-forma-
tion of organs such as the nose and ear using the technique
described above have also been reported [21].

8.5 Body Surface Heterotransplant and Biological Dressing

H.J. DITTLER

Introduction. Animal experiments with heterologous omental

transplants were introduced by SENN [62]. He, as well as THOMP-
SON and POLLOCK [66], used fresh omentum, preserved for up
to 2 weeks in saline or Ringer's solution, to graft wounds of
pleura, lung, liver, spleen, aorta, vena cava, esophageal anasto-
mosis, and bronchial stumps. They reported that 95% of the
transplants healed successfully and recommended their clinical
application. In 1913 DIEL [14] lined the patella with reindeer
tendon in a patient with a tuberculous knee joint in which mobi-
lity was reduced. He then grafted a rabbit omentum between
the regenerated terminal femur and tibia, apparently with a good
functional result.

Trophic Ulcers Based on experimental and clinical examination, RATNER [60]

assumed that the transplanted omentum kept its biological char-
acteristics. Animal omentum placed on infected trophic ulcers
appeared to stimulate the formation of granulation tissue and
epithelialization.

Osteomyelitis After omental transplantation to an infected wound or the site

of osteomyelitis, he found an almost complete disappearance
of the purulent discharge and pain. RATNER thought that in
addition to the protective effect, the omentum exerted a bacter-
iostatic and biochemical effect and was even of benefit in ampu-
tation neuromas.

Burns In experimental studies he used heterologous omentum for the

treatment of burns. Animal omentum preserved at a tempera-
ture of +4° C was placed on the surface of the burn. It was
then covered by a vaseline ointment dressing, which was
changed every 3-4 days. During the course of wound healing
new omental flaps were grafted 3 or 5 times. Pain decreased,
no serious infection occurred, and the wounds were soon cov-
ered by a thin epithelium, which did not only grow from the
edges but also from the center. However, the number of cases
was only small. We tried in recent experimental studies to eluci-

205
 date the value of the omentum as a biological dressing for
burns.
The damage depends on the temperature, duration, and charac-
ter of the heat source [1]. Apart from the local coagulation
necrosis, the thermal damage causes pathophysiological changes
which may influence all organs and lead to a "burn disease,"
which may be overwhelming with toxic shock.
By the release of vasoactive substances, such as histamine, bra-
dykinin, kallikreinin, thermolabile skin proteases, and prostag-
landins, the capillary wall loses its semipermeable qualitity.
Local fluid loss is high within the first 48 h. In addition, osmoti-
cally active plasma protein and electrolytes leave the vascular
compartment and lead to generalized edema. In the course of
burn disease the high protein loss soon leads to a negative nitro-
gen balance. It is important to cover the area of the burn to
prevent fluid loss and infection. Heterologous transplants of
omentum have been used as biological dressings by us [15].

Experimental Design. Before clinical application it was necessary

to undertake animal experiments. V AUBEL and his colleagues,
working in Berlin, inflicted third-degree burns on rabbits by
means of a standardized branding device. After an average of
24 h, the necroses were removed surgically and bleeding was
stopped. Then omental membranes from the pig, removed under
sterile conditions, were placed on the wound surface. The
wounds were left open in order to induce the membrane to
dry onto the wound surface. Wire cages made of stainless steel
wire protected the open wound. Within a few hours after the
grafting, the surface of the membrane started to dry. After the
2nd day, the omentum was completely dry and covered the
entire wound. After about 2 weeks it became opaque and lumpy.
When incised at the edge, the omental dressing could be under-
mined bluntly and removed in one piece (Fig. 114, page 310).
On the remaining wound surface fine diffuse hemorrhages were
seen along with granulation tissue with a good blood circulation,
which covered almost the whole surface.

Technique and Clinical Experience. In two patients with extensive

third-degree burns, porcine omentum was used several times
as temporary wound dressing after debridement, until grafting
had been completed. In one 32-year-old male patient with 35%
full thickness burns, the extensive wound surface was covered
with porcine omentum while debridement was undertaken over
a period of about 3 weeks. The transplants formed scabs and
adhered firmly to the wound surface. When changing them,
Fig. 114 see page 310 they could easily be scraped off with a scalpel, and healthy

206
 granulations were present underneath. However, the patient
died after 4 weeks, due to bronchopneumonia. A 37-year-old
female patient had 15% full thickness and 20% partial thickness
burns. Due to the bad general condition of the patient, the
removal of the necrotic slough could only be started 10 days
after the burning. Smaller areas were primarily grafted with
split skin. The wound extended from the right clavicle to the
right iliac crest and posterior midaxillary line. This defect was
covered with porcine omentum, which had been kept for 3 h
in electrolyte solution (Fig. 115, page 310). Despite adequate
hemostasis before application of the omentum, small posthem-
orrhagic areas appeared. This had also been noted in the pre-
vious patient. The omental graft bulged out in several places
and incisions were necessary in order to relieve the hematomas.
The omentum was left exposed and dried out, covering the
wound tightly. Ten days later the dried omentum was removed
by sharp incision together with some deeper necrotic zones. The
wound was again covered with a fresh omental graft and after
another 10 days the dried omentum was, once more, removed.
The wound surface was well granulated and could be grafted
with autologous split skin (mesh graft). Healing was satisfactory
and no sensitivity to porcine antigen could be detected clini-
cally.
The experimental and clinical experiences described here are
still insufficient to allow a final judgement of the application
of the omentum as a dressing in burns. However, the serious
biological problems which result from fluid and protein loss,
toxins, and infection make further trials with the omentum im-
portant. Especially as the membranes such as porcine skin, fetal
calf skin, amnion, and synthetic substances all have their limita-
tions and complications.

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210
 Protective and
Reconstructive Surgery
with the Omentum in Man

9 Surgical Principles and Techniques

D. LIEBERMANN-MEFFERT and H. WHITE

Sites 1. Reconstruction with the omentum can be undertaken for le-

SIOns:
a) In the peritoneal cavity (Fig. 116a)
b) Extraperitoneally
In the mediastinum and cranium
Exteriorized on the body surface (Fig. 116 b)
Principles 2. The principles of the operation are:
a) Preparation of the donor site such as local clearance by
radical excision of the tumor or lesion
b) Repair or substitution with omentum, when exteriorized
coverage with primary or secondary skin grafting
Methods 3. Methods of reconstruction are (Fig. 117):
a) Use of the omentum on its intact vascularization and with-
in its anatomical reach (omentopexy),
b) With lengthening on a vascular pedicle (transposition)
c) Free transfer of the omentum employing microvascular
techniques (transfer with vascular connection)
d) Free transfer of omental tissue without vascular anasto-
mosis (free transfer)

9.1 General Aspects

9.1.1 Indications and Contraindications

Indications Reconstruction with the omentum is indicated in any case where

an extremely large, contaminated, and intractable defect can
be adequately covered or filled with omental tissue, for example
m:
- Sequelae of accidents including open fractures and bleeding
surfaces of parenchymatous organs and burns
- Contaminated wounds and infection including diabetes, oste-
itis, and protection of vascular prosthesis

211
Fig. 116. The various sites
of intra- and extraperitone-
al lesions for which
omental transposition and
transfrer has been used
successfully

Cavities or exposed skeletal structures after excision of benign

and malignant tumors
Sequelae of radiation such as ulceration, fistulae, and residual
cavities including the presacral space after pelvic exenteration
and following cystectomy (surgery in radiotrophic and ther-
mally damaged tissue)
Extended local recurrence
- Reconstruction when autologous tissue is preferred to foreign
material

212
Fig. 117. For reconstructive
purposes the omentum has
been used successfully:
lengthened on its vascular
pedicle (I), as a free graft
with vascular microanasto-
moses (II), and, less fre-
quently, as a free graft (Ill)

I
\
t
TRANSPOS ITION
IT
.I"'"
TRANSFER

Benefit The omentum:

- Supplies blood to the poorly vascularized viscera and soft and
hard tissues
- Resolves inflammatory processes and resists infection
- Fills spaces of resected organs
- Improves healing and shortens hospital treatment
Surgery using the omentum is often combined with complicated
primary operations on patients in a bad condition and may
represent a final attempt to help in a desperate clinical situation.
Laparotomy and mobilization of the omentum is a straightfor-
ward procedure but this may be undertaken in conjunction with
major surgery, such as pelvic exenteration or extensive removal
of tumor bulk or post-traumatic debridement at different sites.
Patients with cancer are frequently committed, by the nature
of their disease, to several operations. Reconstruction with the
omentum is very often a one- or two-stage maneuver which
reduces the number of interventions. It may offer the only hope
of making patients socially and personally acceptable (Fig. 118),
and in this respect may be of value in improving the quality
of life and easing some of the stresses which may lead to depres-
SIOn.
Risk For the various types of lesions special indications are given
in the respective sections. Repair of defects with the omentum
involves laparotomy. The procedure, therefore, has some risk
for the patient and the alternative operation should be carefully
considered.

213
Fig. 118. Purpose of Aims and advantages
omental plastic surgery. of omental surgery
The procedure is helpful
when it lengthens the pa-
tient's life expectancy and
improves the quality of
life without unjustified risk

Rehabilitation

Social
acceptability

Contraindications Contraindications include:

1. Patient's Condition. There are general contraindications
which are the same as for all major surgery. In addition
there are specific contraindications:
General debility of the patient
- Portal hypertension and liver cirrhosis
- Active peptic ulceration and other gastric pathology
- Splenic pathology such as Hodgkin's disease

2. Omental Deficiencies
- The omentum is too small in size
- It is fibrosed or shrunken due to previous abdominal opera-
tions
- The omentum is diseased (epiploitis, infarction, tuberculosis)
- Omental or recipient vessels are obliterated

9.1.2 Assessment and Preparation for Surgery

Assessment History, Physical, and Clinical Examination. In addition to a

general examination to ensure fitness for surgery, exact assess-
ment of the clinical finding is necessary: laboratory studies and
X-ray screening for metastases must be carried out as the patient
may have associated but still undetected metastatic disease. The
contraindications for reconstructive surgery (Sect. 9.1.1) must

214
 be checked, for example, by liver scans and X-ray examinations
of the stomach.
Site and Size of the Defect. The operability, which depends on
local situation, tumor stage, and the possibility of skin coverage,
should be assessed. This may include biopsy for histology and
microbiology to check local tumor invasion and staging. Bacte-
riological culture is occasionally necessary.
Photographic Records. This is suitable as a routine procedure
when it is planned to exteriorize the omentum. Standardized
views should be taken of the defect; it should be possible to
take follow-up pictures in the identical position at a later date
to assess objectively the results from the functional and aesthetic
points of view.
Omental Condition. The intactness of the omentum should be
considered. DAS [48, 49] postulated that the patient's age and
sex could be used to predict whether the omentum would reach
the lesion. However, there are such great variations in omental
volume, size, shape, and consistency (Sect. 3.3) that decisions
on the different lengthening methods cannot be made preopera-
tively. Age itself is no contraindication. Previous operations and
infections, such as peritonitis, may have caused adhesions.
Omental adhesions are very frequent. They can usually be
divided surgically and are not a contraindication for omental
transposition and transfer. Laparoscopy (Sect. 6.4) is not usual-
ly required as a preoperative assessment. However, it may be
of value in certain cases where other problems, such as liver
metastasis or other intra-abdominal pathology may require as-
sessment. For diagnosis of omental diseases, biopsy and occa-
tionally arteriography (see Sect. 6.2) may be of value.
Preparation Informed Consent. The patient and relatives must be aware of
for Surgery the severity of the primary disease. The nature of the operation
and the prognosis must be explained. The patient himself must
know about:
- Alternative or additional methods of treatment
- Loss of fluid in the dressings, when the omentum is exterior-
ized
- Necessity for fluid replacement
- Possible postoperative symptoms such as gastric fullness,
dumping, and reflux
The problems which have occurred in connection with his severe
disease and which may at least be partially solved, so that he
can lead a worthwhile existence, regaining self-reliance and reso-
cialization (" I can cope ").

215
Preoperative Care The patient should be made as fit as possible before surgery.
This may include:
- Intravenous feeding and blood transfusion
- Control of pain
- Local skin preparation for example with p.v.p. iodine
- Antibiotics are not routinely necessary
When omental transposition is being undertaken in conjunction
with bowel surgery, e.g., pelvic exenteration, routine bowel pre-
paration will be required.

Organizing, Timing of the Operation, and Planning. The preoper-

ative preparation includes planning not only for the timing of
the omental transposition or transfer but also for the staged
secondary skin grafting or other procedures, such as division
of pedicle. For the operation itself the usual precautions for
abdominal surgery must be observed. The danger of powder
granulomata must be avoided by washing gloves. When extra-
abdominal transfer of the omentum with micro anastomosis is
considered, a second team of surgeons is required to prepare
the defect and undertake the anastomosis.

Special Instruments. Two sets of instruments are usually required

to avoid contamination of the abdominal wound either with
organisms or with malignant cells. A large variety of instruments
- perhaps including bone sets - may be required.

Anesthesia. Premedication is given in the usual way about 1-2 h

before the operation. Most often general endotrachial anesthesia
is required. The selection of anesthesia for the operation is the
responsibility of the anesthesist. Relaxation is important for the
laparotomy and almost invariably a nasogastric tube is a wise
precaution and makes the postoperative period more comfort-
able. Intravenous fluid replacement is necessary, especially as
fluid will be lost postoperatively from the exteriorized omentum.
Intraoperative blood transfusion and intravenous pressure mon-
itoring may be necessary. The anesthesist should be prepared
in the chest wall reconstruction for an unexpected hemopneu-
mothorax.

Position. For the approach to the omentum the patient is placed

on the operating table in the supine position. This position may
be changed subsequently according to the exposure required
for particular situations.

Superficial Disinfection. Disinfection of the abdominal wall -

and when the omentum has to be exteriorized - of the entire

216
 area of defect is necessary and should be done with particular
care.

9.1.3 Access to the Omentum

Abdominal Wall Good exposure is important; planning of the abdominal inci-

Incisions sions (Fig. 119 a-e) will depend upon individual preference.
However, the midline approach is most satisfactory, which may
be deviated to avoid the xiphisternum and extended around
the umbilicus. Transposition of the omentum requires careful
planning because additional incisions may become necessary at
the site of the new location. The midline incision can be extended
up to the throat and down to the pubis. When the omentum
is being transposed to the chest (Sect. 9.2.1.3) it may be prefera-
ble to lead it through the rectus muscles and make a small
lateral incision in order to develop the subcutaneous channel.
Occasionally for the approach to the liver, chest, and pelvis,
a transverse upper abdominal incision is preferable and in some
instances a separate transverse lower abdominal incision is add-
ed. In pediatric surgery transverse upper abdominal incision
provides an excellent approach to the omentum and all the ab-
dominal organs of the neonate. For omentoportoduodenostomy
(Sect. 9.2.1.1) a subcostal incision which can be extended trans-
versely is preferable.

Fig. 119a-1, Incisions (a-I)

used in operations involv-
ing the omentum. The
dotted lines show secondary
incisions used to reach the
defect directly or through a
subcutaneous tunnel b

217
 r e:: ~ .. ,
,
,
I
I

-
..
_ ..

\
I

J\ ~ l~
,y f
?~
-- J 1--
; Yj Y

Fig. 1J9c-J

218
Exploration of the
Abdominal Cavity
Operative Technique
of Mobilization
Fig. 120a-c. Detachment
from the transverse colon.
An assistant holds the trans-
verse colon. The omentum
is placed on traction by
the operator, who separates
it away from the colon
along the avascular line a,
(arrowed) whenever possible
leaving the epiploic append-
ages attached to the colon h.
This can be done partly by
blunt, partly by sharp dis-
section c
Prior to omental detachment careful and systematic exploration
of the abdomen is required, even if laparoscopy has been under-
taken previously:
- The omentum may be the site of a small implantation of
metastasis or of inflammation and if so, it is not suitable
- The liver must be examined for metastasis
- Metastatic liver and peritoneal deposits and suspicious lymph
nodes should be excised and submitted to frozen section
- The size of the omentum, vascular pattern, and patency
should be checked
Omental adhesions are frequent and may complicate mobiliza-
tion before transposition; usually, however, they can be divided
surgically and do not provide a contraindication.
Preparation of the Omentum. For repair of organs at the level
of the umbilicus, the omentum is usually of sufficient length.
If it is found to be too short for a distant requirement, attach-
ment from the transverse colon and partial division of the apron
(Sect. 9.2.1) provides added length. The technique of freeing
the omentum from the transverse colon and stomach is basically
the same in all situations.
Detachment from the Transverse Colon (Fig. 120). The omental
apron is lifted upward to open the lesser sac through the posteri-
a c
219
 or part of the greater omentum. The plane (arrow) of dissection
should coincide - whenever possible - with the site of embryonic
fusion because that line, which is usually on the caudad mesen-
teric border of the transverse colon, is avascular and easy to
separate (Fig. 120a). Occasionally, however, the interferes with
the fatty epiploic appendages of the colon and it may be difficult
to discern the plane of fusion (Fig. 120b). The appendages
should be left attached to the colon; attempts to remove them
together with the omentum are often complicated by bleeding
due to the generous blood supply of the epiploic appendages.
Bleeding points must be ligated, which makes it even more diffi-
cult to determine the plane of dissection.
Sharp dissection is often necessary - especially in the middle
of the transverse colon - although blunt dissection (Fig. 120 c)
along the fusion line is desirable. This may be done with a
small sponge and the fingers, a procedure which is most easily
accomplished toward the left side of the transverse colon and
which permits rapid, atraumatic dissection without significant
loss of blood.
As a result of freeing from the middle portion of the transverse
colon, the omentum and the serosa of the transverse colon may
be lacerated; this happens especially when the omentum is thin
(Fig. 121 a, b). Immediate repair with a few absorbable sutures
is advisable. Care is taken to avoid damage to any diverticula
of the transverse colon.

Intraoperative Care
of the Omentum
Hemostasis is important, and bleeding points are tied individual-
ly. Care has to be taken to avoid tension and not to compress
the delicate vessels. Throughout the operation the omentum
should be kept moist at body temperature. For exteriorization
the omentum is kept wet in a laparotomy pack. A plastic intesti-
nal bag as illustrated in a patient with transposition to the chest
(Fig. 122e) avoids drying out until the omentum is led through
a subcutaneous tunnel (Fig. 123) and applied to the site of the
defect.

Closure of the If the pedicle of the transposed omentum, for example, is to

Abdominal Wall be used in chest wall reconstruction or at the neck it is important
not to constrict the vessels in the pedicle. Figures 122a-k illus-
trates most of the important points of technique in an intraoper-
ative series in one patient (see page 312-313).

Drainage Drainage of the abdominal cavity after laparotomy is a matter

of choice. In the case of omental exteriorization a drain may
Fig. 121 a, b. See page 311 be placed for 24-48 h in the subcutaneous channel. These drains
Fig. 122a-k. See page 312-3 should be brought out through healthy skin.

220
Fig. 123. The omentum
being led through a subcu-
taneous tunnel to the site
of the defect. (WHITE)

9.1.4 Repair of the Defect

Principles The repair of the defect requires the following steps:

1. Tissue Excision at the Site of Defect. The repair or substitution

of intra- and extra-abdominal tumors and fistulae may pose
special problems, but all should be treated by a wide tissue
excision. The repair of superficial tumors includes the excision
of the malignant lesion with a margin of at least 2.0 cm of
macroscopically healthy tissue (Fig. 122f) at each side of the
defect and adequate deep clearance. This reduces the risk of
local recurrence; assessment by frozen section is useful. In ad-
vanced local fungating disease or after radiotherapy, LASER ex-
cision of the lesion has been found to be useful [204] in addition
to conventional surgical techniques.

Fig. 122a- k. See page 2. Coverage with the Omentum. After debridement of the lesion
312/313 the pedicled or free omentum is spread over the defect, or added

221
Fig. 124a--c. Even with a
comparatively large chest
wall and pleural defects the
omentum provides satis-
factory functional cover.
a Before application to the
chest wall. Forceps point to
the pericardium. b, c Dur-
ing inspiration and expira-
tion - notice the bUlging
omentum (WHITE)

to stabilizing material, draped carefully, and sutured loosely

to the wound edges. When stabilizing material is not used, the
transposed omentum will move with respiration (Fig. 124a-c).
Stitches should be placed about 1 cm proximal to the omental
margin and at distances of 2-3 cm. Histo-acryl or fibrin glue
can be used when the omentum is exteriorized. Care has to
be taken to avoid tension and not to compress the vessels. This
management is basically the same whether the omentum is
sutured in the peritoneal cavity or extraperitoneally to skin
defects.

3. Skin Grafts can be placed immediately on the omentum, but

a second stage skin grafting 2 or 3 weeks after omental transpo-
sition or transfer improves the skin acceptance and reduces wrin-
kling of the skin grafts. The surface of the omentum to be
grafted is then smaller as a result of shrinkage and epithelializa-
tion from the wound edges [193]. It becomes flat and dry with
healthy granulation. All kinds of skin grafts may be applied.

222
 Although mesh graft has been tried with success, split skin grafts
are most frequently used [11, 29, 90, 96, 133, 193]. Grafting
with full thickness skin and subcutis have shown poor results
[207]. The skin grafts are sutured loosely over the omentum.
This may be with continuous or interrupted sutures.

Dressings are a matter of choice. Nonadhesive dressing or tulle

gras with moist packs are effective. More recently the transpar-
ent plastic dressings have been found to be useful (Fig. 122g,
see page 312-313).

9.1.5 Postoperative Care, Sequelae, and Follow-up

Postoperative Supplementary Procedures. Treatment of patients who have un-

Treatment dergone omental operations follows the pattern used for any
abdominal operation. Special attention must be paid to the site
of the previous defect. Surgery may often have required a long
anesthesia with transfusion. Therefore, in these cases, electro-
lytes, fluid balance, and urinary output have to be monitored
during the first postoperative days. Following laparotomy and
mobilization of the omentum, a temporary ileus may occur,
and a nasogastric tube and regular suction are therefore recom-
mended until bowel sounds are established.

Prophylactic Low Dose Heparin. Postoperative deep vein throm-

bosis or thrombosis in the omental pedicle and anastomosed
vessels is a potential danger. Prophylactic low doses of heparin
(5,000 units s.c. 8 hourly) have been used to minimize the risk.
Occasionally low molecular weight dextran is added. Any acute
thrombosis should be treated actively if there are no contraindi-
cations.

Prophylactic antibiotic application is not routinely used but may

of course be of value in particular cases.

Adjuvant chemotherapy and radiotherapy are related to the type

of malignant tumor in each particular case.

Mobilization The patient should be mobilized as rapidly as possible, and

of the Patient there appears to be no contraindication to getting out of bed
on the first postoperative day unless a skin graft is endangered,
for example, after transposition to the inguinal region. If early
ambulation is not possible, efforts must be made to prevent
venous thrombosis by active and passive physiotherapy, ban-

223
 dages, elastic stockings, frequent turning of the patient, and
leg exercises. If the omental transposition involves a joint, this
should be put through passive and active physiotherapy as soon
as possible.

Complications Complications are usually related to the extent of the malignant

disease itself or pulmonary problems. However, one case of vol-
vulus after omental surgery has been reported [88]. In addition
hemorrhage from or thrombosis of the omental vessels may
occur as well as herniation along the pedicle when exteriorised.

Functional Sequelae Changes in Blood Count and Serum Albumin. Postoperative he-
matological examination [98] after omental transposition to the
thoracic wall showed that some patients develop a normo-
chromic anemia. Intra- and postoperative blood loss from the
recipient and donor site as well as infection may be a contribu-
tory factor.
Especially patients suffering from the effects of metabolic distur-
bance and cachexia associated with malignant disease showed
hypoproteinemia after exteriorization of the omentum to the
chest by exudation from the omental surface and albumin leak.
Following skin grafting these problems are self-correcting.

Follow-up and It must be remembered that the skin grafted over the omentum
Documentation develops no sensation, and this can be a disadvantage especially
in areas where this is important, such as the scalp and extremi-
ties.
The long-term results of omental surgery are not well document-
ed in the literature and many of the cases undertaken may well
have had a poor prognosis because of extensive malignant dis-
ease. Prospective documentation is of great value: Photographic
records of surface defects and CT scans of intra-abdominal
omental transposition allow a worthwhile assessment to be
made.

9.2 Particular Surgical Procedures

9.2.1 Surgical Principles and Techniques:

Omentopexy, Omental Mobilization,
and Transposition

Omentopexy Omentopexy is defined as the application of the omentum to

the stomach, duodenum, liver, and kidney within its normal
anatomical reach and while remaining attached to/or being de-
tached from the transverse colon. Sometimes it is convenient

224
 to divide the apron in the long axis so that only part is brought
to the desired site.

Indications Limitation of Infections. In the stomach and duodenum the

omentum can be used to patch or reinforce the site of perforated
ulcer. In gangrenous appendicitis or similar situations the sur-
rounding surface is inflamed and this predisposes to omental
adhesions. In these cases a few absorbable sutures are used to
hold the omentum in place in an attempt to contain the sepsis.

Filling of Cavities and Coverage of Defects. In the liver the

omentum is used to fill a cavity after removal of, for example,
an echinococcus cyst, a malignant tumor, or liver abscess. The
splenic capsule can be patched when risk of bleeding is a poten-
tial danger after surgery. The kidney and ureters can be pro-
tected by omentopexy.
However, distal ureters are more easily reached by transposition.
This is especially important in gynecological operations.

Drainage In the area of the biliary ducts the omentum is used

for drainage in congenital abnormalities such as biliary atresia.
Omentopexy has been tried for drainage of portal hypertension
and as an outside drainage channel for perforated gastroduo-
denal ulcers (Neumann cuff [142]). But to a large extent results
have been disappointing, and because of better surgical tech-
niques omentopexy is not widely used. However, under certain
circumstances, omentopexy may be the only choice left.

Operative Coverage of the Lesion. The omentum is brought to the prepared

Technique or roughened recipient site and sutured loosely to the lesion,
avoiding any compression and kinking (see Sect. 9.1.3).

Postoperative Care and Follow-up (see Sect. 9.1. 5)

Transposition Transposition is defined as the application of the omentum to

various sites, by dissection from the greater curvature and by
further internal division, in which a vascular pedicle of origin
is preserved.

Routes The omentum can be brought to any site in the abdomen using
the retro-colic route (paracolic gutter, Fig. 139 b, see page 246)
- this route is preferable because it reduces the risk of hernia,

225
 torsion of the pedicle, and adhesions - or the transperitoneal
route (Fig. 139 a, see page 246). The omentum may be led to
the mediastinum through the hiatal opening of the esophagus
and exteriorized to cover defects of the body surface through
a tunnel in the rectus muscle and subcutis.

Indications and In those cases with large defects as listed in Sect. 9.1 the
Contraindications omentum should be considered when it is anatomically possible
to reach the desired site with an adequate pedicle. Although
free omental grafts and more recently microsurgical anasto-
moses have been used it is clearly better not to disconnect the
local blood supply if it can be avoided. In addition to the general
contraindications of omental grafting there may occasionally
be problems in routing the pedicle to the desired site without
torsion or tension - especially when blood vessels are abnormal
or degenerate. In these cases microanastomosis may be pre-
ferred.

Guidelines Diagnostic Preoperative Procedures. Abdominal incisions and ex-

ploration of the abdominal cavity are along the general lines
discussed in Sect. 9.1.3.
With transposition it is especially important to:
- Determine whether the omentum will satisfactorily reach the
desired location. One has to consider the tendency of the
omentum to retract after fixation.
- Check the course and pulsation of the gastroepiploic vessels,
and during mobilization care has to be taken not to damage
the origin or continuity of the main epiploic vessels. The vari-
able vascular pattern is shown in Sect. 4.3.
- Avoid any compression, torsion, and tension of the omentum
- Fold the omental bulk along its long axis when filling cavities
or when sutured to the recipient area to prevent ischemia
by kinking vessels

Careless handling and mobilization damage the omentum and

lead to necrosis.

Mobilization; Pedicle When planning the method of lengthening the omentum, the
for Transposition smallest amount of tissue which is required for transposition
should be used. Clearly it is an advantage to leave as much
omentum undisturbed to serve its normal function. The shortest
route to the defect also gains length and prevents kinking of
the pedicle.

226
Separation Detachment from the Transverse Colon is shown in Sect. 9.1.3.
from the Stomach The omentum can be separated from the greater curvature of
the stomach from either side, retaining the gastroepiploic vessels
outside or within the omental apron (Fig. 125a, d). The gastro-
epiploic arcade may be incorporated in the mobilized omentum:
- Completely by dissecting close to the greater curvature
(Fig. 125d)
- Partially along some of the curvature (Fig. 125 b)
- Totally excluded by dissecting outside the gastroepiploic
arcade (Fig. 125a) if the feeding pedicle and the anastomoses
are adequate

Separation from Left to Right. As proposed by ALDAY and

GOLDSMITH [6] and DAS [48] this is said to be easier, because
on the right the antral portion of the omentum fuses to the
head of the pancreas. In addition, the gastroepiploic artery on
the right side is usually larger than that on the left, providing
better blood supply to the apron (see Sect. 4.3).

Separation from Right to Left. Although dissection of the antral

portion from the head of the pancreas takes longer, there are
some advantages because the omentum on the left side has:
- A greater volume
- Usually large recesses by which a greater effect oflengthening
may be achieved
- Origin nearer to the thoracic wall
- Demonstrably less distortion of the stomach by traction of
the pedicle

Separationfrom Right or Left by a Midline Incision. By a midline

incision from the lower margin of the apron up to the greater
curvature (Fig. 125c, e) only part of the omentum may be mobi-
lized.

Hints When separating the gastroepiploic arteries from the stomach,

the vessels between the two should be carefully and individually
ligated and divided close to the gastric wall, leaving a cuff suffi-
ciently large, so that the gastroepiploic vessels are not con-
stricted; the critical ligatures are those on the gastroepiploic
side, and mass ligature causes foreshortening of the omentum
and hemorrhage. Bleeding of omental vessels rapidly leads to
a hematoma which spreads throughout a large portion of the
omentum. The right gastroepiploic artery especially has to be
separated fully from the stomach to its gastroduodenal origin.
Traction on the pedicle may tear off small undivided gastric
branches and may cause bleeding postoperatively.

