Ninh T. Nguyen
Stacy A. Brethauer
John M. Morton
Jaime Ponce
Raul J. Rosenthal
Editors
The ASMBS Textbook
of Bariatric Surgery
Second Edition
123
The ASMBS Textbook of Bariatric Surgery
Ninh T. Nguyen • Stacy A. Brethauer
John M. Morton • Jaime Ponce
Raul J. Rosenthal
Editors
The ASMBS Textbook
of Bariatric Surgery
Second Edition
Editors
Ninh T. Nguyen
Department of Surgery, Division of
Gastrointestinal Surgery
University of California, Irvine Medical Center
Orange, CA
USA
John M. Morton
Bariatric and Minimally Invasive
Surgery Division
Yale School of Medicine
New Haven, CT
USA
Stacy A. Brethauer
Department of Surgery
The Ohio State University
Columbus, OH
USA
Jaime Ponce
Bariatric Surgery, Metabolic and Bariatric Care
CHI Memorial Hospital
Chattanooga, TN
USA
Raul J. Rosenthal
Department of General Surgery, The Bariatric
and Metabolic Institute
Cleveland Clinic Florida
Weston, FL
USA
ISBN 978-3-030-27020-9 ISBN 978-3-030-27021-6
https://doi.org/10.1007/978-3-030-27021-6
(eBook)
© Springer Nature Switzerland AG 2020
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is
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Preface
The American Society for Metabolic and Bariatric Surgery (ASMBS) is comprised of a
dynamic group of surgeons, physicians, and integrated health members, all of whom are constantly challenged to improve the care of patients with obesity. As acknowledged in a landmark
2013 decision by the American Medical Association, clinically severe obesity is a disease
process that is associated with multiple life-threatening conditions that may lead to premature
death. As repeatedly and consistently demonstrated by literature evidence, metabolic and bariatric surgery has shown to be the only long-lasting effective treatment for obesity and its
related comorbidities.
The field of bariatric surgery has changed tremendously over that past three decades since
the ASMBS’s founding in 1983. Application of minimally invasive surgery had revolutionized
the way we perform modern-day bariatric surgery. Once a large midline incision has changed
to multiple small surgical incisions with enhanced recovery, shortened length of hospitalization, and reduced morbidity and mortality. In the late 1990s, less than 12,000 bariatric operations were performed yearly in the United States, with high rates of morbidity and mortality.
This number of operations has increased exponentially over the subsequent years, and currently more than 225,000 operations are being performed annually. The initial growth directly
correlates with the development and transition from the open to minimally invasive bariatric
surgery, and by 2005, the number of laparoscopic Roux-en-Y gastric bypass cases performed
in the United States surpassed that of the open Roux-en-Y gastric bypass. Since 2010, the laparoscopic sleeve gastrectomy has proven to be a safe and effective bariatric operation and is now
the most commonly performed bariatric operation in the Unites States and worldwide.
Along with advancement in surgical technique, the quality of bariatric surgery had also
improved with implementation of accredited centers designated by the ASMBS and the
American College of Surgeons. This dynamic field of bariatric surgery will continue to grow
with enhanced understanding of the mechanisms of action of our bariatric operations and
offering of other minimally invasive approaches including endoscopic bariatric procedures. As
the needs of the society and its members evolve, the ASMBS continues its commitment to
serve the educational needs of our members. Our annual meeting is the primary venue to disseminate new information and educational materials to clinical professionals. To enhance and
augment these educational offerings, we published the comprehensive ASMBS textbook of
bariatric surgery, first edition in 2014. The development of this book reflects the commitment
of the ASMBS leadership’s goal of providing the most up-to-date education for our members.
Designed to be the most inclusive textbook on the topic of bariatric surgery and integrated
health services, the textbook is comprised of two volumes. The first volume is devoted to the
science and practices of bariatric surgery, while the second volume focuses on the medical,
psychological, and nutritional management of the bariatric patients. Since 2014, the practice
of bariatric surgery has continued to change at a rapid pace, and we are excited to provide you
with the second edition of the textbook on the science and practices of bariatric surgery and
obesity management. This second edition has expanded from 5 to 8 sections to include new
sections on quality in bariatric surgery, endoscopic bariatric surgery, and management of bariatric complications with expansion from 43 to 56 chapters.
v
vi
Preface
Similar to the first edition, each chapter in this book was written by a world-renowned
expert in the field. A comprehensive textbook that adheres to the highest standards is a major
undertaking, and we, the editors, are grateful and indebted to every author who has devoted
time and effort to research the most important evidence-based information and report it in a
concise and easy-to-read chapter. We believe that this second edition of the ASMBS Textbook
of Bariatric Surgery will continue to be the leading source of scientific information for surgeons, physicians, residents, students, and integrated health members today and for years to
come. We hope you enjoy the textbook and would love to hear your comments.
Orange, CA, USA
Columbus, OH, USA
New Haven, CT, USA
Chattanooga, TN, USA
Weston, FL, USA
Falls Church, VA, USA
Philadelphia, PA, USA
Danville, PA, USA
Ninh T. Nguyen, MD
Stacy A. Brethauer, MD
John M. Morton, MD, MPH
Jaime Ponce, MD
Raul J. Rosenthal, MD
Jeanne Blankenship, RD
David Sarwer, PhD
Christopher Still, MD
Contents
Part I Basic Considerations
1Epidemiology and Discrimination in Obesity���������������������������������������������������������� 3
R. Armour Forse, Monica M. Betancourt-Garcia, and Michelle Cordoba Kissee
Introduction����������������������������������������������������������������������������������������������������������������� 3
Definition of Obesity��������������������������������������������������������������������������������������������������� 3
Epidemiology of Obesity ������������������������������������������������������������������������������������������� 5
Racial, Ethnic, and Income Disparities����������������������������������������������������������������������� 8
Trends in Obesity ������������������������������������������������������������������������������������������������������� 9
Discrimination in Obesity������������������������������������������������������������������������������������������� 10
Conclusion ����������������������������������������������������������������������������������������������������������������� 13
Question Section��������������������������������������������������������������������������������������������������������� 13
References������������������������������������������������������������������������������������������������������������������� 13
2The Pathophysiology of Obesity and Obesity-Related Disease������������������������������� 15
Robert W. O’Rourke
Introduction����������������������������������������������������������������������������������������������������������������� 16
Pathophysiology of Obesity ��������������������������������������������������������������������������������������� 17
Pathophysiology of Obesity-Related Disease������������������������������������������������������������� 25
Conclusion ����������������������������������������������������������������������������������������������������������������� 33
Question Section��������������������������������������������������������������������������������������������������������� 33
References������������������������������������������������������������������������������������������������������������������� 34
3History of the Development of Metabolic/Bariatric Surgery��������������������������������� 37
Elias Chousleb, Jaime A. Rodriguez, and J. Patrick O’Leary
History of Bariatric Surgery��������������������������������������������������������������������������������������� 37
Metabolic ������������������������������������������������������������������������������������������������������������������� 42
Minimally Invasive Techniques ��������������������������������������������������������������������������������� 43
Hormonal Weight Loss����������������������������������������������������������������������������������������������� 44
Accreditation��������������������������������������������������������������������������������������������������������������� 45
Conclusion ����������������������������������������������������������������������������������������������������������������� 45
References������������������������������������������������������������������������������������������������������������������� 45
4The History of the American Society for Metabolic and Bariatric Surgery��������� 47
Robin P. Blackstone
Introduction����������������������������������������������������������������������������������������������������������������� 47
The Era of Inquiry 1967–1988����������������������������������������������������������������������������������� 47
The Era of Rapid Growth 1989–2004������������������������������������������������������������������������� 50
Integrated Health��������������������������������������������������������������������������������������������������������� 51
Growth of the Society������������������������������������������������������������������������������������������������� 52
Medical Liability��������������������������������������������������������������������������������������������������������� 53
The Era of Quality and Engagement from 2004 to Present ��������������������������������������� 53
International Affiliations��������������������������������������������������������������������������������������������� 58
vii
viii
Contents
The ASMBS Foundation��������������������������������������������������������������������������������������������� 58
Obesity Week ������������������������������������������������������������������������������������������������������������� 58
Conclusion ����������������������������������������������������������������������������������������������������������������� 59
References������������������������������������������������������������������������������������������������������������������� 59
5Physiological Mechanisms of Bariatric Procedures������������������������������������������������� 61
David Romero Funes, Emanuele Lo Menzo, Samuel Szomstein,
and Raul J. Rosenthal
Introduction����������������������������������������������������������������������������������������������������������������� 61
Mechanism of Action������������������������������������������������������������������������������������������������� 62
Malabsorption������������������������������������������������������������������������������������������������������������� 62
Caloric Restriction ����������������������������������������������������������������������������������������������������� 62
Energy Expenditure���������������������������������������������������������������������������������������������������� 63
Changes in Eating Behavior��������������������������������������������������������������������������������������� 63
Entero-Hormones, Incretins, and Intestinal Adaptation��������������������������������������������� 63
Mechanisms of Diabetes Resolution��������������������������������������������������������������������������� 67
Neuroendocrine Mechanism��������������������������������������������������������������������������������������� 67
Vagus Nerve ��������������������������������������������������������������������������������������������������������������� 67
Bile Acids (BA)����������������������������������������������������������������������������������������������������������� 68
Gastrointestinal Microflora����������������������������������������������������������������������������������������� 68
Adipose Tissue ����������������������������������������������������������������������������������������������������������� 69
Leptin ������������������������������������������������������������������������������������������������������������������������� 69
Adiponectin����������������������������������������������������������������������������������������������������������������� 70
β(Beta)-Cell Changes������������������������������������������������������������������������������������������������� 70
End-Organ Changes ��������������������������������������������������������������������������������������������������� 70
Gastrointestinal-Renal Axis ��������������������������������������������������������������������������������������� 71
Bariatric Surgery and the Control of Blood Pressure Through the GI-Renal Axis����� 71
Conclusion ����������������������������������������������������������������������������������������������������������������� 72
Question Section��������������������������������������������������������������������������������������������������������� 72
References������������������������������������������������������������������������������������������������������������������� 72
6Indications and Contraindications for Bariatric Surgery��������������������������������������� 77
Christopher DuCoin, Rachel L. Moore, and David A. Provost
Introduction����������������������������������������������������������������������������������������������������������������� 77
Indications for Metabolic and Bariatric Surgery�������������������������������������������������������� 77
Specific Considerations����������������������������������������������������������������������������������������������� 79
Conclusion ����������������������������������������������������������������������������������������������������������������� 80
Question Section��������������������������������������������������������������������������������������������������������� 80
References������������������������������������������������������������������������������������������������������������������� 80
7Preoperative Care of the Bariatric Patient��������������������������������������������������������������� 83
Renée M. Tholey and David S. Tichansky
Introduction����������������������������������������������������������������������������������������������������������������� 83
Patient Selection��������������������������������������������������������������������������������������������������������� 83
Cardiac Evaluation����������������������������������������������������������������������������������������������������� 84
Preoperative VTE Evaluation������������������������������������������������������������������������������������� 84
Sleep Apnea and Obesity Hypoventilation Evaluation����������������������������������������������� 85
Evaluation of Upper Gastrointestinal Anatomy ��������������������������������������������������������� 86
Psychological Evaluation������������������������������������������������������������������������������������������� 86
Informed Consent������������������������������������������������������������������������������������������������������� 87
Conclusion: Standardized Care Pathways������������������������������������������������������������������ 87
Question Section��������������������������������������������������������������������������������������������������������� 87
References������������������������������������������������������������������������������������������������������������������� 88
Contents
ix
8Anesthetic Considerations����������������������������������������������������������������������������������������� 89
Hendrikus J. M. Lemmens, John M. Morton, Cindy M. Ku, and
Stephanie B. Jones
Introduction����������������������������������������������������������������������������������������������������������������� 89
Preoperative Evaluation ��������������������������������������������������������������������������������������������� 89
Respiratory Issues Relevant to Anesthesia Management������������������������������������������� 89
Cardiovascular Issues Relevant to Anesthesia Management ������������������������������������� 90
Pharmacological Considerations��������������������������������������������������������������������������������� 91
Induction Agents��������������������������������������������������������������������������������������������������������� 91
Inhaled Anesthetics����������������������������������������������������������������������������������������������������� 93
Neuromuscular Blocking Agents ������������������������������������������������������������������������������� 94
Reversal Agents of Neuromuscular Blockade ����������������������������������������������������������� 95
Monitoring ����������������������������������������������������������������������������������������������������������������� 95
Preoperative Sedation������������������������������������������������������������������������������������������������� 96
Airway Management��������������������������������������������������������������������������������������������������� 96
Aspiration Risk����������������������������������������������������������������������������������������������������������� 97
Pneumoperitoneum: Implications for Ventilation, Hemodynamics,
and Urine Output��������������������������������������������������������������������������������������������������������� 97
Fluid Management ����������������������������������������������������������������������������������������������������� 98
Postoperative Considerations������������������������������������������������������������������������������������� 98
Postoperative Nausea and Vomiting��������������������������������������������������������������������������� 99
Postoperative Analgesia ��������������������������������������������������������������������������������������������� 99
Question Section��������������������������������������������������������������������������������������������������������� 100
References������������������������������������������������������������������������������������������������������������������� 100
9Components of a Metabolic and Bariatric Surgery Center ����������������������������������� 103
Wayne J. English, D. Brandon Williams, and Aaron Bolduc
Introduction����������������������������������������������������������������������������������������������������������������� 103
The Metabolic and Bariatric Surgery Accreditation and
Quality Improvement Program����������������������������������������������������������������������������������� 103
Essential Components of a Metabolic and Bariatric Surgery (MBS) Center������������� 104
Specialty Consultants and Preoperative Clearances��������������������������������������������������� 111
Electronic and Remote Access to the Metabolic and Bariatric Surgery Center��������� 112
Metabolic and Bariatric Surgery in Adolescents�������������������������������������������������������� 112
Common Deficiencies Encountered During the MBSAQIP Site Survey������������������� 114
Conclusion ����������������������������������������������������������������������������������������������������������������� 115
Question Section��������������������������������������������������������������������������������������������������������� 115
References������������������������������������������������������������������������������������������������������������������� 116
10Evaluation of Preoperative Weight Loss������������������������������������������������������������������� 117
Hussna Wakily and Aurora D. Pryor
Introduction����������������������������������������������������������������������������������������������������������������� 117
Principle Behind the Support of Preoperative Weight Loss��������������������������������������� 117
Review of the Data Supporting and Refuting the Benefit of Preoperative
Weight Loss���������������������������������������������������������������������������������������������������������������� 118
Additional Considerations with PWL������������������������������������������������������������������������� 121
Study Limitations������������������������������������������������������������������������������������������������������� 121
ASMBS Position Statement��������������������������������������������������������������������������������������� 121
Conclusion ����������������������������������������������������������������������������������������������������������������� 122
Question Section��������������������������������������������������������������������������������������������������������� 122
References������������������������������������������������������������������������������������������������������������������� 122
x
11ASMBS Position Statements ������������������������������������������������������������������������������������� 123
Stacy A. Brethauer and Xiaoxi (Chelsea) Feng
Introduction����������������������������������������������������������������������������������������������������������������� 123
Summary of Current Position Statements������������������������������������������������������������������� 123
Question Section��������������������������������������������������������������������������������������������������������� 133
References������������������������������������������������������������������������������������������������������������������� 134
Part II Primary Bariatric Surgery and Management of Complications
12Laparoscopic Gastric Bypass: Technique and Outcomes��������������������������������������� 139
Kelvin D. Higa and Pearl K. Ma
Introduction����������������������������������������������������������������������������������������������������������������� 139
Preparation of the Patient������������������������������������������������������������������������������������������� 140
Positioning and Trocar Placement ����������������������������������������������������������������������������� 140
The Components��������������������������������������������������������������������������������������������������������� 142
Routing of the Roux Limb and Closure of Mesenteric Defects��������������������������������� 144
Outcomes ������������������������������������������������������������������������������������������������������������������� 144
Conclusion ����������������������������������������������������������������������������������������������������������������� 146
Question Section��������������������������������������������������������������������������������������������������������� 146
References������������������������������������������������������������������������������������������������������������������� 146
13Laparoscopic Sleeve Gastrectomy: Technique and Outcomes������������������������������� 149
Natan Zundel, Juan D. Hernandez R., and Michel Gagner
Introduction����������������������������������������������������������������������������������������������������������������� 149
Preparation and Surgical Technique��������������������������������������������������������������������������� 150
Postoperative Period��������������������������������������������������������������������������������������������������� 152
Results������������������������������������������������������������������������������������������������������������������������� 152
Sleeve Gastrectomy or Gastric Bypass?��������������������������������������������������������������������� 156
Discussion������������������������������������������������������������������������������������������������������������������� 157
Conclusions����������������������������������������������������������������������������������������������������������������� 157
Question Section��������������������������������������������������������������������������������������������������������� 157
References������������������������������������������������������������������������������������������������������������������� 158
14Biliopancreatic Diversion with Duodenal Switch: Technique and Outcomes������� 161
Ranjan Sudan
Introduction����������������������������������������������������������������������������������������������������������������� 161
Preoperative Assessment��������������������������������������������������������������������������������������������� 161
Technical Details��������������������������������������������������������������������������������������������������������� 162
Postoperative Management����������������������������������������������������������������������������������������� 164
Complications������������������������������������������������������������������������������������������������������������� 165
Outcomes ������������������������������������������������������������������������������������������������������������������� 166
Conclusion ����������������������������������������������������������������������������������������������������������������� 166
Question Section��������������������������������������������������������������������������������������������������������� 167
References������������������������������������������������������������������������������������������������������������������� 167
15Single Anastomosis Duodeno-ileostomy������������������������������������������������������������������� 169
Amit Surve, Daniel Cottam, Hinali Zaveri, and Samuel Cottam
History������������������������������������������������������������������������������������������������������������������������� 169
Surgical Technique����������������������������������������������������������������������������������������������������� 170
Postoperative Care ����������������������������������������������������������������������������������������������������� 172
Weight Loss Outcomes with SADI-S������������������������������������������������������������������������� 172
Complications������������������������������������������������������������������������������������������������������������� 173
Rare Complications and Their Management ������������������������������������������������������������� 175
Nutritional Outcomes������������������������������������������������������������������������������������������������� 175
Contents
Contents
xi
T2DM Resolution������������������������������������������������������������������������������������������������������� 175
SADI as Revision Procedure�������������������������������������������������������������������������������������� 177
Review of Literature��������������������������������������������������������������������������������������������������� 177
Conclusion ����������������������������������������������������������������������������������������������������������������� 177
Question Section��������������������������������������������������������������������������������������������������������� 178
References������������������������������������������������������������������������������������������������������������������� 179
16Laparoscopic One Anastomosis Gastric Bypass: History of the
Procedure Surgical Technique and Outcomes��������������������������������������������������������� 181
Helmuth T. Billy, Moataz M. Bashah, and Ryan Fairley
History������������������������������������������������������������������������������������������������������������������������� 181
Introduction����������������������������������������������������������������������������������������������������������������� 182
Patient Selection and Preparation������������������������������������������������������������������������������� 183
Surgical Technique����������������������������������������������������������������������������������������������������� 184
Creating the Gastric Pouch����������������������������������������������������������������������������������������� 184
Reversal of One Anastomosis Gastric Bypass ����������������������������������������������������������� 187
Benefits of a Single Anastomosis Procedure ������������������������������������������������������������� 188
Complications������������������������������������������������������������������������������������������������������������� 189
Resolution of Comorbidities and Nutritional Complications������������������������������������� 191
Outcome Comparison Roux-Y Gastric Bypass vs Sleeve Gastrectomy vs One
Anastomosis Gastric Bypass��������������������������������������������������������������������������������������� 191
Insurance Coverage USA������������������������������������������������������������������������������������������� 192
Summary��������������������������������������������������������������������������������������������������������������������� 192
Question Section��������������������������������������������������������������������������������������������������������� 192
References������������������������������������������������������������������������������������������������������������������� 193
Part III Management of Bariatric Complications
17Management of Gastrointestinal Leaks and Fistula����������������������������������������������� 197
Ninh T. Nguyen and Shaun C. Daly
Introduction����������������������������������������������������������������������������������������������������������������� 197
Etiologies ������������������������������������������������������������������������������������������������������������������� 197
Presentation and Diagnostic Evaluation��������������������������������������������������������������������� 198
Management��������������������������������������������������������������������������������������������������������������� 199
Nonoperative Treatment��������������������������������������������������������������������������������������������� 199
Reoperation and Drainage������������������������������������������������������������������������������������������� 199
Endoscopic Stent��������������������������������������������������������������������������������������������������������� 200
Endoscopic Stent Technique��������������������������������������������������������������������������������������� 200
Chronic Fistula����������������������������������������������������������������������������������������������������������� 202
Conclusion ����������������������������������������������������������������������������������������������������������������� 202
Question Section��������������������������������������������������������������������������������������������������������� 202
References������������������������������������������������������������������������������������������������������������������� 202
18Gastrointestinal Obstruction After Bariatric Surgery ������������������������������������������� 205
Neil A. King and Daniel M. Herron
Introduction����������������������������������������������������������������������������������������������������������������� 205
Obstruction After Roux-En-Y Gastric Bypass����������������������������������������������������������� 205
Gastrojejunal Stricture ����������������������������������������������������������������������������������������������� 206
Obstruction from Internal Hernia������������������������������������������������������������������������������� 207
Small Bowel Obstruction from Scars and Adhesive Bands ��������������������������������������� 209
Incisional Hernia��������������������������������������������������������������������������������������������������������� 209
Intussusception����������������������������������������������������������������������������������������������������������� 209
Obstruction from Intraluminal Blood Clot or Bezoar������������������������������������������������� 210
xii
Contents
General Approach to the Bypass Patient with Obstruction����������������������������������������� 210
Obstruction in the Laparoscopic Adjustable Gastric Band Patient����������������������������� 210
Obstruction After Laparoscopic Adjustable Gastric Band Placement ����������������������� 212
Early Postoperative Band Obstruction����������������������������������������������������������������������� 212
Late Postoperative Band Obstruction������������������������������������������������������������������������� 212
Unusual Types of Band Obstruction��������������������������������������������������������������������������� 212
Obstruction After Sleeve Gastrectomy����������������������������������������������������������������������� 213
Obstruction After Biliopancreatic Diversion with Duodenal Switch������������������������� 213
Obstruction from Implanted Medical Devices����������������������������������������������������������� 214
Conclusion ����������������������������������������������������������������������������������������������������������������� 214
Question Section��������������������������������������������������������������������������������������������������������� 214
References������������������������������������������������������������������������������������������������������������������� 214
19Postoperative Bleeding in the Bariatric Surgery Patient ��������������������������������������� 217
Federico J. Serrot, Samuel Szomstein, and Raul J. Rosenthal
Introduction����������������������������������������������������������������������������������������������������������������� 217
Definition/Causes������������������������������������������������������������������������������������������������������� 217
Diagnostic Algorithm������������������������������������������������������������������������������������������������� 218
Treatment Strategies��������������������������������������������������������������������������������������������������� 219
Special Considerations����������������������������������������������������������������������������������������������� 221
Conclusion ����������������������������������������������������������������������������������������������������������������� 222
Question Section��������������������������������������������������������������������������������������������������������� 222
References������������������������������������������������������������������������������������������������������������������� 222
20Management of Marginal Ulcers������������������������������������������������������������������������������� 225
Richard M. Peterson and Jason W. Kempenich
Introduction����������������������������������������������������������������������������������������������������������������� 225
Pathophysiology��������������������������������������������������������������������������������������������������������� 225
Etiology����������������������������������������������������������������������������������������������������������������������� 226
Diagnosis��������������������������������������������������������������������������������������������������������������������� 227
Medical Treatment ����������������������������������������������������������������������������������������������������� 228
Prevention������������������������������������������������������������������������������������������������������������������� 228
Endoscopic and Surgical Treatment��������������������������������������������������������������������������� 229
Question Section��������������������������������������������������������������������������������������������������������� 233
References������������������������������������������������������������������������������������������������������������������� 233
21Gastric Banding Complications: Management ������������������������������������������������������� 235
Brittany Nowak, Christine Ren-Fielding, and Jeff Allen
Introduction����������������������������������������������������������������������������������������������������������������� 235
Early Complications��������������������������������������������������������������������������������������������������� 235
Late Complications����������������������������������������������������������������������������������������������������� 236
Conclusion ����������������������������������������������������������������������������������������������������������������� 243
Question Section��������������������������������������������������������������������������������������������������������� 244
References������������������������������������������������������������������������������������������������������������������� 244
22Management of Nutritional Complications ������������������������������������������������������������� 247
Michael Choi, Liz Goldenberg, and Alfons Pomp
Introduction����������������������������������������������������������������������������������������������������������������� 247
Macronutrients ����������������������������������������������������������������������������������������������������������� 247
Micronutrients������������������������������������������������������������������������������������������������������������� 248
Conclusions����������������������������������������������������������������������������������������������������������������� 253
Question Section��������������������������������������������������������������������������������������������������������� 255
References������������������������������������������������������������������������������������������������������������������� 255
Contents
xiii
23Early and Late Dumping Syndromes����������������������������������������������������������������������� 257
Samer G. Mattar and Ann M. Rogers
Introduction����������������������������������������������������������������������������������������������������������������� 257
Diagnosis��������������������������������������������������������������������������������������������������������������������� 257
