Management of Morbid Obesity - 1st Edition
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Preface
The field of bariatric surgery has grown exponentially since 1998. Today there are
more procedures performed for morbid obesity than for gastroesophageal reflux dis-
ease. To meet the public demand for bariatric surgery, more surgeons are taking
steps to incorporate bariatric surgery into their surgical practice. Some surgeons
have decided to solely dedicate their practice to bariatric surgery while others are
performing bariatric surgery as part of their general surgical practice. The American
Society for Bariatric Surgery has documented that the number of surgeons perform-
ing bariatric surgery has more than quadrupled between 1998 and 2003.
The growth in bariatric surgery in the United States has not come without
criticism by the public and third-party payors. One of these concerns relates to the
variability in bariatric surgery outcomes and that the surgery is sometimes being per-
formed by inexperienced surgeons at facilities that are not equipped to care for the
morbidly obese. This textbook was written with a focus on the comprehensive
management of the morbidly obese patient and includes presentations on the preo-
perative work-up by a multidisciplinary team, essentials of a bariatric program, and
perioperative care of the morbidly obese. Several chapters discuss technical details
and outcomes of four commonly performed bariatric procedures including vertical
banded gastroplasty, laparoscopic adjustable gastric banding, Roux-en-Y gastric
bypass and the duodenal switch. Detailed management of perioperative and late
complications are discussed. In addition, postoperative nutritional management is
emphasized.
In a time when bariatric surgery is coming under scrutiny, this book can be
used as a concise reference guide for surgeons and those interested in the care of
the morbidly obese. We hope you will enjoy your learning experience, and this book
will help in the ongoing efforts to improve the quality of surgical care for these
challenging patients.
Harvey J. Sugerman, MD, FACS
Ninh T. Nguyen, MD, FACS
iii
Contents
Preface . . . . iii
Contributors . . . . xi
1. Obesity: Pathogenetic Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . 1
John G. Kral
Introduction . . . . 1
Detection and Evaluation of Food . . . . 2
Processing of Nutrients . . . . 2
Nutrient Sensing . . . . 3
Hunger and Motivation . . . . 4
Surgical Treatment of Overeating . . . . 5
Conclusion . . . . 7
References . . . . 7
2. Epidemiology and Comorbidities of Morbid Obesity ............ 9
Crystal T. Schlösser and Sayeed Ikramuddin
Epidemiology . . . . 9
Social Consequences of Obesity . . . . 11
Comorbid Conditions . . . . 11
Neoplasia . . . . 12
Cardiovascular . . . . 12
Pulmonary . . . . 14
Endocrine . . . . 15
Gastrointestinal . . . . 16
Genitourinary . . . . 17
Musculoskeletal . . . . 18
Hematologic . . . . 19
Renal . . . . 20
Neurologic . . . . 20
Infectious/Immunologic . . . . 21
Dermatologic . . . . 21
Psychiatric . . . . 22
Social/Economic . . . . 22
v
vi Contents
Summary . . . . 23
References . . . . 23
3. Treating the Morbidly Obese Patient: A Lifestyle Approach
to a Chronic Condition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Jennifer E. Taylor, Sara A. Pyle, Walker S. Carlos Poston, and
John P. Foreyt
Introduction . . . . 33
Lifestyle Modification . . . . 34
Dietary Changes . . . . 37
Physical Activity . . . . 39
Combining Behavior Modification and Pharmacotherapy . . . . 40