227
228

Internal Lengthening
by Dividing the
Omentum
The Problem of Ex-
tensive Lengthening
Complications
.. Fig. 125a-e. Separation
from the stomach may be
performed from either side,
retaining the gastroepiploic
vessels outside a or within
d the omental apron. Occa-
sionally mobilization of the
whole of the omentum is
not required and smaller
procedures based on the
vascular pattern are suffi-
cient b--e
The precIsIon of clips is generally not great enough, and in
addition, they can become displaced when leading the pedicle
to its destination. They are also not ideal on the exteriorized
omentum.
Methods have been outlined by KIRICUTA [104], ALDAY and
GOLDSMITH [6], and DAS [48]. In view of the variation in vascu-
lar pattern which has been recently demonstrated ([120],
Sect. 4.3) it is clear that lengthening has to be carefully planned
in individual cases. The main arteries have to be preserved.
DAS [48] extended the possibility of lengthening the omentum
by an additional internal "L" shaped incision. In obtaining
such an extensive increase in length, width may be sacrificed
and the size becomes inadequate for covering large defects. Be-
cause the marginal anastomoses are often insignificant ([120],
Sect. 4.3), the blood circulation may also become very poor;
and in this case transfer with microanastomosis should be pre-
fered.
Repair of the Defect, Coverage of the Lesion, and Skin Grafting
(see Sect. 9.1.4)
Postoperative Care, Functional Sequelae and Complications (see
also Sects. 9.1,9.2). Especially when it is exteriorized, the pedi-
cled omentum may cause some gastric dysfunction [183, 196].
Although it is not routinely necessary [183], in these cases the
pedicle should be divided about 6 weeks after transposition to
prevent continued traction on the stomach.
Small areas of thrombosis and necrosis of the omentum related
to transposition to the body surface are not a serious problem
and can easily be debrided at the time of skin grafting. The
authors have not themselves seen a case of total necrosis but
understand that it has occurred. In this situation and when there
are symptoms of pedicle damage after intra-abdominal transpo-
sition laparotomy and examination of the pedicle must be con-
sidered.
It is unlikely that heparinization, anticoagulant therapy, or low
molecular weight dextran would re-establish circulation or
prevent extension of thrombosis. The administration of vaso-
dilatating drugs is without effect.
229
 9.2.1.1 Intra-abdominal Transposition

Liver Injuries, Cysts, and Tumors

U. NEFF and F. HARDER

Liver Trauma Introduction. The value of detached omental tissue as a

"tampon" [68] for hemostasis of the injured liver was investi-
gated by LOEWY in 1900/1901 and later confirmed by GIRGOLAFF
1907 [68]. Russian surgeons used it for the first time for this
purpose in man but on a vascular pedicle [21, 68, 92]. As early
as 1910 BOLJARSKI [21] reported a few patients with no compli-
cations and extremely short hospitalization with this method.
In clinical practice the omentum found its earliest and widest
use in liver injuries, often sustained on the battlefield [122, 147,
179]. FABIAN et al. in 1980 reported results of extensively injured
livers treated with omental transposition [63].
It is usually possible to distinguish between:
Penetrating trauma such as gunshot or stab injury, which has
a mortality below 10% [138]
Blunt trauma occurring mostly after road accidents, with a much
higher mortality, ranging between 20% and 50% [127]. The
right lobe of the liver is involved in about two-thirds of the
cases [111]. A comprehensive review of 510 such cases and their
treatment has been recently given by WALT [201].

Treatment. The surgical principles of therapy are hemostasis,

debridement, and drainage. Initial hemostasis can be achieved
by:

Manual Liver Tissue Compression (Fig. 126b).

Clamping of the Hepatoduodenal Ligament (Pringle Maneuver).
If this is ineffective the aorta must be exposed and compressed
subdiaphragmatically.
Tamponade with Packs. This should be applied only temporarily,
for example, for transportation because of the possibility of
rebleeding and infection following removal.

The definitive treatment may consist of:

1. Simple drainage
2. Suture and ligature
3. Debridement and segmental resection
4. Omental transposition into the cavity [147]
5. Arterial ligation [1, 127]
6. Intracaval shunt [169]

230
Fig. 126. a Posttraumatic
rupture of the right lobe of
the liver. b Manual com-
pression for immediate he-
mostasis. c Omental tam-
ponade and parenchymal
sutures. Sometimes a teflon
or absorbable sheet is used

Surgical Technique. The upper median incision is the approach

of choice [7]. After hemostasis the omentum may be used as
a physiological tamponade to fill the eventual dead space
(Fig. 126c).

Results. In FABIAN and STONE'S series of 113 patients with liver

injuries hemostasis has been achieved in 105 patients by omental
tamponade alone [63]. In four patients it was necessary to ligate
in addition some smaller arteries in the periphery. Two patients
required ligature of the commen hepatic artery and one patient
ligature of the right hepatic artery. Mortality was 8%; the com-
plications were one liver abscess and one case of hemobilia.

Liver Diseases Introduction. Omental transposition is indicated as a physiologi-

cal tamponade for large raw surfaces or cavities after liver sur-
gery such as :
- excision of cysts of parasitic, inflammatory, traumatic, or con-
genital origin
- after abscess incision

231
 resection of a benign or malignant pnmary or metastatic
tumor.
It helps to prevent infection and fistula formation of the bili-
ary ducts.
It is contraindicated when the omentum itself is inflamed,
edematous, or adherent following previous operations.

Cysts Surgical excision of Echinococcus cysts with subsequent omento-

pexy has been attempted for many years since MAUCLAIRE'S
report appeared in 1903 [38, 69, 113, 130, 134]. Larvae of Echin-
ococcus settle frequently in the liver, where they grow in to
a cystic tumor consisting of different layers [166]:
a) the inner germ cell layer, which may grow toward the periph-
ery into the host capsule, b) the outer cystic wall (cuticula)
[13] and c) the pericyst, i.e., host capsule, which is developed
by the host tissue as a connective tissue reaction against the
growing cyst.

Surgical Technique. The danger of cystectomy following damage

of the cyst during excision is its wide peritoneal spread. Surgery,

Fig. 127. a Enucleation of

a cyst including the host
capsule (pericystectomy).
b Resection of multiple
cysts with the margin of
normal liver tissue included
in the specimen (partial he-
patectomy). c Simple curet-
tage of a cyst (marsupiali-
zation) bears increased risk
of recurrence. d Enuclea-
tion without the host cap-
sule (partial cystectomy)
bears risk of biliary fistula c

232
 a
Fig. 128. a Cyst cavity after
peri cystectomy. b Cavity
filled with omental tissue
Fig. 129a- d. See page 314
Abscesses
b
therefore, aims to remove the parasite without dissemination
and to drain or fill-up the dead space with appropriate tissue.
The omentum is ideal for this purpose. The technique used for
removal of the cyst depends on the number, size, location, and
age of the cysts. Once the cyst is enucleated (Fig. 127 a) the
cavity may be filled with omentum [134]. Occasionally multiple
cysts will require partial hepatectomy (Figs. 127b, 131). Marsu-
pialization (Fig. 127 c) and intracapsular cystectomy (Fig. 127 d)
are unsatisfactory methods because of recurrence and the devel-
opment of biliary fistulae. The resulting cavity following pericys-
tectomy and its obliteration with transposed omentum is shown
in Fig. 128 a, and b. An operative series during excision of a
large echinococcal cyst is shown in Fig. 129a-d (see page 314).
Results. T AGLIACOZZO [180] reported on 114 pericystectomies
in 80 patients with no mortality and recurrences in 1-3 years.
However, pericystectomy is a time-consuming method. PISSIOTIS
(personal communication, 1980), in a series of over 200 opera-
tions for echinococcal cysts, found the main advantage in using
the omentum to be a reduced hospitalization time and a much
lower rate of biliary fistula formation (4% instead of 20%).
Almost identical results were reported by PISSIDIS et al. [159].
Introduction. Many liver abscesses, whether pyogenic or parasit-
ic, are small and may be found to be multiple on the various
233
Fig. 130. a Omentum led
into and through a chronic
abscess cavity with scler-
otic walls. b Omentum
sutured to the distal end of
the abscess cavity

234
Fig. 131. Partial resection
of the right lobe of the
liver for multiple cysts

preoperative diagnostic tests including ultrasonography and CT

scanning which are now used. Medical treatment has priority
in management. When this fails or when a large cyst or several
cysts are present, surgery must be considered.

Surgical Technique. Both acute and chronic abscesses present

similar problems for the surgeon. Once located the abscess must
be drained and antibiotic cover given to prevent portal pyemia.
If possible, an extraperitoneal and/or extrapleural approach
should be used. If a transperitoneal approach is used, the
omentum can be mobilized to obliterate the abscess cavity. This
is particularly important in chronic abscesses with a sclerotic
wall which does not collapse after drainage (Fig. 130 a, b). In
one patient in our series who had a post-traumatic liver abscess
with a biliary fistula and recurrent sepsis, all classical methods
to eliminate the focus of infection failed until the omentum
was transposed.

Tumors Introduction. Partial liver resection has been reported for rare
benign tumors as well as primary and secondary tumors. The
indications for liver resection for solitary metastasis of colonic
. .
cancer are now mcreasmg.

235
Fig. 132. a Omentum mo-
bilized on the right gas-
troepiploic pedicle and
applied to the cut surface
of the liver after resection
of the left lobe.
b Omentum similarly
applied to the cut surface
of the liver following resec-
tion of the right lobe

Surgical Technique. Following liver resection, the omentum, mo-

bilized on the right gastroepiploic pedicle, is applied to the cut
surface of the liver after initial hemostasis (Fig. 132a, b). A
postmortem specimen some weeks after massive right partial
hepatectomy for a tumor is shown in Fig. 133.

Organ Preserving Surgery

J. WALDSCHMIDT

Capsule Rupture Following rupture of the capsule of certain organs such as the
liver and kidney, it is important to preserve the organ and reduce

236
Fig. 133. Postmortem speci-
men after right hemihepa-
tectomy for tumor. The
omentum is seen filling the
"dead space." The cut sur-
face of the liver is well
healed and the common
bile duct (arrowed) is pa-
tent (NEFF and HARDER)

hemorrhage. The omentum can be mobilized and used as a

tampon within the capsule. Some attempts have also been made
to preserve the spleen by such methods following rupture of
the capsule. Despite the desirability of preserving the spleen,
the danger must be remembered and secondary rupture may
occur.

Omentoportoduodenopexy for Drainage

Biliary Duct, Recently HIRSIG et al. [93] summarized our poor knowledge of
Atresia and biliary atresia and emphasized that it is not a simple congenital
Hypoplasia malformation of biliary ducts but rather part of a chronic peri-
and postnatal liver disease. Treatment aims at establishing the
drainage of bile into the peripheral lymphatic vessels. Attempts
have been made to drain the bile:
Into the abdominal end of the thoracic duct
Directly into the bowel using a jejunal loop which has been
isolated according to the technique of Roux, stripped of its
muscular coat, and sutured to the porta hepatis so that the
lymph vessels are able to grow into the intestinal wall [171]
- Via the omentum into the bowel
The first attempt to drain bile via omental lymphatics was made
in 1973 by HUNG and HUANG [95]. They transposed the

237
 Obli terated and hypoplast ic
Liver bili ary ductule

-+-IH+,;:=r-- Art e r y

Irf'::::::!::===:::!=~~:::: -I--I--#-.7===.-- E nl arged int rahepa t ic

lymph vessel

Enlarged lymph nodes

in liver hilum

\
Fig. 134. Principle of
lymph drainage. Oblitera-
tion of the bile duct in the
liver results in back pres-
sure and an increase in bile
in the hepatic spaces. This
bile enters the hepatic
lymph ve sci and nodes
and thence reaches the
Transposed omentum
duodenum via the omental
lymphatic ve sels

omentum in dogs to the liver surface. Although they did not

strip the capsule, encouraging results were achieved and histo-
logical examination confirmed a direct communication of lym-
phatics between the liver and omentum.
We owe the decisive progress to MUGGIASCA [139], who per-
formed an omentoduodenoportopexy in a child suffering from
an intrahepatic biliary duct atresia without opening the intesti-
nal lumen. He incised the lymph vessels and lymph nodes in
the porta hepatis and transposed the omentum between this
region and the ventral surface of the duodenum which had been
stripped of its serosal surface (Fig. 134). In this way a satisfacto-
ry hepatoenteral flow of bile was established without opening
the intestinal lumen. The author reported a good result
10 months after performing the operation.

Surgical Technique (after WALDSCHMIDT). The peritoneal cavity

is opened by transverse epigastric incision (Fig. 119 k and 1,
page 216) and the falsiform ligament divided. The portal lymph
vessels and lymph nodes, which are always enlarged, are in-

238
a b

Fig. 135. a The exposed spected and great care is taken to avoid hemorrhage. The hypo-
porta hepatis and fenes- plastic gallbladder, which will contain colorless bile in complete
trated muscle wall of the
duodenum with intact atresia, is cannulated and manometry undertaken. Water-solu-
mucosa ready to receive ble contrast medium is used to demonstrate the extrahepatic
the transposed omentum. biliary ducts. The ventral layer of the peritoneum is now de-
b Completed omental
transposition
tached from the hepatoduodenal ligament. The vascular struc-
tures, possible rudimentary biliary duct, and lymph vessels are
clearly recognizable. During mobilization the hepatic lymph
vessels are divided in several places, and immediately afterward
the lymph flows into the peritoneal cavity. Then all accessible
lymph nodes are incized and folded open.
The muscular wall on the anterior surface of the duodenum
is stripped over an area of 1.5 x 2 em (Fig. 135a). The omentum
is then mobilized on the right pedicle and sutured to the defect
and to the transsected nodes of the porta hepatis and afterward
to the mucosa of the duodenum, which herniates through the
defect in the duodenal musculature (Fig. 135b). In premature
infants the omentum is very small (Sect. 3.2), and it is necessary
to lengthen the omentum by one of the established techniques
or as shown in Fig. 136.

Results and Outcome. Of the 12 children treated in Berlin all

were between 5 and 11 weeks of age. The results are encourag-
ing, two having been followed for 4 years, two for 2 years, and

239
Fig. 136. Suggested tech-
nique for mobilizing
(dotted lines) and achieving
adequate length of the
omentum in neonates
Portal Hypertension
240
five for over 1 year. Of the two who died, situs inversus was
perhaps contributory in one child.
In all children the jaundice disappeared, and the stools became
a normal color within 3 weeks. In parallel with this transaminase
and alkaline phosphatase levels fell. Ascites and esophageal
varices did not develop. In addition the growth and behavior
of the children appeared to be normal.
Omentopexy for Asites
U. NEFF
The methods of treating portal hypertension are shunt opera-
tions and nonshunt operations. Omentopexy belongs to the
"nonshunt" operations.
Introduction. The first omentopexies to the roughened parietal
peritoneum specifically performed for the treatment of ascites
in portal cirrhosis were attempted by DRUMMOND and MORISON
in 1896 [56] and TALMA in 1898 [181].
Surgical Principles. The omentum is interposed between the
portal vein and the vena cava in the hope that a portosystemic
collateral circulation will develop after a few weeks.
 Results. Although there have been a few further successful
results attributed to this method in the literature [19, 20, 42,
43], the overall results are not encouraging [86, 131].
Thirty-five patients undergoing omentopexy for ascites resulting
from portal hypertension have been reported in the last 20 years.
In seven cases of liver cirrhosis or malformation in the portal-
venous system in children [19] four patients treated by omento-
pexy survived with no further procedure. Another consequence
of portal hypertension is bleeding from esophageal varices.
Omentopexy does not affect the underlying hypertension and
this is seen by the fact that bleeding from varices may occur
even after ascites is controlled. This complication occurred in
two patients in BERMAN'S series.
In adults, EL-ZAWAHRY [59] treated ten patients with bilharzia
who had developed portal hypertension and ascites. He had
some success but two patients in the series died, one from bleed-
ing varices and one from cholemia. Limited success was also
reported in the 18 patients treated with omentopexy by COUIN-
AUD [43].
Although the method is relatively simple, the results are not
satisfactory enough to establish the method as an important
technique in managing ascites from portal hypertension. Not
only are the anastomoses which develop relatively inadequate
but in addition the length of time required for their formation
is unacceptable.

Omental Cuff for Cardiopexy (CESNIK 1980)

D. LIEBERMANN-MEFFERT

Hiatal Hernia Nissen's fundoplication and Belsey and Hill's techniques are
established methods for the treatment of hiatal hernia and reflux
esophagitis. Cardiopexy using the omentum in 30 patients has
been described recently ([37], CESNIK, personal communication,
1981).

Surgical Technique. A strip about 8 cm wide is dissected from

the left side of the omentum, leaving its colic attachments. The
strip is led around the lower end of the esophagus and a cuff
is formed.

Follow-up. There were no postoperative complications but fur-

ther reflux occurred in one of 19 patients and prolonged follow-
up is not available as the technique has only been in use for
the last 3 years.

241
 Protection of Intestinal Defects (SENN 1888)

T. ROEDl

Introduction. In the prelaparotomy era the protecting action of

the omentum may often have been decisive for the survival or
death of the patient. If the omentum was effective in covering
up a small perforation of an ulcer or an inflammatory focus
such as the appendix, gallbladder, or diverticulum of the
sigmoid, the inflammatory process was localized and could heal;
otherwise diffuse lethal peritonitis developed. Adhesions be-
tween omental tissue and an intra-abdominal organ indicate
that some sort of inflammatory reaction has previously taken
place (Sect. 7.4). These observations taught surgeons long ago
[26, 60, 142, 143, 173] to use the omentum or epiploic append-
ages to re-inforce and protect anastomoses or defects in the
gastrointestinal tract. More recently, animal experiments
(Sect. 8.3) have shown that wrapping poorly vascularized intesti-
nal anastomoses in the omentum to some extent may prevent
disaster [51,101,112,132]. If the blood supply to the omentum
was intact, revascularization of the bowel wall occurred very
rapidly. In similar experiments CARTER et al. [35] found no ad-
vantage in re-inforcing everted colonic end-to-end anastomoses
with omentum on a vascular pedicle. A free omental graft
(Sects. 8.2.1, 9.2.4) does not give the same security as it may
become necrotic, leading to considerable inflammation and
thereafter scar formation or bowel obstruction.

Gastric and Duodenal The widest use of omental protection in gastrointestinal surgery
Perforation is the covering of perforated duodenal and gastric peptic ulcers
(BRAUN 1897) with the pedicled omentum. Free grafts have also been success-
fully used (Sect. 9.2.4). Originally described by BRAUN [26] as
the only possible way to close a large defect of the stomach
wall, omentopexy has been adapted and modified by a number
of surgeons. NEUMANN [142, 143] used a Nelaton or Tiemann
catheter to drain the stomach contents. He then wrapped
omentum around the catheter to form a protecting sleeve be-
tween the intestine and abdominal wall. SMOLINSKI [175] modi-
fied the technique by using a Kehr's T-drain, whereby leakage
around the drain could be reduced.
KRAUSZ etal. [114] and RIVES etal. [164,165] routinely used
the pedicled omentum to protect gastric and duodenal ulcer
perforation and combined the procedure with proximal gastric
vagotomy (PGV) as definitive surgery. Although SAWYERS et al.
[168] achieved excellent results with this method, they recently
changed to simple closure of the perforation of ulcer excision

242
 and primary suture in combination with PGV. This has also
been our policy for many years, with very good results [140].

Indication. It may be of benefit to cover the site of perforated

gastric ulcer with the omentum, for example, if the patient is
in an extremely bad condition or if there are complications such
as a severe fall of blood pressure or respiratory problems. How-
ever, if possible, omentopexy should be combined with vagoto-
my and protected by a Penrose drain.

Complications. READ and THOMPSON [162] observed gastric

outlet obstruction after covering perforated chronic ulcers with
the omentum. This did not occur in acute ulcers.

Re-inforcement of In- Exceptionally the omentum may be used to cover:

testinal Anastomoses
- Esophagointestinal anastomoses
- A duodenal stump
- A small bowel anastomosis
- Anastomoses of the colon when there is a risk of fistula
- In one case we successfully used an omental flap to protect
the suture line of an esophagogastric anastomosis.
The standard technique for bowel anastomoses is satisfactory
and does not normally require omental protection. However,
when the bowel is severely damaged by irradiaton or has a
poor blood supply support of the anastomosis with the
omentum may be of benefit. The omentum should be applied
very loosely to avoid strictures due to omental shrinkage. Inter-
estingly enough there are no reports of the use of primary
omental re-inforcement in inflammatory bowel disease (CROHN'S
disease), where fistula formation is frequent. This may be due
to the fact that often the omentum seems to be involved in
the disease process, appearing edematous, and is not suitable.

Low Rectal Leakage of rectal anastomoses following anterior resection and

Anastomoses irradiation occurs in approximately 5%-10% of cases [71,116].
(GOLDSMITH 1977) The pedicled omentum has been found to be effective in prevent-
ing anastomotic disruption. The surgical technique is described
in detail in the section on the pelvis and pelvic floor.

Urogential Organs and Pelvic Surgery

R. AUSFELD, H. TILLMANNS, G. RUTISHAUSER, and H. WHITE

Introduction Experiments reported in 1900 by ENDERLEN [61] confirmed that

in cats and dogs, bladder defects could be repaired with the

243

Fig. 137. Omental transpo-
sition to repair a vesicova-
ginal fistula. [202]
Indications
244
I
C o5€d . stula
transposed omentum, which rapidly became covered with uro-
thelium. The potential for revascularization was shown by
PAUNZ in 1929 [151] when he divided the renal artery in dogs
and found that the transposed omentum wrapped around the
kidney would preserve the viability of the renal parenchyma
and kidney function.
The first clinical use of the omentum in urogenital surgery was
the repair of a recurrent vesicovaginal fistula by WALTERS in
1937 (Fig. 137, [184, 202]). However, it was not until the classic
work of KIRICUTA, starting in 1955 and subsequently published
in 1961 [106], that the full potential of omental transposition
came to be realized in the treatment of pelvic fistulae, including
those after radiotherapy. He continued to develop the technique
[106], which was taken up by TURNER-WARWICK and his col-
leagues [190].
Extensive pelvic obliterative surgery has a high morbidity and
it was natural that attempts were made to reduce some of the
complications by the use of the omentum. FERRARIS [65] and
VALLE and FERRARIS [191] used the omentum not only to line
the denuded area but also to contain the intestinal loops in
a sling and prevent them from descending into the pelvis. The
role of the omentum in overcoming retroperitoneal fibrosis ef-
fecting the ureters was explored by TRESIDDER et al. [186].
In addition to the general indications (Sect. 9.1.1) there are some
specific urogenital indications: If large absorptive surfaces, for
Fig. 138. Indications for Indication Desi red effect
and sites of omental trans-
position Heminephrec tomy
Pole resection Separat ion
Autotransplantation

Chronic renal fistula

Protection
against leakage and infection
Urinoma
Transplant re - Resolut Ion of infectIOn
lated problems

Pyeloplasty In
presence of
severe infect ion

Recurrent stone
formation
Staghorn calculr

Adhesion : supple, loose

Solitary kidney
Impending re -
explorat ion
to avoid frozen
adhesion

example, renal parenchyma or suture lines of ureter, bladder,

and urethra, cannot be closed satisfactorily, the omental sling
forms a sheath resistant to infection (Fig. 138); it may help
to prevent dense adhesions and the rigid fibrosis resulting from
extravasation of urine. The reduction of fibrosis makes re-explo-
ration easier, and control of local infection reduces the risk
of further stone formation around the minute fragments which
inevitably remain [178] after removal of staghorn calculi. For-
mation of loose and elastic adhesions allows" urodynamic mo-
tility [188]," because the tissue retains suppleness after healing.
This facilitates re-exposure if necessary.

Preoperative Assessment. No special preoperative assessment is

necessary when the omentum is used except that routinely re-
quired for urological operations.

Principles The omentum usually reaches the upper urinary tract without
of the Operation any dissection from the stomach. When required to reach the
pelvis it must be lengthened at one or other gastroepiploic vascu-
lar pedicle (see Sect. 9.3.1, Fig. 139a, b). Two different routes
of transposition to the urogenital tract are most commonly used:
1. The trans-abdominal Route [106]. By a midline abdominal
InClSIOn the omentum lS mobilized and lengthened

245
Fig. 139a-c. Routes for
omental transposition to
the pelvis. a Trans-abdomi-
nal route. b Retrocolic
route (anterior view).
c Retrocolic route (lateral
view) occupying lateral
space

(Sect. 9.2.1) to bring a wide thick bulk of omentum with

a good blood supply down to the pelvis. The omentum is
kept in place by sutures to the peritoneum, the taeniae of
the colon, and the pelvic floor (Fig. 139a).
2. The Retrocolic Route [190]. From a midline incision the as-
cending and/or descending colon are mobilized and the
omentum is led retroperitoneally in the paracolic gutter along

246
 the ureter to the pelvis (Fig. 139b, c). Or, using a loin ap-
proach, the omentum is pulled to the paracolic gutter through
an incision in the peritoneum lateral to the colon.

Hints In addition to the general techniques of urosurgery and omental

mobilization, TURNER-WARWICK etal. [188] recommended
routine appendectomy so that the pedicle is not endangered
by subsequent appendicitis. One advantage of the retrocolic
route is that the omentum will not become adherent to the
ovaries and Fallopian tubes and possibly reduce fertility in
young females. This route also reduced bowel complications
which may occur when using the trans-abdominal route.
The importance of using absorbable ligature material must be
emphasized. Non-absorbable material exposed to urine has a
very high risk of developing encrustations, leading to stone for-
mation. Omental transposition along the ureter may displace
it considerably. Although function should not be affected, this
must be remembered when interpreting postoperative pyelo-
grams.

Urinary Tract Reconstruction

R. AUSFELD and G. RUTISHAUSER

Kidney, Renal Indications. Omental support is not indicated for routine opera-
Pelvis, and Ureters tions on the kidney and renal pelvis and one should not compli-
cate a simple retroperitoneal operation by opening the peritone-
al cavity. Omental transposition, however, is of particular value
in all the situations listed in Fig. 138 (see also [41, 178, 188]).

Position of the Patient. The patient is placed either in the supine

position for the trans-abdominal approach or in the lateral posi-
tion for the routine loin approach.

Operative Technique. For the trans-abdominal approach either

a midline lower abdominal incision is used and extended lateral-
ly to the top of the 12th rib or a subcostal incision is made,
giving access to the lumbocostal area. The right colonic flexure
- or both flexures if necessary - is mobilized to expose the
kidney. On the right side the duodenum is displaced by Kocher's
maneuver. After kidney surgery, the omental apron is divided
in the midline from the lower fringe upward to the transverse
colon, taking care of the epiploic vessels. Division of the gastroe-
piploic arch and lengthening of the apron as described above
(Sect. 9.2.1) are not usually required for repair in the upper
urinary tract. The mobilized portion is led directly into the retro-

247
Fig. 140. Transposition of
part of the omentum to the
kidney and renal pelvis
Fig. 141. a Transposed
omentum interposed be-
tween the transplanted
kidney and vascular anas-
tomosis. b The contralater-
al as well as the ipselateral
kidney may be used
Fig. 142. Wrapping of the
ureter in the omentum in
retroperitoneal fibrosis
Vascular Protection
of Anastomoses
in Transplantation
248
Fig. 140
peritoneal space, e.g., paracolic gutter. The omental pedicle may
be spread out behind the kidney and renal pelvis (Fig. 140),
wrapped around and sutured, or brought out in front of the
kidney and fixed behind. Care has to be taken that the kidney
is completely enveloped and that the free margins are stitched
together as well as to the retroperitoneal tissues.
Although the kidney is often infected in these situations, periton-
itis is a very uncommon complication [188]. If extravasation
is a danger, a Penrose drain or latex tube is placed in the area
of the kidney before replacing the colonic flexures and abdomi-
nal closure.
Some surgeons prefer a routine loin approach [123, 188]. In
this case the omentum is pulled through an incision in the lateral
ascending or descending colonic mesentery to wrap the kidney
or ureter. Mobilization of half of the omentum and separation
from the colon may be accomplished by this route, but pre-
existing intra-abdominal adhesions and a short omentum can
make this approach difficult.
In transplantation surgery the omentum can be a useful sheath
in separating the kidney from the vascular system. LINKE et al.
[123], for example, reported an uneventful convalescence of a
patient in whom he autotransplanted a kidney into the iliac
region after extracorporal excision of a renal tumor. After this
"bench surgery" the omentum was brought down retroperiton-
eally, filling the space of the excised kidney, and a flap was
interposed between the reimplanted kidney and the vascular
anastomosis (Fig. 141).
Fig. 141 Fig. 142

Recurrent Inflammatory processes of the retroperitoneal spaces frequently

Retroperitoneal cause dense tissue fibrosis [91, 199]. Two types of fibrosis have
Ureteric been classified [199]: the primary idiopathic retroperitoneal fi-
Obstruction brosis and the secondary retroperitoneal fibrosis which is in-
duced by trauma, irradiation, hematoma, and urine extravasa-
tion. In both fibrosis may develop bilaterally, spread up to the
renal pelvis, and obstruct the ureters.
Ureterolysis and corrective plastic surgery become necessary to
preserve renal function and to avoid hydronephrosis. Simple
ureterolysis and placement within the peritoneal cavity is often
followed by recurrent fibrosis. TRESIDDER et al. [186] wrapped
the ureters and renal pelvis in an "omental sleeve" leaving the
ureters retroperitoneally after a full-length ureterolysis with an
initial good effect (Fig. 142). In progressive disease, however,
the omentum may become involved in the process [188], and
therefore this operation may not be effective in all situations.