Treatment ������������������������������������������������������������������������������������������������������������������� 258
Conclusions����������������������������������������������������������������������������������������������������������������� 260
Question Section��������������������������������������������������������������������������������������������������������� 260
References������������������������������������������������������������������������������������������������������������������� 260
Part IV Reoperative Bariatric Surgery for Weight Regain and Complications
24Reoperative Bariatric Surgery����������������������������������������������������������������������������������� 265
Rene Aleman, Emanuele Lo Menzo, Samuel Szomstein, and Raul J. Rosenthal
Introduction����������������������������������������������������������������������������������������������������������������� 265
Reoperative Bariatric Surgery: Classification������������������������������������������������������������� 265
Preoperative Evaluation ��������������������������������������������������������������������������������������������� 269
Review of Operative Reports ������������������������������������������������������������������������������������� 269
Imaging and Functional Studies��������������������������������������������������������������������������������� 270
Dietary and Nutritional Assessment and Counseling������������������������������������������������� 270
Psychological Assessment and Counseling ��������������������������������������������������������������� 270
Preoperative Testing and Clearances�������������������������������������������������������������������������� 271
Approach��������������������������������������������������������������������������������������������������������������������� 271
Technical Aspects������������������������������������������������������������������������������������������������������� 271
LAGB-Related Reoperations ������������������������������������������������������������������������������������� 272
RYGB������������������������������������������������������������������������������������������������������������������������� 274
Loop Gastric Bypass��������������������������������������������������������������������������������������������������� 275
Biliopancreatic Diversion with Duodenal Switch (BPD-DS)������������������������������������� 276
Vertical Banded Gastroplasty (VBG)������������������������������������������������������������������������� 276
Sleeve Gastrectomy����������������������������������������������������������������������������������������������������� 277
Conclusion ����������������������������������������������������������������������������������������������������������������� 277
Question Section��������������������������������������������������������������������������������������������������������� 278
References������������������������������������������������������������������������������������������������������������������� 278
25Reoperative Options After Gastric Banding ����������������������������������������������������������� 281
Zeyad Loubnan, Manish Parikh, and Marina Kurian
Introduction����������������������������������������������������������������������������������������������������������������� 281
Preoperative Workup��������������������������������������������������������������������������������������������������� 281
Surgical Options��������������������������������������������������������������������������������������������������������� 282
Outcomes ������������������������������������������������������������������������������������������������������������������� 282
Other Less Common Surgical Options for Conversion ��������������������������������������������� 284
Conclusions����������������������������������������������������������������������������������������������������������������� 285
Question Section��������������������������������������������������������������������������������������������������������� 285
References������������������������������������������������������������������������������������������������������������������� 286
26Reoperative Options After Sleeve Gastrectomy������������������������������������������������������� 287
Jacques M. Himpens, Gregg H. Jossart, and Dafydd A. Davies
Introduction����������������������������������������������������������������������������������������������������������������� 287
Reasons for Inadequate Response������������������������������������������������������������������������������� 287
Rates of Failure����������������������������������������������������������������������������������������������������������� 289
Demonstration of Aberrant Anatomy and Consequences for Surgical Treatment ����� 289
Managing Inadequate Response��������������������������������������������������������������������������������� 289
xiv
Contents
Conclusion ����������������������������������������������������������������������������������������������������������������� 294
Question Section��������������������������������������������������������������������������������������������������������� 294
References������������������������������������������������������������������������������������������������������������������� 294
27Reoperative Options After Gastric Bypass��������������������������������������������������������������� 297
Abraham Krikhely and Marc Bessler
Introduction����������������������������������������������������������������������������������������������������������������� 297
Evaluating a Patient with Weight Regain/Failure to Lose Weight ����������������������������� 297
Endoscopic Interventions������������������������������������������������������������������������������������������� 298
Surgical Revision Options ����������������������������������������������������������������������������������������� 298
Algorithms ����������������������������������������������������������������������������������������������������������������� 306
Question Section��������������������������������������������������������������������������������������������������������� 307
References������������������������������������������������������������������������������������������������������������������� 307
28Revisional Bariatric Surgery for Management of Late Complications����������������� 309
Patrick J. Sweigert, Fadi Bakhos, Eric Marcotte, and Bipan Chand
Introduction����������������������������������������������������������������������������������������������������������������� 309
Late Complications Following Sleeve Gastrectomy Requiring Revision������������������� 309
Late Complications Following Roux-en-Y Gastric Bypass Requiring Revision������� 313
Late Complications Following Biliopancreatic Diversion with Duodenal Switch
Requiring Revision����������������������������������������������������������������������������������������������������� 317
Conclusion ����������������������������������������������������������������������������������������������������������������� 318
Question Section��������������������������������������������������������������������������������������������������������� 318
References������������������������������������������������������������������������������������������������������������������� 318
29Revisional Surgery Data and Guidelines ����������������������������������������������������������������� 321
Kunoor Jain-Spangler and Ranjan Sudan
Introduction����������������������������������������������������������������������������������������������������������������� 321
Inadequate Weight Loss ��������������������������������������������������������������������������������������������� 322
Weight Regain������������������������������������������������������������������������������������������������������������� 323
Lack of Comorbidity Resolution or Return of Comorbidities ����������������������������������� 323
Anatomic Complications ������������������������������������������������������������������������������������������� 323
Approach to the Reoperative Surgery Patient������������������������������������������������������������� 324
Summary��������������������������������������������������������������������������������������������������������������������� 324
Question Section��������������������������������������������������������������������������������������������������������� 325
References������������������������������������������������������������������������������������������������������������������� 325
Part V Metabolic Surgery
30Operation of Choice for Metabolic Surgery������������������������������������������������������������� 329
Ali Aminian and Philip R. Schauer
Introduction����������������������������������������������������������������������������������������������������������������� 329
Standard Metabolic Surgical Procedures ������������������������������������������������������������������� 332
Clinical Outcomes������������������������������������������������������������������������������������������������������� 332
Mechanism of Action������������������������������������������������������������������������������������������������� 332
Comparison of Metabolic Procedures������������������������������������������������������������������������� 335
RCTs Comparing RYGB to SG ��������������������������������������������������������������������������������� 335
Meta-analysis of RCTs Comparing RYGB to SG for T2DM������������������������������������� 336
Individualized Metabolic Surgery Score��������������������������������������������������������������������� 337
Other Considerations in Decision-Making Between RYGB and SG������������������������� 338
Summary��������������������������������������������������������������������������������������������������������������������� 339
Question Section��������������������������������������������������������������������������������������������������������� 339
References������������������������������������������������������������������������������������������������������������������� 340
Contents
xv
31Outcomes of Metabolic Surgery ������������������������������������������������������������������������������� 341
Rene Aleman, Francesco Rubino, Emanuele Lo Menzo, and Raul J. Rosenthal
Introduction: Definition of Metabolic Surgery����������������������������������������������������������� 341
Outcomes of Metabolic Surgery: Retrospective and Observational Studies ������������� 342
Outcomes of Metabolic Surgery: Randomized Controlled Trials������������������������������� 347
Conclusions����������������������������������������������������������������������������������������������������������������� 349
Question Section��������������������������������������������������������������������������������������������������������� 349
References������������������������������������������������������������������������������������������������������������������� 349
32Operative Outcomes of Metabolic/Bariatric Surgery in Subjects with Type 1
Obesity Index (30–35 kg/m2) ������������������������������������������������������������������������������������� 353
Ricardo V. Cohen, Tarissa Z. Petry, and Estefano A. Negri
Introduction����������������������������������������������������������������������������������������������������������������� 353
Outcomes ������������������������������������������������������������������������������������������������������������������� 353
Innovative Procedures������������������������������������������������������������������������������������������������� 356
Conclusions����������������������������������������������������������������������������������������������������������������� 356
Question Section��������������������������������������������������������������������������������������������������������� 356
References������������������������������������������������������������������������������������������������������������������� 357
Part VI Endoscopic Bariatric Surgery
33The Role of Preoperative Endoscopy in Bariatric Surgery������������������������������������� 361
Daniel Davila Bradley and Kevin M. Reavis
Introduction����������������������������������������������������������������������������������������������������������������� 361
General Considerations����������������������������������������������������������������������������������������������� 362
Preprocedure Setup and Upper Endoscopy Technique����������������������������������������������� 363
Preoperative Endoscopy in Patients Undergoing Index Procedures��������������������������� 363
Preoperative Endoscopy in Revisional Patients ��������������������������������������������������������� 364
Preoperative Endoscopy in Revisional Patients: Marginal Ulcer������������������������������� 364
Preoperative Endoscopy in Revisional Patients: Stricture ����������������������������������������� 365
Preoperative Endoscopy in Revisional Patients: Postoperative Leaks����������������������� 365
Preoperative Endoscopy in Revisional Patients: Band Erosion,
Impaction, and Slippage��������������������������������������������������������������������������������������������� 366
Preoperative Endoscopy in Revisional Patients: Gastroesophageal Reflux
Disease After Bypass or Biliopancreatic Diversion with Duodenal Switch��������������� 366
Preoperative Endoscopy in Revisional Patients: Previous Endoscopic Procedures��� 367
Preoperative Endoscopy in Revisional Patients: Biliopancreatic Access������������������� 368
Forensic Endoscopy ��������������������������������������������������������������������������������������������������� 369
Forensic Endoscopy: Malabsorptive��������������������������������������������������������������������������� 369
Forensic Endoscopy: Restrictive and Malabsorptive ������������������������������������������������� 370
Forensic Endoscopy: Restrictive��������������������������������������������������������������������������������� 371
Collaborative Efforts��������������������������������������������������������������������������������������������������� 372
Conclusion ����������������������������������������������������������������������������������������������������������������� 373
Question Section��������������������������������������������������������������������������������������������������������� 373
References������������������������������������������������������������������������������������������������������������������� 373
34Intragastric Balloon Therapy ����������������������������������������������������������������������������������� 375
Jaime Ponce and Rami E. Lutfi
Background and History��������������������������������������������������������������������������������������������� 375
FDA-Approved Balloons ������������������������������������������������������������������������������������������� 376
Placement and Removal Technique ��������������������������������������������������������������������������� 376
Patient Management��������������������������������������������������������������������������������������������������� 379
Outcomes and Complications������������������������������������������������������������������������������������� 379
Future Technologies��������������������������������������������������������������������������������������������������� 381
xvi
Contents
Conclusions����������������������������������������������������������������������������������������������������������������� 381
Question Section��������������������������������������������������������������������������������������������������������� 381
References������������������������������������������������������������������������������������������������������������������� 381
35Endoluminal Gastric Pouch Revision����������������������������������������������������������������������� 383
Brian Hodgens, Simon Che, and Dean J. Mikami
Introduction����������������������������������������������������������������������������������������������������������������� 383
Endoscopic Treatment������������������������������������������������������������������������������������������������� 384
Conclusion ����������������������������������������������������������������������������������������������������������������� 388
Question Section��������������������������������������������������������������������������������������������������������� 388
References������������������������������������������������������������������������������������������������������������������� 388
36Endoscopic Primary Bariatric Procedures��������������������������������������������������������������� 391
Michelle H. Scerbo, Melissa M. Felinski, Kulvinder S. Bajwa, Erik B. Wilson,
and Shinil K. Shah
Introduction����������������������������������������������������������������������������������������������������������������� 391
Gastric Procedures ����������������������������������������������������������������������������������������������������� 392
Gastric Balloons��������������������������������������������������������������������������������������������������������� 392
Gastroplasty ��������������������������������������������������������������������������������������������������������������� 392
Other Gastric Procedures ������������������������������������������������������������������������������������������� 396
Small Bowel Procedures��������������������������������������������������������������������������������������������� 398
Duodenal Mucosal Surfacing������������������������������������������������������������������������������������� 400
Conclusion ����������������������������������������������������������������������������������������������������������������� 400
Question Section��������������������������������������������������������������������������������������������������������� 401
References������������������������������������������������������������������������������������������������������������������� 401
37Endoscopic Management of Stomal Stenosis����������������������������������������������������������� 403
Crystal E. Alvarez and Keith Scharf
Introduction����������������������������������������������������������������������������������������������������������������� 403
History of Endoscopy������������������������������������������������������������������������������������������������� 403
Preprocedure Room Setup and Endoscopic Technique ��������������������������������������������� 404
Sleeve Gastrectomy����������������������������������������������������������������������������������������������������� 405
Treatment of Sleeve Stenosis ������������������������������������������������������������������������������������� 406
Roux-en-Y Gastric Bypass����������������������������������������������������������������������������������������� 407
Treatment Options for RYGB Stenosis����������������������������������������������������������������������� 409
Conclusion ����������������������������������������������������������������������������������������������������������������� 411
Question Section��������������������������������������������������������������������������������������������������������� 411
References������������������������������������������������������������������������������������������������������������������� 411
Part VII Quality in Bariatric Surgery
38Patient Safety��������������������������������������������������������������������������������������������������������������� 417
Mohamad Rassoul A. Abu-Nuwar, Robert B. Lim, and Daniel B. Jones
Introduction����������������������������������������������������������������������������������������������������������������� 417
Defining Safety����������������������������������������������������������������������������������������������������������� 417
Ensuring Quality and Improvement��������������������������������������������������������������������������� 419
Preoperative Assessment��������������������������������������������������������������������������������������������� 420
Perioperative Care������������������������������������������������������������������������������������������������������� 421
Postoperative Care ����������������������������������������������������������������������������������������������������� 424
Clinical Pathways and Teamwork������������������������������������������������������������������������������� 424
Disclosure of Complications and Error in Post-Adverse Event Management����������� 427
Conclusion ����������������������������������������������������������������������������������������������������������������� 427
Question Section��������������������������������������������������������������������������������������������������������� 428
References������������������������������������������������������������������������������������������������������������������� 428
Contents
xvii
39LABS Project��������������������������������������������������������������������������������������������������������������� 431
Bruce M. Wolfe and Elizaveta Walker
Introduction to the Problem ��������������������������������������������������������������������������������������� 431
History of the LABS Consortium������������������������������������������������������������������������������� 431
Goals of the LABS Consortium��������������������������������������������������������������������������������� 432
Rationale for Research Design����������������������������������������������������������������������������������� 433
Structure and Working Organization of LABS����������������������������������������������������������� 433
Outcome Domains in Bariatric Surgery��������������������������������������������������������������������� 434
Weight Loss and Body Composition ������������������������������������������������������������������������� 434
Diabetes Mellitus and Insulin Resistance������������������������������������������������������������������� 436
Cardiovascular and Pulmonary Disease��������������������������������������������������������������������� 436
Renal Disease������������������������������������������������������������������������������������������������������������� 436
Liver Function������������������������������������������������������������������������������������������������������������� 436
Behavioral/Psychosocial Factors ������������������������������������������������������������������������������� 436
Musculoskeletal and Functional Status����������������������������������������������������������������������� 437
Gender Issues ������������������������������������������������������������������������������������������������������������� 437
Economic Impact ������������������������������������������������������������������������������������������������������� 437
Biospecimens ������������������������������������������������������������������������������������������������������������� 437
Results from the LABS Consortium��������������������������������������������������������������������������� 437
LABS-1 Baseline Data����������������������������������������������������������������������������������������������� 437
LABS-1 Results ��������������������������������������������������������������������������������������������������������� 438
LABS-1 and LABS-2: 30-Day Results����������������������������������������������������������������������� 439
LABS-2 Baseline Data Reports ��������������������������������������������������������������������������������� 440
LABS-2 Outcome Studies������������������������������������������������������������������������������������������� 442
Conclusion ����������������������������������������������������������������������������������������������������������������� 444
Question Section��������������������������������������������������������������������������������������������������������� 445
References������������������������������������������������������������������������������������������������������������������� 446
40Quality in Bariatric Surgery ������������������������������������������������������������������������������������� 449
Robin P. Blackstone, Thomas P. Petrick, and Anthony T. Petrick
Introduction����������������������������������������������������������������������������������������������������������������� 449
The History of Quality in Bariatric Surgery��������������������������������������������������������������� 449
American Society for Metabolic and Bariatric Surgery Bariatric Surgery
Center of Excellence (ASMBS BSCOE) Program����������������������������������������������������� 450
American College of Surgeons Bariatric Surgery Center Network (ACS BSCN)����� 451
The Michagan Bariatric Surgical Collaborative (MiBSC)����������������������������������������� 451
The Evolution of the ASMBS BSCOE����������������������������������������������������������������������� 452
The Maturation of MBSAQIP������������������������������������������������������������������������������������� 454
Additional ASMBS Quality Initiatives����������������������������������������������������������������������� 458
The MBSAQIP Approach to Accreditation����������������������������������������������������������������� 458
The Future of Quality in Bariatric Surgery����������������������������������������������������������������� 469
Question Section��������������������������������������������������������������������������������������������������������� 470
References������������������������������������������������������������������������������������������������������������������� 470
41Patient Experience and Perioperative Pathway in Bariatric Surgery������������������� 473
Nabeel R. Obeid, Ryan Howard, and Dana A. Telem
Introduction����������������������������������������������������������������������������������������������������������������� 473
Access to Care������������������������������������������������������������������������������������������������������������� 473
Program Pathways and Patient Experience����������������������������������������������������������������� 474
Perioperative Care������������������������������������������������������������������������������������������������������� 475
Postoperative Care ����������������������������������������������������������������������������������������������������� 478
Question Section��������������������������������������������������������������������������������������������������������� 481
References������������������������������������������������������������������������������������������������������������������� 482
xviii
42Decreasing Readmissions in Bariatric Surgery������������������������������������������������������� 487
John M. Morton
Introduction����������������������������������������������������������������������������������������������������������������� 487
Rationale��������������������������������������������������������������������������������������������������������������������� 487
Mechanisms for Decreasing Readmission Rates ������������������������������������������������������� 487
Team Approach����������������������������������������������������������������������������������������������������������� 488
Characterizing Readmissions Following Bariatric Surgery��������������������������������������� 489
Discussion������������������������������������������������������������������������������������������������������������������� 491
Next Steps������������������������������������������������������������������������������������������������������������������� 492
Question Section��������������������������������������������������������������������������������������������������������� 493
References������������������������������������������������������������������������������������������������������������������� 493
Part VIII Specific Considerations
43Enhanced Recovery in Bariatric Surgery����������������������������������������������������������������� 497
Xiaoxi (Chelsea) Feng and Stacy A. Brethauer
Introduction����������������������������������������������������������������������������������������������������������������� 497
Pathophysiological Principles������������������������������������������������������������������������������������� 497
Practice Implementation��������������������������������������������������������������������������������������������� 498
Enhanced Recovery Outcomes in Bariatric Surgery��������������������������������������������������� 499
Exclusion and Barriers to Implementation����������������������������������������������������������������� 500
Economic Benefits ����������������������������������������������������������������������������������������������������� 502
Conclusion ����������������������������������������������������������������������������������������������������������������� 502
Question Section��������������������������������������������������������������������������������������������������������� 502
References������������������������������������������������������������������������������������������������������������������� 503
44Biliary Tract Disease in the Bariatric Surgery Patient������������������������������������������� 505
Adam C. Sheka, Keith M. Wirth, and Sayeed Ikramuddin
Introduction����������������������������������������������������������������������������������������������������������������� 505
Pathophysiology of Cholesterol Cholelithiasis����������������������������������������������������������� 505
Epidemiology of Cholelithiasis���������������������������������������������������������������������������������� 506
Rapid Weight Loss and Gallstone Formation������������������������������������������������������������� 507
Incidence of Cholelithiasis in Bariatric Surgery Patients������������������������������������������� 507
Challenges in Management of the Gallbladder at the Time of Bariatric Operation��� 507
Management Pathways in Patients Undergoing Bariatric Surgery����������������������������� 508
Pharmacologic Prevention of Cholelithiasis After Bariatric Surgery������������������������� 508
Access to the Biliary Tree Following Roux-­en-­Y Gastric Bypass����������������������������� 509
Conclusions����������������������������������������������������������������������������������������������������������������� 511
Question Section��������������������������������������������������������������������������������������������������������� 511
References������������������������������������������������������������������������������������������������������������������� 511
45Joint Disease and Obesity: Opportunity for Multidisciplinary
Investigation and Collaboration ������������������������������������������������������������������������������� 515
John M. Morton
Rationale��������������������������������������������������������������������������������������������������������������������� 515
Risk of Obesity for Joint Disease and Joint Replacement Surgery���������������������������� 515
Bariatric and Orthopedic Surgery: Team Approach��������������������������������������������������� 516
Question Section��������������������������������������������������������������������������������������������������������� 517
References������������������������������������������������������������������������������������������������������������������� 517
46Cardiac Risk Factor Improvement Following Bariatric Surgery��������������������������� 519
Riley Katsuki Kitamura, John M. Morton, and Dan Eisenberg
Introduction����������������������������������������������������������������������������������������������������������������� 519
Obesity and Cardiovascular Disease��������������������������������������������������������������������������� 520
Contents
Contents
xix
Preoperative Cardiac Evaluation��������������������������������������������������������������������������������� 522
Bariatric Surgery and Cardiac Risk Factors��������������������������������������������������������������� 522
Conclusion ����������������������������������������������������������������������������������������������������������������� 523
Question Section��������������������������������������������������������������������������������������������������������� 523
References������������������������������������������������������������������������������������������������������������������� 524
47Critical Care Considerations in the Bariatric Patient��������������������������������������������� 527
Stacy A. Brethauer, Lucia H. Nguyen, and David A. Provost
Introduction����������������������������������������������������������������������������������������������������������������� 527
Neurologic������������������������������������������������������������������������������������������������������������������� 527
Pulmonary������������������������������������������������������������������������������������������������������������������� 528
Cardiovascular ����������������������������������������������������������������������������������������������������������� 529
Gastrointestinal����������������������������������������������������������������������������������������������������������� 529
Nutrition��������������������������������������������������������������������������������������������������������������������� 529
Renal��������������������������������������������������������������������������������������������������������������������������� 530
Endocrine ������������������������������������������������������������������������������������������������������������������� 530
Infectious Disease������������������������������������������������������������������������������������������������������� 530
Pharmacology������������������������������������������������������������������������������������������������������������� 531
Hematology����������������������������������������������������������������������������������������������������������������� 531
Conclusions����������������������������������������������������������������������������������������������������������������� 532
Question Section��������������������������������������������������������������������������������������������������������� 532
References������������������������������������������������������������������������������������������������������������������� 532
48Bariatric Surgery in Adolescents������������������������������������������������������������������������������� 535
S. Christopher Derderian, Marc P. Michalsky, and Thomas H. Inge
Introduction����������������������������������������������������������������������������������������������������������������� 535
Definition of Pediatric Obesity����������������������������������������������������������������������������������� 535
Consequences of Obesity in Adolescence������������������������������������������������������������������� 535
Cardiovascular Disease����������������������������������������������������������������������������������������������� 536
Nonalcoholic Fatty Liver Disease������������������������������������������������������������������������������� 536
Glucose Impairment��������������������������������������������������������������������������������������������������� 537
Obstructive Sleep Apnea��������������������������������������������������������������������������������������������� 537
Idiopathic Intracranial Hypertension (IIH)����������������������������������������������������������������� 537
Psychological and Quality of Life Issues������������������������������������������������������������������� 537
Musculoskeletal Disorders����������������������������������������������������������������������������������������� 537
Pharmacotherapy��������������������������������������������������������������������������������������������������������� 537
Incidence and Best Practice Guidelines for Adolescent MBS ����������������������������������� 538
Outcomes of Metabolic and Bariatric Surgery in Adolescents����������������������������������� 540
Summary��������������������������������������������������������������������������������������������������������������������� 541
Question Section��������������������������������������������������������������������������������������������������������� 541
References������������������������������������������������������������������������������������������������������������������� 542
49Pregnancy Issues and Bariatric Surgery ����������������������������������������������������������������� 545
Tripurari Mishra and Shanu N. Kothari
Introduction����������������������������������������������������������������������������������������������������������������� 545
Effects of Prepregnancy Obesity on Fertility and Pregnancy Outcomes ������������������� 545
Obesity and Polycystic Ovarian Syndrome ��������������������������������������������������������������� 546
Impact of Bariatric Surgery on Fertility��������������������������������������������������������������������� 547
Impact of Bariatric Surgery on Mother and Neonate������������������������������������������������� 547
Nutrition Factors After Bariatric Surgery������������������������������������������������������������������� 548
Internal Hernia During Pregnancy ����������������������������������������������������������������������������� 548
Conclusion ����������������������������������������������������������������������������������������������������������������� 551
Question Section��������������������������������������������������������������������������������������������������������� 551
References������������������������������������������������������������������������������������������������������������������� 552
xx
50Robotics in Bariatric Surgery ����������������������������������������������������������������������������������� 553
Keith Chae Kim, Jonathan Douissard, Cynthia K. Buffington, and Monika E.