Surgery . . . . 42
Summary and Conclusions . . . . 43
References . . . . 43
4. Preoperative Evaluation and Intraoperative Care of the Obese . . . . 49
Rodrigo Gonzalez, Scott F. Gallagher, Lisa Saff Koche, and
Michel M. Murr
Introduction . . . . 49
Preoperative Evaluation . . . . 49
Revisional Bariatric Surgery . . . . 55
Intraoperative Care . . . . 56
Conclusion . . . . 57
References . . . . 58
5. Essentials of a Bariatric Surgery Program . . . . . . . . . . . . . . . . . . 61
Samer G. Mattar and Tomasz Rogula
Introduction . . . . 61
Overview of Etiology and Epidemiology of Morbid
Obesity . . . . 61
Criteria for Selection of Patients for Bariatric Surgery . . . . 62
Components of a Bariatric Surgery Program . . . . 63
Hospital Requirements . . . . 71
Bariatric Surgery Database . . . . 72
Bariatric Surgery Program Web Site . . . . 72
Conclusion . . . . 73
References . . . . 73
6. Nutrition and Roux-en-Y Gastric Bypass Surgery . . . . . . . . . . . . . 75
Jeanne Blankenship and Bruce Wolfe
Introduction . . . . 75
Pre-Surgical Nutrition Assessment and Management . . . . 75
Pre-Surgical Nutrition Education . . . . 78
Postoperative Diet Guidelines . . . . 79
Nutrient Absorption and Deficiency . . . . 80
Contents vii
Malabsorptive Procedures . . . . 80
Roux-en-Y (RYGB) . . . . 81
Post-surgical Nutrition Assessment . . . . 84
Nutrition and Surgical Complications . . . . 85
Conclusion . . . . 86
References . . . . 86
7. Laparoscopic Vertical Banded Gastroplasty . . . . . . . . . . . . . . . . . 91
J. K. Champion and Michael Williams
Introduction . . . . 91
Methods . . . . 93
Results . . . . 97
Discussion . . . . 98
References . . . . 100
8. Physiology of Laparoscopy in the Morbidly Obese . . . . . . . . . . . 101
David Magner and Ninh T. Nguyen
Effects of Carbon Dioxide Absorption During
Pneumoperitoneum . . . . 102
Effects of Increased Intra-Abdominal Pressure During
Pneumoperitoneum . . . . 102
Conclusions . . . . 105
References . . . . 105
9. The Pathophysiology of Severe Obesity and the Effects of Surgically
Induced Weight Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
Harvey J. Sugerman
Introduction . . . . 109
Central (Android) vs. Peripheral (Gynoid) Fat
Distribution . . . . 113
Hypertension . . . . 114
Cardiac Dysfunction and Dyslipidemia . . . . 114
Pulmonary Dysfunction . . . . 115
Diabetes . . . . 116
Venous Stasis Disease . . . . 117
Degenerative Joint Disease . . . . 118
Gastroesophageal Reflux and Asthma . . . . 118
Urinary Incontinence . . . . 118
Female Sexual Hormone Dysfunction . . . . 119
Pseudotumor Cerebri . . . . 119
Malignancy Risk with Obesity . . . . 120
Hernia Risk with Obesity . . . . 120
Infectious Problems Associated with Morbid Obesity . . . . 120
NALD/NASH . . . . 121
Quality of Life . . . . 121
Mortality . . . . 121
viii Contents
Conclusions . . . . 122
References . . . . 122
10. Techniques of Laparoscopic Gastric Bypass . . . . . . . . . . . . . . . . 129
Benjamin E. Schneider, Ninh T. Nguyen, and Daniel B. Jones
Introduction . . . . 129
Materials and Methods: Laparoscopic Gastric Bypass
Technique . . . . 129
Discussion . . . . 136
References . . . . 136
11. Outcome of Laparoscopic Gastric Bypass . . . . . . . . . . . . . . . . . . 139
Corrigan L. McBride, Harvey J. Sugerman, and Eric J. DeMaria
Introduction . . . . 139
Literature Review—Case Series . . . . 139
Literature Review—Prospective, Randomized Clinical
Trials . . . . 143
Discussion . . . . 145
References . . . . 150
12. Changing Intestinal Absorption for Treating Obesity . . . . . . . . . . 153