Ureteral Stricture, These diseases are usually caused by injuries following surgery,
Stenosis, and Defects tuberculosis, and irradiation. Unilateral stenosis can be treated
by resection and ureteroureterostomy. In bilateral disease, an
ileal conduit may be required. In both cases the omentum may
be used in an attempt to prevent recurrent problems.
Distally located defects can be reconstructed and bridged with
a bladder flap such as that described by BOAR!. TURNER-
WARWICK [187] preserved the ureterovesical junction with a
"urothelial bladder flap," which he supported with the pedicled
omentum. LINKE et al. [123] resected ureteral defects and au-
to transplanted the kidney in the iliac area. He protected the

249
Fig. 143. a When used to
protect a ureteroileal anas-
tomosis, the omentum is
led along the course of the
ureter. b The omentum is
sutured to the ileal
conduit. c If the omentum
is long enough, it may be
led into the pelvis
Cystectomy
and Ureteroileo-
cutaneostomy
250
suture lines in separating the vessels from the ureteric implant
by interposition of the omentum (Fig. 143 a, b).
Although pelvic floor reconstruction is specifically discussed in
the following section it is necessary to introduce the problem
of surgical reconstruction after cystectomy and operation on
the lower urinary tract. Peritonealization of the cavity after cys-
tectomy can be difficult or impossible, especially if the tissue
has been irradiated. Abscess formation and impaired healing
is common in the hollow space. To fill this space, the omentum
is immediately transposed to the pelvis. This is one of the most
important indications in urosurgery, which adds only 20- 30 min
to the main operation.
Surgical Options. The pedicled gracilis muscle has been used
to fill the" dead space" after cystectomy. However, this proce-
dure is time consuming, the muscle has little volume, and post-
operative mobilization of the patient is more difficult.
Operative Technique. The omentum on the right gastroepiploic
pedicle is commonly used to cover the ureter (Fig. 143 a). This
is largely dictated by the fact that the terminal ileum and the
ileal mesentery, which are used for the ileal conduit, lie to the
right. The omentum is led behind the ascending colon and the
ileal conduit to the site of the ureteroileal anastomosis [152]
and on into the pelvis (Fig. 143 b, c), where it is sutured loosely to
the surrounding tissue . Particular care has to be taken to avoid
any torsion, compression, or tension on the omental pedicle.
Omentocystoplasty Although the omentum is a potential substitute for the bladder
wall, because the urothelium rapidly epithelializes defects cov-
ered with the omentum [82], the clinical results are poor. The
muscle of the bladder tends to contract, reducing the size of
the grafted area. Bladder repair requires a tissue of similar com-
pliance to the bladder, being able to some extent to replace
detrusor function. Bowel used as a cecocystoplasty or ileocysto-
plasty has been shown to be better material for supporting
bladder defects. However, it may be helpful to transpose the
omentum to the site of the repaired defect, especially if the
tissues have previously been irradiated [65].

Pelvis
H. WHITE

Pelvic Floor The techniques of pelvic and exenterative surgery and the pre-
Reconstruction and postoperative care of these patients is well established [176].
As they are in common use among surgeons, the illustrations
in this book are restricted to the technique of omental transposi-
tion, and reference is made only to relevant points.
Although the pelvic peritoneum is damaged during operation,
it is often possible to close it satisfactorily by suturing the edges
together. However, in some procedures and especially in surgery
for malignant disease the peritoneum cannot be closed as the
pelvic floor may also have been damaged. In these cases some
form of reconstruction is necessary. Radical hysterectomy, cys-
tectomy, abdominoperineal resection of the rectum, and pelvic
exenteration are all examples of operations in which large sur-
faces of the pelvis are denuded and deep dead spaces left between
the pelvic musculature and the skin, which may itself on occa-
sion be left open.
Omental transposition usually offers a technically satisfactory
method of reconstructing the pelvic peritoneum and filling the
presacral cavity and may, therefore, reduce the risk of potential
complications such as small bowel prolapse. The method is natu-
rally dependent upon being able to mobilize enough omentum
to reach the pelvis without tension. This may not be possible
after previous abdominal surgery [167].
Surgical Options. Suture of the pelvic floor muscle and where
possible, perineal fat and skin
- Omental transposition and primary or secondary perineal
closure
- Reconstruction with natural materials, e.g., fascia lata
- Reconstruction of synthetic materials, e.g., Marlex mesh
- Pack and secondary healing or suture

251
Replacement of the The greater omentum may be mobilized on either the left or
Pelvic Peritoneum right gastroepiploic pedicles and lengthened on the vascular
arcades (see Sect. 9.2.1) so that there is a satisfactory apron
of omental tissue with a good blood supply to reach the pelvis.
The pedicle may lie either on the left or right of the abdominal
cavity.

Abdominoperineal Following abdominoperineal excision of the rectum with a ter-

Excision minal colostomy, an omental pedicle based on the left gastroe-
piploic artery is useful in reconstructing the pelvic floor [167].
If the terminal left iliac fossa colostomy is not retroperitoneal,
the pedicle may be used to help closing the lateral space (Fig.
139b, c). There is a potential danger in that the omental pedicle,
being fixed proximally and distally, could form a band around
which the small bowel might undergo torsion. This danger can
be reduced by suturing the pedicle to the parietal peritoneum.
At all times great care must be taken to ensure that sutures
which fix omentum do not interfere with the main omental
vessels and that the pedicle is not twisted. When suturing the
omentum to the lateral wall of the pelvic cavity the iliac vessels
and ureters must also be carefully identified.

Anterior Restorative The anastomosis in anterior restorative resection can be covered

Resection by the transposed omentum. The pedicle, based on the left gas-
troepiploic artery, is easily led through the splenic mesocolon
(Fig. 144a) and then in the midline, where distally it will help
to obliterate the presacral space (Fig. 144 b).

After omental transposition it does not appear to be necessary

to nurse the patient postoperatively in the Trendelenburg posi-
tion or confine him to bed for longer than the usual period,
varying from 24 h to 5 days [31, 191]. The position of the
omentum in the pelvis can be identified satisfactorily with com-
puted tomography (Fig. 149). Following abdominoperineal re-
section, the transposed omentum is shown in Fig 145 immediate-
ly after operation. About one year later the omentum is still
filling the pelvis with no prolapse of the small bowel
(Fig. 146).
The omentum can be distinguished from prolapsed bowel with
certainty when the lumen is outlined with contrast medium
(Fig. 147, 148). Recurrent tumor is of a different density and
can be seen to invade adjacent structures (Fig. 149).
Although a number of surgeons are known routinely to trans-
pose the omentum to the pelvis, little in the way of formal
follow-up of this technique has been published. Over the last
3 years we have used this technique in abdominoperineal resec-

252
Fig. 144. a Protection of
low rectal anastomo is.
The omental pedicle is led
through the splenic me 0-
colon and behind the co-
lon. It is important that
the omentum is anchored
distally around the anasto-
mosis (anterior view).
b Protection of low rectal
anastomosis (lateral view)

tion and pelvic exenteration in 23 patients. One had transient

obstructive signs and symptoms which settled conservatively
within 12 h, and no other complications were noted. Complica-
tions following extensive pelvic surgery without omental trans-
position have been carefully analyzed by SPRATT et al. [176],
but their series is so much more extensive that comparison is
inappropriate.
In low rectal anastomoses and especially those performed with
the stapling gun, the distal length of descending colon relies
on the marginal artery for its blood supply and may lack sup-
porting mesentery. The rectal stump at the peritoneal reflection
will also be denuded of supporting tissue during mobilization.
The transposed omentum can be led posteriorily and fixed dis-
tally to make up for these deficiencies and also may be wrapped
around the suture line as already described (Fig. 144). For satis-
factory healing of these low anastomoses, it appears vital that
the hollow of the sacral cavity is filled [72]. Although the residu-
al colon is satisfactory in most cases, the presacral space is
equally well filled with the omentum, and this may even have
some advantage through increased vascularity.

Congenital Congenital malformations may require staged pelvic floor re-

Malformation construction, and omental tissue may be of help in both the
primary surgery and the management of some of the complica-
tions of surgery such as fistulae (see below).

253
Fig. 145. Omental pedicle
lying behind the prostate
and filling the presacral
space. Note the reaction
and base of bladder which
was in contact with peritu-
mor abscess. (CT-scans
9-13 by courtesy of J.E.
HUSBAND, Royal Marsden
Hospital, London)

Anterior
Bladder
Reaction at base of bladder

Sacrum
Posterior

254
Fig. 146. Omental pedicle
9 months later with the
omentum still filling the
presacral space and the
bladder reaction resolved

Bladder Anterior

HIp jOint

R Sacrum
Omentum
Posterior

255
Fig. 147. Prolapsed small
bowel in the pelvis in a pa-
tient without omental
transposition

Bladder Anterior
Pubic ramus

R L

Small bowel
Posterior

256
Fig. 148. Prolapsed small
bowel confirmed with Gas-
trografin contrast medium

Anterior
Bladder

Sacrum
Gaslrografm In small bowel
Postenor

257
Fig. 149. Recurrent tumor
invading the base of the
bladder in a patient with-
out an omental pedicle.
Note the greater density of
the mass and probable
loop of the small bowel
within the tumor mass

Anterior
Bladder
Tumor Inl'Odlng bladder

Tumo r

Small bowel

Posterior

Pelvic Exenteration Omental transposition for reconstruction of the pelvic peritone-

um is a valuable technique after pelvic exenteration, in addition
to the less extensive surgery already discussed. As well as provid-
ing tissue for replacing the pelvic floor, it is useful in filling
the "dead space" left after removal of the pelvic organs. By

258
Fig. 150. a Omental apron
sling (anterior view) envel-
oping small intestines and
preventing prolapse. The
individual points of suture
are variable across the
peritoneal cavity from the
ascending colon and cecum .
to the left paracolic gutter.
b Omental apron sling (lat- .
eral view). The omental
flap is sutured to the pelvic :
peritoneum, psoas muscle,
and periosteum of the
sacrum with a few inter-
rupted absorbable sutures.
The omentum forms a sac
which contains the small
intestines and the descend-
ing colon leading to the
colostomy

containing the small bowel in an omental apron based on the

right gastroepiploic artery and sutured to the posterior abdomi-
nal wall (Fig. 150a, b), it has been found that fistula formation,
which is more frequent after radiotherapy, may drop from a
reported 25% in some centers to 10% [191].
A lateral sling based on the left gastroepiploic artery can be
constructed to support the small bowel following pelvic exenter-
ation in exactly the same way as after abdominoperineal resec-
tion (Fig. 139 a-c). The problems of management of the pelvic
floor after exenteration are reviewed by WEBB et al. [203]. In
this series and those of KARLEN and PIVER [99] and BUCHSBAUM
and WHITE [31] there were few problems although the series
were small.

Urinogenital and Intra-abdominal Fistulae

H. TILLMANNS

Fistulae of Introduction. Fistulae between the pelvic viscera are not frequent
Pelvic Viscera and mostly result from intraoperative injuries or complications
of irradiation. With improvement in surgery and radiotherapy
the fistula rate has dropped but there are still patients in whom
closure of fistulae causes problems.

259

Fig. 151. Location and dis-
tribution of female fistulae
260
Fis t ula Frequency
Vesicocervical 2%
Ureterovag inal 50%
Vesicovaginal 41%
Vesicovaginorectal 4%
(12% with DXT )
Urethrovaginal 3%
Treatment aims at separating the viscera and at closing the
defect while preserving urinary and rectal continence. It has
been suggested that fistulae should not be operated on earlier
than 6 weeks after trauma and 6-12 months after irradiation
[100]. This interval can be shortened when omental interposition
is used [182].
Fistulae in the Female
Fistulae between the pelvic organs (Fig. 151) occur mainly after
hysterectomy and bowel surgery for tumors and after irradia-
tion, but occasionally follow pelvic trauma in heavy childbirth.
Traumatic, postoperative fistulae are usually small communica-
tions, while fistulae occurring after irradiation may have open-
ings of up to 5 cm. The surrounding tissue is very rigid, difficult
to close, and fistula recurrence is frequent. Therefore, interposi-
tion of the omentum is of great benefit [8, 14, 100, 107, 187,
188, 190].
Principles of the Operation and Surgical Options. Most traumatic
and posthysterectomy fistulae in which the tissue has not been
damaged by irradiation can be repaired by careful fistula invagi-
nation (FuETH-MAYO [see 100]), excision, and suture in layers
 (SIMS-SIMON [see 100]) or using a high colpocleisis (LATzKo [see
100]). Colpocleisis includes excision of the fistula and scar tissue,
de-epithelialization of the proximal vagina and sutures to ap-
proximate the vaginal walls. In greater defects and if recurrence
is a potential danger, muscular flaps such as the m. bulbocaver-
nosus flap, m. pubococcygeus flap, m. gracilis flap, and perito-
neum are a possible treatment after radiation or recurrence and
after previous surgery for fistulae [100, 156]. The disadvantages
of these techniques are a reduction in vaginal length, resulting
in dyspareunia, and stress incontinence in up to 25% of patients
[156].
Large, complicated fistulae are sometimes very difficult and may
even be impossible to close. A satisfactory solution for this prob-
lem is the interposition of nonirradiated tissue such as peritone-
um, fat, muscle flap, or omental tissue between the viscera. In
the various transabdominal approaches used to reach the defect,
the intraperitoneal transvesical route is that most commonly
used for omental transposition. A synchronous approach via
the vagina is sometimes required.

Indications. The abdominal approach is indicated [156] Ill:

Large fistulae more than 2 cm in diameter
Involvement of the ostium of the Fallopian tube
Multiple fistulae
Vesicocervical fistulae
Recurrent fistulae
Damaged surrounding tissues

Position. The patient is either in an abdominoperineal position

(Fig. 155 a) with the legs widely abducted or in a variety of posi-
tions which, like the semiprone position, may give better access.

Vesicovaginal Operative Techniques. For the repair of the posthysterectomy

Fistula Vesicovaginal fistula (Fig. 152) a median abdominal incision is
used. The bladder is opened anteriorly and separated from the
vagina by blunt and sharp dissection [14]. The ureteric openings
must be identified, they may be situated near or in the fistula,
and reimplantation may become necessary. The bladder incision
is extended into the fistula, which is excised whenever possible
with a cuff of healthy tissue. If possible the bladder is closed,
but this may be difficult after irradiation, and if there is suffi-
cient tissue the vaginal stump is also closed - preferably at right
angles to the bladder incision. It is less important to close the
vesical defect completely, if the omentum is interposed, because
it forms a sheath protecting against urine extravasation, and
urothelium will grow over the omental tissue [82].

261
Fig. 152. a Vesicovaginal
fistula. b Omentum trans-
posed between the bladder
and vagina in definitive
repair

The omentum is mobilized and brought down through a tunnel

developed behind the bladder (Fig. 152); it is then sutured to
the vagina, bladder, and rectum and is used for reperitonealiza-
tion of the pelvis. Suprapubic bladder drainage may be required
postoperatively for some 2 weeks and the pelvic floor is drained
by Penrose or latex tubes.

Vesicovaginorectal If the fistula involves the bowel (Fig. 153 a) a preliminary de-
Fistula functioning colostomy must be added. The fistula is excised
and the omentum transposed in a manner similar to that de-
scribed above (Fig. 153 b). If the bladder cannot be separated
from the vagina, the vaginal stump is re-opened and the
omentum is pulled through the channel toward the vulva, where
it is fixed by sutures (Fig. 153c). If granulation tissue develops
it can be excised later using diathermy [100]. Urinary drainage
is required for up to 2 weeks.

Recurrent Fistula Recurrent Fistula After Radical Hysterectomy and Radiotherapy.

One danger of radical hysterectomy after a full course of radio-
therapy for advanced carcinoma of the uterus or cervix is post-
operative fistula complicated by hemorrhage. The interposition
of nonirradiated tissue to cover the suture lines and fill the
dead space fosters primary healing and reduces fistula forma-

262
a

Fig. 153 a V .
rectal fi~tul e~ICOvaginO-
transposed ~ Omentum
bladde .etween the
rectumr~mvadgma,
efiniti
and
.
c O mentum I d ve repaIr.
the vagina toe I through
v . c ose v .
agmorectal fi eSICO-
the bladd Istula when
er and .
adherent vagma are c

263

Rectoprostatic and
Rectourethral Fistulae
Fig. 154. a Rectoprostatic
fistula. b Omentum inter-
posed between the prostate
and rectum in definitive
repair. In this case a supra-
pubic catheter as well as a
urethral splinting catheter
is shown
264
tion. It has been shown that if the omentum is transposed to
the pelvis after the Meigs-Wertheim procedure, i.e., pan hyster-
ectomy, resection of the proximal vagina, and excision of the
pelvic lymph nodes, the fistula rate drops from 30% to 10%
[84].
Operative Technique. After hysterectomy and hemostasis the
omentum is led down to the pelvis as described above. It is
then sutured loosely to the vaginal stump and to the peritoneum
between the ureter and sigmoid colon.
Fistulae in the Male
These fistulae (Fig. 154) occur after:
Trauma causing prostatic dislocation such as gunshot wounds,
pelvic fractures, perineal laceration, straddle injury, or urethral
instrumentation, Operations on the prostate or rectum, Congen-
ital malformations, e.g., cloaca
Surgical Options. To close fistulae in the male, pull through
operations [129], skin grafts [137], and interposition of the pedi-
cled omental sling [189] have been recommended.

Fig. 155. a Position for
perineal operation. b Inci-
sions for perineal operation
and site of drainage
Urethral Strictures
a
Position. The patient is placed and prepared as for abdomino-
perineal procedures (Fig. 155a, b).
Operative Technique. Fistula resection, omental transposition,
and construction of an abdominoperineal tunnel for the omental
swing are carried out with an abdominoperineal approach:
U sing a midline incision the omentum is mobilized on a vascular
pedicle and brought down in the right or left paracolic gutter
to the pelvis as described above (Fig. 139). Next, or simulta-
neously with a second team of surgeons [135], the perineum
is explored, the fistula between the urethra and rectum is careful-
ly dissected, and the visceral defects are closed by interrupted
absorbable sutures. After developing a tunnel between the
bladder and prostatic urethra on one side and the rectum on
the other, the omentum is interposed (Fig. 154 b) but care is
taken that the omental pedicle is not under tension or torsion.
Urinary and perineal drainage are important.
Late stricture formation is not uncommon after urethral injury
and may be related to unrecognized periurethral urine extravasa-
tion and infection. Difficult urethral stricture problems, for
example, after prostatic dislocation with subsequent periurethral
fibrosis and difficulty in achieving a satisfactory urethral anasto-
mosis, have been resolved to some extent by wrapping the anas-
tomosis in the omentum [188] or by a urethral island" bladder
flap urethroplasty" wrapped in omentum.
265
 Infect ion of Prophylaxis

140.~~-----\.----- Aortointestinal fistula

'------'\:-- Bleed ing anastomosis

Bifurcation prosthesis - + - - - - - - - J . . . - - l .
--..--~---....--->-I -j' - - - - --t--- Anastomotic aneurysm

Aortofemoral bypass --+-------cJ -t-- - - - + - Mycotic aneurysm

/------f- Exposed inguinal vessels

or prosthesis
Femoral bypass - - --\----+I-tT+I

Fig. 156. Indications for Vascular Protection in Reconstructive Arterial Surgery

omental transposition in
vascular surgery R . VAN DONGEN

General Aspects and Indications. In reconstructive arterial sur-

Fig. 157 a- d. See page 315
gery, there are numerous possibilities for applying the omentum
with the object of preventing or treating complications. We first
transposed the omentum to the groin for septic complications
near the proximal anastomosis of femoropopliteal saphenous
vein bypass grafts 18 years ago. The results of this" biological
wrapping" were so good that we have subsequently also applied
this treatment after prosthetic arterial replacement and in nu-
merous other situations (Fig. 156), for example:
- Prevention and treatment of septic complications
- Affording protection of anastomoses
- Treatment of uncontrollable hemorrhage
- Covering prosthetic grafts and vessels threatened by infection

266
 b

Fig. 158a, b. The omentum Technique. For the transposition of an omental flap to the groin
is wrapped around the area, a suprainguinal incision is often satisfactory (Fig. 157 a-d,
anastomosis as seen here
schematically in a life- see page 315). Usually the omentum is so long and so mobile
threatening hemorrhage that a flap can be brought through a tunnel in front of the
inguinal ligament into the groin region. It is important for the
tunnel to be wide, so that circulation in the flap is not impaired
by compression. In order to avoid damage to the vessels during
transposition, it is advisable to pack the flap- into a condom
before pulling it through. In the groin, the flap is wrapped
around the anastomosis and fixed with a few sutures (Fig. 158 a,
b). Skin closure alone without suture of the deep layers helps
to avoid compression when the groin wound is closed.
If it is not possible to obtain a sufficiently long omental flap
for transposition into the groin using a supra-inguinal incision,
a laparotomy is necessary. After the omentum has been detached
from the transverse colon and pulled through a window in the
transverse mesocolon, it is almost always possible to reach the
groin region. The same technique is applied when the omentum
has to be brought into the retroperitoneal space to cover a bifur-
cation prosthesis (Fig. 159). If it is not possible to obtain a
sufficiently long omental flap in this way or if the femoral region
must be reached, the omentum is lengthened on the left or right
gastroepiploic vessels (Sect. 9.2.1 [79]).

Special Indications. Our experience is obtained from the follow-

ing prophylactic and therapeutic indications and procedures.

Septic Complications The best results are obtained with infection in the groin or tigh
in the Groin Region region after the use of autogenous vein transplants [54, 55].

267
Fig. 159. Aortic prosthesis
wrapped in the omentum

In most cases a functioning graft can be maintained. It is almost

never possible to oversew directly a bleeding anastomosis or
a septic defect in the wall of a vein transplant, both of which
can lead to life-threatening hemorrhage (Fig. 160a, b, see
page 316). The bleeding can be controlled temporarily by a ve-
nous patch, but as a rule renewed bleeding occurs after a few
days. By covering the bleeding region with an omental flap
(Fig. 158 a, b), which is wrapped around the anastomosis and
the adjacent parts of the artery and transplant, it is usually
possible not only to prevent further hemorrhage but also to
overcome the infection.
It is important to transpose the omentum at the first sign of
hemorrhage. However, the procedure can sometimes also be
successful in cases of severe septic hemorrhages.
The good results achieved in the treatment of infections after
venous bypass operations provided the basis for applying the
procedure in cases of septic complications after the use of pros-
thetic vascular grafts in the groin. These cases usually concern
infection of the distal anastomosis of an aortofemoral prosthetic
graft and rarely the proximal anastomosis of a femoral bypass
prosthesis. The treatment was almost always successful when
the infection was limited to the anastomosis and the immediately
adjacent vessel and prosthesis sections. This situation, however,
is seldom seen. More commonly the infection has spread over
the entire prosthesis involving the other anastomosis. In this
case the removal of the entire prosthesis is usually unavoidable.

268
Infection of a Bifur- If the infection is restricted to one of the anastomoses, whether
cation Prosthesis or proximal or distal, an attempt should be made to seal the af-
an Aortofemoral fected anastomosis and stop the infection by omental wrapping
Bypass [22, 55, 80, 141]. In patients in a poor general condition, howev-
er, removal of the prosthesis is unavoidable, and the same
applies if the entire prosthesis is infected. We only succeeded
in one case in maintaining a bifurcation prosthesis which was
infected over its entire length after all three anastomoses and
the prosthesis were wrapped with omentum.

Securing the Aortic After removal of an infected aortic bifurcation prosthesis, the
Stump After Removal care of the infrarenal aortic stump can be problematic. The
of an Infected Bifur- anterior longitudinal ligament can be used for strengthening
cation Prosthesis the aortic stump. This ligament is divided distally, dissected
from the vertebral body, placed around the aortic stump, and
fixed with the same sutures used for closure of the stump. It
may be more reliable to suture an omental flap to the stump
instead of this ligament. In addition, it is advisable to introduce
the rest of the omentum into the prosthesis bed and to fix it
laterally to the edges of the posterior peritoneum [55].

Anastomotic The treatment of an anastomotic aneurysm consists of resection

Aneurysms of the anastomosis together with the adjacent vessel prosthesis,
or venous transplant sections, lengthening of the prosthesis, or
transplant, and establishment of a new anastomosis [23, 55].
Regardless of where such an aneurysm is situated and of the
cause of the false aneurysm, one should wrap the new anastomo-
sis with an omental flap in order to prevent further problems
and to combat infection.

Mycotic Aneurysm After resection of a mycotic aneurysm, the question arises

whether circulation of the lower extremities should be restored
by means of an extra-anatomic (subclavian-(bi)femoral) bypass
graft or by direct interposition of a (bifurcation) prosthesis [40,
55]. Healing took place without any complications in two cases
where we performed direct implantation of a bifurcation pros-
thesis, wrapping the entire prosthesis and all three anastomoses
with transposed omentum.

Exposed Vessels or Vessels, as well as vascular prostheses, transplants, and anasto-

Vascular Prosthesis moses which are exposed as the result of a necrosis of the cover-
in the Groin or ing soft parts and skin are in danger of infection and can rupture
Tigh Region [40, 76]. The same applies after radical dissection of the inguinal
glands. These complications can be prevented by wrapping the

269
 endangered vessels with omental tissue as early as possible and
filling the entire wound with omental tissue. Such an omental
graft is advisable as a prophylaxis after radical dissection of
the inguinal glands.

Insufficient Coverage Sometimes the posterior peritoneum is insufficient to shield an

of a Prosthesis implanted bifurcation prosthesis from the small intestine [40].
Implanted in the This is especially true if the proximal anastomosis has been
Retroperitoneal created side-to-end with the aorta. If a long sigmoid mesentery
Space is present, one can use this to cover the prosthesis. However,
it is easier and more reliable to make use of the omentum,
which is placed over the prosthesis and fixed laterally to the
edges of the posterior peritoneum.

Infected ilioinguinal Infected hematomas in the groin region and the iliac fossa en-
Hematomas near danger the vessels [40]. Here too an omental graft is helpful.
Vessels Less frequently, omental transposition can be used in regions
other than those discussed. Our own experience relates to vascu-
lar grafts of the intestinal and renal arteries, the branches of
the aortic arch, the internal carotid artery, and the popliteal
artery [77].

Aortointestinal If a prosthesis implanted in the retroperitoneal space is only

Fistulae insufficiently covered with the posterior peritoneum or the sur-
rounding tissue, thereby rendering it possible for parts of the
intestine to come into direct contact with the prosthesis or one
of the anastomoses, an erosive defect of the intestinal wall and
perforation may result. This is mostly a perforation of the proxi-
mal anastomosis of a bifurcation prosthesis into the duodenum.
In many cases such an aortointestinal fistula is combined with
an anastomotic aneurysm, but it is uncertain which lesion devel-
ops first. Perforation of a true or a mycotic aortic aneurysm
into a segment of the intestine takes place less frequently.
The treatment of this complication is difficult [45, 55, 67, 177],
and, if there is a deep erosive lesion or an infarction of the
intestinal wall, both the prosthesis and the anastomosis are in
constant risk of infection. The use of the transposed omentum
is effective in such cases. The operation consists of the following
steps: elimination of the aortointestinal fistula, closure of the
intestinal wall defect, and fixation of an omental flap to the
site of closure. Then a new anastomosis is made after lengthen-
ing the aortic part of the prosthesis. Finally a second omental
flap is wrapped around the adjacent parts of the aorta and
the prosthesis. The remainder of the omentum can be used for
Fig. 161. See page 317 closure of the posterior peritoneum. Particular care is taken

270
 that sufficient omental tissue is interposed between the vascular
graft and the intestinal wall.
If there is a perforation of a true or mycotic aneurysm into
an intestinal segment (usually the duodenojejunal junction), the
aneurysm must be resected with the exception of a part of the
wall in the area surrounding the fistula (Fig. 116, see page 317).
After the perforation has been closed and covered with trans-
posed omental tissue, the edges of the remaining aneurysmal
wall in the area surrounding the fistula are approximated over
the omental flap.

Anastomotic The weak nature of the infra renal aortic section may be the
Hemorrhage cause of difficulties in the treatment of hemorrhages from the
proximal anastomosis of an aortic bifurcation prosthesis [40,
55]. When there is an uncontrollable hemorrhage from the prox-
imal anastomosis of an aortic aneurysm the aneurysmal sac
provides sufficient material for producing a cuff which is fas-
tened around the anastomosis. In all other cases, reinforcement
with an omental flap is helpful.

U reteropathology Strictures, erosive lesions, and even perforations of an ureter

After Aorto(bi) after implantation of a prosthesis in the retroperitoneal space
Femoral Vascular are not uncommon [40). After excision of the fibrotic tissue
Prosthesis between the ureter and prosthesis, both should be covered with
the omentum. An erosive defect of the ureteral wall should not
be oversewn but a perforation may be oversewn temporarily.
Careful covering of the damaged area with the omentum almost
always ensures healing without complications.

Hints Omental transposition is never the sole measure in the prophy-

laxis of infection-threatened vessels and prostheses or the treat-
ment of septic complications. All classical rules and therapeutic
measures of septic surgery must always be considered, including
debridement, antibiotic therapy, and drainage. Many of the indi-
cations mentioned relate to prophylaxis. It cannot be empha-
sized strongly enough that one should be very careful in estab-
lishing the indications for omental transposition in each case.
It is not advisable to cover every anastomosis in the groin area
or in the retroperitoneal space with the omentum for prophy-
lactic purposes [121).

Results Table 9 shows the results of omental transposition according

to indication and localization. The benefits in many complica-
tions of vascular surgery suggest that the technique should be
considered as established practice in many circumstances. The
transposed omentum is almost indispensable for the prophylaxis
and treatment of septic complications.