Hagen
Introduction����������������������������������������������������������������������������������������������������������������� 553
Robotics for Bariatric Surgery ����������������������������������������������������������������������������������� 553
Robotic Roux-en-Y Gastric Bypass (RYGB)������������������������������������������������������������� 554
Robotic Sleeve Gastrectomy (SG) ����������������������������������������������������������������������������� 554
Robotic Adjustable Gastric Band (AGB)������������������������������������������������������������������� 555
Robotic Biliopancreatic Diversion with Duodenal Switch (BPD/DS)����������������������� 555
Robotic Revisional Surgery ��������������������������������������������������������������������������������������� 556
Cost of Robotic Bariatric Surgery������������������������������������������������������������������������������� 556
Currently Available Robotic Surgery Systems����������������������������������������������������������� 557
Emerging Robotic Surgery Systems��������������������������������������������������������������������������� 558
Conclusion ����������������������������������������������������������������������������������������������������������������� 559
Question Section��������������������������������������������������������������������������������������������������������� 559
References������������������������������������������������������������������������������������������������������������������� 560
51Body Contouring After Massive Weight Loss ��������������������������������������������������������� 563
Natalie S. Barton, Al S. Aly, and Gregory R. D. Evans
Introduction����������������������������������������������������������������������������������������������������������������� 563
Presentation of the Massive Weight Loss Patient to the Plastic Surgeon������������������� 563
Workup for Post-Massive Weight Loss Plastic Surgery��������������������������������������������� 564
Postoperative Management����������������������������������������������������������������������������������������� 566
The Lower Trunk ������������������������������������������������������������������������������������������������������� 566
The Upper Arms��������������������������������������������������������������������������������������������������������� 567
The Upper Trunk��������������������������������������������������������������������������������������������������������� 570
Thighs������������������������������������������������������������������������������������������������������������������������� 571
Miscellaneous Regions����������������������������������������������������������������������������������������������� 573
Important Issues for the Bariatric Surgeon/Plastic Surgeon Interaction��������������������� 573
Conclusion ����������������������������������������������������������������������������������������������������������������� 574
Question Section��������������������������������������������������������������������������������������������������������� 574
References������������������������������������������������������������������������������������������������������������������� 575
52The Practice of Bariatric Coding and Reimbursement������������������������������������������� 577
Laura Dewender and Ashutosh Kaul
Introduction����������������������������������������������������������������������������������������������������������������� 577
From Global Proportions, Trend, and Cost Issues to Surgical Intervention��������������� 577
The Value of Surgery: The Basics of RVUs and CPTs����������������������������������������������� 578
Bariatric Surgery CPT Codes������������������������������������������������������������������������������������� 579
Coding Nuances ��������������������������������������������������������������������������������������������������������� 579
Insurance Preauthorization: Initial Bariatric Surgery������������������������������������������������� 580
Post-surgery Appeals�������������������������������������������������������������������������������������������������� 580
Participation in Specific Plans ����������������������������������������������������������������������������������� 582
Contracted Rates��������������������������������������������������������������������������������������������������������� 582
Conclusion ����������������������������������������������������������������������������������������������������������������� 582
Question Section��������������������������������������������������������������������������������������������������������� 582
References������������������������������������������������������������������������������������������������������������������� 583
53Medical Malpractice in Bariatric Surgery: The ASMBS Journey to a Closed
Claims Registry����������������������������������������������������������������������������������������������������������� 585
William A. Sweet and Eric J. DeMaria
The Challenge Defined����������������������������������������������������������������������������������������������� 585
ASMBS Efforts����������������������������������������������������������������������������������������������������������� 585
Most Important “Quality Care” Deficiencies and Outcomes Prompting
Bariatric Claims ��������������������������������������������������������������������������������������������������������� 587
Contents
Contents
xxi
The Critical Importance of “History”������������������������������������������������������������������������� 587
Excellence in Consent Process, Rapport-­Building: The Communication
Keys Prior to “Not Guilty” After an Adverse Event��������������������������������������������������� 587
“Anatomy of a Near Miss,” the Sometimes Critical Difficulty of In-Hospital
Communication����������������������������������������������������������������������������������������������������������� 588
Disastrous Team Training and Handoff Management: Don’t Fumble the Handoff��� 589
The Substantial Hazards of Inadequate Postoperative Communications
Planning ��������������������������������������������������������������������������������������������������������������������� 589
GI Bleed Post-RYGB Management Disaster, the most read�������������������������������������� 590
Delay/Failure to Treat and Communication Lapses Are Frequently Paired��������������� 592
A Leak Event Compounded��������������������������������������������������������������������������������������� 592
Question Section��������������������������������������������������������������������������������������������������������� 593
References������������������������������������������������������������������������������������������������������������������� 593
54Obesity Prevention����������������������������������������������������������������������������������������������������� 595
Elizaveta Walker and Bruce M. Wolfe
Introduction����������������������������������������������������������������������������������������������������������������� 595
Obesity and Its Causes ����������������������������������������������������������������������������������������������� 595
Prevention Strategies in Adult Populations����������������������������������������������������������������� 597
Prevention Strategies in Childhood and Adolescent Populations������������������������������� 601
Monitoring and Surveillance of Obesity��������������������������������������������������������������������� 604
Resources ������������������������������������������������������������������������������������������������������������������� 606
Conclusion ����������������������������������������������������������������������������������������������������������������� 607
Question Section��������������������������������������������������������������������������������������������������������� 607
References������������������������������������������������������������������������������������������������������������������� 607
55Training in Bariatric Surgery ����������������������������������������������������������������������������������� 613
Corrigan L. McBride
Background����������������������������������������������������������������������������������������������������������������� 613
Evolution of Bariatric Surgery Fellowship Training��������������������������������������������������� 614
Question Section��������������������������������������������������������������������������������������������������������� 616
References������������������������������������������������������������������������������������������������������������������� 617
56Adjuvant Pharmaceutical Therapy for Perioperative Use in
Bariatric Surgery ������������������������������������������������������������������������������������������������������� 619
John M. Morton, Saber Ghiassi, and Geoffrey S. Nadzam
Introduction����������������������������������������������������������������������������������������������������������������� 619
Rationale: Variation in Treatment Effect��������������������������������������������������������������������� 619
Preoperative Weight Loss������������������������������������������������������������������������������������������� 620
Postoperative Weight Gain����������������������������������������������������������������������������������������� 621
Anti-obesity Medications: Indications and Contraindications����������������������������������� 621
Adjuvant Pharmaceutical Therapy with Bariatric Surgery����������������������������������������� 622
Next Steps������������������������������������������������������������������������������������������������������������������� 622
Conclusion ����������������������������������������������������������������������������������������������������������������� 623
Question Section��������������������������������������������������������������������������������������������������������� 623
References������������������������������������������������������������������������������������������������������������������� 623
Answers������������������������������������������������������������������������������������������������������������������������������� 625
Answers (Chap. 1) ������������������������������������������������������������������������������������������������������� 625
Answers (Chap. 2) ������������������������������������������������������������������������������������������������������� 625
Answers (Chap. 5) ������������������������������������������������������������������������������������������������������� 626
Answers (Chap. 6) ������������������������������������������������������������������������������������������������������� 626
Answers (Chap. 7) ������������������������������������������������������������������������������������������������������� 626
Answers (Chap. 8) ������������������������������������������������������������������������������������������������������� 626
Answers (Chap. 9) ������������������������������������������������������������������������������������������������������� 627
xxii
Answers (Chap. 10) ����������������������������������������������������������������������������������������������������� 627
Answers (Chap. 11) ����������������������������������������������������������������������������������������������������� 627
Answers (Chap. 12) ����������������������������������������������������������������������������������������������������� 628
Answers (Chap. 13) ����������������������������������������������������������������������������������������������������� 628
Answers (Chap. 14) ����������������������������������������������������������������������������������������������������� 628
Answers (Chap. 15) ����������������������������������������������������������������������������������������������������� 628
Answers (Chap. 16) ����������������������������������������������������������������������������������������������������� 629
Answers (Chap. 17) ����������������������������������������������������������������������������������������������������� 629
Answers (Chap. 18) ����������������������������������������������������������������������������������������������������� 629
Answers (Chap. 19) ����������������������������������������������������������������������������������������������������� 629
Answers (Chap. 20) ����������������������������������������������������������������������������������������������������� 629
Answers (Chap. 21) ����������������������������������������������������������������������������������������������������� 630
Answers (Chap. 22) ����������������������������������������������������������������������������������������������������� 630
Answers (Chap. 23) ����������������������������������������������������������������������������������������������������� 630
Answers (Chap. 24) ����������������������������������������������������������������������������������������������������� 630
Answers (Chap. 25) ����������������������������������������������������������������������������������������������������� 631
Answers (Chap. 26) ����������������������������������������������������������������������������������������������������� 631
Answers (Chap. 27) ����������������������������������������������������������������������������������������������������� 631
Answers (Chap. 28) ����������������������������������������������������������������������������������������������������� 631
Answers (Chap. 29) ����������������������������������������������������������������������������������������������������� 632
Answers (Chap. 30) ����������������������������������������������������������������������������������������������������� 632
Answers (Chap. 31) ����������������������������������������������������������������������������������������������������� 632
Answers (Chap. 32) ����������������������������������������������������������������������������������������������������� 633
Answers (Chap. 33) ����������������������������������������������������������������������������������������������������� 633
Answers (Chap. 34) ����������������������������������������������������������������������������������������������������� 633
Answers (Chap. 35) ����������������������������������������������������������������������������������������������������� 634
Answers (Chap. 36) ����������������������������������������������������������������������������������������������������� 634
Answers (Chap. 37) ����������������������������������������������������������������������������������������������������� 634
Answers (Chap. 38) ����������������������������������������������������������������������������������������������������� 634
Answers (Chap. 39) ����������������������������������������������������������������������������������������������������� 635
Answers (Chap. 40) ����������������������������������������������������������������������������������������������������� 635
Answers (Chap. 41) ����������������������������������������������������������������������������������������������������� 635
Answers (Chap. 42) ����������������������������������������������������������������������������������������������������� 635
Answers (Chap. 43) ����������������������������������������������������������������������������������������������������� 636
Answers (Chap. 44) ����������������������������������������������������������������������������������������������������� 636
Answers (Chap. 45) ����������������������������������������������������������������������������������������������������� 636
Answers (Chap. 46) ����������������������������������������������������������������������������������������������������� 636
Answers (Chap. 47) ����������������������������������������������������������������������������������������������������� 636
Answers (Chap. 48) ����������������������������������������������������������������������������������������������������� 637
Answers (Chap. 49) ����������������������������������������������������������������������������������������������������� 637
Answers (Chap. 50) ����������������������������������������������������������������������������������������������������� 637
Answers (Chap. 51) ����������������������������������������������������������������������������������������������������� 637
Answers (Chap. 52) ����������������������������������������������������������������������������������������������������� 637
Answers (Chap. 53) ����������������������������������������������������������������������������������������������������� 638
Answers (Chap. 54) ����������������������������������������������������������������������������������������������������� 638
Answers (Chap. 55) ����������������������������������������������������������������������������������������������������� 638
Answers (Chap. 56) ����������������������������������������������������������������������������������������������������� 638
Index������������������������������������������������������������������������������������������������������������������������������������� 639
Contents
Contributors
Mohamad Rassoul A. Abu-Nuwar, MD Division of Bariatric & Minimally Invasive Surgery,
Beth Israel Deaconess Medical Center, Boston, MA, USA
Rene Aleman, MD Minimally Invasive Surgery and Bariatric Surgery Department, Cleveland
Clinic Florida, Weston, FL, USA
Jeff Allen, MD, FACS, FASMBS General Surgery, Division of Bariatric Surgery, Norton
Healthcare, Louisville, KY, USA
Crystal E. Alvarez, DO Minimally Invasive Surgery, Bariatric Surgery, Department of
General Surgery, Loma Linda University Health, Loma Linda, CA, USA
Al S. Aly, MD Plastic Surgery, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates
Ali Aminian, MD, FACS, FASMBS Department of General Surgery, Bariatric and Metabolic
Institute, Cleveland Clinic, Cleveland, OH, USA
Kulvinder S. Bajwa, MD Department of Surgery, Division of Minimally Invasive and
Elective General Surgery, McGovern Medical School, UT Health, Houston, TX, USA
Fadi Bakhos, MD Department of Surgery, Loyola University Medical Center, Maywood, IL,
USA
Natalie S. Barton, MD Plastic Surgery, University of California, Irvine, Orange, CA, USA
Moataz M. Bashah, MD Division of Metabolic and Bariatric Surgery, Hamad General
Hospital, Hamad Medical Corporation, Doha, Qatar
Marc Bessler, MD Department of Surgery, Columbia University Irving Medical Center, New
York, NY, USA
Monica M. Betancourt-Garcia, MD DHR Health Institute for Research and Development,
DHR Health System, Edinburg, TX, USA
Helmuth T. Billy, MD Metabolic and Bariatric Surgery, Community Memorial Hospital,
Ventura, St. John’s Regional Medical Center, Oxnard, CA, USA
Robin P. Blackstone, MD, FACS, FASMBS Metabolic and Bariatric Surgery, Banner
University Medical Center – Phoenix, Phoenix, AZ, USA
Aaron Bolduc, MD Department of Surgery, Augusta University Medical Center, Augusta,
GA, USA
Daniel Davila Bradley, MD Gastrointestinal Minimal Invasive Surgery, The Oregon Clinic,
Portland, OR, USA
Bariatric Surgery, Portland Providence Medical Center/Legacy Medical Center, Portland, OR,
USA
Stacy A. Brethauer, MD, FASMBS Department of Surgery, The Ohio State University,
Columbus, OH, USA
xxiii
xxiv
Cynthia K. Buffington, PhD Department of General Surgery/Bariatrics, Center for Metabolic
and Obesity Surgery at Advent Health Celebration, Celebration, FL, USA
Bipan Chand, MD, FACS, FASGE, FASMBS Department of Surgery, Division of GI/
Minimally Invasive Surgery, Loyola University Medical Center, Stritch School of Medicine,
Maywood, IL, USA
Simon Che, MD Department of Surgery, University of Hawaii John A. Burns School of
Medicine, Honolulu, HI, USA
Michael Choi, MD Department of Surgery, Weill Cornell Medical Center, New York-­
Presbyterian Hospital, New York, NY, USA
Elias Chousleb, MD, FACS, FASMBS Department of Surgery, Florida International
University, Herbert Wertheim College of Medicine, Miami, FL, USA
Ricardo V. Cohen, MD, FASMBS, FACS The Center for Obesity and Diabetes, Oswaldo
Cruz German Hospital, São Paulo, Brazil
Daniel Cottam, MD Bariatric Medicine Institute, Salt Lake City, UT, USA
Samuel Cottam, HS Bariatric Medicine Institute, Salt Lake City, UT, USA
Shaun C. Daly, MD Department of Surgery, Division of Gastrointestinal Surgery, University
of California, Irvine Medical Center, Orange, CA, USA
Dafydd A. Davies, MD, MPhil, FRCSC Division of Pediatric Thoracic and General Surgery,
The Hospital for Sick Children, Toronto, ON, Canada
Eric J. DeMaria, MD, FACS, FASMBS American Society for Metabolic and Bariatric
Surgery, Division of General/Bariatric Surgery, Department of Surgery, Brody School of
Medicine, East Carolina University, Greenville, NC, USA
S. Christopher Derderian, MD Pediatric Surgery, Children’s Hospital Colorado, Aurora,
CO, USA
Laura Dewender, CPC Coding and Compliance, Advanced Surgeons, Valhalla, NY, USA