Picard Marceau, Simon Biron, Frédéric Simon Hould, Stéfane Lebel, and
Simon Marceau
Introduction . . . . 153
Development of Bariatric Surgery . . . . 154
Biliopancreatic Diversion . . . . 156
Beneficial Effects of Biliopancreatic Diversion . . . . 158
Detrimental Effect of Biliopancreatic Diversion . . . . 162
Conclusion . . . . 164
References . . . . 164
13. Laparoscopic Adjustable Silicone Gastric Banding . . . . . . . . . . . . 167
Jeff W. Allen and Christine J. Ren
Introduction . . . . 167
Patient Selection . . . . 168
Operative Technique . . . . 169
Postoperative Management . . . . 170
Complications . . . . 173
Results . . . . 176
Conclusions . . . . 178
References . . . . 178
14. Outcomes of Laparoscopic Adjustable Gastric Banding . . . . . . . . 181
Paul E. O’Brienz
Introduction . . . . 181
Laparoscopic Adjustable Gastric Banding . . . . 183
Contents ix
Discussion . . . . 188
Conclusions . . . . 189
References . . . . 189
15. Part II of Debate: Laparoscopic Roux-en-Y Gastric Bypass . . . . . 191
Eric J. DeMaria
Introduction . . . . 191
Roux-en-Y Gastric Bypass . . . . 191
Laparoscopic Adjustable Gastric Banding (LAGB) . . . . 194
Conclusion . . . . 203
References . . . . 203
16. Complications of Laparoscopic Bariatric Surgery . . . . . . . . . . . . 207
Daniel M. Herron
Introduction . . . . 207
Leaks . . . . 208
Intestinal Obstruction from Internal Hernia . . . . 209
Bleeding . . . . 210
Stricture Formation . . . . 211
Pulmonary Embolism . . . . 212
Cholelithiasis . . . . 212
Marginal Ulcer . . . . 213
Incisional Hernia . . . . 214
Pressure-Related Complications: Rhabdomyolysis and Compartment
Syndrome . . . . 214
Laparoscopic vs. Open Bariatric Surgery . . . . 214
Conclusion . . . . 215
References . . . . 216
17. Postoperative Follow-Up and Nutritional Management . . . . . . . . . 219
Scott A. Shikora and Margaret M. Furtado
Introduction . . . . 219
Commonly Performed Bariatric Procedures . . . . 219
The Significance of Long-Term Follow-Up . . . . 220
Nutritional Deficiencies . . . . 221
Protein-Calorie Malnutrition . . . . 221
Dehydration . . . . 222
Nausea and Vomiting . . . . 223
Vitamin Deficiencies . . . . 223
Gastrointestinal Issues . . . . 226
Conclusions . . . . 229
References . . . . 230
Index . . . . 233
Contributors
Jeff W. Allen Department of Surgery and the Center for Advanced Surgical
Technologies, University of Louisville School of Medicine, Louisville, Kentucky,
U.S.A.
Simon Biron Department of Surgery, Laval Hospital, Laval University, Quebec,
Canada
Jeanne Blankenship Department of Surgery, University of California Davis School
of Medicine, Sacramento, California, U.S.A.
J. K. Champion Mercer University School of Medicine and Emory-Dunwoody
Medical Center, Atlanta, Georgia, U.S.A.
Eric J. DeMaria Department of Surgery, Duke University, Durham, North
Carolina, U.S.A.
John P. Foreyt Baylor College of Medicine, Houston, Texas, U.S.A.
Margaret M. Furtado Obesity Consult Center, Center for Minimally Invasive
Obesity Surgery, Tufts-New England Medical Center, Boston, Massachusetts,
U.S.A.
Scott F. Gallagher Interdisciplinary Obesity Treatment Group, Department of
Surgery, University of South Florida Health Sciences Center, Tampa, Florida,
U.S.A.
Rodrigo Gonzalez Interdisciplinary Obesity Treatment Group, Department of
Surgery, University of South Florida Health Sciences Center, Tampa, Florida,
U.S.A.
Daniel M. Herron Section of Bariatric Surgery, Department of Surgery, Mount
Sinai School of Medicine, New York, New York, U.S.A.