271
 Table 9. Review of 78 patients treated with omental transplantation for com-
plications of vascular surgery between 1963 and 1981 in the Surgical Dept.,
The Wilhelmina Gasthuis, University Hospital, Amsterdam, The Netherlands

Indication Patients

Total Successful

Treatment of septic complications

Anastomosis in the groin area
- Proximal anastomosis of femoral vein bypass graft 8 6
- Distal anastomosis of aortofemoral prosthesis J 6 2
- Proximal anastomosis of femoral artery bypass
prosthesis
Totally infected bifurcation and aortofemoral 2 1
prosthesis
Other locations 3 2
Aortointestinal fistulae 6 5
25 16 (64%)

Prophylactic use
Protecting aortic stump after removing 5 4
infected bifurcation prosthesis
Anastomotic aneurysm 10 9
Mycotic aneurysm (aorta, carotid artery) 3 3
Protection of exposed vessels or vascular 8 8
prosthesis
Covering bifurcation prosthesis 14 14
Infected ilioinguinal hematomas near vessels 3 3
U reteropathology after prosthetic arterial 4 4
replacement

47 45 (96%)

For hemostasis
Bleeding from proximal anastomosis of bifurcation 6 6
prosthesis

9.2.1.2 Extra-abdominal Transposition

Intrathoracic Transposition
T. RUEDI

Esophagus Introduction. Intrathoracic esophagogastric and esophagoenteric

Y ASARGIL 1956/57, anastomoses have a tendency to leak, which is associated with
GOLDSMITH 1968 a high mortality rate. This may be due to a lack of serosal
coating, poor vascularity of the esophagus, or the absence of
any significant tissue in the mediastinum to reinforce suture
lines. It has been experimentally shown in the dog that anasto-

272
Fig. 162 a, b. Repair of
esophageal defects [78]. a
Marlex mesh graft bridging
an esophageal defect in a
dog. The omentum is
placed behind the prosthe-
sis. b The omentum enve·
lops the prosthesis com-
pletely and is attached with
a few tiches to the esopha-
gus and the hiatu
a

moses at risk [75, 78], full-thickness defects [136], and synthetic

prosthesis replacing part of the esophagus [16, 75, 206] can
be effectively protected with a generous well-vascularized
omental wrap led through the diaphragm into the chest
(Fig. 162). More recently PAPACHRISTOU and FORTNER [150]
formed a gastric antral flap in dogs from the greater curve side
with a long vascular pedicle which was based on the left gastro-
epiploic vessels, to cover defects in the cervical esophagus,
trachea, or pharynx (Fig. 163).

Esophagoplasty
Both techniques have now been used in man: simple omental
transposition in four patients [149] and omental gastric island
flaps in 13 patients ([94] HUGH, personal communication, 1981).

Options. Protection of esophageal anastomoses and reconstruc-

tion of the cervical esophagus with long intestinal pedicles is
limited. Such defects are most often caused by extensive surgery
or tumor irradiation, which may lead to stricture formation .
They can be treated by:
- Free microsurgical transfer of bowel, for example, a jejunal

273
Fig. 163. Gastric antral
island flap (first performed
in dogs). [150]

segment using the internal mammary vessels for vascular con-

nection as described by BRENNWALD and ALLGOWER [27]
- Simple omental transposition [149]
- Omental gastric island flap [94]

Indications and Contraindications. Coverage with omentum may

be indicated after:
- Esophageal perforation, e.g., spontaneous rupture
- Resection of firm fibrous strictures due to acid peptic eso-
phagitis
- Surgery for severe dysphagia with increasingly difficult dilata-
tion
- Stricture recurrence after myotomy
- Benign and malignant tumors
- Irradiation damage
- Closure of large defects

274
Fig. 164. The omentum i
led in front of the stomach
through the hiatus and en-
velops the mid thoracic
esophageal defect from
behind

Contraindications may be mediastinitis, for example, following

iatrogenic esophageal perforation and pleural empyema.
Preoperative Assessment. Apart from general examinations
(Sect. 9.1) chest X-ray and upper gastrointestinal studies are
required.
Positioning (Sect. 9.1) Semiprone at 45°.

Surgical Technique. An oblique thoracoabdominal incIsIOn

through the bed of the eighth left rib gives the best approach
to the omentum and chest.
1. Simple Omental Transposition [149]. After closure of the
esophageal defect the omentum is mobilized from the stomach,
maintaining the right or left gastroepiploic pedicle. The esopha-
geal hiatus in the diaphragm must be incised and enlarged so
that the omentum can be led into the thoracic cavity (Fig. 164)

275
 and even the neck without any tension and compression. It
is then wrapped from behind around the esophageal anastomo-
sis or suture line and fixed with single sutures to the esophageal
wall. A Nissen fundoplication may be added to avoid reflux.
Fundoplication located in the chest causes no postoperative
problems in our experience. Recently the protection of intra-
thoracic stapled anastomoses between the stomach and esopha-
gus with the transposed omentum has been shown to be benefi-
cal [64].

2. Omental Gastric Island Flap [94]. After excision of a stricture

or tumor an oval full-thickness antral patch 2 x 5 cm is removed
from the greater curvature (Fig. 165 a). By dividing the gastro-
epiploic vessels from the greater curvature toward the left a
pedicle based on the left gastroepiploic artery with a mobile
muscle-mucosal patch can be fashioned. This patch should be
supplied by two or three gastric branches. It should also be
free of acid-secreting mucosa because patches taken from the
gastric body containing parietal cells may cause esophagitis in
the areas close to the gastric implant, and ulceration may occur
especially when stimulated with histamine.
To avoid pyloric obstruction the gastric defect is closed trans-
versely (Fig. 165b); if this is difficult a gastroenterostomy can
be performed. After enlargement of the esophageal hiatus the
island flap is passed behind the stomach to the esophagus
(Fig. 165b) via the omental bursa. The patch is fixed with single
sutures to the esophageal defect. Care must be taken to avoid
twisting of the pedicle and not to damage the vagal trunk. A
Nissen fundoplication may be added around the distal end of
the patch, leaving the pedicle free (Fig. 165c).

Danger Point. A very thin or absent gastroepiploic connection

may endanger the ingrowth of the gastric flap.

Prognosis. Results are reported as being excellent with both

techniques. The omento-antral island flap provides a more phys-
iological approach than a Marlex prosthesis in combination with
the transposed omentum. The 13 patients in whom HUGH under-
took esophagoplasty remained well for 6 months to 4 years ([94]
HUGH, personal communication, 1981) after gastric island flap
without reflux symptoms. Three patients have endoscopic evi-
dence of patchy esophagitis proximal to the patch because of
possible imperfect competence of the fundoplication. None of
the patients has restrictured and it seems unlikely that this can
occur at the level of the patch since the patch is not subject
to ulceration and scar. HUGH finds this technique an extremely

276
Fig. 165a-c. Repair of an
esophagal stricture [94].
a A pedicled omental
antral island flap is formed
which is based on the left
gastroepiploic vessels.
b The antral defect is
closed transversely. The
patch is passed behind the
stomach and sutured to the
opened esophageal stricture
(after HUGH). c An endo-
thoracic fundoplication is
added

277
 satisfactory solution for a very small and uncommon group
of patients who have reached the final stage of transmural
esophageal fibrosis, and in whom the only alternative is esopha-
geal resection. The number of patients who require this proce-
dure is small according to HUGH, since most of the esophageal
strictures are reversible after a simple antireflux procedure.

Bronchopleural Although the incidence ofbronchopleural fistulae as a complica-

Fistulae tion following pulmonary resection has been lowered with anti-
(PERIANAYAGAM,1980) tuberculous therapy, there is still a 3% risk [154]. PERIANAYA-
GAM [154] reported on two patients with recurrent broncho-
pleural fistulae and empyema in whom intercostal myoplasty
was unsuccessful. The damaged tissue was covered with the
omentum transposed at the left gastroepiploic vascular pedicle.
Follow-up was uneventful in the two patients treated by this
method.

Postoperative Care. Routine postoperative care follows the rules

of thoracoabdominal approach.

Transposition to the Cranium and Extremities

H. GOLDSMITH

Brain Introduction. The first use of omental transposition to the brain

in man was carried out as a feasibility study on individuals
who had sustained a cerebral infarction 8, 12,30, and 66 months
previously [81]. The first step in the surgical procedure is to
separate the omentum from the transverse colon. Following this,
the omentum is removed from the greater curvature of the stom-
ach leaving the gastroepiploic vessels within the omental apron.
This is a time-consuming portion of the operation since small
blood vessels connecting the greater curvature of the stomach
to the gastroepiploic arcade must be divided and ligated careful-
ly and individually.
After separating the omentum from the greater curvature of
the stomach, a decision is made whether to divide the left or
the right gastroepiploic artery, the left usually being chosen since
it is frequently the smaller. Following this, the omentum is fur-
ther divided in such a manner that its arterial supply is main-
tained primarily along its periphery.
After the omentum is surgically lengthened to the point that
it can reach the top of the skull without tension, incisions are

278
Fig. 166. Patient several
days after omental transpo-
sition to brain. Sutures
in scalp are still in place
(GOLDSMITH)

made along the chest and neck. A long subcutaneous tunnel

is made connecting these incisions so that the omentum can
be placed upon the chest wall and in the neck, after which
it is brought out behind the ear near the proposed craniotomy
site. A craniotomy is then performed and the dura and arach-
noid widely opened. When both cerebral hemispheres are to
be vascularized, an extensive craniotomy can be performed. The
omentum is then laid directly upon the underlying brain and
is secured by several interrupted sutures to the edge of the sur-
rounding dura.

Clinical Results. Of the four chronic stroke patients who under-

went omental transposition to the brain (Fig. 166), it was clini-
cally obvious that the younger patients (42 and 45 years old)
did better in terms of long-term subjective and objective post-
operative changes than did the elderly patients (71 and 76 years
old). It was of interest to note that there were progressive chan-
ges in somatosensory evoked potentials in spite of the long peri-
od that had elapsed since these patients had sustained their