Jonathan Douissard, MD Division of Digestive Surgery, University Hospital Geneva,
Geneva, Switzerland
Christopher DuCoin, MD, MPH, FACS, FASMBS Division of Bariatric & General Surgery,
University of South Florida, Tampa, FL, USA
Dan Eisenberg, MD, MS, FASMBS Department of Surgery, Stanford School of Medicine
and VA Palo Alto Health Care System, Palo Alto, CA, USA
Wayne J. English, MD Department of Surgery, Vanderbilt University Medical Center,
Nashville, TN, USA
Gregory R. D. Evans, MD, FACS Plastic Surgery and Biomedical Engineering, University
of California, Irvine, Orange, CA, USA
Ryan Fairley, DO Surgical Education, Community Memorial Hospital, Ventura, CA, USA
Melissa M. Felinski, DO Department of Surgery, Division of Minimally Invasive and Elective
General Surgery, McGovern Medical School, UT Health, Houston, TX, USA
Xiaoxi (Chelsea) Feng, MD, MPH Department of General Surgery, Cleveland Clinic,
Cleveland, OH, USA
R. Armour Forse, MD, PhD DHR Health Institute for Education and Innovation, DHR
Health System, Department of Surgery, University of Texas Rio Grande Valley, Edinburg,
TX, USA
Contributors
Contributors
xxv
David Romero Funes, MD Department of General Surgery, The Bariatric and Metabolic
Institute, Cleveland Clinic Florida, Weston, FL, USA
Michel Gagner, MD, FRCSC, FACS Department of Surgery, Herbert Wertheim College of
Medicine, Florida International University, Miami, FL, USA
Department of Surgery, Hôpital du Sacré-Coeur, Montreal, QC, Canada
Saber Ghiassi, MD, MPH Department of Surgery, Yale School of Medicine, Fairfield,
CT, USA
Liz Goldenberg, MPH, RD, CDN GI Metabolic and Bariatric Surgery, Weill Cornell
Medicine, New York-Presbyterian Hospital, New York, NY, USA
Monika E. Hagen, MD, MBA Division of Digestive Surgery, University Hospital Geneva,
Geneva, Switzerland
Juan D. Hernandez R., MD, FACS Surgery and Anatomy, Hospital Universitario Fundación
Santa Fe de Bogotá, Universidad de los Andes School of Medicine, Bogotá, Colombia
Daniel M. Herron, MD, FACS, FASMBS Garlock Division of Surgery, Mount Sinai
Hospital, Icahn School of Medicine at Mount Sinai, New York, NY, USA
Kelvin D. Higa, MD Department of Surgery, Minimally Invasive and Bariatric Surgery,
Fresno Heart and Surgical Hospital, University of California San Francisco, Fresno, CA, USA
Jacques M. Himpens, MD, PhD, FASMBS (Hon) Abdominal Surgery, St. Pierre University
Hospital, Brussels, Belgium
Brian Hodgens, MD Department of Surgery, University of Hawaii John A. Burns School of
Medicine, Honolulu, HI, USA
Ryan Howard, MD Department of Surgery, University of Michigan, Ann Arbor, MI, USA
Sayeed Ikramuddin, MD, MHA Department of Surgery, University of Minnesota,
Minneapolis, MN, USA
Thomas H. Inge, MD, PhD Pediatric Surgery, University of Colorado, Denver and Children’s
Hospital Colorado, Aurora, CO, USA
Kunoor Jain-Spangler, MD Department of Surgery, Division of Metabolic and Weight Loss
Surgery, Duke University, Durham, NC, USA
Daniel B. Jones, MD, MS Department of Surgery, Beth Israel Deaconess Medical Center,
Boston, MA, USA
Stephanie B. Jones, MD Department of Anesthesia, Critical Care and Pain Medicine, Beth
Israel Deaconess Medical Center, Boston, MA, USA
Gregg H. Jossart, MD, FACS Department of Surgery, California Pacific Medical Center, San
Francisco, CA, USA
Ashutosh Kaul, MD, FACS, FRCS Department of Surgery, NY Medical College, Valhalla,
NY, USA
Bariatric Surgery, Greenwich Hospital, Valhalla, NY, USA
Minimally Invasive Surgery, Westchester Medical Center, Valhalla, NY, USA
Jason W. Kempenich, MD, FACS Department of Surgery, UT Health San Antonio, San
Antonio, TX, USA
Keith Chae Kim, MD, FACS Department of General Surgery/Bariatrics, Center for Metabolic
and Obesity Surgery at Advent Health Celebration, Celebration, FL, USA
xxvi
Neil A. King, MD Garlock Division of Surgery, Mount Sinai Hospital, Icahn School of
Medicine at Mount Sinai, New York, NY, USA
Michelle Cordoba Kissee, MD Endocrinology, Diabetes, Metabolism and Bariatrics, DHR
Health System, University of Texas Rio Grande Valley, Edinburg, TX, USA
Riley Katsuki Kitamura, MD General Surgery, Palo Alto VA Health Care System, Palo Alto,
CA, USA
Shanu N. Kothari, MD Minimally Invasive Bariatric Surgery, Department of General
Surgery, Gundersen Health System, La Crosse, WI, USA
Abraham Krikhely, MD Department of Surgery, Columbia University Irving Medical
Center, New York, NY, USA
Cindy M. Ku, MD Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel
Deaconess Medical Center, Boston, MA, USA
Marina Kurian, MD Department of Surgery, NYU School of Medicine, New York, NY, USA
Hendrikus J. M. Lemmens, MD, PhD Multispecialty Division, Department of Anesthesia,
Stanford University School of Medicine, Stanford, CA, USA
Robert B. Lim, MD Minimally Invasive Surgery, Department of Surgery, Tripler Army
Medical Center, Honolulu, HI, USA
Zeyad Loubnan, MD Department of Surgery, NYU School of Medicine, New York, NY,
USA
Rami E. Lutfi, MD, FACS, FASMBS Department of Surgery, University of Illinois at
Chicago, Chicago, IL, USA
Pearl K. Ma, MD Department of Surgery, Minimally Invasive and Bariatric Surgery, Fresno
Heart and Surgical Hospital, University of California San Francisco, Fresno, CA, USA
Eric Marcotte, MD, FACS, FASMBS Department of Surgery, Division of GI/Minimally
Invasive Surgery, Loyola University Medical Center, Stritch School of Medicine, Maywood,
IL, USA
Samer G. Mattar, MBBCh, FRCS, FACS, FASMBS Swedish Medical Center, Seattle, WA,
USA
Corrigan L. McBride, MD, MBA Bariatric Services, Department of Surgery, University of
Nebraska Medical Center, Omaha, NE, USA
Emanuele Lo Menzo, MD, PhD, FACS, FASMBS Department of General Surgery, The
Bariatric and Metabolic Institute, Cleveland Clinic Florida, Weston, FL, USA
Marc P. Michalsky, MD Clinical Surgery and Pediatrics, Center for Healthy Weight &
Nutrition, Pediatric Surgery Department, Nationwide Children’s Hospital, Columbus, OH,
USA
Dean J. Mikami, MD Department of Surgery, University of Hawaii John A. Burns School of
Medicine, Honolulu, HI, USA
Tripurari Mishra, MD Minimally Invasive Bariatric Surgery and Advanced Laparoscopy
Fellowship, Gundersen Medical Foundation, La Crosse, WI, USA
Rachel L. Moore, MD, FACS, FASMBS Moore Metabolics & Tulane University Department
of Surgery, New Orleans, LA, USA
John M. Morton, MD, MPH, FACS, FASMBS, ABOM Bariatric and Minimally Invasive
Surgery Division, Yale School of Medicine, New Haven, CT, USA
Contributors
Contributors
xxvii
Geoffrey S. Nadzam, MD, FACS, FASMBS Department of Surgery, Yale School of
Medicine, New Haven, CT, USA
Estefano A. Negri, MD The Center for Obesity and Diabetes, Oswaldo Cruz German
Hospital, São Paulo, Brazil
Lucia H. Nguyen, MD General Surgery, Baylor Scott and White Health, Temple, TX, USA
Ninh T. Nguyen, MD, FASMBS Department of Surgery, Division of Gastrointestinal Surgery,
University of California, Irvine Medical Center, Orange, CA, USA
Brittany Nowak, MD General Surgery, NYU Langone Medical Center, New York,
NY, USA
Nabeel R. Obeid, MD Department of Surgery, University of Michigan, Ann Arbor,
MI, USA
J. Patrick O’Leary, MD Department of Surgery, Florida International University, Herbert
Wertheim College of Medicine, Miami, FL, USA
Robert W. O’Rourke, MD Department of Surgery, University of Michigan, Ann Arbor, MI,
USA
Bariatric Surgery Program, Division of General Surgery, Ann Arbor Veterans Administration
Hospital, Ann Arbor, MI, USA
Manish Parikh, MD Bariatric Surgery, Bellevue Hospital Center, NYU Langone Medical
Center, New York, NY, USA
Richard M. Peterson, MD, MPH, FACS, FASMBS Bariatric and Metabolic Surgery,
Department of Surgery, UT Health San Antonio, San Antonio, TX, USA
Anthony T. Petrick, MD, FACS, FASMBS Geisinger Medical Center, Danville, PA, USA
Thomas P. Petrick, MD Department of Surgery, Chinle Comprehensive Health Care Facility,
Chinle, AZ, USA
Tarissa Z. Petry, MD The Center for Obesity and Diabetes, Oswaldo Cruz German Hospital,
São Paulo, Brazil
Alfons Pomp, MD, FRCSC, FACS, FASMS GI Metabolic and Bariatric Surgery, Weill
Cornell Medicine, New York-Presbyterian Hospital, New York, NY, USA
Jaime Ponce, MD, FACS, FASMBS Bariatric Surgery, Metabolic and Bariatric Care, CHI
Memorial Hospital, Chattanooga, TN, USA
David A. Provost, MD, FASMBS, FACS Division of General and Bariatric Surgery, Baylor
Scott & White Medical Center, Temple, TX, USA
Aurora D. Pryor, MD, FACS Department of Surgery, Stony Brook Medicine, Stony Brook,
NY, USA
Kevin M. Reavis, MD, FACS Foregut and Bariatric Surgery, Division of Gastrointestinal and
Minimally Invasive Surgery, The Oregon Clinic, Legacy Weight and Diabetes Institute,
Portland, OR, USA
Christine Ren-Fielding, MD, FACS, FASMBS General Surgery, Division of Bariatric
Surgery, NYU Langone Medical Center, New York, NY, USA
Jaime A. Rodriguez, MD Department of Surgery, Florida International University, Herbert
Wertheim College of Medicine, Miami, FL, USA
Ann M. Rogers, MD Penn State Surgical Weight Loss Program, Department of Surgery,
Penn State Hershey Medical Center, Hershey, PA, USA
xxviii
Raul J. Rosenthal, MD, FACS, FASMBS Department of General Surgery, The Bariatric and
Metabolic Institute, Cleveland Clinic Florida, Weston, FL, USA
Francesco Rubino, MD Bariatric and Metabolic Surgery, King’s College London Consultant,
King’s College Hospital, London, UK
Michelle H. Scerbo, MD, MS Department of Surgery, Division of Minimally Invasive and
Elective General Surgery, McGovern Medical School, UT Health, Houston, TX, USA
Keith Scharf, DO, FACS, FASMBS Bariatric Surgery, Department of General Surgery,
Loma Linda University Health, Loma Linda, CA, USA
Philip R. Schauer, MD Department of General Surgery, Bariatric and Metabolic Institute,
Cleveland Clinic, Cleveland, OH, USA
Federico J. Serrot, MD Section of Minimally Invasive Surgery, Department of General
Surgery, The Bariatric and Metabolic Institute, Cleveland Clinic Florida, Weston, FL, USA
Shinil K. Shah, DO Department of Surgery, Division of Minimally Invasive and Elective
General Surgery, McGovern Medical School, UT Health, Houston, TX, USA
Michael E. DeBakey Institute for Comparative Cardiovascular Science and Biomedical
Devices, Texas A&M University, College Station, TX, USA
Adam C. Sheka, MD Department of Surgery, University of Minnesota, Minneapolis, MN,
USA
Ranjan Sudan, MD Department of Surgery, Division of Metabolic and Weight Loss Surgery,
Duke University, Durham, NC, USA
Amit Surve, MD Bariatric Medicine Institute, Salt Lake City, UT, USA
William A. Sweet, MD, FACS (Retired) Reading Hospital and Medical Center, West
Reading, PA, USA
Patrick J. Sweigert, MD Department of Surgery, Loyola University Medical Center,
Maywood, IL, USA
Samuel Szomstein, MD, FACS, FASMBS Department of General Surgery, The Bariatric and
Metabolic Institute, Cleveland Clinic Florida, Weston, FL, USA
Dana A. Telem, MD, MPH Clinical Affairs, Comprehensive Hernia Program, Department of
Surgery, University of Michigan, Ann Arbor, MI, USA
Renée M. Tholey, MD Department of Surgery, Thomas Jefferson University Hospital,
Philadelphia, PA, USA
David S. Tichansky, MD Department of Surgery, Thomas Jefferson University Hospital,
Philadelphia, PA, USA
Hussna Wakily, MD Division of General Surgery, Department of Surgery, NY and NJ
Surgical Associates, Queens, NY, USA
Elizaveta Walker, MPH Department of Surgery, Oregon Health & Science University,
Portland, OR, USA
D. Brandon Williams, MD Department of Surgery, Vanderbilt University Medical Center,
Nashville, TN, USA
Erik B. Wilson, MD Department of Surgery, Division of Minimally Invasive and Elective
General Surgery, McGovern Medical School, UT Health, Houston, TX, USA
Contributors
Contributors
xxix
Keith M. Wirth, MD Department of Surgery, University of Minnesota, Minneapolis, MN,
USA
Bruce M. Wolfe, MD Department of Surgery, Oregon Health & Science University, Portland,
OR, USA
Hinali Zaveri, MD Bariatric Medicine Institute, Salt Lake City, UT, USA
Natan Zundel, MD Department of Surgery, Florida International University Herbert
Wertheim College of Medicine, North Miami Beach, FL, USA
Part I
Basic Considerations
1
Epidemiology and Discrimination
in Obesity
R. Armour Forse, Monica M. Betancourt-Garcia,
and Michelle Cordoba Kissee
Chapter Objectives
At the end of the chapter, the reader should be able to
describe:
1. Definition of obesity
2. Epidemiology of obesity
• Global burden of obesity
• Obesity in the United States
3. Disparities in obesity by age, race, ethnicity, gender, and socioeconomic status
4. Obesity-related discrimination, especially in
spheres of employment, health care, and children
5. Effect of discrimination on obese individuals
Introduction
Obesity has become one of the most significant public health
challenges in both economically developed and developing
regions of the world. In 2016, more than 1.9 billion adults
worldwide were overweight, and, of these, more than 650
million were obese, a number that has tripled since the 1970s
[1]. There are an estimated 2.5 people added to the global
population each second, and one of them will be obese or
R. A. Forse (*)
DHR Health Institute for Education and Innovation, DHR Health
System, Department of Surgery, University of Texas Rio Grande
Valley, Edinburg, TX, USA
e-mail: r.forse@dhr-rgv.com
M. M. Betancourt-Garcia
DHR Health Institute for Research and Development, DHR Health
System, Edinburg, TX, USA
M. C. Kissee
Endocrinology, Diabetes, Metabolism and Bariatrics, DHR Health
System, University of Texas Rio Grande Valley, Edinburg, TX, USA
overweight. In the United States it is estimated that 39.8% of
the adult population is obese [2].
Obesity is associated with markedly reduced life expectancy, thus becoming a leading cause of preventable deaths
in the United States. In 2015, high body mass index (BMI)
contributed to 4 million deaths and contributed to 120 million disability-adjusted life-years (Fig. 1.1). High BMI has
been shown to be associated with hypertension, hyperlipidemia, coronary artery disease, abnormal glucose tolerance or
diabetes, sleep apnea, nonalcoholic fatty liver disease, musculoskeletal disorders, kidney disease, and certain cancers
including esophageal, pancreatic, renal cell, postmenopausal
breast, endometrial, cervical, and prostate cancers [3].
Health-care costs associated with obesity are high and
climbing. In 1998, the estimated annual cost of obesity was
$78.5 billion. Today, in the United States alone, obesity and
its related illnesses cost an estimated $191 billion with the
medical costs $2741 higher, annually, for people who are
obese than those of normal weight [4]. Social, psychological,
and economic consequences are also well-recognized. A
large amount of research is focused on the understanding of
obesity, and many public health efforts have been directed
toward controlling its exponential growth.
Definition of Obesity
The World Health Organization (WHO) defines obesity as a
condition of excessive fat accumulation in the body to the
extent that health and well-being are adversely affected [1].
If the amount of body fat exceeds normal physiological values, a person is obese. Although this definition appears simple on the surface, it has major limitations. The physiologically
normal amount of body fat depends on age and on gender
with high variation among individuals. Newborns have
10–15% body fat (BF), and during the 1st year of life, this
increases to about 25%. After that, BF% slowly decreases
again to 15% of body weight at the age of 10 years, when
differences between the sexes become more apparent. During
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_1
3
4
R. A. Forse et al.
Musculoskeletal Disorders
Cardiovascular Diseases
a Disability-Adjusted Life-Years in 1990
Cancers
Chronic kidney Disease
Diabetes Mellitus
b Disability-Adjusted Life-Years in 2015
10
10
8
8
6
Disability-Adjusted Life-Years
(in millions)
Disability-Adjusted Life-Years
(in millions)
1.6%
1.6%
2.1%
4
25.6%
35.4%
0.3%
2
0.6%
0.8% 0.3%
20
6
18.7%
25
3.3%
0.2%
2.5%
0.4%
6.4%
0.8% 0.3%
2.8%
11.5%
2.1%
0
3.1%
30
35
40
45
50
4.2%
2.9%
3.4%
5.8%
33.7%
4
2
4.1%
0
2.8%
20
25
18.0%
4.7%
30
35
40
45
50
Body-Mass Index
Body-Mass Index
Fig. 1.1 Global disability-adjusted life-years associated with a high
body mass index (1990–2015). Shown are the number of global
disability-­adjusted life-years (in millions) related to a high body mass
index (BMI) among adults according to the cause and the level of BMI
in 1990 (Panel a) and in 2015 (Panel b). (Source: GBD 2015 Obesity
Collaborators [3]. Reprinted with permission from Massachusetts
Medical Society)
sexual maturation, girls experience an increase in their body
fat again, up to 25%, whereas boys keep about the same
BF%. During adulthood, BF% increases slowly with age in
both males and females. It is not known whether this age-­
related increase during adult life is a normal physiological
effect or whether it is caused by overeating and/or a sedentary lifestyle.
Body fat can be measured by different techniques including densitometry, hydrometry, dual energy X-ray absorptiometry (DXA), chemical multi-compartment models,
computed tomography (CT), or magnetic resonance imaging
(MRI). These methods are not suited for use under clinical
conditions and in population-based studies. There are a number of other methods available for large-scale use that can
predict body fat (BF)%; these include skinfold thickness
measurements, bioelectrical impedance, the use of body
mass index (BMI) and waist circumference, and the more
recently described body adiposity index (BAI) [5]:
divided by height in m2. Generally, healthy BMI range is
from 18.5 to 24.9 kg/m2. Overweight is defined as a BMI
from 25 to 29.9 kg/m2, and obesity is defined as a BMI of
30 kg/m2 or greater. Obesity can further be subdivided based
on subclasses of BMI, as shown in Table 1.1 [6, 7]. Extreme
obesity is defined as a BMI greater than 40 kg/m2. Waist circumference can also be used in combination with a BMI
value to evaluate health risk for individuals. The waist/hip
ratio relates to the distribution of body fat. Patients with a
waist/hip ratio of less than one tend to have more of a peripheral fat distribution ratio often referred to as having a “pear”
Table 1.1 Categories of BMI and disease risk relative to normal
weight and waist circumference
BAI = ( hip circumference / height1.5 ) - 18.
These methods rely on statistical relationships between
easily measurable parameters and a method of reference,
normally densitometry, deuterium oxide dilution, or
DXA. As the range of BF% varies largely and is dependent
on age and sex, clearly defined cutoff points for obesity,
expressed as BF%, cannot easily be established. There is no
doubt that these clinical measures are limited in terms of
accuracy, but they are very portable and applicable and give
meaningful trends when used over time.
Of the aforementioned parameters, the one that is most
widely applied is BMI, which is determined by weight
Underweight
Normala
Overweight
Obesity
Obesity
Extreme
obesity
Relative disease risk by waist
circumference (type 2 diabetes,
hypertension, cardiovascular
disease)
Men
>102 cm
Men ≤102 cm
(>40 in)
(≤40 in)
Women
Obesity Women ≤88 cm >88 cm (>35
in)
(≤35 in)
BMI kg/m2 class
<18.5
–
–
–
18.5–24.9 –
–
–
25.0–29.9 –
Increased
High
30.0–34.9 I
High
Very high
35.0–39.9 II
Very high
Very high
III
Extremely high Extremely
≥40
high
Modified from [6, 7]
a
Increased waist circumference can also be a marker for increased risk
even in persons of normal weight
1
Epidemiology and Discrimination in Obesity
5
distribution. This fat distribution has lower health risks.
Patients with a waist/hip ratio of greater than one are referred
to as having an “apple” or central fat distribution, and these
patients are considered to have a high health risk [8]. In children (2–19 years of age), overweight is defined as a BMI-for-­
age greater than or equal to the 85th percentile and less than
the 95th percentile on the Centers for Disease Control and
Prevention (CDC) growth charts [9]. Obesity is defined as a
BMI-for-age greater than or equal to the 95th percentile on
the CDC growth charts.
It is well accepted that BMI is an estimate rather than an
accurate measurement. It fails to account for fitness, and
there is a wide variation of body adiposity in the same BMI
range. In general, adiposity has been shown to vary among
men and women (with women having more adiposity for the
same BMI group) and across different age groups (adiposity
increases with age). It has also been noted that in the same
BMI range, Asians and African-Americans have more prevalence of diseases such as hypertension and diabetes. Using
BMI as the only qualifying requirement for bariatric surgery
runs the risk of discriminating against these groups, and care
may be denied to patients who may benefit from if delivery
of care is based upon this imperfect and somewhat arbitrary
measure of obesity.