Frédéric Simon Hould Department of Surgery, Laval Hospital, Laval University,
Quebec, Canada
xi
xii Contributors
Sayeed Ikramuddin Center for Minimally Invasive Surgery, Department of
Surgery, University of Minnesota, Minneapolis, Minnesota, U.S.A.
Daniel B. Jones Harvard Medical School, Beth Israel Deaconess Medical Center,
Boston, Massachusetts, U.S.A.
Lisa Saff Koche Interdisciplinary Obesity Treatment Group, Department of
Surgery, University of South Florida Health Sciences Center, Tampa, Florida,
U.S.A.
John G. Kral Department of Surgery, SUNY Downstate Medical Center,
Brooklyn, New York, U.S.A.
Stéfane Lebel Department of Surgery, Laval Hospital, Laval University, Quebec,
Canada
David Magner Department of Surgery, University of California Irvine Medical
Center, Orange, California, U.S.A.
Picard Marceau Department of Surgery, Laval Hospital, Laval University,
Quebec, Canada
Simon Marceau Department of Surgery, Laval Hospital, Laval University, Quebec,
Canada
Samer G. Mattar Department of Surgery, University of Pittsburgh Medical Center,
Pittsburgh, Pennsylvania, U.S.A.
Corrigan L. McBride Department of Surgery, University of Nebraska Medical
Center, Omaha, Nebraska, U.S.A.
Michel M. Murr Interdisciplinary Obesity Treatment Group, Department of
Surgery, University of South Florida Health Sciences Center, Tampa, Florida,
U.S.A.
Ninh T. Nguyen Department of Surgery, University of California Irvine Medical
Center, Orange, California, U.S.A.
Paul E. O’Brien The Centre for Obesity Research and Education (CORE),
Monash University, Melbourne, Victoria, Australia
Walker S. Carlos Poston University of Missouri-Kansas City and Mid America
Heart Institute, Kansas City, Missouri, U.S.A.
Sara A. Pyle University of Missouri-Kansas City and Mid America Heart
Institute, Kansas City, Missouri, U.S.A.
Christine J. Ren New York University School of Medicine, New York, New York,
U.S.A.
Contributors xiii
Tomasz Rogula Department of Surgery, University of Pittsburgh Medical Center,
Pittsburgh, Pennsylvania, U.S.A.
Crystal T. Schlösser Center for Minimally Invasive Surgery, Department of
Surgery, University of Minnesota, Minneapolis, Minnesota, U.S.A.
Benjamin E. Schneider Harvard Medical School, Beth Israel Deaconess Medical
Center, Boston, Massachusetts, U.S.A.
Scott A. Shikora Obesity Consult Center, Center for Minimally Invasive Obesity
Surgery, Tufts-New England Medical Center, Boston, Massachusetts, U.S.A.
Harvey J. Sugerman Department of Surgery, Virginia Commonwealth University,
Richmond, Virginia, U.S.A.
Jennifer E. Taylor University of Missouri-Kansas City and Mid America Heart
Institute, Kansas City, Missouri, U.S.A.
Michael Williams Emory-Dunwoody Medical Center, Atlanta, Georgia, U.S.A.
Bruce Wolfe Department of Surgery, University of California Davis School of
Medicine, Sacramento, California, U.S.A.
1
Obesity: Pathogenetic Mechanisms
John G. Kral
Department of Surgery, SUNY Downstate Medical Center, Brooklyn, New York, U.S.A.
INTRODUCTION
The critical requirement for species’ survival is securing nutrients. Surviving
organisms either have primarily had characteristics enabling them to withstand all
ambient environmental threats to their existence (‘‘stressors’’) or have evolved
through adaptability. Foremost among species in the latter group is Homo sapiens.
Evolutionary pressure had quantitatively and qualitatively stimulated the develop-
ment of mechanisms to detect, evaluate, ingest, digest, assimilate, store, and release
nutrients to sustain life when humans appeared some 4 million years ago. It is only
during the last 150 years that the efficiency of these mechanisms has become mal-
adaptive, driving a life-threatening, civilization-related, global epidemic of a syndrome
of metabolic obesity.