279

Left median n
Right scalp
Right median n
Left scalp'
Left ulnar n.
Right scalp
Right ulnar n
Left seal p'
Left lat. popl. n.
Right scalp
Right lat. pol. n.
Lett scalp'
5)JVL
Fig. 167. Somatosensory
evoked potentials of a post
omental transposition pa-
tient. Note changes of elec-
trical activity, as mani-
fested by deepening ampli-
tude patterns on the in-
farcted side of the brain
which has received omental
placement. *. omental
transposition to the left
cortex. Patient RL (GOLD-
SMITH)
280
PRE-OP POST-OP
5/24178 2months 7months 10 months
1~~~~
~r~rY-
~~~~-'~
I
~
40ms
brain infarction (Fig. 167). Obviously one could not expect that
a brain infarct had been revitalized by omental transposition,
but it is speculated that perhaps the electrical changes in the
brain resulted from increased blood flow to biolelectrically de-
pressed neurones located at the interface of the cerebral infarc-
tion.
Recent experimental studies have now documented that the
omentum can supply a source of blood to the brain that main-
tains regional cerebral blood flow at a level of at least 75%
of normal in spite of MCA ligation [52]. It has also been shown
that omental transposition can maintain electrical conductivity
within the brain following MCA occlusion, but that there is
disappearance of electrical activity without omental transposi-
tion.
The type of patient who might best benefit from omental trans-
position to the brain is the patient with a diminished cerebral
blood flow but who has not already suffered irreversible or
massive brain damage. These clinical situations would include
individuals with transient ischemic attacks or previous small
strokes. There is even the possibility that omental transposition
might be helpful in patients who have recently suffered an acute
 stroke. The reason for this belief is that once an acute stroke
has occurred, cerebral edema progresses over the following days.
This increasing edema formation eventually exerts pressure
upon the lumen of functional capillaires located at the interface
of the cerebral infarct, eventually causing the initial cerebral
infarction to increase in size with progressive clinical sequelae.
It is suggested that if the omentum was placed on the brain
of a stroke victim within 6-8 h of a stroke, one might suspect
that the omentum would prove helpful in absorbing cerebral
edema since the ability of the omentum to remove fluid from
other areas of the body is known [119]. The minimization of
edema formation could be expected to lessen the progression
of an enlarging cerebral infarct.

Lymphatic and Introduction. The omentum has been rarely used in treating
Vascular Insufficiency pathological conditions involving an extremity. CANNADAY in
of an Extremity 1945 was the first to bring the omentum out of the abdominal
cavity for the purpose of covering a defect on the arm. The
omental pedicle from the abdominal cavity was subsequently
divided and a split-thickness skin graft placed directly on the
omentum with clinical success [34]. KIRICUTA and POPESCU have
also described using the omentum for this purpose [108, 109].
A common clinical reason today for placing the omentum on
an extremity is in the treatment of lymphedema or vascular
insufficiency, which are both conditions requiring replacement
of new lymphatic and/or blood vessels into the involved extremi-
ty.

Lymphedema. Many operations have been described for treating

lymphedema, with the multiplicity of these procedures attesting
to the inability of any operation at the present time to be ex-
pected to give consistent and continued relief. The basic problem
in chronic lymphedema appears to be an anatomical or func-
tional defect of the lymphatic channels draining the involved
extremity. In order to obviate this deficiency, omental transposi-
tion has been used during which the rich lymphatic and vascular
supply of the pedicled omentum is lengthened and placed subcu-
taneously into the lymphedematous extremity. The rationale for
this operation is that it was expected that omental lymphatics
would develop functional connections to the existing lymphatics
within the involved lymphedematous limb and thus aid in the
drainage of stagnant lymph.
Thirty-five patients with chronic lymphedema have been treated
by the author using omental transposition. The surgical steps
used in this procedure, along with the results and complications
of the operation, have been described [79]. It can be expected

281
Fig. 168. Lymphangiogram
showing functionallym-
phatics between the trans-
posed omentum in the left
leg and trunk. Normal
lymphangiogram on right.
[74]

that success with omental transposition for chronic lymphedema

will be seen in approximately one-third to one-half of the pa-
tients in whom the procedure is performed. Lymphangiograms
by several investigators have confirmed that lymphatic anasto-
moses (Fig. 168) do develop between the transposed omentum
and the underlying lymphatics within the lymphedematous ex-
tremity [45, 163].

Peripheral Vascular Insufficiency. Amputation of an extremity

for distal tissue ischemia is a very common procedure. The
omentum has been used to salvage such end-stage ischemic limbs
when all conventional reconstructive revascularization proce-
dures have been exhausted.
In 1967 it was shown experimentally for the first time that the
pedicled omentum could be lengthened and placed in the leg
resulting in the delivery of an additional source of blood to
that extremity [70]. During recent years, clinical success has
been reported in using the intact omentum to treat patients
(Fig. 169) who were considered to have unsalvagable extremities
secondary to extensive arterial occlusions [36, 73]. Recently,
there has been interest in using a free omental graft for revascu-
larization purposes, but this requires microvascular techniques
[144, 148]. Use of microvascular surgery seems unnecessary
since it is a relatively easy surgical technique to lengthen the

282
Fig. 169. Operative photo-
graph showing the intact
omentum exiting from an
incision on the lateral chest
wall prior to being placed
subcutaneously along the
entire right arm. The
towel in the foreground
covers the hand. [731

omentum sufficiently so that it can be placed with its intact

arterial and venous systems far distally into an ischemic extremi-
ty.

Vascular Protection. A highly effective but little-used technique

for protecting vascular grafts from potential infection involves
the complete envelopment of these prostheses and their suture
lines with the intact omentum. This has been done experimen-
tally [80] and clinically [76] (see also Sect. 9.2.1.1.).

Lymphatic Relief

E. VAUBEL

Lymphedema Pathogenesis. The lymphatic drainage of the extremities can be

divided into two systems: the superficial compartment, which
is the skin and subcutaneous tissue, and the deep compartment,
which contains muscles, bones, and neurovascular structures.
Although both systems are connected, the deep fascia forms
a barrier for the lymph flow to the deep compartment [39].
Surgical methods, therefore, usually aim at resecting the fascia
in order to open up an additional pathway for drainage.

283
 Two types of lymphedema are known:
1. Due to reduction in the number of lymphatics and inadequate
clearance of the macromolecular substances [39], known as
"primary lymphedema"
2. Due to obliteration of the lymphatics in the axilla and groin
due to tumor invasion, lymphadenectomy, irradiation, and in-
fection, known as "secondary edema"
In both the pressure rise in the tissue leads to fibrosis of the
connective tissue and thickening of the fascia, a process often
accelerated by recurrent infection. Attempts have been made
to use the lymphatics of the transposed omentum for drainage
in various sites, including the scrotum [32, 39, 53, 79, 153].

Technique. The techniques using the omentum for lymphatic

drainage and vascularization of the extremities are described
above by GOLDSMITH.

Outcome. Although GOLDSMITH records satisfactory results (see

Fig. 168 and text below), lympholymphatic anastomosis could
not be demonstrated by all the examiners [32, 46]. Reoperation
was often necessary because of frequently occurring seromas,
and lymph vessels showed insufficient ingrowth, with omental
tissue floating in fluid-containing spaces.

9.2.1.3 Exteriorized Transposition

Chest, Neck, and Axilla

E. VAUBEL and H. WHITE

Chest Wall Introduction. The surgical treatment of chest wall disease and
Tumors defects is a common and difficult requirement of therapy for
neck and chest wall cancer. KIRICUTA [102] proposed omental
transposition in combination with split skin grafting to cover
extensive defects following excision of breast cancer with local
recurrence or radiation damage. This method is now used in
selected cases [57, 97, 160, 196], instead of the latissimus dorsi
myocutaneous island flap (Fig. 170, see page 318).

Surgical Options. Currently used techniques are

1. myocutaneous flaps (m. latissimus dorsi, m. rectus abdominis,
and deltopectoralis flap (Bakamjian flap));
2. cutaneous flaps (thoracoepigastric flap)
Fig. 170a, b. See page 318 3. omental transposition.

284
Fig. 171. Rotation arcs of
different flaps used to
cover chest wall defects

Indications and Contraindications. Omental transposition is

useful in those situations in which the established methods are
likely to be difficult, lead to complications, or are clearly techni-
cally inadequate. After radiotherapy, previous scarring, over-
enthusiastic local tumor clearance, and even with extensive
tumor and tissue damage in the midline of the neck and thorax,
a healthy bed for subsequent grafting can be easily established
with the omentum [157] for example also in the area around
a tracheostomy stoma where myocutaneous flaps may be precar-
ious (Fig. 171).
Small defects should be repaired by the other established
methods. General limitations and contraindications are dis-
cussed in Sect. 9.2.1. It must be realized that when compared,
for example, with the latissimus dorsi flap, omental transposi-
tion usually requires two stages of repair and a longer time
in hospital (about 3 weeks).

Operative Technique. When used for the chest wall the omental
pedicle may be brought out of the abdominal cavity
- laterally through the rectus sheath (Fig. 172)
- in the xiphisternal angle (Fig. 173 a). If the defect spreads

285
Fig. 172. 0 ment
posed throu h urn trans-
sheath and Ig d ~he
rectus \
taneous tu e I In a subcu-
racic wall dnn; to the tho-
elect

Fig. 172

F·Ig. 173. a Om
posed throu h entum. trans-
Incision alo g .~e mIdline
xiphisternu ngsl e the
pectoralis :~s~1 T~e major
ered to d e IS uncov-
emonst
the axilla rate how
can be
by reflecting th pr?tected
pectoralis m e reSIdual
sutured dee ~sc1e, which is
al border of t~:o the later-
mus dorsi m. latIssi-

F·Ig. 174. a VI
noma in a 62 cerated carci-
tient b N -year-old pa-
. ote 1 k
omental tr wee after
well_granU~a~S~osition the
the oment e surface of
. urn. c Th .
sk. In graft'IS fiIxed e. splIt
h
h Isto-acryl' I WItTh
IC g ue. d
postoperative' . e a
8 months I SItuatIOn
ater (V AUBEL) Fig. 173

286
 \0
00
N
V
01)
(Ij
0.
v
v
[/J

"'0
:::
v
01)
v
......l

1
...".
r--
~
~

287
Fig. 175. a Extremely large
defect after various opera-
tions to eradicate local re-
currences, with intense
scarring 5 days after
omental transposition, in a
36-year-old patient. In this
situation a myocutaneous
flap would not have been
possible. b The same pa-
tient 6 months after mesh
graft transplantation.
(VAUBEL)

to the axilla it may be beneficial to mobilize the residual

pectoral muscle and turn this into the axilla to reduce tension
on the pedicle (Fig. 173 b). Examples of reconstruction are
shown in Figs. 174a-d and 175a, b.
A combination of omental transposition and laterally based
skin flap or latissimus dorsi myocutaneous island flap can
Fig. 176. See page 318 prevent contracture in the axilla (Fig. 176, see page 318).

288
Fig. 177. Open channel
which can be used instead
of a long subcutaneous
tunnel leading the
omentum to the neck (see
Fig. 178 a-d, page 319)

Any pedicle led through the abdominal wall causes an area

of weakness which will predispose to herniation. However, when
the pedicle is led through a small separate lateral incision in
the abdominal wall (Fig. 172a) the chances of herniation are
theoretically reduced and are less in our experience. In addition
any infection tracking along the pedicle from the area of the
defect will not communicate with the laparotomy incision. It
is sometimes a wise precaution to drain the subcutaneous tunnel
if chronic infection is present. Any subsequent division of the
pedicle which may be required can be undertaken easily at the
small lateral incision without re-opening the main laparotomy
InCISIOn.
A long subcutaneous tunnel extending from the abdomen to
the neck, especially if it traverses tissue which has been subjected
to irradiation, may lead to some special problems. The loss
of tissue elasticity together with possible edema or fibrosis may
impair the roof of the tunnel and constrict the pedicle. If this
is thought to be a problem sufficient to endanger the pedicle
it is better that a long tunnel is not fashioned but rather an
open channel is constructed from the abdomen to the distant
defect (Fig. 177, case and series, Fig. 178 a-d, see page 319) [2].
When the defect of chest and neck involves ribs (Fig. 178 a-d
case series, see page 319) and even parietal pleura, it has been
suggested that stability should be given with synthetic mesh
under the pedicle [2]. We have not found this to be necessary.
The omentum adequately plugs the pneumothorax, and with
the surrounding fibrous reaction and organization of the
omentum a perfectly stable bed is provided for the overlying
Fig. 178 See page 319 skin. The chest wall movement is satisfactory, and the procedure

289
Fig. 179. Barium examina-
tion shows constant inden-
tation (arrow) on the
greater curvature, with
mucosal folds crossing the
lesser curvature in a
62-year-old patient [196]

requires no further stabilization unless the sternum has to be

replaced or there are very extensive defects.

Skin Grafting and Dressings (see Sect. 9.1.4)

Postoperative Care (see Sect. 9.1.5)

Functional Sequelae. When the omental pedicle is being led up

to the neck or thoracic wall - and especially when based on
the right gastroepiploic artery - traction on the stomach may
occur. This has been blamed for some of the occasional distur-
bances in gastric function including delayed gastric emptying
and fullness which have been described after this procedure [97,
196]. Radiological findings most commonly seen at the greater
curvature are [170]: (a) finger-shaped indentations, (b) distor-
tion of the gastric antrum, and (c) mucosal folds crossing the
lesser curve side.
These changes (Fig. 179) may mimic gastric carcinoma and the
radiologist should be forewarned. Gastroscopy following trans-
position has shown some abnormalities such as gastric erosions
which are occasionally associated with a small hematemesis.

Complications Related to the Omentum. Problems of abdominal

wall herniation have been discussed above. Twelve hernias have

290
Fig. 180. Breast reconstruc-
tion after subcutaneous
mastectomy with a silicon
prosthesis wrapped in the -0
transposed omentum

occurred in 42 patients when the pedicle was led through the

midline incision; two cases of herniation has so far occurred
in the 20 patients in whom we have led the pedicle through
the rectus. One small hemorrhage, one partial venous thrombo-
sis, three abscesses in a subcutaneous tunnel (before drainage
was routinely undertaken), one case of damage to the marginal
artery of the transverse colon making a segmental bowel resec-
tion necessary, and one total necrosis through torsion of the
omental pedicle occurred in the whole series.

Long-Term Results. The quality of the grafted skin over the

pedicle usually remains healthy and supple. Slight reduction of
omental tissue thickness at the site of grafting occurs after sever-
al months. The vessels in the transposed omentum are still pa-
tent after 6 months. Occasionally a ring of keloid change is
seen around the grafted area. Patients may notice heat (increased
blood flow) in the transposed omeutum during and after a meal.

Reconstruction of Because of its easy mobilization, plasticity, and rich blood

the Breast After supply, attempts have been made to fill the breast following
Subcutaneous subcutaneous mastectomy with the omentum [208] by the tech-
Mastectomy niques described above. The transposed omental tissue may
shrink postoperatively after several months, leading to lack of
symmetry of the breasts. When wrapping a silicon prosthesis
in the transposed omentum (Fig. 180, 181 a-c), shrinkage of the
capsule, displacement of the prosthesis, perforation of the skin,
and breast asymmetry did not occur in the eight patients treated
in this way (FAlX-SCHADE, personal communication, 1981). The
skin which is thinned and impaired by ischemia after subcutane-

291
 ous mastectomy recovered faster when compared with the sim-
ple implantation of the prosthesis. Reduction of the contralater-
al breast may be required.

Reconstruction of Myocutaneous island flaps (Fig. 171, chest) using the latissimus
the Breast After dorsi muscle or a medially pedicled thoracoepigastric flap are
Radical Mastectomy usually applied to cover large defects after mastectomy and ra-
diotherapy. However, there is no standardized and satisfactory
technique for the substitution of the totally removed pectoralis
muscle with exposed ribs, cicatricial contractions, and scar for-
mations of varying shape and size.
ARNOLD et al. [9, 10] transposed the omentum as a soft tissue
mantle for prosthetic materials in the manner described above.
This technique has been improved by implanted fascia lata strips
below the transposed omentum [157]. Augmentation of the
breast and reconstruction of the nipple can be carried out simul-
taneously or at a second operation.

Correction of Deformities of the Anterior Thoracic Wall

E. VAUBEL, R. ACHINGER, and J. TOOMES

Funnel Chest The frequency of thoracic wall deformities ranges between

0.06% [146] and 3.5% [115]; most are funnel chest, of whom

292
~ Fig. 181 a-c. Intraoperative
view after subcutaneous
mastectomy. a The
omentum is exposed for
wrapping the silicon pros-
thesis. b Preoperative and
c postoperative view on the
seventh postoperative day.
(Courtesy of Dr. FAIX-
SCHADE)
Result
Pharyngo- and
Oropharyngostoma
(ABBES 1974)
10% need bony reconstruction because of cardiac or pulmonary
disorders. The operation should be carried out between the ages
of 4 and 7 years, because later correction has been shown to
provide disappointing cosmetic results [161].
Options. Alloplastic or autologous material implanted into the
hollow space of the funnel chest may be the method of choice
and has been used in patients between 15 and 25 years. The
application of alloplastic material was complicated by painful
capsule fibrosis, pain due to rigidity of the material when
bending forward, and displacement of the prosthesis. Trans-
posed omentum, recently used in six patients, seems to prevent
these problems.
Surgical Technique. Preparation for surgery and moblization of
the omentum has already been described (see Sects. 9.1, 9.2.2).
The omentum may be kept on the right or left gastroepiploic
pedicle according to the site of the deformity. For midline defor-
mities the linea alba is incised at the lower border of the defect,
creating a tunnel for the omentum (Fig. 173). In lateral deformi-
ties the tunnel is made in the rectus sheath in the manner shown
in Fig. 172. The subcutaneous tissue in the area of the deformity
is removed close to the thoracic wall. Skin elasticity restores
the contour above the tunnel. The hollow space is filled up
with the omentum. Because of its tendency to retract the
omentum is sutured carefully to the subcutis using loose sutures
knotted over swabs. More rapid fixation is achieved using fibrin
adhesive. Supporting bandages should be worn by the patient
after mobilization for 3 weeks.
No tissue shrinkage has been observed 21/2 years after omental
transposition.
Throat
D. LIEBERMANN-MEFFERT
VALLICIONI (1973), ABBES et al. [2, 3, 4] and later KIRICUTA
[110] used the omentum to close large stomas due to pharyngo-
larnygectomy and cobalt therapy for cancer of the larynx, pyri-
form sinus, retromolar, and gingival area. ABBES and co-workers
transposed the omentum on a safe vascular pedicle; they pre-
ferred incision of the skin to KIRICUTA'S subcutaneous tunnel.
Because in one of the first patients there was one partial necrosis
of the omentum due to constriction in a narrow tunnel [2].
293
Fig. 182. Abdominal wall
repair with Marlex mesh
and overlying transposed
omentum between the
mesh and skin

Recently the omentum has been transferred and connected suc-

cessfully with microvascular anastomoses to the throat area [17].
Fixation of the omentum which was immediately covered by
skin grafts caused no problem. In some cases omental support
was aided by a deltopectoral flap. No drains were used.

Abdominal Wall

E. VAUBEL

Abdominal While the chest usually offers sufficient stability, reconstruction

Wall Abscess of the abdominal wall is difficult in patients with abdominal
wall abscess, third degree and electric burns, and after radical
tumor excision. It may be complicated by hernias which are
frequent after secondary healing above granulated or grafted
intestinal surfaces.

Options. Large abdominal wall defects can be covered with myo-

cutaneous flaps, rotation skin flaps, or the omentum in combi-
nation with alloplastic material.

Burn Experience with the Omentum. After treatment of shock,

DELARUE et al. [50] used the omentum to cover an extensively
large, 25 - 2 cm sized abdominal wall defect caused by an electric
burn (18,000 V). Although the blood circulation of the fascia
was greatly damaged in this patient, the wound healed within
10 days after skin grafting. Because local electric burns often
lead to intestinal necrosis, systematic laparotomy has been rec-
ommended, and reconstruction with the omentum in this situa-
tion, therefore, adds no risk to the patient.
Desmoid Tumors The omentum has also shown to be useful for defects following
excision of large fibroma or desmoid tumors in the abdominal
wall or groin area [12, 24, 155]. Plastic material will be added
(Fig. 182) and staged skin grafting is recommended.

294
Fig. 183. Omental pedicle
led to the elbow and
forearm

Extremities

E. VAUBEL and H.J. DITTLER

Arm Introduction. In 1945 CANNADY [34] first transposed the

omentum to the lower arm, and this was recently taken up
[108, 128, 195]. One unusual case is the report of a successful
transposition to the hand, in which the split skin covered
omental pedicle was subsequently transplanted as a jump flap
to cover a calcaneal defect [105].

Surgical Options. Although the myocutaneous latissimus dorsi

island flap to the upper arm, and the pedicled groin flap or
skin flaps from the abdominal wall to the hand and lower arm
are satisfactory methods of defect cover, certain difficulties are
experienced in using classical pedicles for covering defects
around the elbow and middle arm. Omental transposition is
extremely valuable in preparing a suitable bed for skin grafting.
In this region the pedicle allows the arm to be kept in a natural
position and a degree of motility to be maintained which would
otherwise be lacking and predispose to contracture formation.

295
 a

Fig. 184. a Omentum being

applied to the upper arm.
The defect resulted from
the excision of a radiation
ulcer at the site of a
sarcoma. Note the
humerus and surrounding
radiation skin changes.
b Testing the local blood
supply 3 weeks after opera-
tion by clamping the pedi-
cle. c The defect 1 week
after division of the pedicle
(VAUBEL)

Fig. 185. See page 320 c

296
Fig. 186. Angiography at
the site of the celiac axis
showing local anastomosis
and venous backflow over
the brachial vein (arrow)
(VAUBEL)

This benefit is especially valuable in the old patient in whom

loss of function may lead to a permanent disability. The desira-
bility may become a necessity when extensive areas of the trunk
which would normally be suitable pedicle sites are involved in
burn defects.
Indications. Although there are some reports of successful
omental transposition to the hand and lower arm [108], this
technique is only indicated in the middle of the arm and around
the elbow joint for (a) third degree and electric burns, (b) injury
in combination with burns, (c) radiation and chemotherapy
ulcers, and (d) tumors. The omentum on a pedicle may be
helpful when coverage with skin flaps from the abdominal wall
is unsatisfactory in the case of radio-ulnastabilization with exter-
nal fixation.

297

Fig. 187. Omentum 7 days
after transposition to the
chest wall with a dried,
condensed, and demarcated
superficial zone (above).
The connection of the
omentum with cutis and
subcuticular layers can be
seen (right). H & E, x 22.5
(GROSS)
298
Operative Technique. The omental pedicle is led to the appro-
priate arm via an incision lateral to the rectus sheath (Figs. 183,
184a-c, 185a-c, see page 320, technique Sects. 9.1, 9.2.1). The
arm is immobilized with a plaster of Paris or Desault bandage
and the axilla padded (Fig. 184 b). After some 2 weeks the
omental pedicle is occluded with an non-crushing intestinal
clamp (Fig. 184 b) or rubber sling (Fig. 185 c, Fig. 185 see
page 320) for limited periods of 2 h 3 times daily to establish
that the local anastomoses are adequate to allow division of
the main pedicle. At this time the bed is usually well enough
vascularized to allow split skin grafting.
Postoperative Care. While the bridging pedicle is present there
is no need for it to be protected with a covering of skin. A
tulle gras dressing similar to that described in Sect. 9.1.4 is suffi-
cient.
Mobilization. Active movements of the joint are encouraged
after 10 days.
Postoperative Angiography. The filling of the pedicle (Fig. 186)
and venous back flow to the axilla confirm the development

Fig. 188. Extensive necrosis
and edema with tissue re-
action 24 days after
omental transposition to
the upper arm. Superficial
exudate formation and de-
hydration (right). H & E,
x 28 (GROSS)
of anastomotic connections by 2 weeks. This establishes that
division of the pedicle, which is tested routinely by occlusion,
is safe.
Complications. Special complications have not yet been de-
scribed.
Histopathology of the Exteriorized Omentum
U. GROSS and E. VAUBEL
The histopathology of the transposed or transferred omentum
is undocumented. Pathomorphological findings, namely serous
transudation, fibrosis, fibroplasia, sclerosis, and focal necrosis
of the transposed or transferred omentum are merely mentioned
[57, 103, 105, 133, 194]. Our own histopathological investiga-
tions are based on six cases studied 7 days to 12 months postop-
eratively. The most striking late characteristic after omental
transposition is the irregular and partly reticular fibrosis of the
displaced fatty tissue.
299
Fig. 189. Linear fibrosis In the early stage, an expansion of the areas of vascularized
and cellular perivascular connective tissue due to an edema, a cellular inflammatory infil-
reaction with recent scar
tissue formation (below) tration, and capillary bleeding are observed; the superficial layer
24 days after omental of the fatty tissue exposed to air becomes condensed. The con-
transposition. H & E, x 32 nection of the surface of the transposed omentum with pre-
(GROSS)
existing and surgically damaged tissue and the tissue continuity
resulting from the organization of exudate are visible as early
as 7 days after the transposition (Fig. 187). The edema and the
inflammatory changes of the transposed omentum are still pre-
sent after 24 days (Fig. 188). However, by this time breakdown
of the irreversibily damaged transposed fatty tissue and its re-
placement by scar tissue with macrophages containing fat or
of lipophagic granulomas occurs. In the edematous omentum
and in the surrounding connective tissue, fibrosis and sclerosis
occur as well as a cellular inflammatory infiltration by leuko-
cytes and macrophages in the area of the vessels (Fig. 189).
A moderate-grade leukocytic infiltration can be observed at the
surface (Fig. 190).

300
Fig. 190. Recent fibrosis
(middle and below) with
leukocyte and histiocyte
migration to the superficial
tissue (above) 24 days after
omental transposition. H &
E, x 91 (GROSS)

In the late stage, between the transplanted skin and the trans-
posed omentum a dense, plate-like, and cell-deficient, hyalinized
connective tissue layer rich in collagen fiber can be recognized
(Fig. 191). Omental fatty tissue with the characteristic lobular
structure can be found underneath (Fig. 191). It is remarkable
that focal perivascular lymphoreticular tissue which corresponds
to milky spots can only be found very occasionally.

301
Fig. 191. Transposed
omentum below. Skin graft
above and between the two
is a dense fibrous scar-like
tissue. 18 mon ths after
grafting. H & E, x 32
(GROSS)

9.2.2 Free Omental Transfer with Microvascular

Anastomosis

J. BRENNWALD

Introduction. The use of the omentum as a pedicled graft outside

the abdominal cavity has proved to be valuable in many cases.
However, it is difficult to reach and cover defects such as those
on the scalp which are distant from the origin of the gastroepip-
loic pedicle. McLEAN and BUNeKE [133] first transferred the
free omentum to the scalp using microvascular anastomoses,

302
Fig. 192. a Freely trans-
ferred and micro surgically
connected omentum, which
covers a large scalp defect.
End-to-side anastomoses
are shown for both artery
and vein. b Correction of
hemifacial atrophy. End-
to-side arterial anastomosis
is shown
Technique
and there have since been many reports of similar techniques
being used in the following sites for a variety of conditions
[10,11,17,62,90,200,207]:
- Scalp (Fig. 192)
- Brain (for revascularization and drainage for hydrocephalus)
- Face (reconstruction of the tumor excision, hemifacial atro-
phy)
- Oral cavity and pharynx
Brachial plexus (revascularization in postradiation change)
Arm (drainage of lymphedema)
- Thoracic wall
- Lower extremity (revascularization and osteomyelitis)
- Neoformation of organs, for example in combination with
bone
The more extensive use of free cutaneous myocutaneous flaps
developed by DANIEL [47] enabled surgeons to cover defects
at most sites in the body without a laparotomy. If sensation
in the graft area is needed a neurosensory free flap can be used.
However, in extensive large defects the free omental transfer
covered with split-thickness skin grafts remains an important
technique, and is perhaps the method of choice in repairing
large scalp defects.
After assessment of the site, requiring cover and preparation
of the recipient vessels under magnification, the laparotomy is
undertaken. The selection of the donor vessel in the omentum
303

-~-
--~---
c
Fig. 193a-d. Technique of
the end-to-side anastomo-
sis. a Excision of a segment
in the recipient vessel
slightly larger than the
vessel. b Two stay stitches
in the corner of the se-
lected segment in longitudi-
nal axis are performed
first. c Anterior and poste-
rior stitches are placed on
each side. d Intermittant
stitches can then be in-
serted
304
b
-u-
d
is determined chiefly by the vessel diameter. The right gastro-
epiploic artery is larger (1.5-2.0 mm) than the left gastroepiploic
artery (1.0-1.5 mm). The omentum and pedicle are then careful-
ly dissected and magnification of the vessels is a great help.
The vein is clamped first so that the vessels remain filled with
oxygenized blood. No cooling or perfusion of the transplant
is necessary as the graft is transferred immediately to the recipi-
ent site. Under the microscope the graft vessels are anastomosed
to the recipient vessels. We prefer an end-to-side anastomoses
for both artery and vein (Fig. 193). This preserves the donor
vessels and, flow studies show a higher patency rate with end-to-
side anastomoses. When an end-to-end anastomosis is required,
Acland's technique [5] has been used successfully.
In order not to interfere with the microsurgery work it is advis-
able not to close the laporatomy wound during the short time
in which the microvascular anastomoses are undertaken. Any
disturbance prolongs the ischemic time of the graft, which seems