Epidemiology of Obesity
Global Burden of Obesity
Overweight and obesity are increasing public health challenges in both economically developed and developing
regions of the world, with nearly one third of the world’s
population (1.9 billion adults and children) overweight or
obese [1] (Fig. 1.2). This is a substantial increase from 1980
when only 5% of men and 8% of women were obese [10]. It
Male
Female
Global
revalence of Overweight and Obesity
P
in the United States
The strongest data on obesity prevalence rates over time in
the United States come from the results of the National
Low SDI
Low-middle SDI
Middle SDI
High-middle SDI
High SDI
2010
2015
C Obesity in Adults According to Year
20
15
Prevalence (%)
Fig. 1.2 Prevalence of
obesity at the global
level, according to
sociodemographic index
(SDI). Age standardized
prevalence trends at the global
level and according to SDI
quintile from 1980 to 2015
among adults. (Source: GBD
2015 Obesity Collaborators
[3]. Reprinted with
permission from
Massachusetts Medical
Society)
is estimated that if recent trends continue, by 2030 up to
57.8% of the world’s adult population (3.3 billion people)
could be either overweight or obese [11]. In general, the
prevalence of overweight and obesity is higher in economically developed countries; however, the prevalence has continuously increased across all levels of development,
regardless of economic growth [3, 11].
Approximately 604 million adults are obese, and the
global prevalence is higher in women than in men [3]. More
than 50% of the world’s obese population live in only ten
countries, including the United States, China, India, Russia,
Brazil, Mexico, Egypt, Germany, Pakistan, and Indonesia
[12]. Obesity has been thought of as a high-income country
problem, but the prevalence of overweight and obesity is also
on the rise in developing countries, particularly in urban settings. This is in part fueled by industrialization, the creation
of mass transit systems, lifestyle changes, and the promotion
of unhealthy “fast foods” in these countries in the last two
decades. Many developing nations are now facing a “double
burden” of disease as is seen in much of Asia, Latin America,
the Middle East, and Africa. While they continue to deal with
the problems of infectious disease and undernutrition, they
are experiencing a rapid upsurge in noncommunicable disease risk factors such as obesity and overweight. It is not
uncommon to find undernutrition and obesity existing side
by side in the same community and the same household.
Conversely, accelerated growth rates in overweight and obesity seen from 1992 to 2002 have slowed in developed countries [12].
10
5
0
1980
1985
1990
1995
2000
Year
2005
6
R. A. Forse et al.
Health and Nutrition Examination Surveys (NHANES). The
NHANES program of the National Center for Health
Statistics (NCHS), Centers for Disease Control and
Prevention, includes a series of cross-sectional nationally
representative health examination surveys beginning in 1960
[13–17]. In each survey, a nationally representative sample
of the US civilian non-institutionalized population was
selected using a complex, stratified, multistage probability
cluster sampling design. In the 2009–2010 and 2015–2016
surveys, household interview and a physical examination
were conducted for each survey participant including height
and weight measured as part of a comprehensive set of body
measurements by trained health technicians, using standardized measuring procedures and equipment excluding pregnant women and persons missing a valid height or weight
measurement [2, 18]. In the 2009–2010 survey, age was
based on age at the time of interview and grouped into
20–39 years of age, 40–59 years of age, and 60 years and
older. Race and ethnicity were self-reported and for purposes
of this report were classified as non-Hispanic white, non-­
Hispanic black, Mexican-American, other Hispanic, and
others.
Results from the 2009–2010 National Health and
Nutrition Examination Survey (NHANES), using measured
heights and weights, indicate that an estimated 33.0% of US
adults aged 20 and over are overweight, 35.7% are obese,
and 6.3% are extremely obese [18]. In 2009–2010, the age-­
adjusted mean BMI was 28.7 (95% CI, 28.3–29.1) for men
and also 28.7 (95% CI, 28.4–29.0) for women [18]. Figure 1.3
shows the trends in overweight and obesity among adults
from 1960 to 2010 [16]. In this figure it is interesting to note
that the rate of overweight has been more or less stable, but
there have been significant increases in the rates of obesity,
with obesity rates having very recently overtaken the rate of
prevalence of overweight in the adult population.
The National Center for Health Statistics analyzed obesity in an updated 2015–2016 study. The participants in the
2015–2016 survey were grouped into 20–39 years of age,
40–59 years of age, and 60 years and older. Race and ethnicity were classified as non-Hispanic white, non-Hispanic
black, non-Hispanic Asian, and Hispanic. The data for adults
suggests a steady prevalence of obesity from the 1960s
through the 1980s, with a steady increase in obesity since the
late 1980s and today in the United States, with the estimated
age-adjusted prevalence moving upward from a previous
level of 23.0% in 1988–1994 to approximately 39.8% in
2015–2016 [2, 16]. The age-adjusted prevalence of obesity
was 37.9% among adult men and 41.1% among adult women
[2]. The highest prevalence of obesity was seen in the 40–59
age group for both men and women. One of the national
health objectives for the Healthy People 2020 initiative is to
reduce the prevalence of obesity among adults by 10–30.5%
[19]. Figure 1.4 depicts the trends in obesity prevalence
among adults and youth from 1999 to 2016.
Data suggest that those who are obese may be gaining
weight at a more rapid pace than those who are not. Data
from the Behavioral Risk Factor Surveillance System (a
random-­digit telephone survey of the household population
of the United States) shows that it is not just that more
Americans are becoming obese but that it is the most severe
obesity that is increasing the most in relative terms. From
2000 through 2005, the prevalence of obesity (self-reported)
increased by 24%, the prevalence of a self-reported BMI
greater than 40 increased by 50%, and the prevalence of a
BMI greater than 50 increased by 75% [20]. The greatest
relative increase has been in the proportion of individuals
with a BMI greater than 50 kg/m2. The most recent NHANES
data also confirm this trend: the percentage of the population
with a BMI greater than 40 has increased from 0.9% in the
1960s to approximately 6% at the current time [17].
60
Percent
50
40
Overweight
30
20
10
0
Obese
Extremely obese
19601962
19711974
19761980
Fig. 1.3 Increasing trends in overweight, obesity, and extreme obesity
among US men ages 20–74 years, spanning the years 1960–1962
through 2009–2010. Age adjusted by the direct method to the 2000 US
Census population using age groups 20–39, 40–59, and 60–74.
Overweight is a body mass index (BMI) of 25 kg/m2 or greater but less
than 30 kg/m2. Obesity is a BMI greater than or equal to 30 kg/m2.
19881994
2001- 2005- 20092002 2006 2010
Extreme obesity is a BMI greater than or equal to 40 kg/m2. (Data
sources: CDC/NCHS, National Health Examination Survey I 1960–
1962; National Health and Nutrition Examination Survey (NHANES) I
1971–1974; NHANES II 1976–1980; NHANES III 1988–1994;
NHANES 1999–2000, 2001–2002, 2003–2004, 2005–2006, 2007–
2008, and 2009–2010. Data from Fryar et al. [16])
1
Epidemiology and Discrimination in Obesity
Fig. 1.4 Trends in obesity
prevalence among adults aged
20 and over (age adjusted)
and youth aged 2–19 years:
United States, 1999–2000
through 2015–2016. (Source:
Hales et al. [2])
7
40
Percent
30
37.7
30.5
30.5
32.2
34.3
35.7
34.9
16.8
16.9
16.9
17.2
2007–
2008
2009–
2010
2011–
2012
2013–
2014
33.7
39.6
Adults1
20
13.9
15.4
17.1
15.4
18.5
Youth1
10
0
1999–
2000
2001–
2002
2003–
2004
2005–
2006
2015–
2016
Survey years
Epidemiology of Childhood Obesity
sity was seen at all race, ethnicity, and income levels [15],
those of Hispanic origin and non-Hispanic black children
There were more than 213 million children aged 5–19 years had a higher prevalence compared to non-Hispanic white
old that were overweight and 125 million children with obe- and non-Hispanic Asian children [2].
sity as of 2016 [21]. In a study that included data from 200
Overweight children and adolescents are more likely to
countries and territories in all regions of the world, obesity be overweight or obese adults. Those with a BMI between
prevalence increased in every region. Rates rose from 0.7% the 75th and 84th percentiles were up to 20 times more likely
to 5.6% in girls and from 0.9% to 7.8% in boys since 1975 than their leaner counterparts of becoming overweight or
[21], and the rates of increase were highest in early adult- obese as young adults [23]. Childhood obesity can lead to
hood between the ages of 15 and 24 years old [30]. The high- immediate psychosocial and metabolic problems but may
est global standardized mean BMI in children and adolescents also have lasting effects on health, especially if this weight is
were found in high-income English-speaking regions carried into adulthood. A complex interaction of genetic fac(22.4 kg/m2) and Polynesia (23.1 kg/m2) [21].
tors such as variation in DNA sequence or expression and
Children in developing countries are more vulnerable to epigenetic factors including in utero environment, behavior,
inadequate prenatal, infant, and young child nutrition. At the lifestyle, ethnic variability in body composition, and values/
same time, they are exposed to high-fat, high-sugar, high-­ perceptions has led to an increase in the prevalence of obesalt, energy-dense, micronutrient-poor foods, which tend to sity and its assocaited chronic diseases such as high blood
be lower in cost. Additionally, urbanization and mechaniza- pressure, high cholesterol, diabetes, cardiovascular disease,
tion, higher rates of television viewing and electronic device and many cancers.
use, and increasing pressure among children in developing
countries to perform scholastically have led to a sharp decline
in physical activity. Interaction of these factors with chang- Obesity and Age
ing dietary patterns results in drastic increases in childhood
Obesity rates are high in most age groups. For both men and
obesity and metabolic syndrome.
In the United States in 2015–2016, the prevalence of obe- women, the prevalence of obesity is higher among middle-­
sity in children 2–19 years of age was 18.5% and affected aged adults (42.8%) between 40 and 59 years of age than
about 13.7 million children and adolescents, with the highest younger adults 20 and 39 years of age (35.7%) [2]. The rate
prevalence among adolescents 12–20 years of age [22] of increase, however, is higher in early adulthood between 15
(Fig. 1.5). The prevalence of obesity decreased with increas- and 24 years of age [3]. Obesity rates, in general, increase
ing level of education and income in the household ranging with age until approximately 75 years of age, when rates
from 18.9% among children and adolescents in the lowest decline. The decline in obesity rates in the elderly could be
income group and 10.9% among those in the highest income attributed to a decrease in lean body mass and a tendency to
group [2]. While an increase in prevalence of childhood obe- gain fat in the older patient, which plateaus as the older
8
R. A. Forse et al.
Fig. 1.5 Prevalence of
obesity among youth aged
2–19 years, by sex and race
and Hispanic origin: United
States, 2015–2016. (Source:
Hales et al. [2])
Non-Hispanic white
30
Non-Hispanic black
Hispanic
Non-Hispanic Asian
28.0
1–3
25.8
1,2
25.1
1,2
25
1,2
23.6
22.0
1,2
Percent
20
15
19.0
14.6
14.1
11.0
13.5
11.7
10.1
10
5
0
Total
patient establishes a new weight set point. In addition, there
is increasing mortality from obesity-related conditions with
age; a significantly higher all-cause mortality has been noted
in obese individuals compared to normal weight subjects,
with one study predicting that mortality was likely to occur
9.44 years earlier for those who were obese (BMI, ≥30) [24].
Racial, Ethnic, and Income Disparities
Increasing BMI and increasing obesity prevalence are affecting the entire adult population with no group being immune
[25, 26]. Increasing rates of obesity are seen across men and
women of all ethnic groups, of all ages, and of all educational and socioeconomic levels. Still, racial, ethnic, and
socioeconomic disparities are seen in the prevalence of obesity, and some subgroups in the population are affected to a
greater extent than others.
Boys
Girls
the 12-year period from 1999 through 2010 but has slowed in
recent years [2].
For women, the age-adjusted prevalence is 41.1%, and the
range is from 14.8% among non-Hispanic Asian women to
54.8% among non-Hispanic black women, and a prevalence
of 50.6% in Hispanics (Fig. 1.6) [2]. Within all race/ethnicity
groups, women have a higher prevalence than men.
Interestingly, non-Hispanic black women also experienced a
decline in prevalence since the 2011 survey from 56.9% to
54.8% [2].
These disparities are likely a combination of differences
in socioeconomic status, environmental and social risk factors among racial groups, and genetic, epigenetic, and metabolic factors, which suggest a hereditary nature of disease
and similar obesity patterns in families [14, 15].
Obesity and Socioeconomic Status
The prevalence of overweight and obesity in both adults and
children is higher in economic developed countries [11].
However, when dividing countries into quintiles of economic
There are significant racial and ethnic disparities in obesity status, the most rapid relative increase in obesity occurred in
prevalence among US adults. Among men, overall age-­ individuals living in countries with low and low-middle
adjusted obesity prevalence is 37.9%, but within race/ethnic- sociodemographic characteristics [3].
ity groups, prevalence ranges from 10.1% among
On an individual level, obesity prevalence decreases as
non-Hispanic Asian men to 43.1% among Hispanic men income increases [14] with obesity among adults approxi(Fig. 1.6). Between the 1988–1994 and 2015–2016 surveys, mately 8% lower in the highest income group (>350% of
the prevalence of obesity among men increased, from 20.3% the federal poverty level) compared to those living on less
to 37.9% in non-Hispanic white men and 23.9–43.1% among than 130% of the federal poverty level. The largest contrast
Hispanic men [2]. Prevalence for non-Hispanic black men in prevalence is observed between women with income
rose from 21.1% in 1988–1994 to 37.3% in 2007–2008 but >350% of the federal poverty level and those 130% below
has since dropped slightly to 36.9%. For men, the overall the federal poverty level, 29.7% versus 45.2%,
prevalence of obesity showed a significant linear trend over respectively.
Obesity and Race
1
Epidemiology and Discrimination in Obesity
Fig. 1.6 Age-adjusted
prevalence of obesity among
adults aged 20 and over, by
sex and race and Hispanic
origin: United States,
2015–2016. (Source: Hales
et al. [2])
9
Non-Hispanic white
60
Non-Hispanic black
Hispanic
Non-Hispanic Asian
54.8
1,2
1,2
50
46.8
50.6
47.0
1,2
1,2
43.1
1,4
Percent
40
1
37.9
1
37.9 1,3,436.9
38.0
1
30
20
12.7
10
14.8
10.1
4
0
Total
Education has a large influence on obesity rates. Age-­
adjusted prevalence of obesity among college graduates is
27.8%, while prevalence for those who were high school
graduates or less is 40.0% [27].
It is interesting to note that some of these trends differ
when considering race and ethnicity. For instance, women
in general have higher obesity rates than do men regardless
of income or education level, except for college-educated
high-­
income non-Hispanic white men who have higher
obesity rates than their non-Hispanic white female counterparts. Non-Hispanic Asian individuals have prevalence
rates at approximately 11%, and this remains consistent for
both men and women regardless of income or education
level [27].
Trends in Obesity
Close examination of trends in obesity shows that this epidemic arose from gradual yearly weight gain in the population produced from a slight consistent degree of positive
energy balance (i.e., energy intake exceeding energy expenditure). Using longitudinal and cross-sectional data sets, it
was found that the average adult in the United States has
gained an average of 1–2 lb/year for the past two to three
decades [28]. Assuming that an excess of 3500 kcal produces 1 lb of weight gain and assuming that excess energy
was stored with an efficiency of 50%, that weight gain in
90% of the adult population is attributable to a positive
energy balance of approximately 100 kcal/day. Thus, it
seems that the obesity epidemic arose gradually over a long
period because of a slight but consistent degree of positive
energy balance.
Our bodies are designed to work best in a setting in which
food was inconsistent and high levels of physical activity
Men
Women
were required to secure food and shelter and for transportation. In previous times, this biology was adequate to allow
most people to maintain a healthy weight without conscious
effort. Body weight regulation was achieved for most with
simple physiological control. The situation is different in
today’s environment. Securing food and shelter and moving
around no longer requires the high levels of physical activity
needed in the past. Technology has made it possible to be
productive while being largely sedentary.
Advancements in workplace technology and reduction
of manual labor have resulted in decreased energy expenditure. Factors such as urban design, land use, public transportation availability, density and location of food stores
and restaurants, and neighborhood barriers such as safety
and walkability contribute to unhealthy lifestyles.
Significant changes have taken place in the food environment with increased accessibility of inexpensive foods.
Prices of calorie-dense foods and beverages have decreased
considerably in contrast to increasing prices of fresh fruits,
vegetables, fish, and dairy items, contributing to increased
consumption of unhealthy foods in increasing portion sizes.
Significant marketing and advertising of unhealthy, energydense foods by the food industry contribute to excessive
food consumption. Under such conditions, weight gain can
only be prevented with conscious efforts to eat less eat
healthier and/or to be physically active.
Obesity rates are increasing among people in all income
and educational levels, but absolute rates are lower in those
with higher incomes and higher education levels. The finding that minority and low-income individuals are disproportionately affected by obesity is not surprising. The most
inexpensive foods are those containing high levels of fat and
sugar. The biological preference for these foods combined
with easy availability contributes to overeating. Further,
minority and low-income individuals may engage in less
10
physical activity than other sectors of the population [29].
One reason for this disparity may be because problems with
neighborhood safety in low-income areas may prevent
adults and children from engaging in outdoor physical activities. People who have more financial resources combat
these circumstances more easily and, consequently, maybe
more physically active and less obese than those with fewer
resources.
Discrimination in Obesity
Obesity Discrimination
Overweight and obese individuals are vulnerable to negative societal attitudes, stigma, and prejudice. Reported
experiences of weight/height discrimination included a
variety of settings in major lifetime events and interpersonal relationships. Weight bias has been documented in
multiple settings including places of employment, healthcare facilities, educational institutions, mass media, and
close interpersonal relationships with friends and family
members [30–33]. Obese individuals, especially the
severely obese, often confront bias in these various settings. They are frequently the target of ridicule even in their
early years in school. Some estimates even suggest that
25% of severely obese women were sexually abused. Obese
people have difficulty finding jobs [32], and, when they find
employment, they all too often have high levels of absenteeism, poor performance at work, and high health-care
costs. Similarly, within their families, the levels of conflict
regarding relationships, parenting, and sexuality are high.
Data from the two versions of the National Survey of
Midlife Development in the United States (MIDUS) have
shown increasing incidence of weight-based discrimination
from 7% in 1995–1996 to 12% in 2004–2006 [30]. Data for
this were drawn from a nationally representative multistage
probability sample of community-based English-speaking
adults in the contiguous United States.
Weight-based discrimination is the third leading cause of
prejudice, next only to age and race. In contrast to more
widely recognized social stigmas such as gender or race that
have legal sanctions in place to protect individuals from discrimination, there are no laws to prohibit weight discrimination, with the exception of a few states. It is unknown how
weight discrimination compares in strength or prevalence to
discrimination based on these attributes. Because weight
stigma remains a socially acceptable form of bias, negative
attitudes and stereotypes toward obese persons have been
frequently reported by employers, coworkers, teachers, physicians, nurses, medical students, dietitians, psychologists,
peers, friends, family members, and even among children
aged as young as 3 years [30].
R. A. Forse et al.
Employment Discrimination
Obesity discrimination is widespread in employment.
Employment discrimination may be related to the increasing focus on employee weight and its contribution to
employers’ overall costs stemming from increased healthcare costs and decreased productivity from absenteeism,
which is perceived among coworkers as laziness and lack
of dedication that may lead to heightened discrimination.
In 2007, obesity and morbid obesity were associated with
an estimated cost of $4.3 billion in the United States with
the estimated annual cost of absenteeism being $1026 for a
male worker with BMI >40 and $1262 for a female worker
with the same BMI [32]. In addition, employing morbidly
obese individuals is associated with additional cost to
employers; for example, a bariatric chair able to hold 500 lb
is estimated to cost $1295, and a bariatric toilet rated at
700 lb is estimated at $1049. Employers have started implementing wellness programs and incentives to control
health-care cost. Evidence suggests that medical costs fall
by about $3.27 for every dollar spent on wellness programs
and that absenteeism costs fall by about $2.73 for every
dollar spent [34]. Wellness programs have their own disadvantages; especially those that impose financial risk on
unhealthy employees are likely to be regressive because the
prevalence of unhealthy conditions typically targeted by
wellness programs is highest among people with low socioeconomic status.
Data from various surveys consistently document lower
labor market participation of overweight and obese individuals. While employers and coworkers may use the data
mentioned previously to justify bias against obese workers,
this mentality may adversely impact the psychological
well-­being of the individual, which in turn can result in lost
days at work and decreased productivity. Roehling et al.
found that overweight respondents were 12 times more
likely, obese respondents were 37 times more likely, and
severely obese respondents were 100 times more likely
than normal weight respondents to report employment discrimination [32]. In addition, women were 16 times more
likely to report weight-related employment discrimination
than men [32]. A meta-analysis of 32 experimental studies
that investigated weight discrimination in employment settings was recently conducted [31]. Typically, such experimental studies ask participants to evaluate a fictional
applicant’s qualifications for a job, where his or her weight
has been manipulated (through written vignettes, videos,
photographs, or computer morphing). Outcome variables
examined in these studies included hiring recommendations, qualification/suitability ratings, disciplinary decisions, salary assignments, placement decisions, and
coworker ratings. Across studies, it was demonstrated that
overweight job applicants and employees were evaluated
1
Epidemiology and Discrimination in Obesity
more negatively and had more negative employment outcomes compared to non-overweight applicants and employees [31]. After adjusting for sociodemographic and
health-related variables, an increase in BMI is shown to be
associated with a lower percentage of total working years,
a lower rate of employment, and a lower probability of
regaining employment.
Discrimination between normal weight individuals and
those overweight or obese has been demonstrated, and there
is now evidence that shows society holds very different body
standards for men versus women. As a result, the two sexes
are discriminated against differently. A 2010 study that compared income earnings across the BMI spectrum found that
very thin women are rewarded for being underweight
(decrease in weight of 2 standard deviations) and earn
approximately $22,000 more than average weight women
[3]. However, men who were 2 standard deviations below
average resulted in the opposite with an earnings decrement
of $17,535 [3]. Overweight and obese women lost roughly
between $9000 and $19,000 more than average weight
women, but men with an increase in weight of 2 standard
deviations actually earned $14,889.00 more than average
weight men [3]. Our society has standards of attractiveness
that are substantially slimmer for women than men who then
consequently experience opposite incentives regarding
weight. Overweight women are perceived as fat, lazy, undisciplined, and unsuccessful, while overweight men are perceived as strong, competent, reliable, and tough and are
rewarded for gaining weight until the point of obesity. Those
that do not resemble the stereotypical gender norms experience financial consequences proportional to their deviation
from these norms.