With this ‘‘ergocentric’’ (as in energy) view, it is reasonable to postulate that
threats to nutrition, and thus to the integrity of an organism, are the ultimate stres-
sors stimulating adaptation. The surgical treatment of obesity, as do all treatments of
the disease, seeks to override the many protective mechanisms that have evolved
through natural selection.
Tragically, in these affluent times, and largely ignored, social mechanisms have
similarly evolved to ‘‘protect’’ the non-obese against the relative voracity of obese
people, whose appetites threatened the previously limited food supplies of the group;
bias, harassment, and frank ostracism of the obese became instinctive. With abun-
dance of food, these ‘‘protective’’ mechanisms have remained and become social
stressors for the obese. Perpetuation of these biases underlies the denial of obesity
as a disease, limiting resources to treat or prevent it, thus maintaining a vicious cycle
contributing to the disease.
The purpose of this chapter is to review publications relevant to ingestive beha-
vior, the largest contributor to obesity, and thus the most logical target of surgical
treatment. It is true that energy expenditure also contributes to the nutritional state
and can be enhanced by some forms of surgery, but its contribution to energy
balance is far smaller than caloric intake, except in the presence of complications
or maladaptive behavior.
1
2 Kral
DETECTION AND EVALUATION OF FOOD
Plants and the most primitive unicellular organisms, with few exceptions, rely on
chance encounters with nutrients in proximity to their stomata, although chemotactic
mechanisms are involved in the tropism of plants and the protrusion of pseudopodia
from amoebae. Plants are equipped with stomata and guard cells that regulate water
flux and carbon gain (1), and have been demonstrated to rely on intracellular
calcium-release channels for physiological processes (2). Similar channels are present
in animals’ enterocytes. In the brain, information processing, requiring increased
blood flow for providing substrate, uses neurons that raise intracellular Ca2þ ions
(3), demonstrating the fundamental role of calcium as a signal of the nutritive state
of cells.
Early in phylogeny, the stoma was equipped with special cells for sensing nutri-
ents. The brain has evolved from a collection of sensitive nerve cells surrounding the
stoma (mouth) or the entry to the digestive system (4), enabling the identification,
selection, and ingestion of nutrients and fluid. The anterior lobe of the pituitary is
derived from pouching of the oral ectoderm, and is the source of the most important
appetitive peptides. The primary function of the brain is to secure nutrition for the
survival of the individual; the secondary function is to ensure reproduction for the
survival of the species. Interestingly, there is evidence for reciprocity and cooperation
between sexual behavior and ingestive behavior (5), and the related neural pathways
associated with reward peptides colocalize in the brain.
The five classical senses vision, smell, touch, taste, and hearing contribute to the
detection and evaluation of nutrients (solid or liquid) and water. It is teleologically
attractive to hypothesize that the reliance of all senses on dopaminergic pathways
mediating reward [e.g., (6)], implies a commonality of purpose, namely reinforcing
nutritionally positive or rewarding stimuli. Only recently has it been determined that
the process of estimating or evaluating rewards depends on dopamine neurons (7).
The evaluation of nutrients also requires the recognition of toxicity. The most
important ‘‘tool’’ for this function is the tongue with its sense of taste. Recent
research has identified the receptors necessary for detecting bitter taste, the most
important characteristic of dangerous and inappropriate food (8).
PROCESSING OF NUTRIENTS
After detection and evaluation, followed by the ‘‘decision’’ (whether cognitive or
reflexive) to reject or ingest a substance, processing begins. The expansion of the
ectodermal stoma made possible by multicellularity, gave rise to the endodermal
gut for food absorption via specialized cells (9). A different early function of the gut
has been largely ignored, namely storage of excess nutrients. Interestingly, several spe-
cies of snakes still exhibit an extraordinary storage capacity in the wall of the gut (10).
The mesoderm did not arise from the endoderm until after about 40 million years.