to decrease its survival rate. If drains are planned at the recipient
site, care has to be taken not to impair the flow in the vessels.
Anticoagulants are only required for systemic problems and not
for prophylaxis against local thrombosis. When there is a large
defect requiring a long period of reconstructive surgery prophy-
lactic antibiotics for 48 h are useful.
 Reconstruction of Skull and Scalp Defects

H. WHITE

Scalp Defects Options. Defects of the scalp can usually be covered with a
variety of local skin flaps. After loss of more than two-thirds
of the scalp, however, reconstruction is difficult. The techniques
which are currently used for repair are:
- Free transfer of groin flaps
- Retransplantation of the scalp
- Overgrafting of granulations growing from cortical defects
- Omental transfer with vascular anastomosis (see Sect. 9.3.3)

Indication. Reconstruction with the omentum has been recorded

giving satisfactory cosmetic results in selected cases [15, 30, 33,
89, 96, 133]. The method offers the advantages of:
- No disfiguring defect at the donor site
- Suppleness correcting irregularities of the wound surface pre-
serving function of the muscles of facial expression
- The ability to cover defects of any size
- Similar diameter of donor and recipient vessels, ranging be-
tween 1 and 2.5 mm
- Optional length for vascular pedicles
- Reconstruction with the omentum may be considered in:
- Tumors such as neurofibroma [133], basal cell carcinoma [30,
118], and dermatofibrosarcoma [118]
- Sequelae of irradiation such as radionecrosis of the scalp and
skull [89]
- Sequelae of accidents such as scalping injury [90, 96, 118],
electric injuries and third degree burns [33], depressed fracture
with severe skin contusion, and through-and-through gunshot
wounds [10].

Principles and techniques of the operation are along the general

principles already outlined (see Sect. 9.1 and 9.2). The right gas-
troepiploic artery taken as its origin with an attached piece of
omentum is most often used [11, 15, 29, 30, 89, 118, 200], but
occasionally the smaller left gastroepiploic artery has been suc-
cessfully anastomosed [11, 15, 133]. The temporal artery and
vein, the external carotid artery, and retromandibular or exter-
nal jugular vein have all been used as recipient vessels.
(Fig. 192). Apart from the technique described above the follow-
ing points are important:
Retroauricular access to the temporal vessels is recommended
in order to avoid injury to the facial nerve [118].

305
 The transferred omentum is covered immediately after its fixa-
tion with a split skin graft because meningitis is a potential
danger in all scalp and skull lesions.
Recently ARNOLD and IRONS have used the omentum in the
reconstruction of massive cranio-facial defects. They described
one patient who lost one eye, half the maxilla and mandible
and most of the nose from a shot-gun injury [10]. For repair
they took a portion of the stomach along the greater curvature
with the attached omentum containing the right gastroepiploic
vessels and joined these to the stumps of the facial vessels. The
stomach wall was used to replace the buccal mucosa and the
omentum to support a split skin graft. The distroyed facial bones
were reconstructed with ribs packed around with omentum
which maintained the viability of the bone grafts.

Sequelae. ARNOLD (personal communication 1981) reported that

the gastric secreting cells within the gastro-omental flap pre-
sented no problem and that digestion was unaffected by the
gastric resection. One of ARNOLD'S patients gained weight fol-
lowing surgery.
It is of interest that when the patient gaines weight, the omental
graft enlarges. This could be critical in such situations where
the omentum has been transferred as microvascular transplant
in the face for hemi facial atrophy (ROMBERGS Disease).

9.2.3 Free Omental Grafts

H. TILLMANNS, D. LIEBERMANN-MEFFERT, and H. WHITE

Definition A free graft is a piece of the omental apron which is transferred

without either a pedicle or a local vascular anastomosis to either
site of the body.

Introduction Nicholas SENN in 1887 [174] first pointed out the possibility
of using the omentum for the repair of tissue defects. He showed
in animal experiments that omental tissue, although detached
from its blood supply, survived and preserved its own character
[25, 185, 197]. Many experiments and reports of clinical experi-
ence using free omental grafts, plugs, and wrap-around sheets
for repair or protection of damaged organs have been reported
since SENN [18, 35, 83, 85,117,124,125,142,143,198,205].
The size of the graft is important for ingrowth [66], but thick
fatty grafts become necrotic [25, 126]. Hemorrhage under the
graft impaired the chances of survival [28], but it was shown
not to be important whether the omentum was attached to a

306
Fig. 194. The sites of free
omental grafts in the pelvis
(from left to right): ovary,
pouch of Douglas, and
uterus

raw or smooth surface [25, 58, 185]. A disadvantage of an

omental graft is its progressive fibrotic transformation [28, 83,
125], which may, for example, cause small bowel stricture [66].
Fibrosis of the omental graft makes it an unsatisfactory method
for the long-term treatment of coronary artery disease [158].

Indications Although there are many theoretical reasons for preferring

omental transposition with a pedicle rather than free grafts,
there are some situations in which free grafts have classically
been used (Fig. 194):
- Large serous defects in gynecological surgery, for example
at the site of myomectomy or after excision of endometriosis
in the pelvis. This has been of value when the defects are
in the pouch of Douglas [145, 172].
- Protection of the ureter but only when there is a risk of ureter-
ovaginal fistula after irradiation. Stricture of the ureter may
be a late complication [87, 145].
Contraindications are (see Sect. 8) (a) an extreme fatty omentum,
(b) small bowel, (c) wounds badly damaged by irradiation, (d)
contaminated wounds, and (e) badly vascularized tissues.

Surgical Techniques U sing the abdominal or perineal approach a thin membranous

omental portion should be chosen for a free graft to minimize
the risk of fat necrosis. Because of the subsequent shrinkage
the graft must be about 1 cm larger diameter than the recipient
site, but the tissue must be taken from a part of the intact

307
 omentum which will not subsequently impair the blood supply
of the residual tissue. The graft is attached with absorbable
sutures (Sect. 9.1).

Results Although it is not used commonly enough for series to have

been reported, it has been observed at relaparotomy that the
region of the free graft is adhesion free with a few clusters of
fat cells in the area [172].

9.3 Limitations of Omental Transposition

and Transfer

H. WHITE

In the right circumstances omental surgery is a valuable tech-

nique, but other more conventional methods such as myocutan-
eous flaps should always be considered before having recourse
to the omentum.
In planning any surgical procedure, it is necessary to remember
the morbidity and mortality and whether a lesser operation
would give benefit with fewer risks and complications. Omental
surgery carries potential risks which must be carefully assessed.
For exteriorization of the omentum laparotomy is required with
all the attendant morbidity as well as the possibilty of torsion
of the pedicle, and herniation may occur, where it is led through
the abdominal wall. Occasionally venous congestion and throm-
bosis are a problem.
If the omentum is greatly lengthened to reach a distant site
the amount of tissue left for cover is small. In lean subjects
the omentum may be very thin and frail and provide an inade-
quate cover even when not lengthened. The lymph drainage
of the omentum is poor and sensory innervation absent. This
must be taken into account when planning surgery and the limi-
tations of using the tissue on the scalp are evident and microvas-
cular techniques require surgical expertise which is not univer-
sally available. Finally the amount of shrinkage of the trans-
posed and transferred omentum is variable and must be allowed
for when covering defects.

308
Color Plates of Chapter 9

309
Fig. 114. Removal of the
omental graft after
2 weeks; fresh granulations
of the wound surface.
(DITTLER)

Fig. 115. Porcine omentum

before placement on a
third-degree burn wound
after necrosis removal.
(DITTLER)

310
Fig. 121 a, b. Technique
shown at operation. The
small defect in the
omentum was subsequently
repaired. (WmTE)

311
312
Fig. 122a-k. Sequence at operation. (WHITE, a Patient, 25 years after initial treatment for primary breast cancer with excision and local radiotherapy.
Recurrent disease treated with further radiotherapy immediately before toilet mastectomy. b Xeromammogram showing tumor eroding sternum. c Mobiliza-
tion from transverse colon. d Omentum led through abdominal wall and laparotomy incision closed. e Omentum placed in plastic intestinal bag during
mastectomy. f Mastectomy specimen. g Patient immediately after surgery with plastic dressing covering omentum. h Granulating surface of the omentum
10 days after surgery. i Skin donor site 10 days after grafting. j Chest wall 10 days after skin grafting. k Patient 2 months after surgery. Notice the
fullness of the omentum in the subcutaneous tunnel and slight herniation where the omentum is led through the abdominal wall
Fig. 129. a Echinococcal
cyst and surface of the
right lobe of the liver.
b Cyst following perciystec-
tomy including the host
capsule. c Cavity after re-
moval of the cyst.
d Omentum filling the cyst
cavity (NEFF and TON-
DELLI)

Fig. 157 a-d. The omentum

is mobilized by a supra-
inguinal access and packed
into a condom. b The
condom is brought to the
inguinal region through a
wide tunnel in front of the
inguinal ligament. c Top
left is the inguinal incision.
In the groin the condom is
removed from the
omentum. d The omentum
is wrapped around the
anastomosis and the proxi-
mal part of the venous
graft and fixed with a few
stiches (VAN DONGEN)
~
Fig. 160. a Infected proxi-
mal anastomosis of a fem-
oral venous bypass graft.
b Magnification of the
proximal anastomosis with
hemorrhage from the ve-
nous graft (VAN DONGEN)

316
Fig. 161. Perforation of the
aortic aneurysm into the
duodenum. The figure
shows the erosive defect of
the duodenal wall with two
perforations. An edge of
the aneurysma wall adja-
cent to the site of perfora-
tion is left (VAN DONGEN)

317
Fig. 170a, b. Breast carci-
noma with extended severe
radiation damage and great
discomfort in a 51-year-old
patient (WHITE)

Fig. 176. Combination of

omental transposition and
latissimus dorsi myocutan-
eous island flap to prevent
contraction of the axilla.
Second stage 8 months
after omental transposition
(V AUBEL)

318
Fig. 178. it Supraclavicular
in radiation damage with
total necrosis of the clavi-
cle in a 57-year-old patient.
Situation after omental
transposition through a
midline incision on the 5th
b and 18th c postoperative
days. d Final skin closure
and split skin graft in the
neck region (VAUBEL)

319
Fig. 185. a An extensive
burn and crash injury with
exposed radius. b The same
patient 2 weeks after sur-
gery showing a healthy
pedicle and c the technique
testing the local blood
supply by occluding the
pedicle with rubber slings
immediately before division
(DITILER)

320
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 Historical Review

10 History

10.1 Historical Glance at the Terminology

U. TROEHLER

The term for the omentum which first appears in Western cul-
Dertron ture is "dertron" in HOMER'S Odyssey in the eighth century
B.C. 1 : in Hades the giant Tityos was eternally punished for
his crimes by vultures which plunged deeply into the dertron
to feed on his liver [54]. Related to "dero" (to flay) and
"derma" (skin) this term reflected the membraneous character
of the omentum.

" Dertron" also occurs once in the HIPPOCRATIC texts from the
fifth and fourth centuries B.c. [52a]. More frequently, however,
Epiploon the authors used the term" epiploon" [52 b]. ARISTOTLE ( '" 384
to '" 322 B.c. [3, 4]) and GALEN (128 to '" 200 A.D. [34a] re-
ferred) to the" epiploon" and thought this to be the appropriate
term in meaning" the thing floating or drifting on the surface"
of the bowels [34 b]. This etymology is, however, probably
wrong as "epiploon" is related to "pelma" or sole of the foot
rather than to "plein" or "sail" [99]. "Epiploon" is still the
French medical term for the omentum.

GALEN'S contemporary JULIUS POLLUX, teacher of rhetoric at

Athens, transmitted colloquial Greek expressions reflecting the
resemblance of the omentum to a fisherman's net. These have,
however, so far not been found in medical texts [99]. On the
Omentum other hand the introduction of the Latin term "omentum" as
a synonym of the Greek word" epiploon" is found in the medical
part of the encyclopedia compiled in Latin by the Roman writer
CORNELIUS CELSUS in the first century A.D. CELSUS called an
omental rupture an epiplocele whereas he described the organ
itself as "omentum, ex inferiore parte leve et adstrictum, ex super-
1 Nothing is known, according to present knowledge, from texts of ancient
Egypt concerning the name or function of the omentum (Prof. W. WESTEN-
DORF, University of G6ttingen, personal communication, 1980)

331
 iore mollius. Cui adeps quoque innascitur ... " [17 a, b]. Another
Roman encyclopedist, PLINY THE ELDER (23-79 A.D.) also used
the term "omentum" [83] as had done the poet CATULLUS
100 years before [16].
" Omentum" is the medical expression now current in English.
Yet, its etymology remains somewhat obscure. The Strasbourg
student FRIDERICUS REEBMANN noted in his doctorate thesis" De
omen to sana et morbido" (1753), that some Latinists believed
"omentum" to be related to "omen" since it played an impor-
tant part in the ancient custom of haruspicium [85]. As attrac-
tive as this hypothesis may have been [56] - and still is [97]
- it can hardly be maintained today. First, the Roman augurs
prophesied the future mainly by observing the flight of birds;
yet practices from other Mediterranean regions might have in-
fluenced Latin vocabulary. Secondly, as REEBMANN was aware,
"omentum" had been related to "operimentum" (cover, i.e.,
of the intestines), and had thus occasionally been used to de-
scribe the meninges covering the brain.

Philologists in the eighteenth century also suggested that

"omentum" was derived from "supra maneo" (I remain above,
i.e., the intestines) or from" opimus" (fat). Modern etymolog-
ists, however, trace it back to an earlier hypothetical term" ovi-
mentum" from" induo" (I clothe or cover) [28].

The term "zirbus" from the Arabic "tharb," which denoted

the omentum in medieval medicine, also means fat. We find
"zirbus" in exclusive use from A VICENNA (980-1037) and the
mid-twelfth century manuscripts from Salerno [99] until the
early fourteenth century: It was HENRI DE MONDEVILLE
(1260-1320) who reintroduced" omentum" as a synonym of
Zirbus "zirbus:" " Zirbus et omentum idem sunt," he wrote in his Ana-
tomia (1304) [72]. This was probably no coincidence since MON-
DEVILLE lectured at MONTPELLIER. This city, as well as Salerno,
was one of the early European Universities in close contact
with the Arab world, through which the occident gradually re-
covered parts of the medical knowledge of antiquity. Indeed,
the great GUY DE CHAULIAC (,...., 1300 to ,...., 1368), who was one
of the most knowledgable writers, in surgery at that time, duly
reintroduced the term "epiploon" alongside "zirbus" and
"omentum" [19].

Whilst" zirbus" disappeared during the sixteenth century, Latin

texts now started to include terms alluding to other features
of the position, function, or structure of the omentum. Thus
it was called "mappa ventris" (napkin of the abdomen),

332
 "clipeus" (shield) [85], and the Greek picture of the fisherman's
net appeared again in the term "rete" or "reticulum" [15].
Rete Remarkably enough, just as in antiquity, "rete" was first linked
with everyday rather than with medical language. "Zirbus seu
omentum. .. rete a vulgaribus dicitur" wrote BERENGARIO DE
CAPRI in 1522 [99]. VESALIUS used almost the same wording
in 1543 in his famous Fabrica [105]. It was only with THOMAS
BARTHOLIN'S widely read Anatomia (1660) that" rete" became
accepted alongside other expressions [6]. Hence it has found
Netz its way into current scientific Italian and German (Netz).

If we turn to an early medical book written in the vernacular

we find in AMBROISE PARE a summary of the terms and met-
aphors hitherto used: "De l'omentum, dit du vulgaire coe/e, et
des arabes zirbus," was the title of the relevant chapter in his
Chirurgie (1564), in which he further wrote of the" Epiploon,
... , pource qu'i/ nage et est tendu entierement par dessus tous
les intestins Ie plus souvent: laquelle ressemble a une rets aprendre
poissons" [79]. Various vernacular expressions can in fact be
found in both medical and nonmedical literature since the four-
Caul/ Crepin/ Rodol teenth century - Caul in English, Crepine and Rodol in French,
Gi1del and Gi1del in German [56, 57, 77, 88, 97, 109] - some of which
have fallen into disuse in modern idioms.
This survey on the history of one term illustrates that Western
medicine has inherited from antiquity in different ways: while
all the current expressions for the omentum can be traced back
at least to the time of CELSUS [18], there are" cultural" diversi t-
ies in their modern usage. Is it not tempting to speculate why
" omentum" is used in English, "epiploon" in French, and
" N etz" in German?

10.2 Historical Survey

M.L. PORTMANN, D. LIEBERMANN-MEFFERT" and H. WHITE

10.2.1 The Classical Period and Ideas of Anatomy,

Function, and Surgery

It was the custom in ancient Egypt to embalm the human body

after death. However, anatomical knowledge at this time was
very limited (Fig. 195). The omentum was first mentioned in
HOMER'S Odyssey (eighth century B.C. [54]), but it is not until
the Greek writings of the fourth century B.C. that we find any
detailed description of the omentum [3, 4, 52].

333
Place Reference Age Terminology Anatomy Functions

Egyp

Greece Odyssey 8 BC dertron

1
Hippocrates· I. BC epiploon Fatty Iissue

1
c:
Ari stotle 3 BC Attachment to Heat exchanger. .2
stomach U
Lubricator . Fat storage, c:
Rome Pliny 1 AD omentum Membrane. .2

I
Accelerator 0
Galen 2 AD Peritoneal purse. \.1/
of digestion z
Avicenna 1000 Zirbus Vessels ~6::::' I

I
./

Iddle
ages
Mondi no
Brunschw ig
1300 Zirbel
11.80 Gudel
rete
elz
Attachment
colon
0
I I
D

~
,
Rena ls - Leonardo do Vinci 1506 1a
First Iliu strotlon 6
sance Vesa l 151.3 .J::.
11\
c:
0
.J::.
u
First detailed ~ .7 Ruler of the
Riolan 1580 0, E c: description
abdomen.
c: ~ ~
SCientific Cruve i lhier 181.1
'" 0\
Absorption . Defence
Diseases
against Inflammation
age Ranvier 1871. " Milky spot s .. and in fect IOn
1900

Fig. 195. Knowledge of the
omentum over the centur-
ies, HIPPOCRATIC writings
HIPPOCRATIC writings [52a] contain a number of references to
the omentum and particularly case reports of abdominal injuries
in which the omentum became excluded and gangrenous. AR-
ISTOTLE (384-322 B.C.) records that the omentum is fatty materi-
al present in all warm-blooded animals, and he believed that
it accelerated digestion because of its warmth [3, 4].
At this time it was suggested that in obese women the omentum
pressed upon the uterus and prevented conception. Other specu-
lative theories of omental function included the view that in
pregnant women, the gravid uterus pressed upon the stomach
and caused ingested fat to flow in the omentum. When the
uterus expanded further it was thought that this fat ascended
to the breasts and turned into milk (On the Nature of the Child,
52b). It had also been observed that there was a depletion of
omental fat in malaria but even despite such observations, no
definite function could be ascribed to the omentum [52b]. The
opinion of the Alexandrine school expressed by ERASISTRATOS
(ca. 304-250 B.c.) that the omentum had no special function
(Fig. 195) must represent the overall view at that time [27].
PLINY THE ELDER (23-79 A. D.) first used the term "omentum"
in Latin (Fig. 195) to describe the fatty membrane covering the
stomach and intestines [83]. CELSUS [18], writing at the same
time, described the physical signs of irreducible hernias contain-
ing omentum and gave the first details of surgery. He drew
attention to the need to determine whether or not the extruded
omentum was gangrenous and required resection before being
replaced in the peritoneal cavity. He also emphasized the need

334
 for the surgeon to open the sac in both inguinal and inguinoscro-
tal hernias to determine the amount of omentum which had
prolapsed. If only a small amount was in the sac, it could be
replaced by a finger probe; with a large omental prolapse he
recommended either that it was treated by caustics or ligated
so that it died away and dropped off. According to CELSUS
[18], an umbilical hernia could only be treated between the ages
of 7 and 14 years. The technique used was first to cause the
hernia to prolapse by straining and then mark the lower margin;
after this the hernia was reduced and the sac with adherent
skin ligated along the lower margin and subsequently treated
with caustics and cautery.
GALEN (128-199 A.D.) gives the most accurate description of
the omentum in classical times [34a]. He described peritoneal
folds of varying size in two sheets having the shape of a purse
or bag. The main artery and vein supplying the omentum were
known to follow the greater curvature of the stomach from
the duodenum to the spleen with the smaller branches passing
down between two mesenteric leaves. He considered that the
chief function of the omentum was to warm the intestines and
lubricate the peritoneum as well as act as a site of fat storage.
In support of the theory that the omentum warmed the intes-
tines, he described a gladiator who had an abdominal injury
and after having a large portion of the omentum resected, felt
cold easily and could not bear to have his abdomen uncovered.
When resecting the extruded omentum, GALEN [34 b] empha-
sized his belief that the ligatures should be placed on healthy
tissue when resecting the gangrenous omentum because of the
risk of hemorrhage and that the ends of the ligature should
be left hanging out of the sutured wound so that they could
subsequently be pulled out.

10.2.2 Tradition in the Middle Ages

The classical ideas were preserved and passed on to the middle

ages:

Anatomy AVICENNA (980-1037), who was born in Persia, gives a detailed

anatomical account of the omentum in the "Canon of Medi-
cine" [5]. However, his description is largely derived from earlier
writers such as GALEN [34]. THEODORIC, writing about 1267,
described the omentum as being formed of delicate membranes
interlaced by veins and arteries which were tributaries of the
hepatic vein and branches of the aorta respectively [100].

335
 Perhaps the most notable mediaeval anatomist who wrote about
the omentum was MONDINO DE' LUZZI (1275-1326). He had in-
stituted dissection at the University of Bologna. Despite this,
he hardly questioned GALEN'S views. His own account of the
anatomy described the omentum as arising in the region of the
diaphragm at the peritoneal reflection and being attached to
the stomach, spleen, and particularly the colon [73].

Function ALI IBN-ABAS, who like Avicenna was also born in Persia, de-
scribed the omentum and its functions in Liber Regius in the
tenth century [2]. He still accepted that it warmed the stomach
and intestines. HENRI DE MONDEVILLE (1260-1320) believed that
digestion in man was less effective than in animals because of
man's thin and hairless skin and that the omentum to some
extent compensated for this [72].

Surgery The knowledge of ancient surgical techniques was also kept

alive through the ages. PAULUS OF AEGINA, writing in the seventh
century, gives a detailed account of treating abdominal wounds
involving the omentum [81]. When the Byzantine Empire fell
to the conquering Arabs, surgical knowledge, along with certain
aspects of the culture, was absorbed and preserved. The Nestor-
ians, taking refuge in Persia from the persecutions of the Ortho-
dox Church, carried the knowledge and ideas to the Orient.
It is not surprising, therefore, that we find good accounts of
omental resection in various publications from distant centers
at this time. ALBUCASIS (936-1013) in his Altarif, published in
Spain, discussed the accepted techniques [43 a], as did BRUNO
DA LONGOBURGO (1252), who practiced in Padua and Verona
and wrote Chirurgia Magna [43 b]. The importance of the
omentum in the surgical repair of hernias is recorded by ROGER
FRUGARDI in Ars Chirurgica written in the second half of the
twelfth century [43 c]. WILLIAM OF SALICETO [92], a contempo-
rary, in his Handbook of Surgery (1476), discussed the differen-
tial diagnosis of intestinal and omental hernias. There was an
audible murmur over the bowel which was absent when the
omentum filled the hernial sac. He used the term "rete" in
connection with an omental hernia and described it as felling
like a net wrapped up in a cloth of linen. Hernias which con-
tained omentum were more tender than those which contained
bowel.
A pupil of SALICETO, LANFRANCHI OF MILAN, who died in 1315,
laid the foundations of French surgery, which was predominant
in Europe from the fifteenth century to the Napoleonic Wars
[43d]. Little however, was, added to the views of GALEN about
either the function or the surgery of the omentum. GUY DE

336
 CHAULIAC (1298-1368) warned of the risk of hemorrhage in
surgery of the omentum, which was, of course, also recognized
by GALEN, who stressed that ligatures should be placed on
healthy tissue when resecting the gangrenous omentum [19].
The first outstanding German surgeons, HIERONYMUS BRUNSCH-
WIG [12] (1450-1533) and HANS VON GERSDORFF [36] (1517),
who both lived in Strasbourg, undoubtedly derived much of
their knowledge from the French school. BRUNSCHWIG [12] gave
a detailed account of abdominal injuries with pikes, arrows,
and swords, but apart from stressing the need to establish the
depth of penetration had little to add to the techniques of resec-
tion already established. The Middle Ages kept alive the ideas
of the classical times (Fig. 195). During this time the descriptions
and techniques of antiquity were recorded and copied ready
for the age of anatomical enlightenment and surgical advance
characterized by the Renaissance.

10.2.3 Observation and Experience in the Renaissance

Anatomy At the beginning of the sixteenth century, BERENGARIUS OF

CARPI (1470-1550) was teaching in the University of Bologna
[43e]. He began to question the work of earlier authors such
as MONDINO [72]. He suggested that contact with air caused
gangrene. Although he claimed repeatedly to have resected the
omentum without ligature or cautery, he acknowledged that
the traditional methods were safer.
The illustrations published in 1523 by BERENGARIUS [43 e] were
still somewhat primitive and stylized, although LEONARDO DA
VINCI (1452-1519) had already made a life-like drawing between
1504 and 1506 (Fig. 196 [63]). Leonardo had the benefit of
ample dissection material, which was probably obtained from
the Hospital of Santa Maria N uova. Although he made accurate
drawings with copious notes, they were not published until more
than 200 years after his death and, therefore, in this respect
he influenced his contemporaries but little. Many of his anatom-
ical drawings, including that of the omentum, are preserved
in the library of Windsor Castle [63].
ANDREAS VESALIUS (1514-1564), the founder of modern anato-
my, was able to criticize the Galenic tradition as a result of
first-hand knowledge gained from dissection. His book De
humani corporis fabrica (1543) has accurate and beautiful illus-
trations representing the omentum [105]. In it the omentum
is compared to a birdcatchers sack, and attention was drawn
to the two components of the greater omentum (Fig. 197). He

337
 H \

.
/,
"

338
 Fig. 197. Illustration of the
omentum by ANDREAS VE-
SALIUS [105]. (Courtesy of
the U niversitatsbibliothek,
Basel)
Function
Surgery
.... Fig. 196. First illustration
of the omentum (1504) by
LEONARDO DA VINCI.
(Library of Windsor
Castle, England, facsimile)
described the superficial layer extending along the greater curva-
ture of the stomach to the spleen and the deep layer arising
from the deep surface of the stomach. It was clear that the
two layers were not attached to the intestines, except the trans-
verse colon. He described the main tributaries of the portal
vein, the largest being on the right, coming from the colon.
He also observed arteries and nerves accompanying the veins,
and the origin of the nerves appeared to be the sixth cranial
nucleus. VESALIUS also believed that the omentum had glands
which excreted liquid. He drew attention to the different amount
of omental fat in obese and slender subjects.
Between 1565 and 1604 HIERONYMUS FABRICIUS AB AQUAPEN-
DENTE (1537- 1619) taught anatomy and surgery in Padua [30].
He wrote about the omentum in considerable detail and re-
garded it as a receptacle into which waste products from the
stomach, liver, and spleen were discharged (cited in [85]).
The most outstanding surgeon of the period was AMBROISE PARE
[79, 80] (1510--1590). In writing about hernias, he described a
relaxation or rupture of the peritoneum which allowed the
omentum to extrude and form a swelling which was not disco-
lored, felt somewhat rubbery to the touch, and was almost pain-
less. In order to prevent the omentum herniating after reduction,
he advocated that the defect should be tightened by a needle
339
 LiD,VIr.!J' '

FIG.

v

Anatomy
.. Fig. 198. Ideas of omental
vessels by JULIUS CASSERIUS
Placentinii [14]. (Courtesy
of the Univer-
sihitsbibliothek, Basel)
and thread and advised scarification around the hernia to accel-
erate the healing process. He recommended plasters and trusses
rather than the fanciful remedies suggested by some surgeons,
such as swallowing magnetic filings and then spreading honey
and iron filings on the hernia in the hope that they would be
sufficiently attracted by the magnetic ones to reduce the hernia.
PIERRE FRANCO (1500-1561) was rather radical in the repair
of hernias [31], advising ligation of the omental pedicle and
even resection of the testicle if the omentum extended to the
scrotum and was adherent to the testicle. He was, however,
aware of the dangers of opening the bowel if this was also
present in the sac and advised a small exploratory incision as
a check.
Despite the advance in anatomical knowledge of the period,
the technique of repair which FABRICIUS AB AQUAPENDENTE [30]
recommended differed little if at all from those of his predeces-
sors, and we know from many sources, such as the case reports
from Basel and Freiburg by JOHANNES SCHENCK VON GRAFEN-
BERG (1530-1598), that the attemped surgical repair of even large
hernias was commonplace [93].
10.2.4 Modern Trends
ADRIAAN VAN DEN SPIEGHEL (1578-1625) gave a very compre-
hensive description of the omentum [98], but was unable to
confirm the glands which VESALIUS had described. In looking
for a route of communication between the liver and omentum,
VAN DEN SPIEGHEL suggested the small hepatic lobe beneath the
porta hepatis (lobulus Spigelii). Because of its proximity to the
omentum and the very thin capsule, his contemporaries accepted
this theory.
The skills of making anatomical preparations had reached a
climax in the art of FREDERICK RUYSCH (1638-1731 [91]). By
injecting wax into the arteries, the course of the blood vessels
became clearly visible, and errors in describing the vessels made
as recently as 1677 by FRANCIS GLISSON (1597-1677 [38]) could
be corrected (CASSERIUS, Figs. 198, 199). RUYSCH'S techniques
of preparation were so delicate that he was able to dry the
omentum like a piece of silk and prove that in life it was not
perforated between the vessels and that the earlier descriptions
of it being a net or "rete" were incorrect. The anatomical
knowledge of the time was summarized in 1695 by JOHANNES
VIERZIGMANN [107] working at the University of Altdorff, in
341
 TAB '. VI . Lib :ur

342
... Fig. 199. The omentum by
JULIUS CASSERIUS Placen-
tinii [14]. (Courtesy of the
Universitatsbibliothek,
Basel)
Function
Pathology
his thesis De Omento. The one point on which he appeared