Health-Care Discrimination
Health-care costs associated with obesity are high, and the
estimated annual cost of obesity was $147 billion in 2008
with the medical costs for people who are obese being $1429
higher annually than those of normal weight in the same year
[35]. Studies demonstrate negative stereotypes and attitudes
toward obese patients by a range of health-care providers and
fitness professionals [33]. There is also research indicating
that providers spend less time in appointments and provide
less health education with obese patients compared with
thinner patients. There is evidence indicating that these attitudes begin during medical school. Medical students perceive overweight and obese patients as ugly, lazy, sloppy,
depressed, and a main target of derogatory humor in the hospital setting [36]. In response, obese individuals frequently
report experiences of weight bias in health care. Obese
patients also indicate that they feel disrespected by providers, perceive that they will not be taken seriously because of
11
their weight, report that their weight is blamed for all of their
medical problems, and are reluctant to address their weight
concerns with providers.
A number of studies demonstrate that obese persons are
less likely to undergo age-appropriate preventive cancer
screenings. Lower rates of preventive health care exist even
after control for factors such as less education, lower
income, lack of health insurance, and greater illness burden.
In a survey of obese women about their perceived barriers to
routine gynecological cancer screenings, weight was
reported to be a major barrier to seeking health care with
perception of disrespectful treatment and negative attitudes
from providers, embarrassment about being weighed, and
receiving unsolicited advice to lose weight, and it was also
reported that gowns, examination tables, and other medical
equipment were too small to be functional for their body
size [37].
Obesity Discrimination in Children
The psychological and social consequences of being overweight or obese are likewise experienced by children.
Obesity stigmatization and discrimination occurring in
adulthood actually emerges in children as early as 2 years
old [40]. Children can be victims of physical (e.g., kicking,
pushing, hitting), verbal (e.g., being teased, name calling,
derogatory remarks), or relational (e.g., being ignored or
avoided, social exclusion, being targets of rumors) aggression [41]. Studies have shown that preadolescent obese
boys and girls are more likely to be victims of bullying
because they deviate from appearance ideals [42].
Overweight and obese peers are associated with negative
adjectives and less preferred as friends than the normal
weight children, and the prejudice was stronger toward
females than males [43]. Interestingly, these attitudes persist despite the child’s own body size. In fact, overweight
children have demonstrated stronger stigmatism than those
who are not overweight [44]. There are two studies that
suggest even parents have biases against their own children
with obesity by not providing the same support emotionally
and financially than would be given to average weight children [45, 46].
Furthermore, these prejudices follow them through
adulthood and can have major social impacts. One survey
found that a few extra pounds could reduce a woman’s
chance of getting married by 20% [47]. This study also
noted overweight females completed fewer years of school,
had lower household incomes, and had 10% higher rates of
household poverty [47]. It is clear that a child’s perception
of an endomorph is established early in childhood and discrimination of these individuals begins early in life, especially in girls.
12
Effect of Discrimination on Obese Individuals
Perceived weight stigma and discrimination have a vast
impact on the quality of life of overweight individuals [30].
A number of studies have consistently demonstrated that
experiencing weight stigma increases the likelihood of
engaging in unhealthy eating behaviors and lower levels of
physical activity, both of which exacerbate weight gain and
obesity. For instance, as a result of discrimination in the
sphere of health care, overweight patients might be reluctant
to seek medical care, be more likely to cancel or delay
medical appointments, or put off important preventative
­
health-­care services [33].
besity Discrimination and Psychological
O
and Physical Health
Emerging research suggests that weight stigma invokes psychological stress, which contributes to poor physical health
outcomes for obese individuals and is a risk factor for depression, anxiety, low self-esteem, and body dissatisfaction [31].
Adults who experience weight-based stigmatization engage
in more frequent binge eating, are at increased risk for maladaptive eating patterns, and are more likely to have a diagnosis of binge eating disorder.
Obesity has been associated with impaired quality of life.
A 1997 study measured the impact of obesity on functional
health status and subjective well-being. Health-related quality of life, as measured by the Medical Outcomes Study
Short Form-36 Health Survey, of more than 300 obese persons seeking treatment for obesity at a university-based
weight management center was compared with that of the
general population and with that of other patients with
chronic medical conditions [38]. Obese participants (mean
BMI of 38.1) reported significantly lower scores (more
impairment) on all eight quality-of-life domains, especially
bodily pain and vitality. The morbidly obese (mean BMI of
48.7) reported significantly worse physical, social, and role
functioning; worse perceived general health; and greater
bodily pain than did the mildly obese (mean BMI of 29.2) or
moderately to severely obese (mean BMI of 34.5) [38]. The
obese participants also reported significantly greater disability attributable to bodily pain than did participants with other
chronic medical conditions.
There is also emerging evidence for physiological effects,
with weight discrimination having been shown to be related
to increased blood pressure, chronic inflammation, greater
disease burden, and even increased risk of mortality [39].
There is a common perception that weight discrimination
might encourage individuals with obesity to lose weight, but
research suggests the opposite to be true. Both adults and
children who experience weight-related discrimination are
R. A. Forse et al.
actually more likely to engage in behaviors that promote the
progression of obesity, including disordered eating, poor
adherence to healthy food choices, increased energy intake,
and avoidance of physical activity, thus further increasing
the prevalence and severity of obesity through a vicious
cycle of weight gain and discrimination [39].
Obesity Discrimination and Public Health
It has been shown that the more a disease is perceived as
under volitional control, the more stigmatizing it is—with
obesity generally being perceived as highly volitional.
Numerous studies have documented harmful weight-based
stereotypes that overweight and obese individuals are lazy,
weak-willed, unsuccessful, and unintelligent, lack self-­
discipline, have poor willpower, and are noncompliant with
weight loss treatment. Society regularly regards obese persons as architects of their own ill-health, personally responsible for their weight problems because of laziness and
overeating. Because of these common perceptions, weight
stigmatization is regarded as justifiable (and perhaps necessary) because obese individuals are believed to be personally
responsible for their weight and that stigma might even serve
as a useful tool to motivate obese persons to adopt healthier
lifestyle behaviors, with weight stigma being suggested by
some as a method for obesity control [39].
Although assumptions about personal responsibility in
obesity and justification of weight stigma are prevalent in our
national mindset, considerable scientific evidence has
emerged to challenge them. Many significant contributors to
obesity are beyond the control of individuals. In addition to
the important role of genetic and biological factors regulating body weight, multiple social and economic influences
have significantly altered the environment to promote and
reinforce obesity. It has been shown that most behavioral and
dietary interventions produce a modest 10% weight loss with
a high rate of weight regain. This is associated with improvements in obesity-related health consequences such as diabetes, hypertension, and cardiovascular disease but is unlikely
to alter appearance or translate into a non-obese BMI and is
unlikely to be significant to reduce obesity-related stigma
and discrimination.
Obesity stigma creates significant barriers in efforts to
address the epidemic. Current public health approaches to
tackling this epidemic focus on providing education to the
affected individuals rather than providing a comprehensive
plan to tackle this epidemic. This approach is based on the
assumption that Americans lack sufficient knowledge of the
personal behaviors leading to weight gain. This is apparent
in comparing the federal institution’s policies regarding obesity when compared to other disease states. For example,
National Institute of Health’s (NIH) projected spending for
1
Epidemiology and Discrimination in Obesity
HIV/AIDS in 2012 was $3.075 billion. When compared to
this, obesity, which affects more individuals and poses
numerous health risks, is allocated $830 million. The NIH is
comprised of 27 institutes and centers, each with a specific
research agenda, which focus on pressing and significant
health issues. Some of these institutes include the National
Cancer Institute, Eye Institute, the Human Genome Research
Institute, the Institute of Allergy and Infectious Disease, and
Institute of Mental Health to name a few. However, there is
not an institute dedicated to obesity, arguably one of the most
serious chronic diseases on both the national and international level. Federal and state legislative initiatives related to
obesity have failed to address societal and environmental
contributors for obesity. There is also a significant lack of
attention to stigma associated with obesity and its consequences for individuals in public health efforts against this
epidemic. Stigmatization of obese individuals poses serious
risks to their psychological and physical health, generates
health disparities, and interferes with implementation of
effective obesity prevention efforts. To optimize obesity prevention and intervention efforts, these assumptions must be
addressed within the sphere of public health, with recognition of the harmful impact of weight stigma on quality of life
and the need to eliminate stigma from current and future
public health approaches to the obesity epidemic.
Experimental research has shown that providing individuals with information emphasizing personal responsibility for
obesity increases negative stereotypes toward obese persons,
whereas information highlighting the complex etiology of
obesity (such as biological and genetic contributors)
improves attitudes and reduces stereotypes [31].
Conclusion
There is a clear need for increased public awareness and education about the complex etiology of obesity and the significant obstacles present in efforts to achieve sustainable weight
loss. The prevailing societal and media messages that reinforce blame on obese persons need to be replaced with messages that obesity is a chronic disease with a complex
etiology and is a lifelong condition for most obese persons.
Supporting individuals with adaptive ways to cope with
weight stigma can facilitate weight loss outcomes.
Question Section
1. Overweight is defined as a BMI (kg/m2) of _______.
A. 20–24.9
B. 30–34.9
C. >35
D. 25–29.9
13
2. Which of the following is true?
A. Medical costs for obese individuals are the same as
individuals with normal weight.
B. Patients with “apple” distribution are considered to
have a lower health risk than “pear” distribution.
C. Women have more adiposity for the same BMI group.
D. Adiposity decreases with age.
3. Which of the following races/ethnicities has the highest
prevalence of obesity?
A. Non-Hispanic White
B. Non-Hispanic Asian
C. Hispanic
D. Non-Hispanic Black
4. Discrimination related to obesity has been documented in
which of the following spheres?
A. Employment
B. Health-care facilities
C. Educational institutions
D. Close interpersonal relationships
E. All of the above
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2
The Pathophysiology of Obesity
and Obesity-Related Disease
Robert W. O’Rourke
Abbreviations
AgRP
ARCN
ATM
BAT
BMI
CART
CNS
DIT
ER
GIP
GLP-1
GWAS
HFC
LCFA
LHA
MAPK
MCH
MSH
NAFLD
NEAT
NO
NPY
NREE
POMC
PUFA
PVN
REE
ROS
SAT
SNP
SVF
Agouti-related peptide
Arcuate nucleus
Adipose tissue macrophages
Brown adipose tissue
Body mass index
Cocaine- and amphetamine-regulated transcript
Central nervous system
Diet-induced thermogenesis
Endoplasmic reticulum
Glucose-dependent insulinotropic polypeptide
Glucagon-like peptide-1
Genome-wide association analysis
Hypothalamic feeding center
Long-chain fatty acids
Lateral hypothalamic area
Mitogen-activated protein kinases
Melanin-concentrating hormone
Melanocyte stimulating hormone
Nonalcoholic fatty liver disease
Non-exercise-induced thermogenesis
Nitric oxide
Neuropeptide Y
Non-resting energy expenditure
Pro-opiomelanocortin
Polyunsaturated fatty acids
Paraventricular nucleus
Resting energy expenditure
Reactive oxygen species
Subcutaneous adipose tissue
Single nucleotide polymorphism
Stromal-vascular cell fraction
R. W. O’Rourke (*)
Department of Surgery, University of Michigan,
Ann Arbor, MI, USA
Bariatric Surgery Program, Division of General Surgery,
Ann Arbor Veterans Administration Hospital, Ann Arbor, MI, USA
e-mail: rorourke@med.umich.edu
TEE
UCP
UPR
VAT
WAT
Total energy expenditure
Uncoupling proteins
Unfolded protein response
Visceral adipose tissue
White adipose tissue
Chapter Objectives
• Part I
1. Understand the mechanisms that regulate body
weight and their contribution to the obesity phenotype, including regulation of satiety and hunger, metabolic rate, and thermogenesis.
2. Understand the evidence that demonstrates that
obesity is a genetic phenomenon, including data
from twin studies and genome-wide analyses.
3. Understand the concept of thrifty genes, the
thrifty genotype, epigenetics, and the evolutionary influences that contribute to the human tendency towards excess adiposity.
4. Understand the terms homeostasis, allostasis,
and homeorhesis and how these terms describe
the behavior of biologic systems.
• Part II
1. Understand the early events in adipose tissue
that contribute to adipose tissue dysfunction
including hypoxia and nutrient excess.
2. Understand how endoplasmic reticulum stress,
oxidative stress, and inflammation evolve in adipose and other tissues and how these phenomena
conspire to induce metabolic dysfunction at the
tissue level.
3. Understand the concepts of adipose tissue buffering and overflow and their contribution to the
pathogenesis of metabolic disease.
4. Understand the basic concepts behind the pathogenesis of liver disease, vascular disease, diabetes, and cancer in obesity.
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_2
15
16
R. W. O’Rourke
Introduction
Obese people… already subject to adverse health effects are
additionally victimized by a social stigma predicated on the
Hippocratic nostrum that weight can be controlled by ‘deciding’
to eat less and exercise more. This simplistic notion is at odds
with substantial scientific evidence illuminating a precise and
powerful biologic system that maintains body weight within a
relatively narrow range. Voluntary efforts to reduce weight are
resisted by potent compensatory biologic responses. -Jeffrey
Freidman [1]
The current epidemic of obesity is partly caused by the fact
that we all possess an ancient metabolism selected to protect us
from starvation, and hence, quite unsuited to our modern lifestyle…the metabolisms of most of humankind have been honed
by famine and starvation...hunger and famine have been an everpresent influence on genetic selection. -Andrew Prentice [2]
Obesity has been a part of the human condition since our
genesis. Stone figurines depicting obesity found throughout
Europe are among the earliest human artifacts [3] (Fig. 2.1).
Obesity is not a new phenomenon but rather part and parcel
of the human condition, and in our modern environment,
the majority of the population is overweight or obese [4].
Lifestyle modification achieves significant durable weight
a
loss only rarely. Why is this failure rate so high? Friedman
alludes to powerful biologic systems that defend body
weight, systems rooted in the midbrain and molded by a
genetic heritage that was forged, as Prentice states, by the
selective pressure of famine present during our evolution.
An understanding of the pathophysiology of obesity and
metabolic disease will guide development of novel therapeutic interventions. Perhaps equally important, an understanding of the origins of the epidemic and an appreciation
that obesity in most cases results not from a defect of individual willpower but rather from a physiology shaped by
eons of genetic selection and thrust into a modern “obesogenic” environment provide a basis for empathy towards
those afflicted with a debilitating condition. This chapter
reviews the physiologic mechanisms that lead to the obesity
phenotype, answering the question “How do we become
obese?” We go on to discuss genetic, evolutionary, and
environmental forces that molded these regulatory systems
to create the modern epidemic, answering the question
“Why do we become obese?” If obesity was simply a cosmetic condition, we might end there, but obesity is associated with a wide range of pathology. We will explore the
b
Fig. 2.1 (a) Mammoth ivory figurine, Swabian Jura, Germany circa 35,000 B.C. (b) Venus of Willendorf, circa 22,000 B.C.
2
The Pathophysiology of Obesity and Obesity-Related Disease
17
pathophysiology of metabolic disease and the effects of
nutrient excess on cellular metabolism and systemic
physiology.
Pathophysiology of Obesity
Pathophysiologic Mechanisms
ow Do We Become Obese?
H
Why do diets fail? Why do dieters hit a “wall” that resists
further weight loss? Why, in short, can we not simply
“decide” to eat less? The answers to these questions are
rooted in the physiologic systems that regulate body weight.
Humans are creatures of behavior, and so the most important
of these mechanisms control food-related behavior. But the
processes that regulate energy homeostasis are so central to
our biology that they interface with every aspect of physiology. These processes include control of food intake, energy
expenditure, thermogenesis, adipocyte biology, and a host of
other metabolic processes.
ontrol of Food Intake: The Leptin Paradigm
C
The reason we become obese, at the most basic level, is that
we eat more calories than we metabolize. The most important weight regulatory mechanism in humans is the collective system that controls food intake. Hunger, defined as the
desire to eat, and satiety, defined as the lack of hunger,
describe fundamental aspects of eating behavior. While conceptually useful, at the cellular and molecular level, these
definitions are less precise, as satiety and hunger mediators
utilize distinct yet intimately associated signaling pathways.
Furthermore, the dichotomy between satiety and hunger is
overly simplistic, as feeding behavior is highly complex and
includes subtle behaviors such as eating speed, food preferences, hunger irritability, and sensory and emotional
responses to food. We often consider such behaviors to be
under conscious control, but in fact the neural networks that
control these behaviors reside in the midbrain, an area that
from an evolutionary perspective long predates the frontal
cortex, the seat of conscious thought and cognition. Eating
behavior is regulated predominantly at a subconscious level.
We can, for a time, consciously control our food intake and
lose weight with dieting, but with few exceptions, such
efforts are limited in magnitude and followed by weight
regain, as midbrain counter-regulatory systems are activated
that vigorously defend body weight.
In 1994 Dr. Jeffrey Friedman cloned the leptin gene [5].
Friedman studied the Ob mouse, a hyperphagic obese strain
described in the 1950s that lacked a circulating factor that,
when restored from wild-type mice in parabiosis experiments, reversed the obese phenotype (Fig. 2.2). Friedman
identified circulating factor as the 16kD protein leptin and
Fig. 2.2 The Ob mouse
found the leptin gene to be mutated and nonfunctional in the
Ob mouse. Restoration of exogenous wild-type leptin protein to Ob mice reversed obesity. Friedman’s group cloned
the human leptin gene, and within a few years, two obese
human kindreds were identified with similar leptin mutations
in whom administration of exogenous leptin reversed obesity
[6]. These results were met with much excitement, and leptin
was considered a potential treatment for obesity in the general population. It was soon found, however, that single
monogenic leptin mutations are a rare cause of common
human obesity. Exogenous leptin, while a cure for Ob mice
and Ob humans, had no therapeutic effect in most obese
humans. In fact, common human obesity is characterized by
elevated leptin levels and resistance to leptin’s satiety effects,
a phenomenon not dissimilar from insulin resistance [7, 8].
The discovery of leptin transformed our understanding of
energy metabolism. Leptin mediates a complex communication between the gut, adipose tissue, and brain that regulates
food intake. Secreted by adipose tissue in response to a meal,
leptin circulates through the bloodstream to bind its receptor
in the hypothalamus and effect satiety. Serum leptin levels
are low after a nighttime fast; breakfast generates an adipose
tissue leptin secretory response that induces satiety and limits food intake for a few hours, after which leptin levels wane
and we find ourselves hungry by lunch and the cycle repeats.
In this manner, leptin controls short-term food intake. Leptin
also regulates long-term food intake and adipose tissue
stores. Peak postprandial leptin levels are determined by the
adipose tissue mass available to secrete leptin, which in turn
dictates the magnitude and kinetics of the satiety response.
When adipose tissue mass is reduced with dieting, postprandial leptin levels decrease, chronically attenuating the postprandial satiety response, leading to a progressive increase in
food intake until adipose tissue mass and postprandial leptin
levels are restored to baseline levels. This mechanism provides a cogent explanation for weight regain after dieting.
he Hypothalamic Feeding Center
T
As early as 1940, hypothalamic ablation experiments in rats
that induced hyperphagia and obesity first demonstrated the
18
R. W. O’Rourke
central role of the hypothalamus in weight regulation. Leptin tem (CNS) regions, as well as remote organs including adibinds receptors within the arcuate nucleus (ARCN) of the pose tissue and liver, that relay information regarding
hypothalamic feeding center (HFC) and activates anorexi- short-term prandial status and long-term energy stores. In
genic (satiety-inducing), catabolic pro-opiomelanocortin response, the HFC orchestrates diverse behavioral, meta(POMC), and cocaine- and amphetamine-regulated tran- bolic, and physiologic responses via efferent projections to
script (CART)-producing first-order neurons in the dorsolat- multiple brainstem and higher level central nervous system
eral ARCN. POMC is posttranslationally processed to yield networks that regulate food intake. These communication
the anorexigenic peptides α-, β-, and γ-MSH. Leptin simul- networks overlap with CNS regions involved in emotional
taneously inhibits secretion of the orexigenic (hunger-­ responses, cognition, sensory processing, and memory. Food
inducing) mediators neuropeptide Y (NPY) and agouti-related intake activates reward centers, hedonic circuits that drive
peptide (AgRP) by the ventromedial ARCN. First-order consumption of foods high in fat, sugar, and salt in the
ARCN neurons in turn project to second-order neurons, absence of caloric deficiency; visual food stimuli activate
including those within the paraventricular nucleus (PVN) dedicated memory and visual circuits linked to emotional
and lateral hypothalamic area (LHA), which in turn elabo- responses [10]. Food acquisition is such an important task in
rate secondary signaling mediators. The PVN generates an our evolutionary history that it involves all areas of the brain
anorexigenic, catabolic program via expression of CRH, and all aspects of behavior and physiology.
TSH, and oxytocin, which increase satiety and energy expenditure via multiple endocrine and autonomic nervous system A Complicated Family of Mediators
pathways. The LHA, in contrast, generates an orexigenic, Leptin opened the door to the discovery of a family of proanabolic program via expression of orexins A and B and teins that regulate food intake, broadly classified as adipomelanin-concentrating hormone (MCH). Each of these path- kines, gut hormones, and cytokines (Table 2.1). Adipokines
ways inhibits the other at the level of first-order neuron trans- are secreted predominantly by adipose tissue, gut hormones
mitter effects on second-order neurons [9] (Fig. 2.3).
by the gastrointestinal tract and viscera, and cytokines by
The HFC exhibits an intrinsic set point that vigorously leukocytes. These proteins share phylogenetic and functional
defends adipose tissue stores, the so-called adipostat. The overlap and classification systems remain in flux. For examHFC is influenced by multiple afferent inputs from all organ ple, leptin is a member of the long-chain helical chain cytosystems, including diverse neighboring central nervous sys- kine family, of which IL-6 and IL-11 are members; the term
adipocytokines is sometimes used to reflect the close relationship between adipokines and cytokines. In many cases
Orexigenic,
Anorexigenic,
these mediators are secreted by multiple tissues and cell
anabolic signals
catabolic signals
types. TNF-α is expressed predominantly by macrophages
but also by adipocytes; ghrelin is secreted primarily by gastric fundus cells but is also expressed at low levels by the
MCH,
orexins
A,B
CRH, TRH, oxytocin
placenta, kidney, pituitary, endometrium, macrophages, and
hypothalamus; adipocytes are the dominant source of leptin,
LHA
Second order neurons
PVN
but small amounts are also secreted by the placenta, muscle,
and stomach.