Early in gut development, however, the pancreas, enhancing absorption, and the
liver, synthesizing structural, transport, and functional proteins, developed from
the foregut. A poorly recognized fact is that the liver took over the lipid-storing capa-
city of the gut and likely pre-dates the mesodermal formation of adipose tissue. Con-
sequently it should not be surprising that the liver responds to diverse stressors by
fatty metamorphosis (steatosis). Furthermore, lipodystrophy, adipose tissue knock-
out models, and lipectomy all lead to fatty infiltration of the liver.
Obesity: Pathogenetic Mechanisms 3
NUTRIENT SENSING
The most important aspect of energy balance and the central ‘‘problem’’ of obesity is
determining the signal(s) driving ingestive behavior. Obviously the preceding elements
of consummatory behavior do not require ‘‘consciousness’’ at any level; primitive
organisms do not exhibit chronic overnutrition, as in obesity. Before addressing the
topic of ‘‘hunger,’’ operationally defined here as the cognitive correlate of undernutri-
tion, it is important to consider the most basic signals of nutritive state. In this context,
‘‘set-point’’ theory has been a valuable construct.
Set-point theory evolved from the concept of sensors of body stores of macro-
nutrients: lipostatic, glucostatic, or aminostatic or –privic signals regulating ingestive
behavior. According to set-point theory there is a fixed level of body weight or some
component of body composition toward which the organism will strive after devia-
tions incurred by starvation or over-consumption (11). Since all three classes of
macronutrients can function as signals, it is more logical to speak of a system based
on energy: an ergostatic or nutristatic theory. In analogy with the carotid artery
glomus cell, which is exquisitely sensitive to fluctuations in oxygen tension in the
blood (12), considerable interest has been directed toward identifying nutritive sen-
sors or ‘‘nutristats.’’ Incidentally, the glomus cell itself responds to hypoxia by influx
of calcium and release of dopamine, as described earlier for the regulation of sub-
strate flux in plants and animals. Rather than engaging in the debate over whether
glucostatic or lipostatic mechanisms take precedence, it is more enlightening to
survey the most recent findings on nutrient signaling.
In a putative ranking of organs according to critical function, the brain comes
to mind first, followed by the heart and the lungs, although it is questionable whether
any ranking serves a practical purpose. Most ‘‘rankings’’ of nutrients begin with
carbohydrate, owing to its role as the preferred substrate for the brain, and indeed,
the tightly regulated blood glucose level is a key component in survival. Just recently
the molecular mechanisms of glucose homeostasis were discovered, not surprisingly,
in the liver (13). Thus, a ‘‘glucostat’’ has been detected.
Since most organs are made up of protein, the analyte best representing lean
body mass, its importance is generally recognized, as evidenced in the interest in
‘‘protein-sparing’’ diets. The indispensable or ‘‘essential’’ amino acids are logical
candidate signals serving a hypothetical ‘‘aminostat.’’ Indeed, most species sense a
diet deficient in indispensable amino acids within minutes (14). A basic mechanism
functioning as an aminostat has also been discovered recently (15).
The last macronutrient, lipid, has as its basic and circulating components, fatty
acids, some of which are essential. In the context of energy balance, especially its dys-
regulation in obesity, there has been a long-standing interest in ‘‘lipostatic’’ mecha-
nisms. Lipid sensors were first discovered in a different context, however. Lipids are
integral components of pathogenic microorganisms and have been identified as sig-
nals inducing septic shock. The toll-like receptor 2 (TLR2) is required for detecting
various pathogens unrelated to any nutrient-sensing function. This aspect does not
seem to have been investigated, although it is intriguing to speculate that TLR2
mediation of prostaglandin E2 release (16), with attendant vasodilation, might have
a nutritive function.
Owing to the close relationships between lipids and glucose regulation, it is
difficult to separate a specific lipostatic mechanism responsible for energy homeosta-
sis. Nevertheless, long-chain fatty acids have been postulated to have an etiologic
role in obesity and type 2 diabetes mellitus (T2DM), and they are metabolized in