to be at variance with his colleagues was the existence of lym-
phatics, despite their description some years earlier by several
workers and their recent "confirmation" by WHARTON
(1614-1673 [111]).
The central figure in omental research at this period was
JACOBUS BENIGNUS WINSLOW (1669-1760), who worked in Paris
[112]. He established the anatomy of the omental reflections
beyond doubt. In Exposition Anatomique de fa Structure du
Corps Humain, published in 1732, he described the greater and
lesser omentum. We also find the first description of the lesser
sac and the foramen which came to bear Winslow's name. The
Swiss physician ALBRECHT VON HALLER (1708-1777) described
the colic omentum in leones Anatomicae (1743 [44, 45, 49, 50]).
Much of the work which enabled the omental attachments to
the stomach, duodenum, colon, and spleen to be so accurately
recorded was undoubtedly undertaken on human subjects. It
is likely that the experiments inflating the lesser sac through
the foramen were in animals, but unfortunately we do not know
the species.
When JEAN RIOLAN (1580-1657, cited in [96] found that omental
resection did not lead to the patients suffering from cold, he
questioned the traditional function of the omentum. While
HELKIAH CROOKE [20] in England still proclaimed that the
omentum was an important heat exchanger, Riolan referred to
it as the "ruler of the whole abdomen," and half a century
later, JEAN LOUIS PETIT (1674-1750) suggested in the Academie
des Sciences [82] that the omentum played little part in warming
the body but rather acted like a lubricant in smoothing per-
istaltic movements.
The omentum was so often found in association with pus that
JOHANN VESLING (1598-1649 [106]) believed that it produced
pus and serous fluid. Speculation on the function of the omental
fat led MARCELLO MALPIGHI (1628-1694 [67]) to suggest that
there was a system of adipose vessels which distributed fat to
the distant parts of the body. These, of course, were never found,
but by the mid-seventeenth century THOMAS WHARTON
(1614-1673 [111]) from England, THOMAS BARTHOLIN
(1616-1680 [6]), a Danish anatomist, HERMANN BOERHAAVE
(1668-1738 [8]), and HALLER (1708-1777 [44]) had all described
a "lymphatic system" which they thought played a role in the
transport of fat.
In 1628 SENNERT (1602-1637), professor from WITTENBERG, gave
one of the first surveys of diseases of the omentum [96]. The
343
 TAB . xxxvu .

344
~ Fig. 200. Surgical treatment
of abdominal injuries with
omental prolapse by
JOHANN SCUL TETUS, Sr.
[94] showing how to suture
omental injury. (Courtesy
of the Medizin-Historische
Bibliothek, Basel)
Surgery
Embryology
formation of national and international scientific societies led
to a comparatively rapid dissemination of ideas throughout
Europe. The Miscellanea Curiosa published by the German
academy Leopoldina and the Philosophical transactions of the
Royal Society of London are examples of such reports which
were widely distributed. Inflammation and abscesses (FRAN<;ms
ROUSSET, 1535-1590, cited in [96]; BONET, 1620-1689 [9];
JOHANN CHRISTIAN FROMMANN, 1685 [32]), injuries (VIER ZIG-
MANN, 1653-1727 [107]), and omental tumors (THEOPHILE
BONET, 1620-1689 [9]; JOHANN DANIEL GEYER, 1687 [37]; VIER-
ZIGMANN [107]; JOHN HUXHAM, 1694-1765 [55]) are well docu-
mented in these reports. The first comprehensive review ap-
peared in the thesis" De omenta sana et morbido" by FREDERI-
CUS REEBMANN in 1753 [85].
GIOVANNI BATTISTA MORGAGNI (1682-1771) made many refer-
ences to the omentum [74]. He included clear descriptions of
omental adhesions to the intestines, uterus, and even torsion.
Often, after a long disease, the omentum was known to become
almost fat free, and by that time there were many reports of
tumors, abscesses, inflammation, and parasitic infiltration
(REEBMANN 1753 [85]. Such was the interest in the pathogenesis
of various conditions of the omentum that it was to influence
the experimentation and thought of workers in this field
throughout the nineteenth century.
Developments in surgical technique were minimal. JOHANN
SCULTETIUS (1595-1645) of VIm advocated [94] the traditional
methods of replacing the healthy omentum in the abdominal
cavity after an injury but resecting gangrenous parts using liga-
tures hanging out of the abdominal wound during wound
healing (Fig. 200). LORENZ HEISTER (1683-1758) merely sug-
gested placing the ligatures on the omental pedicle, on the bowel,
or on dressings of different colors [47]. In this way he argued,
the tails which were ultimately pulled out could be distinguished
from one another. DIONIS [23], a surgeon who practiced in Paris
in the early eighteenth century, first diagnosed strangulated
omentum in a hernia and was able to resect it. The development
of pain in a previously trouble-free swelling was said in 1740
by RENE-JACQUES CROSSANT DE GARENGEOT [35] to indicate
strangulation in an omental hernia.
10.2.5 The Scientific Age
MECKEL (1781-1833) was the first to devote his attention to
the development of the omentum [70]. He observed that it was
345
 absent in the early embryo but began to develop on the greater
curvature at the end of the 2nd month. This observation was
later confirmed by HIS (1831-1904), and it was noted that initial-
ly the omentum was without fat and consisted of two anterior
and two posterior layers [53]. JOHANNES MUELLER (1801-1858)
claimed that there was an embryonic rotation of the viscera
and that the omentum came to lie between the transversely or-
ientated stomach and the adjacent transverse colon [75]. This
was, however, not universally accepted and even KOELLIKER
(1817-1905), a pupil of MUELLER, disputed his master's view
that the posterior leaf of the omentum embraced the transverse
colon [61].

Anatomy In 1812 FRORIEP (1779-1847 [33]) published a remarkable study

on the structure of the peritoneum and omentum. The work
was largely based on the dissection of stillborn babies and con-
firmed the arrangement of the lesser sac and foramen of
Winslow. Interest in the omentum continued and in 1836 HEN-
NECKE [quoted in 48] was awarded a prize by the University
of Gottingen for his review of the anatomy, pathology, embryo-
logy, and function of the omentum. Although he remained
doubtful about the innervation of the omentum, he was abso-
lutely certain that a lymphatic plexus existed.
In 1882 HYRTL (1811-1894) described ([56] the lesser omentum
as having two layers and the greater, despite its extreme thinness,
as having four layers. A similar observation was made by
LANDAU (1902), who pointed out that the recessus omentales
persisted in the adult more commonly on the left [62].

Physiology The function of the omentum was somewhat neglected in the

nineteenth century. VON SOEMERRING (1755-1830 quoted in [48])
asserted that it had a function in lubricating the intestines and
pointed out that when the omentum was removed surgically
the intestines usually adhered to one another. Some of the old
ideas on protecting the intestines against cold and injury were
also revived. The ability to surround and isolate foreign bodies
was not only accepted but well illustrated by a specimen in
the anatomical museum in Vienna, described by ROBERT
(1814-1878 [87]). The preparation showed a human stomach
perforated by a spoon which had been wrapped in the omentum
and so isolated from the rest of the peritoneal cavity.
A most important observation related to the function of the
omentum was that by RANVIER (1835-1922 [84]). He described
milky spots in 1874 and stressed their role in the ability of
the omentum to protect against infection.

346
 Experimental proof of the importance of the omentum in intra-
abdominal infection was to come from the work of ROGER
(1860-1946) when he compared the ability of normal rabbits
and guinea pigs to withstand peritonitis induced by the intraperi-
toneal injection of staphylococci with those in which the
omentum had been removed [89].
In 1899 MILIAN (1871-1945) proved experimentally that carmine
and foreign organic material injected into the peritoneal cavity
was taken up by the omentum within half an hour [71]. In
1904 HEGER [46] studied the fate of iron filings introduced into

Fig. 201. Diseases of the

omentum: metastases of a
gastric carcinoma by CRU-
VEILHIER [21]. (Courtesy of
the Medizin-Historische
Bibliothek, Basel)

347
 the peritoneal cavity with X-rays and found that they eventually
became encysted. The functional importance of the omentum
had been elegantly confirmed by DE RENZI (1839-1921) when
he ligated the splenic pedicle in experimental animals and found
that it became enveloped in the omentum and the animals sur-
vived. However, animals in which the omentum had previously
been resected died (see Sect. 5, [86]).

Pathology CRUVEILHIER (1791-1874), one of the outstanding pathologists

of the age, published a detailed atlas of pathology in 1829 which
included tumors (Fig.201), hydatid disease, and tuberculosis
[21]. Both he and other pathologists of the period, including
HENNECKE (1836 [48]), commented on the shrinkage of the
omentum which can occur in tuberculous peritonitis. The large
and fat-laden omentum often found in the obese was thought
to account for some of the functional gastrointestinal problems
resulting from traction of the stomach and spleen because of
the excessive weight of the omentum.
With the introduction of asepsis in surgery by LISTER (1827-1912
[64]) in 1867 and more effective anesthetics, reports of omental
pathology became more frequent. These were reports of torsion
- such as that in 1882 by OBERST (1849-1925). This was thought
to develop gradually and eventually lead to infarction if the
blood supply was obstructed [76].
VIRCHOW'S (1821-1902) observations on tumors [108] were im-
portant in leading to the first classifications of omental neo-
plasms. Between 1889 and 1892 four groups of omental tumors
- the benign lipomas and fibromas, the malignant metastatic
tumors, and the mixed malignant tumors such as liposarcomas
were distinguished, and the very rare primary omental neo-
plasms, for example, endotheliomas, were discussed.

Surgery Surgery for Omental Diseases

Until the introduction of antiseptic techniques in surgery in 1867
by LISTER [64], operations on the abdominal cavity were only
undertaken as last resort. There are good accounts of strangu-
lated hernias in the lectures of DUPUYTREN (1778-1835), which
were published between 1830 and 1834 [25]. When surgery was
undertaken for hernia, the smallest procedure was attempted
with mass ligation, and often the pedicle was left in the neck
of the sac as a tampon and sutured to the walls. Gradually
more individual vessels were ligated, especially after the intro-
duction of the carbolized catgut ligature in 1869 by LISTER [64].
The omentum was usually returned completely to the peritoneal
cavity as recommended by MALGAIGNE (1806-1865), although

348
Fig. 202. Development of
reconstructive surgery
using the omentum. The
idea of using the omentum
for protection originates
from JOBERT DE LAMBALLE,
who described its readiness
to form adhesions with the
injured bowel. Since 1887
free and pedicled omentum
has been used sporadically
in surgery. However, it was
the work of KIRICUTA and
GOLDSMITH, who treated ir-
radiation defects of the
chest wall and abdomen
with the pedicled
omentum, and the develop-
ment of microvascular sur-
gery for its free use at far
distant sites, which paved
the way for the omentum
to become a "material" of
interest in surgery. (TA-
Diagram: LIEBERMANN)

he later had reservations about this technique [66]. The old

practice of cauterization, however, died hard and still appeared
in the manual of surgery published by VELPEAU (1795-1867
[104]) in 1832. Although the death rate from herniotomy and
reduction of the omental contents remained high, being a little
over 22% at the end of the nineteenth century [10], the founda-
tions of modern understanding and techniques had been laid.

10.3 Plastic Surgery

H. WHITE and D. LIEBERMANN-MEFFERT

When surgical techniques become widely established they are

often regarded as a new development. However, their origins
can usually be traced back several decades and this is true of
both free grafts and transposition of the omentum (Fig. 202).
In 1829 JOBERT DE LAMBALLE [22] recorded the value of the
omentum in covering bowel injuries, and by 1888 SENN [95]
had recommended free omental grafts to protect unsafe suture

349
 lines. The value in acute gastroduodenal ulceration [7, 11],
hepatic injury [65], and hydatid disease of the liver [68] was
soon apparent. At about this time omentopexy to the liver was
also undertaken for drainage of ascites [24]. This paved the
way for more extensive use of the omentum in the abdominal
cavity, and reports of its use for repair of the bladder [26, 51]
and vesicovaginal fistula [101, 11 0] were soon published, fol-
lowed more recently by reports of its use in the pelvic floor
[42, 90].
The good vascular supply of the omentum led to its attempted
use for cardiac revascularization [78]. Distant organs, however,
could not be reached satisfactorily, and CANNADAY [13] was
the first to undertake lengthening. This enabled a whole range
of new sites to be encompassed, such as the esophagus [113],
oropharynx [1, 103], and brain [40], and also made possible
the protection of vascular anastomoses [39].
The versatility of the omentum, which could be exteriorized
[13, 60], was well realized and led KIRICUTA [59] to use it for
repairing chest wall defects after extensive surgery for breast
cancer. Some of the more elegant and valuable uses of omentum
in urogenital tract surgery have been developed in recent years
by TURNER-WARWICK et al. [102]. A few areas of endeavor,
such as the treatment of lymphedema [41], have been less suc-
cessful. However, the development of microvascular surgery for
use in facial reconstruction [69] and organ reconstruction [29]
has opened up areas of new promise.

350
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Subject Index
Abdominal Cavity 1,4
-, Drainage 220
-, Exploration 141,219
-, Transposition 23~272
Abdominal Wall, Abscess 294
-, Burn 294
-, Closure 220
-, Defects 294
-, Desmoid Tumors 294
-, Incisions 141,217,218,245
-, Transposition, Herniation
224, 289, 290, 291
-, -, Surgical Technique 294
Abdominoperineal Resection
202, 251, 252, 259
Abnormalities 111-118,237-
240, 264
-, Attachment to Viscera
112-114
-, Congenital 111-118,120
-, Defects 115, 120, 121, 123
-, Malformations 111,112
-, Symptoms 116, 117
-, Treatment 117,118
Absorption 66-90, 189-199
-, Cell Mechanisms 52, 77
-, Edema, Brain 189-199
-, Experiments 67-84, 189-199
-, Fat 29, 188, 299
-, Fluid 74, 80
-, Fluid Exchange 67-89
-, Lymphatic Drainage 66,67,
70-74
-, Lymphedema 281-284
-, Molecular Substances 63, 74
-, Necrotic Tissues 65
-, Particulate Material 67,90
-, Pathways 77
-, Peritoneal Cavity 66, 77,
84--88
Access to Omentum 217-220,
247, 275, 307
Accessory Spleens 170
Actinomycosis 129, 139, 141
Activation, Milky Spot 55, 56
Adhesions 64, 65, 126-128,
215
-, Clinical Picture 127
-, Congenital 126
-, Detachment 118
-, Etiological Factors 64,107,
126, 127, 135
-, Examination 107
-, Fibrinogen Exudation 64, 65,
298-301, 307
-, Hernial Sac 126
-, Inflammatory Response 127,
129
-, Injuries of Omentum 64,
118-120
-, Mechanical Barrier 126, 127,
245
-, Mechanism 64
-, Pathology 64, 65, 127
-, Pelvic Organs 127, 308
-, Posttraumatic 126, 127
-, Splenic Flexure Traction
Syndrome 127
-, Symptoms 128
-, Transposition 215
-, Treatment 128,215
Adhesives 222, 293
Adipose Tissue, see Fat Tissue
Adjuvant Chemotherapy 166,
223
Agenesis 111
Anastomoses, Dye Injection
19~197
-, Esophageal 200, 272-278
-, Intestinal 199, 242, 243
-, Leakage 243, 272
-, Low Rectal 243, 253
- , Microvascular, Transfer 211,
302-306
-, -, Surgical Technique 304
-, of Omental Vessels 31-36
-, Revascularization 188-198
-, at risk, Esophagus 272-274
-, Vascular, Re-implanted
Kidney 248, 249
Anastomotic Hemorrhage 266,
271,316
Anatomy 1-63
--, Cat 8, 9
-, Configuration 1
-, Definitions 1
-, Dog 7,8
-, Guinea Pig 8, 11
-, Historical Aspects 30, 38, 39,
333, 335, 337, 340, 346
-, Laboratory Animals 6-12
-, Macroscopic Appearance 1,
2,6-12,21-27
-, Microcirculatory 67-72
-, Microscopic Picture 1, 2,
14--17
-, Mouse 9, 12
-, Pig 6
-, Rabbit 8, 10
-, Rat 9,12
-, Size 23
-, Stroma 26
-, Tissue Composition 1, 2, 26-
30
Anesthesia 141, 216
Aneurysms 266,269,317
-, Anastomotic 269
-, Aortic 268, 269, 317
-, Mycotic 269
-, Transposition Technique 266,
269
Angiogenic Factor 66
Angiogram Anatomical
Variations 31-35
-, Benign Tumors 162
-, Diseases of Omentum 106,
162, 165
-, Post-Operative, Transposition
298
-,-,Brain 193
-, -, Extremities 193, 297, 298
-, -, Lymphangiogram 282
-, Technique 31, 37, 106
Animals, Anatomy 6-12
-, Experimental 67, 187
-, Omental Size 23
-, Phylogenetic Distribution 5
Anterior Restorative Resection
243, 252, 253
Antibiotics 141,216, 223, 235,
304
Antibody Formation 56, 9~92
Antibody Secreting Cell 56, 91
Anticoagulants, see Heparin
Antigenic Stimulation, Immune
Response 92
Antral Patch Esophagoplasty
200, 272-278
Aortic Prosthesis 268
Aortic Stump 269
357
Aortointestinal Fistula 266, 270,
317
Aplasia, Omentum 111
-, Splenic Ligament 111
Appearance, Macroscopical
1-27
-, Animals 6-12
-, Man 21-27
-, -, Adult 24-27
-, -, Child 20--23
-, -, Fetus 18-20
Appendectomy, Routine 147,
247
Arterial Surgery 265-272,
315-317
-, Indications 266, 269
-, Prophylaxis 266
-, Results 272
-, Septic Complications 267,
270,315
-, Transposition, Technique 266,
315
Arteries of Omentum 2, 30--38
-, Anastomoses 31-36, 47
-, Angiogram 30-35
-, Animals 6-12
-, Arcade Formations 31-36
-, Assessment 30
-, Child 21, 22
-, Distribution 30, 37
-, Epiploic 30--37
-, -, Appendages 36
-, Gastroepiploic 30--37
-, Lengths 31
-, Man, Adult 30--38
-, Marginal Supply 36
-, Variations 30--37
-, Vascular Diameter 31, 37, 69,
75
Arterio-venous Communications
38, 47, 74, 75
Arterioles 69
Ascites, Omentopexy 240,
241
-,Omentitis 129, 130
Attachments 3-6
-, Deficient 112-116
-, Development 13-20
-, Embryological 5, 13-20
-, Graft Ingrowth 188
-, Ligaments 3, 18-20
-, Pathological 3, 112-116
-, -, Ascending Colon 112
-, -, Cecum 118
-, -, Small Bowel 116
-, -, Symptoms 116
-, -, Transverse Colon 112
-, -, Treatment 118
-, Secondary 18, 19
-, Topographical Relations 4, 6
358
-, Transverse Colon 3, 18, 20,
22
-, -, Embryological 5, 18-20
-, -, Fusion Line 5, 220
-, to Viscera 3, 4
Autotransplantation, Kidney
248,249
-, -, Transposition Technique
249
-, Spleen 92-95, 118
Bacteria 55, 74, 90, 129
Bacterial Infection 129
Basal Lamina, see Basement
Membrane
Basement Membrane 42,43, 71,
77, 78, 83, 85
-, Capillaries 69, 77, 83, 85
-, Lymphatics 71
-, Mesothelium 42, 78, 85
Bilharziasis 136, 141, 241
Biliary Duct Atresia 237-240
-, Principles of Lymphdrainage
238
-, Prognosis 239, 240
-, Transposition, Technique 238,
239
Birds 5
Bowel Complications,
Transposition 247
Brain 278-281
-, Blood Flow 280
-, Electrical Activity,
Postoperative 280
-, Lengthening of Pedicle 278
-, Prognosis 279
-, Revasularization 189
-, Routes for Pedicle 278, 279
-, Stroke 278-281
-, Transposition Technique 278,
279
Breast Cancer 284-291, 312,
313,318,319
-, Complications 290, 291
-, Dividing Pedicle 289
-, Functional Sequelae 285-289,
318,319
-, Herniation 290, 291
-, Indications 285-289,318,319
-, Options 284
-, Prognosis 291
-, Routes for Pedicle 285-289,
319
-, Stability 289
-, Transposition, Techniques
285-290,312,313,318,319
Breast Reconstruction 291, 292
- Simple Mastectomy 292
- Subcutaneous Mastectomy
291
-, Transposition Technique
285-292
Bronchopleural Fistula,
Transposition 278
Burn 205-207,294,310,320
-, Heterotransplant 205-207,
310
-, Omental Transfer, Technique
206
Bursa Omentalis, see Omental
Bursa
Capillaries 36, 47, 67-84,
187-189
-, Basement Membrane 77
-, Classification 69-71
-, Degeneration 49, 188
-, Fenestrated 47, 75, 76, 82
-, Fluid Exchange 78-84
-, -, Filtration 80, 83
-, Microvascular Pressure 80--83
-, Milky Spot System 38, 47,
74-78
-, Neovascularization 64-66,
187-198
-, Permeability 79-82
-, Vascular Diameter 31, 37,69
Capillary Barrier 83, 85
-, Flow 75, 80
-, Ingrowth, Graft 64-66,
187-191
-, Pressures 75-79
Capsule Rupture 236, 237
Cardiopexy, Hiatal Hernia 241
-, Omental Cuff 241
Cat 8,9
Cavities, Residual 212, 231-235,
251,315
Cell, Content, Milky Spot 47,
48, 51-55
-, -, Tissue 28, 29
-, Exposure 45
-, Migration 45, 54-56, 74, 131
-, Movement 45, 56, 74
-, Population, Omentitis 130
-, Transformation 49, 53, 56
-, Transport 52
Cells 28, 29, 41-56
-, Endothelial Cell 70, 71, 76-
78,82, 83
-, Eosinophilic Leukocyte 54
-, Fat 28, 29, 55
-, Fibroblast 28, 29,43, 52, 53,
188
-, Leukocyte 55, 300, 301
-, Lymphocyte 28, 29, 45, 46,
50--52, 54, 56, 91, 130
-, Macromolecular Transport
44, 52, 56, 74
-, Macrophage 28,29, 50-54,
56,130,147,300
-, Mast Cell 28, 29, 54
-, Mesenchymal Cell 54
-, Mesothelial Cell 41,42,44,
45,50
-, Plasma Cell 28, 29, 54, 91,
130, 147
-, Reticular Cell 28, 29, 50, 53
Cellular Defence 54, 90, 147
-, Infiltration 130, 131, 298-301
-, Response 55, 56
Cerebral Infarction 278-281
-, Acute Stroke 280
-, Chronic Stroke 279
-, Lengthening of Pedicle 278
-, Postoperative Electric
Activity 280
-, Routes for Pedicle 278, 279
-, Transposition, Surgical
Technique 278, 279
Cestodes 137
Chemotherapy, Adjuvant 141,
166,223
Chest-Wall Defects 284-290,
318, 319
-, Complications 289-291
-, Dividing Omental Pedicle 289
-, Functional Sequelae 291
-, Longterm Results 291
-, Operative Techniques,
Transposition 285-288, 312,
313
-, Routes for Pedicle 221, 285,
286,289,319
-, Stability 289, 299
-, Surgical Options 284, 285
Chondroma 153
Clearance, Creatinine 85
-, Defect 211,221,312
-, Inulin 86
-, Peritoneal 84-86
-, Ultrafiltration 86
-, Urea 84
Cloaca, Transposition 264
Coloptosis 118
Composite Island Flaps, Omental
Gastric 276
-, Omental Myocutaneous 204,
205, 304-306
-, Omental Osteo-Cutaneous
204, 205, 305, 306
Computed Tomography 103,
106,107, 141,224,235
-, Internal Hernias 123
-, Omental Tumors 141, 162,
163,165
-, Presacral Space 254-258
Congenital Malformation
111-118,237-240,253,264
Coverage with Omentum 221,
see also Surgery of Omentum
Cranio-facial Defects 306
-, Gastroomental Flap 306
-, Options 303, 305
-, Recipient Vessels 305
-, Sequelae 306, 304
-, Surgical Principles 305
-, - Techniques 302-305
-, Viability of Bone Grafts 306
Cranium, Transfer 302-306
-, Transposition 278-281
Cystectomy, Transposition 250,
251
-, -, Surgical Technique 250
Cysts 154-156, 163, 164,235
-, Assessment 108, 163, 164
-, Classification 155
-, Definition 154
-, Distribution, Age and Sex
154
-, Echinococcus, see Hydatid
-, Histology 155
-, Hydatid 137,141,142, 164,
231-233, 235, 314
-, Incidence 154
-, Laboratory Finding 161
-, Liver, Transposition 231-233,
314
-, Macroscopic Appearance 155,
156
-, Prognosis 156, 164
-, Symptoms 104, 163
-, Treatment 164
Dead Space 231-236, 250, 258,
259, 314
Debridement 221, 313
Defect, Abdominal Wall 294
-, Contaminated 211
-, Craniofacial 302-306
-, Esophageal 273-278
-, Fistulae 260-265
-, Intestinal 242, 243, 253
-, in Omentum 115, 117-120
-, Pelvic 243, 251-265
-, Peritoneal 200, 250-252, 258,
307
-, Repair 118,221-223,225,
252, 287, 288, 296, 310, 313,
320
-, Skull 303-306
-, Transomental Prolapse 117,
122
-, Ureter 249
-, Urinary Bladder 200, 231
Defence 46-56,90,91, 199,200
-, Cellular 54, 90, 147
-, -, Foreign Body Reaction
90-92
-, Leukocytes 55
-, Macrophages 45-56,90
-, Mechanisms 49, 55, 56,
90-92, 147
-, Milky Spot 48, 55, 56
-, Phagocytosis 55, 56, 90-92
-, Plasma Cells 54, 92
Deposits 167-175
-, Accessory Spleens 170
-, Decidual Nodules 173
-, Endometriosis 170
-, Fat Accumulation 169
-, Pregnancy in Omentum
170-173
-, Splenosis 169, 170
-, Tumor Metastases 159, 160,
167-169
Dertron, old Terminology (T A)
331,334
Desmoid Tumors 294
-, Transposition, Technique 294
Development of Omentum
13-22
-, Attachments 13, 18-22
-, -, Fusion Line 5,220
-, -, Secondary 18, 19
-, -, Transverse Colon 19, 20
-, Dorsal Mesogastrium 14-17
-, Fat 21,22
-, Foramen of Winslow 16
-, Histology 14-17,20
-, Historical Aspects 13, 345
-, Ligaments 13-20
-, -, Gastrocolic 20
-, -, Gastrosplenic (lienal) 16,
17
-, Macroscopic Picture 18-22
-, Malformations 111-115
-, Milky Spots 49, 56
-, Omental Bursa 13, 14, 19
-, Primitive Ligaments 13, 15
-, Recesses 13-22
-, Tissue 14-17,20
Diabetes, Transposition 211
Dialysis 84-89
-, Creatinine Clearance 85
-, Dialysate Flow 85, 86
-, Inulin Clearance 86
-, Omental Complications 88-89
-, Peritoneal Clearance 85, 86
-, -, Transport 84-88
-, Pharmacokinetics 88
-, Ultrafiltration 84-87
- Urea Clearance 84, 85
Diffusion, Basement Membrane,
Barrier 42, 85
-, Interendothelial Pathway 77
Diseases of Omentum 103-109,
111-185
-, Abnormalities 111-118
359
Diseases of Omentum, Adhesions
126---128
-, Angiography 106
-, Classifications 104, 129, 142,
143, 147-149, 155
-, Clinical Definition 103
-, Clinical Signs 103-105, 127,
139-141, 161-163,165, 167
-, Computed Tomography 106,
107, 123, 144, 162, 163, 165
-, Cysts 104,154-156, 163, 164
-, Endoscopy 107-109, 165
-, Fat Necrosis, Pancreatitis 134
-, Hernias 120-126
-, Infarction 142-147
-, Inflammatory Lesions 105,
129-142
-, Injuries 115, 118-120
-, Laboratory Findings 140,
146,161, 163, 165
-, Laparoscopy 107, 119
-, Laparotomy 109,119
-, Mass Lesions 103
-,Omentitis 129-142
-, Parasites 135-139
-, Pregnancy 170-173
-, Radiography 105, 140, 161,
163, 165
-, Solid Tumors 103, 108
-, Symptoms 103, 116, 125, 127,
139, 161-163, 165, 167
-, Torsion 142-147
-, Treatments 117,118,120,
125, 127, 141, 147, 162, 164,
166, 167, 169
-, Tuberculosis 107, 129, 135,
214
-, Tumors 147-169
-, -, Benign 147-154
-, -, Malignant 156---159
-, -, Metastatic 159-161,
167-169
-, Ultrasonography 106, 141,
162, 163, 165
-, Vascular Lesions 104
Dividing Omental Pedicle
227-229, 278, 283, 296, 298,
320
Dog 7,8
Drainage 198, 220, 225
-, Abdominal Cavity 220
-, Ascites 240
- Biliary Duct Atresia 237-240
-, Hydrocephalus 198
-, Lymphatic 38-40, 67, 70,
238
-, Lymphedema 281-284
-, Neumann Cuff 225,242
-, Omentopexy 225, 237-240
-, Peritoneal 40, 84-88
360
-, Pelvic Cavity 265
-, Recepient Site 220, 286, 289,
291,304
-, Subcutaneous Tunnel 220,
286, 289
-, Venous 38
Dressings 205, 223, 287, 313,
314
Echinococcus 137, 141, 142,
164, 230-233, 235
Edema Absorption, Brain
189-193
-, Lymphedema 281-284
-, Spinal Cord 194-197
-, Transposition Technique 195,
196
Elbow Joint 295-297
Embryology 13-20, 345
Encapsulation 65, 244
Endometriosis 170-173
Endoscopy 107-109, 165
Endothelial Cell 71,76---78,
82-85
-, - Electronmicroscopic Image
71, 77
- Channels 70, 71
- Lining 71, 77, 85
- Pores 76, 77
- Sacculations 70, 71
Endothelium, Basement
Membrane 77, 78, 85
-, Fenestrae 77, 82, 85
-, Fluid Exchange 76---78, 85
-, Intercellular Junctions 83
-, Interendothelial Gaps 83, 85
-, Transendothelial Channels 77,
82
Eosinophilic Granulocytes 28,
29, 54, 131
Epiploic Appendage 3-5, 36,
219-220
-, Arteries 30-37
Epiploitis, see Omentitis
Epiploon, Terminology 331
Epithelialization 200
-, Transposition 222,261,313
-, Urinary Bladder 200, 261
Epitheloid Leiomyoma 150
Esophageal Anastomoses 200,
272-278
-, Full Thickness Defects 273
-, Leakage 272
-, Prosthesis 273
-, Strictures 274
Esophagoplasty 200, 272-278
-, Gastric Antral Omental Island
Flap 200, 273-278
-, Indications 274
-, Options 273, 274
-, Prognosis 276, 278
-, Simple Transposition 273-276
Exenterative Surgery,
Transposition 251-258
Experimental Animals 187
Experiments 63-96, 187-207
-, Absorption (Drainage) 52,
66---67,90-92, 189-199
-, -, Brain 189-193
-, -, Edema 67, 189-197
-, -, Effect of Omentectomy 65,
90
-, -, Fluid 66, 67
-, -, Fluid Exchange 67-84
-, -, -, In vivo Examination 67
-, -, -, Technique of
Preparation 67-69, 79-81
-, -, Foreign Body Uptake 66,
67
-, -, Hydrocephalus 189, 199
-, -, Necrotic Tissues 65
-, Angiogenic Property 66
-, Burn 205,310
-, Composite Grafts 200, 204,
205
-, Defence 90
-, -, Foreign Body Response
90-92
-, -, Immunological Concepts
90
-, -, Phagocytosis 90-92
-, Epithelialization 200
-, Graft Incorporation 64-66,
187-189
-, -, Attachment 188
-, -, Fat Absorption 188
-, -, Fibrotic Transformation
188
-, -, Recepient Sites 187
-, -, Recepient Tissues 187
-, -, Size of Graft 189
-, -, Storage 189
-, Hemostatic Effect 65
-, Heterotransplant, 205-207,
310
-, Immunological Concepts
90-92
-, Movement 63, 64
-, Protection of Defects
199-200, 242
-, Reconstruction 200-207
-, -, Composite Graft 204, 205
-, -, Free Graft 187-189, 198,
199, 204-207
-, -, Pedicled Graft 187-204
--, -, Pyloro-Rectal Valve
200-204
-, (Re)vascularization 65, 66,
187-198,244
-, -, Brain 189-193
-, -, Capillary Ingrowth 64-66,
187-191
-, -, Graft Implants 92-96
-, -, Myocardium 197-198
-, -, Spinal Cord 193-197
-, -, Surgical Techniques
189-191, 194
-, -, Ureter 198
Exposed Vessels, Transposition
269, 315
Exteriorised Omentum 220,281,
284-306
-, Histopathology 299-302
-, Skin Grafts 222, 287, 313
Extraskeletal Osteosarcoma 159
Extremities 281-284, 295-298,
320
-, Angiogram 297
-, Clamping of Pedicle 296, 320
-, Dividing Pedicle 296, 299
-, Indications 274, 297
-, Routes for Pedicle 295, 296
-, Surgical Options 295
-, Transposition Technique 283,
296, 298, 320
Exudate Production 64, 65, 78,
299
-, Exteriorized Omentum 224,
299-301
Fat, Absorption 64, 188, 300
-, Cell 28, 29,47,49, 55
-, Collection, Abnormal 131,
133, 169
-, Content, Animals 1, 6--12
-, -, Child 1,21,22
-, -, Man, Adult 1, 24-28
-, -, Newborn 1, 21
-, Necrosis (Pancreatitis) 55,
107, 108, 134
-, -, Incidence 134
-, -, Pathology 108, 134
-, Tissue 1,2,6--12
-, -, Function 49, 55
-, -, Transformation 49, 188,
300
Fibers 26--30
-, Function 71, 72
Fibrin Formation 64, 131, 188
Fibrinogen Exudation 64, 127,
131, 188, 289-301
-, Fibrous Adhesion 127, 188,
298-302
Fibroblasts 28, 29, 43, 47, 52,
53, 130
Fibroma 150
Fibromatosis 150
Fibrosarcoma 156, 157
Fibrotic Transformation 127,
133, 139, 188,299-302,307
Fibrous Histiocytoma 157
Fibrous Tissue Elements 28, 29,
45, 71
Filariae Nematodes 138
Fistulae 244, 259-266
-, Aorto-intestinal 266--270
-, Biliary 233-235
-, Broncho-pleural 278
-, Chronic Renal 245
-, Drainage 265
-, in Female 260-264
-, -, Frequency 259, 260
-, -, Indications 261
-, -, Location 260
-, Intra-abdominal 259
-, in Male 264-265
-, -, Indications 264
-, Principle of Operation 260,
261
-, Recto-prostatic 264, 265
-, Recto-urethral 264, 265
-, Recurrent 261,263,264
-, Surgical Options 260, 261,
264
-, Transposition Techniques
259, 261-266
-, Urethral Strictures 265
-, Vesico-vaginal 260, 261
-, Vesico-vaginorectal 260, 262,
263
-, Ureterovaginal 260
-, Urethrovaginal 260
Fluid, Exchange 66--90
-, Capillary Pressures 75-79
-, Concepts 78-84
-, Dialysis 84-88
-, Hydrostatic Pressures 79-81
-, "in vivo" Microscopy 67,68,
79-89
- Leakage, Edema 196
- Loss, Burn 207
- -, Transposition 215
-, Omentectomy 90
-, Pathophysiology 67-84
-, Pathway 84-89
-, Peritoneal Clearance 84, 85
-, Pores 78, 82
-, Production of Exudate 64, 65,
78
- Replacement 215
-, Technique of Observation
67
-, Technique of Preparation 67
-, Transendothelial Channels 77,
82
- Transport 84, 89
-, - Mechanisms 82-84
Foramen of Winslow 5
-, Development 16
-, Internal Hernias 118, 121
Foreign Body, Response 55, 56,
91,92
-, Adhesion Formation 64
Foreign Material, -i.p.-Injection
56, 66, 67, 90
-, Infection 129
-, Uptake 66, 67, 90
Free Omental Graft 187,
197-200, 306--308
-, Definitions 307
-, Experiments 63-66, 187-189,
200
-, Limitation 308
-, Transfer Techniques 307
Functions (Potentials) 63-96
-, Abdominal Policeman 63, 343
-, Ability to Encapsulate 65
-, Absorption, Peritoneal Cavity
66--89,197, 198
-, Adhesiveness 64
-, Antibody Formation 56,
90-92
-, Capillary Ingrowth 65, 66
-, Chemotaxis 64
-, Defense Mechanisms 56, 63,
90--92
-, Fluid Exchange 67-89
-, Hemostasis 65
-, Historical Aspects 63-67, 90,
333, 336, 339, 343, 346
-, Mechanical Barrier 126, 127
-, Movement 63
-, Neovascularization 64-66
-, Normal Steady State 42,
67-89
-, Pathological Conditions 63,
90-92, 187-189
-, Phagocytosis 63, 90
-, Plasticity 63
-, Protection, Mechanical 63,
343
Fungi 138
Funnel Chest 292, 293
-, Options 293
-, Transposition Technique 293
Gaps, Endothelial 77, 78, 85
-, Mesothelial 44-48, 76, 78, 85
Gastric Carcinoma, Metastasis
160, 168, 169
-, Histology 159
-, Incidence 159, 160
-, Omentectomy 166, 169
Gastric Dysfunction,
Transposition 215, 290
Gastric Omental Island Flap
276
-, Prognosis 276
-, Surgical Technique 276
Gastric Reflux 215
361
Gastrocolic Ligament 3, 4, 20,
112, 113
- Separation 112, 113
Gastroduodenal Perforation
242,243
-, Neumann Cuff 225,242