+
+
Most but not all adipokines, gut hormones, and cytokines
NPY, AgRP
POMC, CART, α -MSH
regulate food intake. Leptin appears to play a dominant role
in regulating long-term satiety, while the gut hormones CCK,
Dorsolateral
Ventromedial
PYY, and ghrelin dominate short-term food intake including
First order neurons
ARCN
ARCN
variables such as meal size and duration [9]. Ghrelin is
+
secreted during fasting and binds receptors in the hypothalamus to induce an orexigenic signal. Other mediators have
Leptin
only modest effects on food intake. Adiponectin, an adipokine secreted by adipocytes, stimulates insulin secretion,
Fig. 2.3 A simplified schematic of the hypothalamic feeding center:
inhibits pancreatic beta-cell apoptosis, and attenuates inflamFirst-order ARCN neurons communicate with second-order PVN and
LHA neurons to coordinate behavioral and metabolic output. PVN sig- mation. Consistent with these beneficial effects, serum adinaling is primarily anorexigenic and catabolic and enhanced by leptin ponectin levels are inversely correlated with obesity and
and insulin, while LHA signaling is primarily orexigenic and anabolic metabolic disease.
and inhibited by leptin and insulin. Both pathways negatively regulate
In addition to regulating food intake, satiety and hunger
the other. Other peripheral and central mediators (not shown) stimulate
mediators
manifest multiple other functions. Leptin induces
first- and second-order neurons, including insulin, ghrelin, CCK, GLP-­
1, serotonin, endogenous cannabinoids, and norepinephrine
macrophage, monocyte, and T-cell proliferation and cytokine
2
The Pathophysiology of Obesity and Obesity-Related Disease
19
Table 2.1 Proteins involved in weight regulation
Mediator
Adipokines
Adiponectin
Apelin
Primary source
Satiety
Glucose homeostasis
Immunity
Minimal satiety effects
Probably anorexigenic,
data sparse
Unknown
Leptin
Adipocytes
Pro-inflammatory,
macrophage homing
Generally pro-inflammatory
Lipocalin 2
Adipocytes,
monocytes,
macrophages
Adipocytes
Anorexigenic,
hypothalamic leptin
resistance in obesity
Unknown
Insulinomimetic
Inhibits glucose-induced insulin
secretion
Diabetogenic, likely through
pro-inflammatory properties
Generally insulinomimetic
Anti-inflammatory
Anti-inflammatory
CCL2
Adipocytes
Adipocytes, brain,
heart, kidney, lung
Adipocytes
Diabetogenic via pro-­
inflammatory effects
Pro- and anti-inflammatory
effects
Unknown
Unknown
Probably diabetogenic –
causality not well-established
Diabetogenic via pro-­
inflammatory effects
Diabetogenic
Unknown
Insulinomimetic
Anti-inflammatory,
suppresses Wnt signaling
Plasminogen activator
inhibitor-1 (PAI-1)
Resistin
Retinol-binding protein
4 (RBP-4)
Adipocytes,
macrophages
Adipocytes,
hepatocytes,
macrophages
Adipocytes,
pancreas
Unknown
Probably anorexigenic
Pro-inflammatory
Pro-inflammatory
Secreted frizzled-­
related protein 5
(SFRP5)
Visfatin
Adipocytes
May induce satiety, data
conflicting
Insulinomimetic
Pro-inflammatory
Gut hormones
Amylin
Pancreatic β cells
Anorexigenic, increases
energy expenditure
Probably pro-inflammatory,
conflicting data
Duodenal, jejunal I
cells, CNS
Gastric fundal cells
Duodenal, jejunal C
cells
Anorexigenic, regulates
meal termination
Orexigenic
Anorexigenic
Co-released with insulin in
response to food, inhibits insulin
secretion
Probably insulinomimetic
Anti-inflammatory
Diabetogenic
Induces insulin secretion,
conflicting data
Anti-inflammatory
Pro- and anti-inflammatory
effects, conflicting data
Cholecystokinin (CCK)
Ghrelin
Glucose-dependent
insulinotropic peptide
(GIP)
Glucagon-like
peptide-1 (GLP-1)
Glucagon
Ileal L cells, CNS
Anorexigenic
Insulinomimetic
Anti-inflammatory
Pancreatic α cells
Pancreatic β cells
Increases blood glucose levels,
insulin secretion
“Insulinomimetic”
Probably pro-inflammatory
Insulin
Anorexigenic, increases
energy expenditure
Anorexigenic, increases
energy expenditure
Oxyntomodulin
Ileal L cells
Probably insulinomimetic
Pancreatic polypeptide
(PP)
Peptide tyrosine
tyrosine (PYY)
Cytokines
IFN-γ
Pancreatic F cells
Ileal L cells
Anorexigenic, increases
energy expenditure
Anorexigenic, increases
energy expenditure
Anorexigenic
Insulinomimetic, increases
hepatic insulin sensitivity
Insulinomimetic
T cells, NK cells
Unknown
Generally diabetogenic
Macrophages
Adipocytes,
macrophages,
lymphocytes
Macrophages,
lymphocytes
Adipocytes,
macrophages,
lymphocytes
Anorexigenic
Unknown, likely
anorexigenic in context
of cachexia
Unknown
Diabetogenic
Generally diabetogenic although
effects are context dependent and
conflicting
Insulinomimetic
Anti-inflammatory
Anorexigenic, mediates
cachexia response
Diabetogenic
Pro-inflammatory
IL-1
IL-6
IL-10
TNF-α
Generally anti-inflammatory,
CNS administration may
promote inflammation
Unknown
Unknown
Anti-inflammatory, inhibits
NFκB activation
Pro-inflammatory, induces
macrophage inflammation
Pro-inflammatory
Generally pro-inflammatory
20
expression, with a bias towards generating pro-­inflammatory
responses [11]. Leptin controls endocrine function, potentiating pituitary-hypothalamic axis activity and regulating steroid metabolism. Leptin is implicated in cognitive function,
learning, and memory; leptin-deficient humans suffer mild
cognitive deficits that are corrected with exogenous leptin
replacement [12]. The incretins are a class of gut hormones
that includes glucose-dependent insulinotropic polypeptide
(GIP) and glucagon-like peptide-1 (GLP-­1). GIP is secreted
by K cells in the duodenum and jejunum in response to a
glucose load, induces insulin secretion by pancreatic β cells,
and stimulates fatty acid synthesis in adipocytes. GLP-1 is
secreted by L cells in the ileum and has insulinomimetic
properties, decreasing peripheral insulin resistance and
potentiating pancreatic insulin secretion. GLP-1 also inhibits
gastric emptying and induces satiety [13]. Altered secretion
of incretins secondary to anatomic changes in the intestinal
tract has been implicated in metabolic responses to bariatric
surgery, although exact mechanisms remain unclear.
Furthermore, GLP-1, GIP, and other gut hormones have
immunoregulatory functions. Similar functional diversity
characterizes adipocytokines. TNF-α induces insulin resistance and altered lipid metabolism and promotes anorexia in
cachexia and inflammatory states [14]. In general, adipose
tissue cytokines and adipokines are either pro-inflammatory
and diabetogenic (e.g., TNF-α, IL-6, IL-8, IL-1, resistin) or
anti-inflammatory and insulinomimetic (e.g., IL-10, IL-1Ra,
adiponectin), with the former upregulated and the latter
downregulated in obesity. Exceptions exist: the orexigen
ghrelin, for example, has anti-­inflammatory properties but
induces insulin resistance [15].
Multiple other mediators regulate feeding behavior,
including insulin, endogenous opioids, adrenergic agonists,
and cannabinoids. Redundancy, complex regulatory control,
and functional pleiotropy involving virtually all physiologic
systems characterize the broad family of molecules that regulate food intake.
Energy Expenditure
While dominant, control of food intake is not the sole mechanism of weight regulation. Obese patients often report eating little but suffering from a “slow metabolism.” The
magnitude of the effect of differences in energy expenditure
on human body weight variability is debated but, while less
than contributions from differences in the regulation of food
intake, nonetheless contributes. Metabolic rate has been
studied in response to weight loss in healthy volunteers using
indirect calorimetry. In conditions of energy deficit, total
energy expenditure (TEE), comprised of resting energy
expenditure (REE, 60–70% of TEE, defined as energy used
for basic physiologic functions at rest) and non-resting
energy expenditure (NREE, 30–40% of TEE, defined as
energy used for activity above and beyond REE), is decreased
R. W. O’Rourke
beyond that expected by loss of fat and fat-free mass alone.
These changes are secondary to equal decreases in NREE
and REE and accompanied by a corresponding decrease in
voluntary physical activity. Similar changes are observed in
obese subjects who achieve 10–20% body weight loss,
whose TEE decreases up to 20% more relative to predicted
values from loss of fat and fat-free mass [16, 17]. Obese subjects who maintain weight loss have lower resting metabolic
rates than lean subjects, changes that persist for years, and
mandate constant dietary vigilance [18]. In contrast to diet-­
induced weight loss, bariatric surgery-induced weight loss
may be paradoxically associated with increased TEE in
rodents and humans. In the absence of surgery, however,
compensatory decreases in energy expenditure counteract
caloric restriction and provide yet another explanation for
the failure of dietary weight loss efforts.
Studies of overfeeding and weight gain in obese subjects
demonstrate converse changes with notable differences.
First, overfeeding leads to a compensatory increase in TEE
primarily due to increased NREE, in contrast to weight loss,
in which equal decreases in NREE and REE are observed
[16, 19]. Second, voluntary overfeeding studies in twin
cohorts demonstrate a significant genetic contribution to
individual variability in weight gain in response to overfeeding [20]. Third and importantly, increases in TEE in response
to overfeeding appear to be transient, lasting months then
reverting to baseline, unlike sustained weight loss for which
such changes tend to be long-lasting. Furthermore, while
compensatory increases in TEE oppose weight gain, this
effect is weaker than that of decreased TEE with weight loss.
Taken together, these observations suggest that regulation of
metabolic rate is more robust in conditions of negative rather
than positive energy balance – the system is better designed
to prevent leanness than avoid adiposity, a common theme.
The mechanisms underlying the regulation of energy
expenditure and metabolic rate are complex, but sympathetic
nervous and hormonal systems are dominant. Voluntary
choice controls NREE to some extent, but much like food
intake, we consciously control our activity levels to a lesser
degree than we may imagine. Differences in autonomic nervous system activity contribute to variability in metabolic
rate: overfeeding increases and underfeeding decreases sympathetic nervous system activity in rodents, and variability in
sympathetic nervous system activity is observed in humans,
with higher levels predicting successful weight loss [21].
Obese subjects manifest alterations in thyroid hormone and
catecholamine balance that are associated with decreased
metabolic rates [22]. At the cellular level, these variables
control energy expenditure by regulating thermogenesis.
Thermogenesis
In 1783 Laplace and Lavoisier invented the first calorimeter
and measured energy balance in animals, demonstrating that
2
The Pathophysiology of Obesity and Obesity-Related Disease
biologic systems obey the first law of thermodynamics, such
that energy intake equals the sum of energy storage and
energy expenditure. Energy expenditure in turn may be
approximated by the sum of energy used to drive physical
activity and cellular processes, and energy dissipated as heat.
As Lavoisier famously concluded, “Life is combustion.” All
cellular biochemical reactions are less than 100% efficient
and thus generate heat. Thermogenesis occurs in all cells but
is most active in brown adipose tissue (BAT) and skeletal
muscle. Skeletal muscle thermogenesis occurs during exercise, during movement not associated with exercise (non-­
exercise-­
induced thermogenesis, NEAT), and during
cold-induced shivering. Skeletal muscle energy utilization
efficiency during exercise is increased in subjects who lose
weight and decreased in subjects who gain weight [17].
Furthermore, lower levels of NEAT have been demonstrated
in obese humans [23], suggesting that differences in skeletal
muscle thermogenesis contribute to the pathogenesis of obesity. BAT is a dominant site of thermogenesis, in which it
underlies non-shivering thermogenesis, a critical thermoregulatory mechanism in rodents and neonatal humans. BAT,
relative to white adipose tissue (WAT), is associated with
higher thermogenic potential, increased mitochondrial number and function, decreased lipid storage, and improved
metabolism [24]. Diet-induced thermogenesis (DIT), a postprandial increase in metabolic rate observed in rodents and
humans, is an important component of the thermogenic
response. At the cellular level, DIT increases mitochondrial
heat production and decreases energy extraction, limiting
exposure to postprandial increases in nutrient flux. Humans
demonstrate significant variability in the magnitude of DIT,
with obese humans having lower DIT responses [25].
While all biochemical reactions generate heat, membrane
ion leaks that occur in all cells and triglyceride-fatty acid
futile cycling within skeletal muscle are examples of processes that involve significant thermogenesis. Uncoupling of
electron transport from oxidative phosphorylation within
mitochondria is a dominant-regulated thermogenic process.
Mitochondria, evolved from intracellular parasites to become
endosymbiotic cell organelles, utilize oxidative phosphorylation coupled to electron transport along their inner membrane to generate ATP from glycolytic energy substrates. The
efficiency of this process is regulated by uncoupling proteins
(UCPs) that uncouple oxidative phosphorylation from electron transport, creating a proton leak that effectively runs the
mitochondrial engine in neutral, generating heat rather than
ATP. UCPs adjust mitochondrial efficiency and act as a thermoregulatory mechanism. This control mechanism extends
across animal and plant phyla: uncoupling occurs in potatoes
in response to cold weather [19]. Three dominant human
UCP isoforms are identified. UCP-1 expression is restricted
to BAT; UCP-2 is widely expressed in multiple tissues, while
UCP-3 is expressed in the BAT, skeletal muscle, and brain.
21
In humans the correlation between UCP function and thermogenesis specifically, and metabolic rate in general, is
imperfect. Skeletal muscle UCP expression is paradoxically
upregulated in response to starvation, for example, confusing
the role of uncoupling in response to nutrient deficit [26].
The type and quantity dietary constituents, along with variables such as environmental temperature and photoperiod,
also influence UCP-1 expression, adding to complexity.
Finally, the magnitude, duration, and direction of changes in
UCP-1 expression in BAT in response to overfeeding in
rodents are heterogeneous and strain-dependent, reinforcing
the importance of genetic background on the regulation of
metabolic rate. Nonetheless, a transgenic mouse overexpressing UCP-1 under control of the adipose tissue-specific
AP2 promoter is resistant to obesity [27], and polymorphisms in UCP genes correlate with obesity and metabolic
disease in humans [28], supporting a role for UCPs in obesity pathogenesis.
dipocyte Biology and Other Metabolic
A
Processes
Differences in the kinetics of adipocyte hypertrophy, proliferation, differentiation, and metabolism contribute to variability in body weight. It was once thought that adipocytes
did not proliferate or increase in number in adults, but recent
data demonstrate otherwise. Obese subjects, especially those
with early-onset childhood obesity, have a greater number of
adipocytes than lean subjects, as well as preadipocyte precursors with a metabolically adverse phenotype and
decreased proliferative potential [29]. The regulatory systems described above comprise only a partial list of the many
physiologic processes that occur within adipose and other
tissues that control energy balance, all of which are regulated
by homeostatic systems with differing amplitudes and kinetics that contribute to variability in human body weight.
Homeostasis
Despite the power of weight regulatory systems, we have a
degree of control over our body weight, and as such within
individual limits, personal choice plays a role in the pathogenesis of obesity. But the magnitude of the effect of personal choice is less than we may believe, as food intake is
subject to tightly regulated subconscious mechanisms. The
limits imposed by these mechanisms are powerful and
indeed represent a fundamental characteristic of all biologic
systems, all of which have one goal: the maintenance of
homeostasis. Perfect homeostasis is of course elusive: our
heart rate is not a constant 72 beats per minute; rather we are
constantly buffeted by external forces that drive us away
from the homeostatic mean. In the case of energy homeostasis, this buffeting comes in the form of periodic alterations in
food resources, physical activity, illness, temperature, and
innumerable other environmental and physiologic variables.
22
R. W. O’Rourke
The term allostasis, proposed by Sterling and Eyer in 1988,
describes how biologic systems evolved to achieve stability
not through strict adherence to a homeostatic mean but rather
through a dynamic response to external stimuli, the allostatic load, that achieves controlled variability around a
homeostatic mean within a defined allostatic range. The
robustness of biologic systems derives from this capacity for
dynamic allostasis. Biologic systems function well within
their allostatic range, deviation from which may be lethal.
Furthermore, most humans, most strains of laboratory
rodents, and many wild animals gradually gain weight over
the course of their lives, suggesting not only a predisposition
to excess weight but also towards gradual lifelong increase.
Biologist Conrad Hal Waddington proposed the term
homeorhesis, in contrast to homeostasis, to describe regulation of a system along such a trajectory [30] (Fig. 2.4).
Leptin represents a paradigm for allostatic behavior but is by
no means unique; all aspects of metabolism, indeed all biologic processes, are governed by allostasis. When we ask
obese patients to lose significant weight with diet and exercise, we are asking them to step outside their allostatic range,
an impossible task from a biologic perspective. This is why
efforts to address the obesity crisis at the individual level fall
short. This is why diets fail. To impact on the obesity epidemic, we must understand the genetic, evolutionary, and
environmental influences that define metabolic allostatic
range and how these factors conspire so vigorously to defend
body weight.
Evolutionary and Genetic Contributors
hy Do We Become Obese?
W
Rare humans suffer a paucity of adipose tissue secondary to
congenital and acquired lipodystrophy syndromes. These
patients have voracious appetites, require high caloric intake
to maintain lean body weight, and suffer from diabetes and
steatosis, stressing the central role of adipose tissue in
metabolism and demonstrating that its absence is as detrimental as its excess. The explanation for why humans are
prone to excess adiposity but stringently protected from
underweight conditions is rooted in genetics and influenced
by powerful environmental and evolutionary selective
pressures.
Despite knowing that it is unhealthy, humans, along with
many animals not capable of such knowledge, will eat to
excess if surplus food is available. Hedonic circuits, mentioned above, and metabolic thrift, discussed below, are
examples of physiologic and evolutionary mechanisms
underlying this phenomenon. But why did evolution select
for such behavior if it is detrimental to health? The reason is
that evolution did not mold us to optimize long-term health
or longevity. Rather, evolution selects for physiology and
behavior that optimizes reproductive fitness. Despite its detrimental long-term effects, surplus nutrition, to a point, optimizes reproductive fitness in youth, as evidenced by
increased fertility rates and younger age of onset of puberty
in Western societies [31]. Reproduction is energy-intensive
Allostatic load
Homeorhetlc
trajectory
Body weight,
satiety, leptin
levels, other
mediator levels, all
metabolic and
biologic processes,
and many of the
stimuli that
regulate them
Homeorhetic
mean
Allostatic range
Allostatic load
Fig. 2.4 Homeostasis, allostasis, homeorhesis: Levels of leptin and
other mediators, the outcome measures they regulate (food intake, thermogenesis, and all other metabolic and physiologic processes), as well
as physical activity and many environmental and physiologic stimuli
that regulate these processes, all cycle in an allostatic manner around a
homeostatic mean, or alternatively in some cases, along a homeorhetic
trajectory (e.g., body weight over the course of a lifetime). External
stimuli (the allostatic load) cause deviation from the homeostatic mean.
Optimal functioning of a biologic system occurs within its allostatic
range, defined as the degree to which a biologic system can tolerate
deviation from its homeostatic mean without disruption
2
The Pathophysiology of Obesity and Obesity-Related Disease
and evolution selected for a propensity to maximize energy
resources to ensure adequate reproductive potential. Humans,
unlike other animals, have the ability to self-reflect and, to an
extent, “decide” to eat less and thus possibly increase long-­
term health and longevity, but as discussed, this ability is
constrained by allostatically governed mechanisms. The distinct and separate goals of reproductive fitness and long-term
health and longevity, the former hardwired by evolution, the
latter unique to human cognition, lead to our conflict with
overeating.
Metabolic Thrift
James Neel at the University of Michigan proposed the
thrifty genotype hypothesis in 1962 [32]. Neel postulated that
throughout evolution, the constant pressure of famine led to
selection of genes that regulated metabolism in a thrifty
manner: polymorphisms in metabolic genes were selected
for if they imparted a tendency towards efficient energy storage and metabolism, while polymorphisms that imparted a
tendency towards a less efficient metabolism were strongly
selected against. Metabolic thrift provided a robust reproductive advantage in a food-sparse leptogenic environment
but leads to a blossoming of the obesity phenotype in an obesogenic environment in which food is plentiful, exactly what
we observe today. Polymorphisms resulting from random
Darwinian mutation that predisposed to overweight, obesity,
and thrift accumulated in the human genome, while those
predisposing to leanness and a lack of thrift became rare. The
thrifty gene hypothesis has evolved and remains debated.
Thrifty gene candidates are sparse and proof of causality
remains elusive. Alternative hypotheses such as predation
release and genetic drift may also contribute to obesity [33,
34]. Despite these controversies, the thrifty genotype hypothesis provides a coherent explanation for the human predisposition towards overweight and obesity and its dramatic recent
increase.
Why Adipose Tissue?
Animals employ diverse strategies for metabolic thrift,
including hibernation, high reproductive rates, and high
caloric intake. Among these strategies, storage of calories for
future use is common. Storage may be ectopic: hamsters
store up to 50% of their body weight in their cheek pouches.