-, Omentopexy 225, 242, 243
-, -, In Combination with PGV
242
Gastroepiploic Arteries 30-37
Gastroschisis 111, 112, 120, 126
Gastrosplenic Ligament 3, 17
Graft, Capillary Ingrowth
64-66, 188
-, Free Omental 307
-, -, Recepient Sites 187
-, Heterotransplant 205-207
-, Incorporation 187
-, Matrix 92-96
-, Skin 222, 223, 281-287, 313
-, Splenic Autotransplantation
92-95
-, Storage 189
-, Synthetic 291, 292, 294
-, Tumor Implant 96
Guinea Pig 8, 11
Gynecological Surgery 259-266,
306-308
Heart, Ischemic,
Revascularization 197, 198
Hemangioendotheliosarcoma
158
Hemangioma 151
Hemangiopericytoma 151, 158
Hematopoietic Tissue Tumors
154
Hematomas, Infected 270
Hemifacial Atrophy 303-306
-, Transfer Technique 303
Hemostasis 65, 220, 230, 236,
237,272
Hemostatic Factor 65
Heparin 223,229,304
Hernias 120-126
-, Congenital 120, 121
-, External 124-125
-, Incarcerated Omentum 122,
124
-, Internal 121-124
-, -, Diaphragmatic 120-124
-, -, Foramen of Winslow
121-124
-, -, Posttraumatic 122
-, -, Transomental Strangulation
of Bowel 121, 122
-, Symptoms 121, 125
-, Traumatic Prolapse 125, 126
-, Treatment 125-126
362
Herniation, Transposition 224,
289, 290, 291
Heterotransplant 205-207, 310
Histiocytes see Macrophages
Histiocytoma 157
Histopathology, Exteriorised
Omentum 298-301
Historical Review 333-350
-, Anatomy 333, 335, 337, 340,
346
-, Embryology 13, 345
-, Function 333, 336, 339, 343,
346
-, Pathology 343, 348
-, Physiology 346
-, Surgery 333, 336, 339, 345,
348, 349
Howel Jolly Bodies 93, 95
Hydatid Cysts 137, 141, 142,
164, 231-233, 235
Hydrocephalus 198
- Transfer Technique 199
Hypoplasia, Gastrocolic
Ligament 111
-, Omental Apron 111,112
Hysterectomy 251, 261-264
Immune Response 56, 91, 92
-, Antigenic Stimulation 92
-, Concepts 56, 91
-, Foreign Body Reaction 56, 92
-, Milky Spot 55, 56
-, Plasma Cells 54, 91, 130, 147
Immunization, Intraperitoneal
56,90-92
Implant, Pregnancy 170-173
-, Splenic 92-95, 169-170
-, Splenosis 169
-, Tumor Cell Inoculation 96,
159
Infarction, Cerebral 189-198,
278-281
-, -, Transposition Techniques
190-193,281
-, Heart 197, 198
-, -, Surgical Techniques 197
- of Omentum 142-147,214
-, -, Assessment 107, 146
-, -, Incidence 145
-, -, Pathogenesis 145, 146
-, -, Pathomorphology 107, 146
-, -, Primary 145
-, -, Secondary 146
-, -, Symptoms 104, 146
-, -, with Torsion 143
-, - without Torsion 145
-, -, Treatment 147
Infected Bifurcation Prosthesis
268,269
Infected Hematomas 270
Infection, Examination 107
-, Barrier 126, 127,225,235,
242,243
Inflammatory Response,
Adhesions 129, 249, 298-301
- Leukocytes 55,65,299
-, Milky Spot Changes 49, 55
Ingrowth, Capillary 64-66,
187-198
-, of Graft 188
Injuries of Omentum 118-120,
337
-, Closed Blunt 118-119
-, Open, Abdominal 125
-, Symptoms 119
-, Treatment 120
Innervation 41
Interposition of Omentum 250,
260-265
Intestinal Anastomosis 199, 242,
243,274
- Defects, Transposition 242,
243
Intraperitoneal Injection 56, 90
-, Bacteria 90
-, Fluid 90
-, Foreign Material 56, 90
-, in Omentectomized Animals
90
-, Particles 90
-, Technique 56
Irradiation Sequelae 212,
284-292
Island Flaps, Omental, Gastric
200, 276, 306
-, -, Myocutaneous 204, 288,
289, 305, 318
-, -, Osteocutaneous 204, 306
-, -, Skin 204, 303
Kidney, Impending Re-
exploration 245
-, Re-implanted Vascular
Anastomosis 248
-, Staghorn Calculi 245
-, Transposition 245, 247-249
Laboratory Animals 6--12
Laboratory Examination, Benign
Tumors 161
-, Cysts 163
-, Infarction 146
-, Malignant Primary Tumors
165
-, Omentilis 140
-, Splenic Autotransplantation
93-95
-, Torsion 146
Laparoscopy 103,107, 119, 165,
215
-, Benign Tumors 162
Laparotomy 109, 142, 162-166
-, Drainage Abdominal Cavity
220
Laser Excision 221
Leiomyoblastoma 150
Leiomyoma 150
Leiomyosarcoma 158
Lengthening of Omentum
226--229
-, Internal 228, 229, 283
-, Precautions 229
-, Technique 226--229, 245-247
Lesser Omentum 1, 2, 4
- Sac, see Omental Bursa
Leukocytes 55, 65, 130, 134,
298-301
Ligaments 3
-, Aplasia 111
-, Embryological Development
13-18
-, Gastrocolic 3, 4
-, Gastrosplenic 3, 4, 17
-, Phrenocolic 3
-, Primitive 13
Lipoma 150
Liposarcoma 158
Liver Surgery 230-236, 314
-, Abscess 233-235
-, Ascites 240, 241
-, Biliary Duct Atresia 237-240
-, Biliary Fistula 233, 235
- Cyst 231-233, 235, 314
- Echinococcus, 'Dead Space'
232, 233, 235, 314
-, Partial Resection 235-237
-, Tamponade 230-235
-, Transposition Techniques
230-236
- Trauma 230, 231
Location of Defects 212
-, Omentum 1-4
-, -, Normal State 3,6--12,
20-23
- - Pathological Conditions 3,
111-116
Low Rectal Anastomoses 243,
253
-, Transposition Technique 253
Lymphangiogram,
Transposition 282
Lymphangioma 151, 157
Lymphatic
- Anastomoses 282, 284
- Channels 39,40, 70-73
- Microcirculation 70-74
- Microvasculature 69-68
- Peripheral Insufficiency
282-284
- Relief 283
- Sacculatious 41, 70, 71
- Transposition 281
Lymphatics 2,38-41,71-74
-, Absorption Potential 67
-, Assessment 39
-, Basement Membrane 71
-, Construction 40,41, 70, 73
-, Contraction 72-73
- Diameter 40, 70-73
-, Distribution 40, 70
-, Drainage 38-40, 74
-, Fluid Movement 72-74
-, Function 72-74
-, Histology 70, 71, 73
-, Microcirculatory Function 74
-, -, Flow 40, 70-84
-, -, Peristaltic Movement 72
-, -, Pressure 72, 73
-, Migration of Cells 74, 96
-, Milky Spots 2, 39, 41, 47, 71
-, Terminal Structures 39, 40,
41,47, 70-72, 75, 84
-, Uptake of cells 74, 76
-, Valves 39-41,72,73
-, Vasomotion 72, 74, 84
Lymph Drainage 39,40, 72-74,
238
Lymphedema 281-284
Lymphatic Anastomoses 282,
284
-, Pathogenesis 283, 284
-, Prognosis 284
-, Transposition, Technique 281
Lymph Node 2, 40, 46
Lymphocytes 28,29,45-47,
50-52, 54, 56, 74, 91, 130
Lymphoid Cells 91,92
Lymphoreticular Elements
49-52
- Organ 46
Macrophages 28, 29, 43, 45-49,
51-56, 78, 90, 130, 147, 300
-, Electronmicroscopic Image
46,51,53
-, Function 47,49
Malformations 111-118,253
-, Cloaca 264
-, Congenital 111-118,120,121,
253
-, Symptoms 116
-, Transposition Technique 253
-, Treatment 117,118
Mass Lesions 103
Mast Cell 28, 29, 54
Mastectomy, Transposition 291,
292
-, Simple 292
-, Subcutaneous 291
Matrix for Grafts 92-96
-, Pregnancy in Omentum
170-173
-, Skin Graft 221-223, 286--306,
313, 318-320
-, Splenic Implant 92-95, 169,
170
-, Tumor Implant 96, 159, 160,
167-169
Membrane, Basement 42,44,
69, 71, 77, 83, 85
Membranes 1,6--11, 20-22,
26,-28, 41-45
-, Pericolic (Jackson) 112-114
-, Serous 41
Mesenchymal Cell 52, 54, 55
Mesentery 1,4,5,41,112-114
-, Common Ventral Ileocecal
113,114
Mesothelial Cell 41-47, 50, 55
-, Basement Membrane 42-44,
85
-, Electronmicroscopic Image
42, 43-45
-, Fluid Exchange 42,67-78,85
-, Function 47, 78
-, Macromolecular Transport
44, 52, 55, 85
-, Surface Potential 44
Mesothelioma 151
- (Diffuse), Malignant Primary
159
Mesothelium (Lining) 1, 2, 36,
41-51, 56, 78
-, Discontinuity 44-46, 78, 85
-, Function 42
-, Intercellular Gaps 41,44-47,
74, 76--78, 85
-, - Junctions 41-44, 76
-, Milky Spot Area 44
-, Stomata 44-46
-, Tissue Thickness 43, 44
Metastases, Tumor 159-161,
167-169,214
Methods of Reconstruction
Using Omentum 211, 213
Microvascular Anastomosis,
(Omental Transfer) 302-306
-, Composite Grafts 306
-, Cranio-facial Defects 306
-, Definition 211, 213, 302
-, Gastroomental Flap 306
-, Options 303, 305
-, Recepient Vessels 305
-, Sequelae 306
-, Surgical Principles 305
-, - Technique 302-305
Microvascular Circulation
67-84
-, Anatomy 69-71,73
-, Arrangement 69-72,74-78
363
Microvascular Circulation
Arterial 69
- -, Lymphatic 70-74
- -, Venous 69, 70
-, Blood Flow 68, 80, 84
-, Capillary Pressures 72, 75, 80
-, -, Filtration 80
-, Endothelial Wall 71, 85
-, Experimental Model 67, 68,
78-83
-, Function 69, 72-74
-, "intra vital" Microscopy 67,
68, 78-83
-, Production of Exudate 78
-, Vessels, Classification 69, 70,
72
-, -, Diameter 31, 37, 69, 70, 75,
80
Migration, Cell 45, 55, 72, 74,
96
-, Omentum 63
-, Parasites, Toxocariasis 138
-, Substances 56
-, Tumor Cells 96, 159, 168
Milky Spot 1, 2, 26, 36, 44-56,
74-78
-, Activation 55, 56
-, Active Secondary 49, 55
-, Antibody Formation 56,90-
92
-, Arterio-venous Anastomoses
38, 47, 74, 75
-, - Communication (Shunt) 74
-, Basement Membrane 44, 74,
77
-, Blood Flow 74-76, 80
-, Calcification 49
-, Capillary Arrangement 47,
74,75
-, -, Diameter 75,80
-, -, Fluid Exchange 67, 74-78
-, -, Pressures 75
-, Cell Composition 36, 45-55,
147
-, -, Electronmicroscopy 45-47,
50,51
-, Characteristics 46, 48
-, Classification 46
-, Comparative Anatomy 74
-, Constituents 41,47,49,69,
70,74-78
-, Crypt (Gap) 46,47
-, Defence Mechanism 46,49,
55, 56, 90-92, 147
-, Definition, Functional 48
-, -, Morphological 48
-, Endothelium, Basement
Membrane 77, 85
-, Fenestrated Capillaries 36, 47,
75, 76, 77, 82
364
-, Fibrosis 49
-, Function 48
-, Identification 48
-, Immune Response 56,91,92
-, Immunization 56, 91
-, Inactive 49, 55, 76
-, Incidence 48
-, Involution 49
- Life Cycle, Irritation 49
-, Location 2, 26, 48
- Lymph Node, Difference 39,
46
-, Lymphoreticular Organ 46
-, Macrophages 46,47,49,
51-56, 78
-, Macroscopic Appearance 10,
26, 46
-, Mesothelial Gaps 39, 44-47,
76
-, - Lining 46
-, Microscopic Image 46, 47, 50,
51
-, Microvascular Arrangement
47, 69, 74-78
-, Normal Steady State 50, 51
-, Number 48
-, -, of Vessels 75
-, Primary 49
-, Size 48, 96
-, Stimulation 49, 51, 52, 56,96
-, Surface Topography 49, 53,
55
-, Transformation 49, 56
-, Vascular System 36, 38, 39,
47,68-74
Mobilization, Fat 55
-, Elbow Joint 295
-, Omental Pedicle 201,219,
220, 226, 229, 245-248, 250,
311,312
-, Patient, Transposition 223,
298
Monocyte 28, 29
Mouse 9, 12
Movement, Cells 47, 55, 56, 74
-, Intestines, Adhesions 64
-, Intravascular Velocity 74, 80
-, Omentum 63, 64
Myocardium, Revascularization
197, 198
Myocutaneous Island Flap 285,
288, 292, 303, 318
Myxoma 150
Neck, Transposition 284
Necrosis, Omental Tissue 127,
226,229,291,293,299-301,
307
-, Fat 134
Nematodes 137
Neoformation of Organs 303,
305
Neovascularization 63, 188, 189,
195, 196
Netz, Terminology 333
Neumann Cuff 225, 242
Neurinoma 153
Neurofibroma 153
Nodular Panniculitis 131, 133
Omental Apron 3-5
- Bursa 3-6, 13-16,219
-, Composite Island Flaps 204,
205, 276, 304-306
- Deficiencies 111-114, 214
- Epithelialization 200
- Exteriorization 284-306
- Gastric Island Flap 276
-, Free Graft 306-308
-, Lengthening 226-229, 283
-, Mobilization 219, 226-229,
246, 311, 312
-, Potentials, see Functions
-, Prolapse 125
-, -, Iatrogenic Internal 125
-, -, Open Posttraumatic 125
-, Recesses 4, 5, 19, 20
-, Transfer 302-308
-, Transposition 224-298
-, Volume 23, 24, 227
Omentectomy 162, 166,219,220
-, Cysts 164
-, Experiments 65, 90
-, Extended 166
-, Metastases 167, 169
-,Omentitis 141
-, Palliative 166
-, Peritoneal Absorption 65, 90
-, Tumors 162, 166-169
- Risks 164
Omentitis 129-142,214
-, Assessment 105, 107, 108,
140, 141
-, Classification 129
-, Definition 129
-, Etiology 129
-, Examination 107, 108, 140
-, Fat Necrosis 134
-, Frequency 129
-, Histology 130-134
-, Idiopathic 130
-, Macroscopical Picture 107,
130, 131
-, Nodular Mesothelial
Hyperplasia 131
-, Parasitic Diseases 135, 141
-, Peritoneal Ultrafiltration 88
-, Postoperative 130
-, Symptoms 108, 139
-, Treatment 141
-, -, Conservative 141
-, -, Operative 141, 164
-, -, Prognosis 142
-, Tuberculosis 135, 141, 214
Omentocardiopexy
(Myocardium) 197
Omentocystoplasty 251
Omentopexy 211, 224, 225
-, Ascites 240, 241
-, Contraindication 211
-, Definition 224
-, Drainage 225
-, Indications 211,224,225,
237, 240-243
-, Portal Hypertension 240, 241
-, Surgical Technique 225
Omentoportoduodenopexy 237
Omentum, Definitions 1, 2
-, Greater, Anatomy 1-56
-, Lesser 1,2,4, 14
-, Location 3
-, Phylogenetic Distribution 5
-, Size' 23
-, Terminology, Historical
Aspects 331-333
-, Tissue Constituents 1, 2,
26-30
Oral Cavity 303, 305
Organ Preserving Surgery 236,
237
Oropharyngostoma,
Transposition 293, 294
Osteomyelitis 205
Osteosarcoma, Extraskeletal 159
Ovarian Carcinoma, Omental
Metastasis 159,161, 167, 168
-, Omentectomy 166-168
-, Prognosis 168
-, Symptoms 167
Pancreatitis, Fat Necrosis 107,
108, 134
Panniculitis, Nodular 131
Parasitic Diseases 129, 135-142
-, Assessment 140, 141
-, Cestodes 137
-, Filariae Nematodes 138
-, Fungi and Actinomycetes 139
-, Nematodes 137-138
-, Pentasomids 139
-, Prognosis 142
-, Protozoa 139
-, Symptoms 139
-, Treatment 141, 142
-, Trematodes 136, 137
Pathology 111-175
-, Historical Aspects 343, 348
Pelvic Surgery 243-244, 251-265
-, Adhesions 129
-, Anterior Restorative 252, 253
-, Computed Tomography 252,
254-258
-, Dead Space 258
-, Exenteration 258, 259
-, Floor 251-259
-, Hysterectomy 251,260, 262,
264
-, Low Rectal Anastomosis 243,
253
-, Malformations 253
-, Omental Apron Sling 259
-, Options 250, 251
-, Peritoneum, Replacement
251,252,307
-, Routes for Omental Pedicle
245-247, 253
-, Transposition Technique
251-259
Perforation, Gastroduodenal,
Transposition 242
Peritoneal Absorption 66, 67
- Clearance 86
- Defect 200
- Fluid Exchange 40,67-88
- Replacement 251, 252, 258,
307
Phagocytosis 47,49, 54-56, 63,
78, 90, 91, 135
Pharyngostoma, Transposition
293,294
Pig 6, 205-207, 310
Plasma Cell 28, 29, 47, 50-54,
56, 91, 92, 130, 147
-, Mechanism of Antibody
Secretion 56
-, Transformation 49
Plasticity 63
Pores, see Gaps
Portal Hypertension 240, 241
-, Histological Changes 173, 174
-, Omentopexy 240,241
-, Prognosis 241
Positioning of Patient 216
Postoperative Care 223, 312
Potentials, see Functions
Postsplenectomy Immune
Deficiency 92
-, Autotransplantation of
Spleen 92-96
-, Laboratory Findings 93, 95,
96
-, Indications 92
-, Overwhelming Sepsis (OPSI)
92
-, Surgical Technique 93, 94
Precautions with Omentum,
Intraoperative 88,89,141,
220, 222, 226, 227, 245, 246,
250,276,313
-, Postoperative 223-224
-, Preoperative 216
Pregnancy in Omentum 170-173
-, Primary Omental 170, 171
-, Secondary Omental 171-173
-, Symptoms 172
-, Treatment 171, 172
Preoperative Care 216
Principles of Reconstruction
Using Omentum 211
Prosthesis, Aortic (Bifurcation)
Transposition 268, 273
-, Esophageal, Transposition
273
-, Exposed Vessels in Groin Area
Transposition 269, 315
-, Synthetic Prosthesis
Replacement 273, 283
Protection 199, 200, 242
-, Experiments 199, 200
-, Immune Response 91, 92
-, Mechanical 126,127
Protective Surgery Using
Omentum 311-320
-, Anastomoses, Esophageal
272-278
-, -, Intestinal 199, 200, 242,
243
-, -, Kidney Re-implanted 248,
249
-, -, Rectal 252, 253
-, -, Vascular 265-272
-, Fistulae 259-266
-, Mechanical 126
-, Organ Preserving Surgery 236
-, Perforation, Gastro-duodenal
242
-, Prosthesis, Esophageal 211,
269
-, -, Vascular 265-269, 282, 283
-, Wounds, Contaminated 211,
269
Pyelogram, Transposition,
Postoperative 247
Pyeloplasty, Transposition 245
Pyloro-Rectal Valve 200-204
-, Surgical Technique 201, 202,
204
Rabbit 8, 10
Radiography 103, 105, 106, 140,
244
-, Benign Tumors 161
-, Cysts 163
-, Malignant Tumors 165
-, Technique 105, 106
Radiotherapy 166, 168, 223
Radiotrophic Tissue,
Transposition 212
Ranvier, L (Milky Spots) 38,
39, 46, 47, 346
365
Rat 9, 12
Recesses of Omental Bursa 5,
20
-, Definition 5
-, Development 13-22
Reconstructive Surgery 187,
200,205,211-320
-, Abdominoperineal Resection
251, 252, 259
-, Breast Cancer 284-291, 312,
313,318,319
-, Cranium 278-281, 302-306
-, Dead Space 231-233, 258,
259,314
-, Esophagoplasty 200, 272-278
-, Exenterative Surgery 243-245,
251-259
-, Experiments 187-207
-, Fistulae 259-266
-, Funnel Chest 292
-, General Aspects 211-224
-, Indications 211, 212
-, Hysterectomy 261-264
-, Irradiation Ulcer 212
-, Island Flaps, Omental
Composite 204, 276, 277, 306
-, Location of Defect 212
-, Mastectomy 291
-, Methods 211
-, Pyloro-Rectal Valve 200-204
-, Pelvic Floor 251,252
-, Surgical Principles 211
-, Tumor Surgery 212
-, Urinary Tract 245-251
Recurrence, Extended Local
Tumor 212, 221
Recurrent Retroperitoneal
Ureteric Obstruction 249
Reflections, Peritoneal 4
Renal Pelvis, Transposition 245,
247
Repair of Defect 221-223, 306,
313
-, Adhesives 222,293
-, Clearance 221, 312
-, Coverage 221, 313
-, - with Omentum 221-222,
225
-, - with Skin Graft 222, 223
-, -, with Synthetic Material
291, 292, 294
-, Dead space 232-235, 258,
314
-, Debridement 221, 313
-, -, Laser 221
-, Drainage 286, 289
-, Principles 221, 313
-, Revascularization of Tissues
189
-, Shrinkage 222, 293
366
-, Skin Grafts 118, 220, 225,
229,252
-, Stabilization 222, 289, 292
-, Tamponade 231, 235, 314
Replacement, Dead Space 212,
231-235, 251, 252, 258
-, Pelvic Peritoneum 252, 307
Residual Cavities 212, 231, 251,
252
Revascularization 187-198, 244
-, Brain 189-193,279,280
-, Cerebral Infarction (Stroke)
192, 279, 280
-, Histological Examination 191,
192, 195-197
-, Ischemic Heart 197
-, - Free Omental Graft 198
-, - Pedicled Omentum 197
-, Spinal Cord 194-197
-, Surgical Techniques 189-191,
194
-, Ureter 198
Rete, Terminology (TA) 333
Reticular Cell 28, 29, 50, 53
-, Transformation 53
Retroperitoneal Fibrosis 244
Rhabdomyosarcoma 158
Rotation Arcades 285
Routes for Omental Pedicle 226,
245-247, 285-289, 312
-, Brain 189, 190, 278, 279
-, Chest-Wall 221,285-290, 312
-, Extremities 281, 283, 295-298
-, Kidney 247-249
-, Sacral Cavity 253, 262-264
-, -, Retrocolic Route 246, 247
-, -, Transabdominal Route
245, 246
-, Subcutaneous Tunnel 189,
190,220,221,283,286,289,
312
-, Throat 293
Sacral Cavity 251-265
-, Routes for Omental Pedicle
246, 247, 253, 262-264
-, Transposition Techniques
246, 253, 262-264
Scalp, Defects 303, 305
-, Indications 305
-, Transfer 303, 305
Scar Formation 187, 188, 298-
301, 307
Second Stage Skin Grafting 222,
287,313
Sensory Reception 41, 224, 303
Shape, Omental Variations 23,
24
Shrinkage 64, 65, 222
Size, Defect 215, 222, 223
-, Man 20-23, 84, 112
-, -, Preoperative Assessment 223
-, Milky Spots 48, 75
-, Omental Graft 188, 189, 307
-, Omentum, Laboratory
Animals 5, 23
-, Shrinkage 64, 65, 222, 291,
307
Skin Graft 118,220,221,223,
225, 229, 252, 281, 290, 313
-, Full-thickness 223
-, Grafting Technique 222, 281
-, Mesh Graft 223
-, Second Stage Skin Grafting
222, 287, 313
-, Shrinkage 222, 291
'-'-, Split Skin 223, 281
-, Sutures 223,287, 313
-, Timing 222, 306
Skull, Defects 303-305
Sonography 106, 141, 161, 163,
165, 235
Spinal Cord 189, 194-197
-, Revascularization 196
-, Transposition Technique 194,
195
Splenic Autotransplantation
92-95
-, Complications 95
-, Computed Tomography 95
- Flexure Traction Syndrome
127
-, Implant, Immune Response
93
-, Operative Techniques 93, 94
-, Preparation of Implant 93
-, Prognosis 95
Splenosis 92, 169, 170
Stabilizing Material 222, 289,
291, 292, 306
Staghorn Calculi 245, 247
Stimulation, Antigenic 56, 92
-, Immune Response 55, 56, 91
-, Plasma Cells 56
Stomata, Mesothelial Lining 45
Strictures, Esophageal 274
-, Ureteral 249
- Urethral 265
Stroke 189-198, 278-281
-, Acute 281
-, Chronic 279
-, Prognosis 189-191,279
-, Transposition Technique
189-191,279, 280
Stroma 26
Structural Peculiarities,
Childhood 20
Surface Epithelialization 222,
313
Surgery, Historical Review 333,
336, 339, 345, 348, 349
-, Omental Diseases 141, 142,
147,162,164,166-169,171,
172
Surgery Using Omentum 211-
320
-, Access to Omentum 217,218,
247, 275, 307
-, Adhesives 222, 293
-, Adjuvant Chemotherapy 223
-, Advantages 214
-, Aims 214
-, Antibiotics 216, 223, 304
-, Assessment 214,215
-, Benefit 213, 233
-, Complications 224,289-291,
293
-, Contraindications 214, 232
-, Debridement 221
-, Detachment from Transverse
Colon 219, 220, 224, 227, 246,
247, '311,312
-, Disadvantages 224, 303
-, Disinfection 216
-, Dissection Line 220
-, Drainage Abdominal Cavity
220
-, -, Recepient Sites 220, 286
-, Dressings 223, 287, 313
-, Epithelialization 200, 222, 313
-, Experiments 187-206
-, Fibroblastic Transformation
188, 299-302, 307
-, Functional Sequelae 215, 223,
224
-, Hemostasis 220
-, Heparin 223, 229
-, Indications 211-214,225,226
-, Life Expectancy 213, 214
-, Limitation 308
-, Methods of Reconstruction
211, 305
-, Mobilization of Patient 223,
250
-, Neoformation of Organs 303,
305
-, Omentectomy 166,219,220
-, Omentopexy 211, 240, 224,
225
-, Positioning of Patient 216,
247, 261, 265
-, Postoperative Care 223
-, Precautions with Omentum
220, 222, 226, 227, 245, 246,
276,313
-, Preoperative Care 216
-, Preparation 214,215
-, Principles 224
-, Radiotherapy 223
-, Repair of Defect 210,
221-224
-, Risk 213
-, Sensation of Omental Tissue
224, 303
-, Separation from Stomach 227
-, Stabilizing Material 222, 289-
293, 306
-, Surgical Instruments 216
-, Timing of Operation 216
-, Tissue Reactions 188,
298-301, 307
-, - Shrinkage 188,291,293,
307
-, Transfer 302-308
-, Transposition 224-298
Taches Laiteuses see Milky Spots
Tamponade with Omentum
231-235
Teratoma 154
Terminology, Historical Aspects
331-333
Thalassemia 173, 175
Throat, Transposition 293
Thrombosis of Omentum 229,
291,304
Tissue, Acceptance 188
-, Composition, Milky Spot 41,
47
-, -, Omentum 1,2,24-29,
41-55
-, Connective 28,29,41,71
-, Constituents 28, 29
- Deposits 169-173
-, Development 13-22
-, Excision 211,221
-, Fibers 26-28
-, Fibrous 28, 188
-, Framework 26-28
-, Granulation 130, 135, 146,
298-302
-, Irradiation Damage 212, 244
-, Reaction after Transfer/
Transposition 188, 298-301,
307
-, Recepient for Graft 187
-, Shrinkage 291,293, 307
-, Texture 28
Tomography see Computed
Tomography
Topographical Relations 3-12
-, Animals 5-12
-, Attachments 3, 4, 6
-, Man 3
-, Phylogenetic Distribution 5
-, Similarities between Man and
Animals 6
Torsion of Omentum 142-144
-, Assessment 104
-, Classification 142-144
-, Epidemiology 111, 142, 143
-, Incidence 143, 145
-, Pathogenesis 142, 143
-, Pathomorphology 146
-, Primary 143
-, Recurrent Splenic 118
-, Secondary 143
-, Symptoms 104,116,142,146
-, Treatment 118, 146
Transfer 302-308, see also
Surgery Using Omentum
-, Definition 211, 213, 302, 307
-, Experiments 187,188,198,199
-, Limitation 308
-, Necrosis 187-189,307
-, Omental Mobilization 219,
220, 226-228
-, Precautions 226
-, Using Microvascular
Anastomosis 302-306
- -, Composite Grafts 204, 303,
306
-, -, Cooling of Omental Graft
304
-, -, Heparin 304
-, -, Indications 302, 303, 305
-, -, Options 303, 305
-, -, Recepient Vessels 303-305
-, -, Sequelae 306
-, - Surgical Techniques 304,
305, 306
-, Vascular Ingrowth 187, 188
-, Viability of Graft 304, 306
-, Without Microvascular
Anastomosis 306-308
-, -, Contraindications 307
-, -, Heterotransplant 205-207,
310
- -, Indication 306, 307
-, -, Operative Technique 307
-, -, Recepient Sites 187, 212
Transformation, Cell 55, 56
-, Fibrotic 188,291,298-301,
307
-, Milky Spot 49, 55, 56
-, Omental Tissue 49, 188
Transomental Strangulation
121, 122
Transport, Cellular 52, 74
-, Fluid 44, 52, 74, 77-89
-, Macromolecular Substances
44, 52, 56, 74, 82-84
-, Particles 44, 52, 55, 56, 74
Transposition 224-298, 312,
313, see also Surgery Using
Omentum
-, Access to Omentum,
Abdominal Incisions 217,
218,246-248, 225
367
Transposition Assessment
214--216
-, Brain 189-193,278-281
-, Chest Wall 284--293, 312, 313
-, Combined with Myocutaneous
Island Flap 288, 318
-, Complications 224, 229,
289-291
-, -, Abdominal Wall
Herniation 224, 289-291
-, -, Gastric Dysfunction 229,
290
-, -, Necrosis 127,229,291,307
-, Definition 211,213
-, Detachment from Transverse
Colon 219,220,224,227,246,
247, 311, 312
-, Dividing Pedicle 201, 225,
228, 229, 278, 283, 289, 296,
298, 320
-, Dressings 223, 287, 313
-, Experiments 187-200
-, Exploration 219
-, Exteriorized 211, 281,
284--299
-, Extraabdominal 211, 272-306
-, Functional Sequelae 224, 247
-, General Aspects 211
-, Guidelines 226
-, Histopathology, Exteriorised
Omentum 299-301
-, Intra-abdominal 230--272
-, Intrathoracic 272-284
-, Limitations 308
-, Longterm Changes of
Omentum 291
-, Longterm Results 198, 224
-, Omental Mobilization 219,
220, 226-229, 240, 245-247,
278, 311
-, - Lengthening Extensive 229
-, -, Internal 226-229, 278, 283,
296, 320
-, Pelvic Surgery 251-265
-, Precautions with Omentum
88, 89, 141, 220, 222, 226, 227,
245, 246, 276
-, Radiotherapy 223
-, Repair of Defect 221,223,313
-, Routes for Pedicle 226,
245-247, 253, 278, 279, 285,
289, 293
-, Separation from Stomach
227-229
-, Sequelae 223
-, Skin Graft, Timing 222
-, Stabilizing Material 222, 289
-, Subcutaneous Tunnel 194,
217,220,221,279,289,290,
293
368
-, Supplementary Procedures
223
-, Tissue, Reactions 188,
298-301
-, Urogenital Tract
Reconstruction 243-251
-, Vascular Surgery 250
Trophic Ulcers 250
Tuberculosis 108, 129, 135, 214,
249
-, Adhesions 135
-, Incidence 135
Tuftsin Values 93, 95
Tumor-like Changes 169-175
-, Abnormal Fat 169
-, Accessory Spleens 170
-, Decidual Nodules 173
-, Endometriosis 173
-, Pregnancy 170--173
-,Splenosis 169,170
TumorDeposits 159,167-173
-, Assessment 165
-, Classification 167
-, Definition 159
-, Gastric Carcinoma 160, 168,
169
-, Macroscopic Picture 159, 160
-, Metastases 159, 160, 167-169,
214
-, Ovarian Carcinoma 167, 168
-, -, Omentectomy 167-169
Tumors 147-173
-, Benign 147-154,161-163,
169-173
-, -, Assessment 103, 108
-, -, Chondroma 153
-, -, Classification 148, 149
-, -, Definition 147
-, -, Distribution, Age, Sex 150
-, -, Epitheloid Leiomyoma 150
-, -, Fibroma 150
-, -, Fibromatosis 150
-, -, Hemangioma 151, 152
-, -, Hemangiopericytoma 151,
152
-, -, Hematopoietic Tissue 154
-, -, Histology 149
-, -, Incidence 147-149
-, -, Laboratory Findings 161
-, -, Leiomyoma 150, 151
-, -, Lipoma 150
-, -, Lymphangioma 151, 157
-, -, Macroscopic Picture 149,
151
-, -, Mesothelioma 151
-, -, Myxoma 150
-, -, Neurofibroma 153
-, -, Neurinoma 153
-, -, Omentectomy 162
-, -, Prognosis 163, 149
-, -, Recurrence 149
-, -, Symptoms 103, 104, 147,
161
-, -, Teratoma 154
-, -, Transposition 212
-, -, Treatment 162, 163
-, Malignant Primary 156-159,
165-167
-, -, Assessment 108, 156
-, -, Classification 148
-, -, Definition 156
-, -, Extraskeletal Osteosarcoma
159
-, -, Fibrosarcoma 156, 157
-, -, Fibrous Histiocytoma 157
-, -, Hemangioendotheliosarcoma
158
-, -, Hemangiopericytoma 158
-, -, Incidence 156
-, -, Laboratory Finding 165
-, -, Leiomyosarcoma 158
-, -, Liposarcoma 158
-, -, (diffuse) Mesothelioma 159
-, -, Omentectomy 166
-, -, Prognosis 167
-, -, Rhabdomyosarcoma 158
-, -, Symptoms 165
-, -, Transposition,
Contraindication 214
-, -, Treatment 165
- -, Solid 103
-, -, Soft Tissue 147-149
Ulcer, Irradiation Sequelae 212
-, Perforation Gastro-duodenal
242
-, Trophic 250
Ultrafiltration 85-88
Ultrasonography 106, 107
U rea Clearance 84--88
Ureter Defect 249
-, Stenosis 249
-, Stricture 249
-, Transposition 245, 247, 249
U reteroileocutaneostomy,
Transposition 250
Urethral Strictures 265
Urinary Bladder 200, 243, 251
Urinary Tract Reconstruction,
see Urogenital Organs
Urogenital Fistula 259-265
Urogenital Organs,
Transposition 243-245
-, Assessment 245
-, Cystectomy 250
-, Fistula Chronic Renal 245
-, -, Pelvic Viscera 244, 259
-, Heminephrectomy 245
-, Impending Re-exploration
245
~,Indication 244, 245, 247, 250
~, Postoperative Pyelogram 247
~, Principles of Operation 245
~,Pyeloplasty 245
~, Recurrent Retroperitoneal
Ureteric Obstruction 249
~ Recurrent Stone Formation
245
~, Re-implanted Kidney 248
~, Renal Pelvis 247
~, Retroperitoneal Fibrosis 244,
249
~, Routes for Omental Pedicle
225, 245-247
~, Routine Appendectomy 247
~ Solitary Kidney 245
~, Staghorn Calculi 245
~, Surgical Techniques 247, 248,
250
~, Transplant Related Problems
245,248
~, Ureteral Strictures 249
Vascular Architecture 30~39
Vascular Surgery 265~272
~, Anastomotic Hemorrhage
271, 272
~, Aneurysms, Transposition
266,269
~, Aortic Stump 269
~, Aorto-intestinal Fistula 270,
271
~, Exposed Inquinal Vessels 266,
267,269,283,315
~,Hints 271
~,Indications 265~267
~, Infected Hematoma 270
~ Insufficiency, Peripheral,
Transposition 266,281, 282
~,Prognosis 272
~, Prophylaxis, Infection 266
~, Prosthesis, Aortic (Bifurcation)
Transposition 268, 270
~, Septic Complications 267,
268
~, Transposition 269, 315
~, Transposition Technique
266-269, 315
Vascularization see also
Revascularization 64, 65,
187~198
~, Capillary Ingrowth 65, 66,
187, 188, 191
~, Experiments 187
~, of Graft 187, 198
~, of Omental Pedicle 211, 229
Vasodilatating Drugs 229
Veins 38, 39, 69, 70
Vessels 1, 2, 28-40, 67~84
~,Animals 6-12
~, Assessment 30, 38
~, Arterial Anastomoses 31~36,
47
~,~, Diameter 37, 75
~, ~, Distribution 30-35
~, Arterio-venous Anastomoses
38, 47, 75, 76
~, ~ Shunts 74
~, Bleeding 227
~, Capillaries 67~84
~, Classification 69
~, Lymphatics 39, 71~74
~, Microvascular Arrangement
36, 69~72, 74, 75, 80
~, Milky Spot System 36, 47,
68~70, 74, 76
~, Venous Drainage 38
Viability of Graft, Bone 205,
306
~,Omentum 188, 304
~, Organs 65, 244
~, Skin 222, 287, 313
Wound Excision 211, 221
~, Repair see Repair of Defect
Yersinia Enterocolica 129
Zirbus, Terminology (T A) 332
369
 H. D. Becker, W. F. Caspary
Postgastrectomy and Postvagatomy Syndromes
1980. 84 figures (mainly in 2 colors), 55 tables. XII, 188 pages.
ISBN 3-540-09445-8

1. L. Chassin
Operative Strategy in General Surgery
An Expositive Atlas
Illustrated by C. Henselmann
1980. 528 figures, 10 tables. XXIII, 558 pages. ISBN 3-540-90452-2

Colorectal Cancer
Editor: W. Duncan
1982.50 figures, 51 tables. Approx. 195 pages. (Recent Results in Cancer
Research, Volume 83). ISBN 3-540-11395-9

H. M. Delany, R Jason
Abdominal Trauma
Surgical and Radiologic Diagnosis
With contributions by N. Carnevale, W. Delph, C. M. Moss, A. Rudavsky
1981. 259 figures. XVI, 224 pages. ISBN 3-540-90502-2

Endoscopy and Biopsy in Gastroenterology

Techniques and Indications
Editors: P. Friihmorgen, M. Classen. Translated from the German by
H. V. Ammon, K H. Soergel. With contributions by numerous experts.
With a Foreword by L. Demling
1980. 108 figures, 24 tables. X, 198 pages. ISBN 3-540-09645-0

Gastric Cancer
Editors: C. Herfarth, P. Schlag
1979. 161 figures, 144 tables. XV, 374 pages. ISBN 3-540-09467-9

G.P.Marzoli, S.Vesentini
Warren's Operation
With the cooperation of F. Frasson, G. Fugazzola, G. Mangiante, R Maso
1981. 46 figures. XII, 77 pages. ISBN 3-540-10785-1

P. Otto, K Ewe
Atlas of Rectoscopy and Colonoscopy
Translated from the 2nd German edition by B. Clowdus
1979. 124 four-color figures in 21 plates and 31 figures within the text,1 table..
X, 110 pages. ISBN 3-540-09296-X

1.Papillon
Rectal and Anal Cancers
Conservative Treatment by Irradation - an Alternative to Radical Surgery
ISBN 3-540-11626-5
In preparation
Springer-Verlag
Berlin V. I. Sreenivas
Acute Disorders of the Abdomen
Heidelberg Diagnosis and Treatment
With a Foreword by C. E. Welch
New York 1980. 33 figures. XIx, 200 pages. ISBN 3-540-90483-2
Comprehensive E. W.Humphrey, D. L. McKeown
Manual of Pulmonary Surgery
Manuals of Surgical 1982. 215 figures (190 in full color). Approx. 250 pages. ISBN 3-540-90735-7

Specialties Manual of Ambulatory Surgery

Editors: K 1. Kassity, 1. E. McKittrick. Illustrated by 1. Koelling
Edited by Richard H. Egdahl 1982. 230 figures (190 in full color). XVIII, 266 pages. ISBN 3-540-90700-9

Manual of Liver Surgery

byW.P.Longmire, Jr., RK Tompkins. Illustrated by T.B1oodhart
1981. 230 figures (142 in full color). XVII, 267 pages. ISBN 3-540-90212-0

B. 1. Harlan, A. Starr, F. M. Harwin

Manual of Cardiac Surgery
Volume 1
1980. 193 figures (183 in full color), 8 tables. XV, 204 pages.
ISBN 3-540-903934
Volume II
1981. 130 figures in full color. XV, 143 pages. ISBN 3-540-905634

E. 1. Wylie, R 1. Stoney, w. K Ehrenfeld

Manual of Vascular Surgery
Volume 1
1980.557 figures( 471 in fulll color). XII, 264 pages. ISBN 3-540-90408-5

C. E. Welch, L. W. Ottinger, 1. P. We1ch

Manual of Lower Gastrointestinal Surgery
1980. 215 figures (138 in color), 7 tables. XVI, 276 pages. ISBN 3-540-90205-8

A. T. K Cockett, K Koshiba
Manual of Urologic Surgery
Illustrated by I. Takamoto
1979. 532 color illustrations. XVIII, 284 pages. ISBN 3-540-90423-9

B. 1. Masterson
Manual of Gynecologic Surgery
With contributions by K E. Krantz, W. 1. Cameron, 1. W. Daly, 1. A. Fayez,
E. W. Franklin. Illustrator: D. McKeown
1979. 204 figures (192 in color), 12 tables. XV, 256 pages. ISBN 3-540-90372-0

R E. Hermann
Manual of Surgery of the Gallbladder,
Bile Ducts, and Exocrine Pancreas
With contributions by A. M. Cooperman, C. B. Esselstyn Jr., E. Steiger,
R T. Holzbach
1979. 197 color figures (123 figures in black and white), 16 tables.
XIV, 306 pages. ISBN 3-540-90351-8

W. S. McDougal, C. L. Slade, B. A. Pruitt, Jr.

Manual of Burns
Medical Illustrators: M. Williams, C. H. Boyter, D. P. Russel
Springer-Verlag 1978. 214 color figures, 4 tables. X, 165 pages. ISBN 3-540-903194

Berlin A. 1. Edis, L. A. Ayala, R H. Egdahl

Heidelberg Manual of Endocrine Surgery
1975. 266 figures, mostly in color. 242 color plates. XIII, 274 pages.
New York ISBN 3-540-07064-8