Humans in contrast, along with many other species, store
energy in the form of adipose tissue. Adipose tissue is present across phyla, including yeast and insects [29], but is particularly well-developed in vertebrates. Adipose tissue is
particularly energy dense – humans can store less than
1 day’s worth of calories in skeletal muscle in the form of
glycogen but over 2 month’s worth of calories in fat in adipose tissue. Humans invest significant resources into a single
offspring with each pregnancy, and human development is
characterized by a prolonged period of rapid postnatal
23
growth and brain development that requires a constant supply of calories. Nutritional deficits during this period have
widespread detrimental effects and exerted a strong reproductive disadvantage during evolution. Adipose tissue provides a constant source of calories during this critical period,
reflected by the fact that human percent body fat is highest
during this rapid neonatal growth phase. Adipose tissue thus
protects our fragile, singleton, energy-hungry offspring.
Finally, humans are to some extent a migratory species:
much of our evolution was shaped by the out-of-Africa emigration that led to pan-global colonization 50,000–
75,000 years ago [35]. Adipose tissue allowed us to weather
variability in food supplies during famines and migrations.
For all these reasons, adipose tissue is a particularly good
strategy for metabolic thrift in humans.
he Genetic Basis of Obesity
T
Obesity has a strong genetic basis. In addition to leptin mutations, over 20 rare inborn genetic syndromes are associated
with human obesity. In virtually all, obesity is one of a number of phenotypic abnormalities, emphasizing the interaction
of weight regulation with all aspects of physiology. Causative
genes have yet to be identified for Prader-Willi, Bardet-­
Beidl, Cohen, and Alstrom syndromes, while in other syndromes, specific genes have been implicated, many associated
with feeding behavior, stressing the dominance of these systems in obesity pathogenesis. Some disorders are monogenic
and include mutations in genes encoding POMC, PCSK1,
and MC4R. But in contrast to monogenic obesity syndromes
and similar to many chronic diseases, common human obesity is a complex polygenic phenotype, significantly complicating analysis.
Despite these challenges, statistical genetics methods
have accurately quantified the cumulative genetic contribution to obesity and demonstrate a high level of hereditability.
Quantitative genetic analysis of twin cohorts is a powerful
tool that is widely used to quantify genetic contribution to
complex polygenic diseases and clinical phenotypes. Twin
studies rely on comparison of thousands of monozygotic and
dizygotic twin pairs to quantify the contribution of genetic
influences to phenotypic traits based on Mendelian genetic
inheritance with a high degree of analytic power. Further
detail can be gleaned by study of twin pairs separated at
birth. When applied to obesity, multiple studies consistently
demonstrate that genetic factors dictate approximately 70%
of the tendency towards a particular body habitus phenotype,
while nongenetic, presumably environmental factors contribute approximately 30% [20]. Twin studies also reveal
enlightening aspects of food-related behavior. For example,
differences in suckling time, eating speed, food preferences,
and crying frequency manifest at birth and correlate strongly
with genetics, suggesting that such behaviors are hardwired
before the onset of environmental influences [36].
24
While twin studies, as well as genetic linkage and familial
aggregation analyses, demonstrate a strong genetic contribution to obesity, other methodologies are required to identify
specific thrifty genes. Genome-wide association analysis
(GWAS) involves DNA sequencing of the genome in thousands of humans to identify single nucleotide polymorphisms (SNPs) followed by correlation of SNP prevalence
with phenotypic and clinical characteristics. GWAS permits
correlation of specific DNA SNPs with clinical and disease-­
related traits. While powerful, a number of issues currently
limit the utility of these techniques. First is the aforementioned polygenic nature of obesity. Over 200 specific genetic
mutations are associated with obesity in mice and over 50
candidate genes have been identified in humans, likely only
a minority of the total genes involved. These polymorphisms
are found throughout the genome in and near genes associated with multiple physiologic processes, but the individual
effect size of each locus is weak, contributing less than 1–3%
to the tendency towards obesity and confounding analysis of
the functional role of any single gene on global phenotype.
Tens of thousands of subjects are required to adequately
power studies to identify SNPs with such low effect magnitudes. In addition, multiple loci interact in concert, further
increasing complexity and confounding assignment of specific functions. Finally, many SNPs lie in noncoding regulatory regions of the genome, areas that are currently poorly
understood and present challenges with respect to interrogation and functional analysis. Despite these limitations,
GWAS has begun to identify thrifty gene candidates. Among
these emerging candidate genes, MC4R represents a singularly important locus. Over 90 polymorphisms have been
identified within the human MC4R gene locus which together
account for up to 6% of cases of common human obesity and
are transmitted in monogenic Mendelian fashion with incomplete penetrance [37]. Study of similar high-frequency SNP
loci has the potential to identify important markers and
mechanisms of disease. Future challenges include identifying and functionally defining other coding and noncoding
SNPs and quantifying their contribution to obesity.
Metabolic Diversity
If we all share the same tightly regulated weight control
mechanisms, then why are some lean but others obese? The
multiple thrifty polymorphisms in metabolic genes scattered
throughout our genomes combine to cause subtle regulatory
and functional differences in the many proteins that carry out
the tasks of metabolism, providing our species with broad
metabolic diversity [38, 39]. Metabolic diversity explains the
heterogeneity of the obesity phenotype, with variability in
onset and triggers (e.g., adolescence, pregnancy, menopause), severity, anatomic site of excess adiposity, association with metabolic disease, the capacity to lose weight in
response to diet, exercise, and surgical therapy and the body
R. W. O’Rourke
mass index (BMI) range in which individuals exist. The obesity phenotype is heterogeneous because its underlying
mechanisms are equally so. This has led some to propose the
term obesities [40]. Why did metabolic diversity evolve in
humans? First and foremost, we are not a niche species. We
inhabit virtually every environment on the globe, and our
metabolic heterogeneity allows us to weather differing environments. For example, in their native environment, Inuit
Eskimos maintain lower serum LDL levels, higher HDL levels, and lesser degrees of insulin resistance compared with
non-Inuit populations despite a high fat diet and higher
degree of obesity, suggesting that adaptive genes designed to
manage their unique diet were selected for in the Inuit
genome [41]. South Pacific Asians are thought to have a high
prevalence of insulin resistance due to selection of genes that
prevented hypoglycemia during fasting associated with long
ocean voyages [42]. Metabolic diversity provides a genetic
savings bank that allows for rapid selection of thrifty alleles
over a few generations during famine or emigration to new
environments, a strength of our species and one of the reasons that we have populated the planet.
Environmental and Epigenetic Contributors
nvironmental Influences, Obvious and Subtle
E
Despite the importance of genetics, environment plays a central role in obesity pathogenesis. Dominant among environmental contributors is the shift to modern processed food.
Processed food is ubiquitous, plentiful, and cheap; contains
high levels of refined sugar, fat, and salt; is calorie-dense and
highly palatable; and is engineered to appeal to sensory,
physiologic, and emotional inputs. Marketing strategies and
food industry, lobbyist, and subsidy policies that maintain
accessibility and affordability of the very foods that contribute most to obesity positively reinforce consumption. The
dramatic pan-societal decrease in physical activity exacerbates the problem. Our Paleolithic ancestors consumed 30%
more calories than modern humans but engaged in much
higher levels of physical activity [43]. Human physical activity levels decreased but remained much higher over past centuries than in the last, during which time most humans
engaged in regular strenuous physical activity in the context
of agriculture: over 40% of the US population engaged in
farming before 1900, compared to less than 2% currently
[44], and the trend of progressively decreasing physical
activity continues.
These problems are exacerbated by disruption of circadian rhythms. Physical activity during our evolution cycled
in response to circadian rhythms and feast-famine cycles of
early hunter-gatherer and agrarian societies in much the
same way leptin levels cycle though allostatic deviation.
Such cycling is characteristic of multiple physiologic and
2
The Pathophysiology of Obesity and Obesity-Related Disease
behavioral processes, disruption of which contributes to obesity. Temporal eating patterns regulate endocrine physiology
and can be entrained: providing an extra meal beyond energy
requirements to rodents and humans for a period of time will
lead to an anticipatory orexigenic ghrelin surge 1 h prior to
the scheduled meal and is associated with increased food
intake and weight gain [45]. This periodicity extends to the
cellular level, as adipocyte proliferation and other metabolic
and physiologic processes exhibit similar cycling [46].
Circadian cycling of physical activity, sleep, and eating patterns are disrupted in modern society. The contribution of
these disruptions to obesity is evidenced by the correlation
between night work, obesity, and metabolic disease.
Less obvious factors contribute. Indoor temperatures have
increased and stabilized over past decades; sleep patterns are
disrupted, and as the obesity epidemic progresses, assortative mating patterns magnify its growth [47]. Environmental
influences are complex, powerful, and entrenched. A lucrative food industry and a lack of societal resources to encourage healthy food and physical activity choices remain
obstacles to environmental manipulation. Nonetheless,
strong correlation between community food and activity
resources, obesity, and metabolic disease are observed in
multiple studies, and an emerging field of social and environmental engineering has evolved to address this problem [48].
Epigenetics
The phrase “nature versus nurture” suggests dichotomous
processes, but in fact the very the foundation of Darwinian
theory postulates that genetics and environment are intimately linked. Epigenetic regulation of the genome mediates
this link, providing a mechanism for rapid genetic responses
to environmental stimuli on timescales less than those
required for eons of Darwinian evolution by random spontaneous mutation. Epigenetics is defined as post-fertilization
covalent modification of the genome independent of DNA
base-pair mutations and includes DNA methylation, glycosylation, and myristoylation, along with modification of histones, other DNA-associated proteins, and coding and
noncoding RNA that regulate DNA function. Epigenetic
modifications occur in response to environmental stimuli and
are transmitted for one, two, or more generations. Epigenetic
modification of the genome is active during fetal, neonatal,
and to a lesser extent adult development in all cells and
organisms and has profound effects on gene expression,
function, and phenotype.
In 1944 during World War II, the Germans cut off food
supplies to the Netherlands, and for 1 year Dutch citizens
starved. The children of women who gave birth during the
“Dutch Hunger Winter” manifested increased prevalence of
metabolic disease and obesity as adults, whereas children
of the same mothers born before or after the famine manifested a much lower prevalence of metabolic disease [49].
25
Epigenetics
Genetics
Environment
Physiology
Behavior
Phenotype
Fig. 2.5 Complex interactions dictate phenotype: Epigenetic mechanisms mediate environmental effects on genetics. Genetics has diverse
effects on physiology and behavior. Through our behavior we alter our
environment, and our environment in turn has diverse effects on our
physiology
Environmental stimuli “programmed” metabolism in utero
independent of classical Darwinian genetics. Excess nutrition
during pregnancy has similar effects. The risk of adult metabolic disease and obesity is increased over twofold in people
whose mothers had gestational diabetes during their pregnancy compared to siblings born of the same mothers during
nondiabetic pregnancies [50]. Murine and primate models
demonstrate similar effects of maternal overfeeding on metabolic disease in progeny, demonstrating epigenetic modifications that persist generations. The similar epigenetically
mediated metabolic outcome to both maternal overnutrition
and undernutrition may represent an adaptive response to the
fetus “sensing” instability in external environmental food
supplies, whether it be excess or scarcity, leading to rapid epigenetic regulation of the metabolic genome. The thrifty phenotype hypothesis defines epigenetic regulation of metabolism,
in contrast to Neel’s thrifty genotype hypothesis, which is
based on classical Mendelian genetic transmission of thrifty
SNPs. Epigenetic regulation provides a mechanism by which
environmental stimuli rapidly alter the genome to prepare offspring for a dynamic environment. Epigenetics mediates the
link between environment and genetics, an interaction that
determines our physiology and behavior, through which we
in turn modify our environment (Fig. 2.5).
Pathophysiology of Obesity-Related Disease
utrient Excess, Cell Stress, and the Central
N
Role of Adipose Tissue
besity: More than Mass
O
Obesity is associated with a spectrum of pathology collectively referred to as metabolic disease. Metabolic disease
26
involves all organ systems, reflecting the fact that the systems that regulate energy balance are fundamental to biology. Large epidemiologic studies document dose-dependent
increasing risk ratios for metabolic diseases and long-term
mortality with increasing BMI. Despite its strength, however, the correlation between obesity and metabolic disease
is imperfect. Within the obese population, metabolic disease
spans a heterogeneous spectrum. Overweight or lean subjects may suffer metabolic syndrome, while very obese
patients may have minimal disease. Ethnicity also influences
disease risk independent of weight, testament to the role of
genetics in the pathogenesis of metabolic disease. This variability in metabolic disease risk susceptibility is based in
complex variable responses of multiple tissues, including
adipose tissue, to excess nutrient delivery.
Obesity-related diseases were once thought to be the
result of mechanical stress on tissues. Indeed, mechanical
stress contributes to osteoarthritis, sleep apnea, and venous
stasis disease, but even these pathologies result in part from
other mechanisms; for example, inflammation contributes to
the pathogenesis of sleep apnea and osteoarthritis.
Mechanical stress plays little if any role in the pathogenesis
of other metabolic diseases such as asthma, atopy, allergy,
and cancer, all of which are increased in obesity. Metabolic
diseases also develop in lean subjects albeit at lower incidences. So while mechanical stress contributes, it does not
provide the whole story. Rather, metabolic disease results
from nonmechanical stress that occurs at the cellular level in
response to nutrient excess. These stress responses begin in
adipose tissue.
Adipose Tissue Biology
Adipose tissue was once thought of as a homogenous tissue
designed primarily for lipid storage but, in the past few
decades, has emerged instead as a complex metabolic, endocrine, and immune organ. The adipose tissue-gut-central nervous system interaction regulated by leptin serves as an
example of inter-organ communication mediated by adipose
tissue. White adipose tissue (WAT) of mesodermal origin
comprises the majority of human adipose tissue. WAT resides
in discrete anatomic depots each with distinct phenotypes
and functions. Obese humans differ in sites of WAT accumulation, with gynecoid distribution defined by excess subcutaneous adipose tissue (SAT) in the hips and buttocks, android
distribution characterized by excess intra-abdominal visceral
adipose tissue (VAT), and a spectrum of intermediate phenotypes. Excess WAT in general correlates strongly with metabolic disease and long-term mortality, but these risk ratios
are magnified at least twofold for excess VAT compared to
SAT. Reinforcing its importance, VAT but not SAT lipectomy in obese mice ameliorates diabetes [51]. Omentectomy
as an adjunct to bariatric surgery in humans in contrast does
not ameliorate metabolic disease, likely due to the greater
R. W. O’Rourke
degree of complexity of human anatomic adipose tissue
depots and the fact that the omentum comprises a lesser percentage of total VAT mass in humans. A unique aspect of
VAT is its direct anatomic communication with the liver via
the portal venous system, which might explain its detrimental effects without invoking other mechanisms. Important
qualitative differences in metabolism in VAT have been
described, however, including higher levels of inflammation,
lipolysis, β-adrenergic receptor expression, steroid sensitivity, insulin resistance, and adipocyte proliferation and differentiation. These complexities are compounded by the
existence of distinct and functionally less well-defined subdepots within VAT and SAT, including omental, retroperitoneal, mesenteric, and perivisceral subdepots for VAT and
deep, superficial, truncal, and extremity subdepots for
SAT. In addition, adipocytes are not limited to canonical anatomic depots but reside in virtually all tissues including the
bone marrow, perivascular and perivisceral tissues, and all
subcutaneous locations.
Brown adipose tissue (BAT) constitutes a minority of
total adipose tissue stores and is associated with increased
thermogenic capacity and beneficial effects on systemic
metabolism. BAT has been identified in adult humans with
positron emission tomography scanning in cervical, supraclavicular, paraspinous, mediastinal, and perirenal depots,
with increased metabolic activity and thermogenesis induced
by cold and adrenergic stimuli. In contrast to WAT, BAT
mass correlates inversely with metabolic disease risk, and
BAT stores decrease in humans with increasing age and with
increasing obesity [52].
Adipose tissue complexity extends to the cellular level.
Adipocyte stem cells of multiple phenotypic and functional
potentials, including BAT precursors termed beige or brite
(brown-in-white) preadipocytes, reside within WAT and give
rise to adipocytes with different phenotypes. This phenotypic
plasticity is a target for therapy, as human clinical trials of
drugs that induce “browning” or “beiging” of adipose tissue
are in progress. In addition, adipose tissue is comprised not
only of adipocytes but also a stromal-vascular cell fraction
(SVF) that includes endothelial cells, preadipocytes, leukocytes, lymphocytes, and other cell types. Over half of the
SVF is comprised of leukocytes and lymphocytes, which are
a rich source of cytokines, adipokines, and inflammatory
mediators.
utrient Excess and Cell Stress Responses
N
Much like oxygen, the chemical properties that make nutrients efficient vehicles for energy storage and transfer also
impart a high degree of bioactivity and the capacity to participate in energy-intensive and potentially damaging reactions
within cells. To control these bioenergetic molecules, cells
have evolved sophisticated machinery that meters nutrient
flux and limits exposure of cells to nutrients and metabolites.
2
The Pathophysiology of Obesity and Obesity-Related Disease
These protective mechanisms sequester nutrients in highly
regulated organelles, including mitochondria and endoplasmic reticulum. Obesity is associated with chronic increased
cellular flux of nutrients and metabolites that overwhelms
cellular metering processes and induces cell stress responses
that downregulate cell function and eventually induce cell
apoptosis and adaptive responses designed to protect tissues
from individual cells suffering from nutrient toxicity. These
stress responses include three related processes: endoplasmic
reticulum stress, oxidative stress, and inflammation. Stress
responses are universal to all cells, but in obesity, they have
their genesis in adipose tissue.
Initially, adipocytes respond to excess nutrient delivery
with hypertrophy, storing the majority of nutrients in a unilocular cytoplasmic lipid droplet. Hypertrophy is an adaptive
response, but as adipocytes grow to diameters exceeding 100
microns, the diffusion distance of oxygen, cellular hypoxia
ensues. Measurement of adipose tissue oxygen levels is
fraught with technical challenges and conflicting data exist,
but studies in obese mice and humans using platinum-based
electrodes, in vivo staining with hypoxia tracers, and expression of hypoxia-inducible genes confirm hypoxia in obese
adipose tissue [53, 54]. Hypoxia conspires with chronic
nutrient excess to trigger cell stress responses. Foremost
among these responses is the endoplasmic reticulum stress
response. The endoplasmic reticulum (ER) is a complex cell
organelle that coordinates protein and lipid synthesis. Within
the rough ER, chaperone proteins ensure accurate protein
translation and folding during ribosomal translation of RNA
to protein. The ER also manages posttranslational protein
modification, sorting, and transport, RNA processing and
trafficking, and drug metabolism. In orchestrating its many
functions, the ER depends on a constant influx of nutrients to
keep pace with protein synthesis. In this capacity, the ER acts
as a dominant cellular nutrient sensor, adjusting cell physiology to accommodate fluctuations in nutrient resources. The
ER integrates cellular responses to innumerable stimuli,
including hypoxia, temperature, toxins, and, of course, nutrients. The ER is a central clearinghouse for cellular function,
but it can be overwhelmed. If nutrient flux exceeds ER processing capacity, the ER responds with an adaptive stress
response designed to “catch up.” Initially this response
involves upregulation of chaperone protein synthesis to
maintain accurate protein synthesis. If excess nutrient flux
persists, then the ER responds by activating the unfolded protein response (UPR), a complex transcriptional program that
downregulates global cellular protein expression and cell
metabolism. The mitogen-activated protein kinases (MAPK)
JNK and p38 are important downstream effectors of the
UPR, inducing insulin resistance by regulating the activity of
insulin signaling mediators such as insulin receptor and
IRS-1. Finally, if nutrient excess persists and the ER cannot
maintain proper protein synthesis, then the UPR progresses
27
to induce cell apoptosis. The UPR thus protects cells from
manageable increases in nutrient delivery and triggers cell
death when excess nutrient load is insurmountable.
Oxidative stress is activated when formation of reactive
oxygen species (ROS), including superoxides, oxygen and
hydroxyl free radicals, and hydrogen peroxide, byproducts
of mitochondrial respiration, exceeds cellular antioxidant
capacity. Increased ROS formation occurs with nutrient
excess. Initially, the oxidative stress response upregulates
cellular antioxidant mechanisms, including antioxidant
enzymes (e.g., superoxide dismutase, glutathione peroxidase, catalase), scavenging molecules (e.g., ascorbic acid,
vitamin D, urate, divalent metal ions), and thioredoxin and
glutaredoxin scavenging systems. If increased ROS generation continues, the oxidative stress response proceeds to
increase mitochondrial uncoupling to further reduce ROS
production. Further ROS production leads to cross talk
between oxidative stress and ER stress responses and, eventually, cell apoptosis.
Adipocyte apoptosis resulting from chronic cell stress
responses generates sterile inflammation within adipose tissue, as an inflammatory cell infiltrate that includes macrophages, T cells, B cells, NK cells, and eosinophils is recruited
to scavenge dead and dying adipocytes. Adipose tissue macrophages (ATM) are initial responders and dominant effectors of this inflammatory response, congregating around
dead or dying adipocytes in crown-like structures (Fig. 2.6,
[55]). ATM comprise 10–15% of adipose tissue leukocytes,
are increased in obese adipose tissue, and correlate directly
with body weight, with reductions in ATM number observed
with weight loss, including after bariatric surgery [56]. ATM
express multiple cytokines, including TNF-α, IL-10, IL-6,
Fig. 2.6 ATM crown-like structure: Adipose tissue macrophages
(brown) surround an apoptotic adipocyte. (From: O’Rourke et al. [55].
Reprinted with permission from Springer Nature)
28
IL-8, and IL-1β, as well as exerting other effector functions,
all of which in turn regulate diverse aspects of adipocyte
metabolism, inducing insulin resistance and lipogenesis and
decreasing lipolysis. The central role of ATM in systemic
metabolic disease is demonstrated by experiments in which
transgenic adipose tissue-specific knockdown of the macrophage homing molecule CCL2 abrogates insulin resistance
in obese mice, while overexpression of CCL2 induces insulin resistance in lean mice [57, 58]. ATM are highly heterogeneous and are shifted towards a pro-inflammatory
phenotype in obesity. Obesity-specific pathogenic ATM subpopulations have been identified. The integrin CD11c represents an important marker for diabetogenic ATM. CD11c+
ATM are increased in obese mice and humans and induce
insulin resistance in adipocytes in vitro, and in vivo ablation
of CD11c+ macrophages in obese mice ameliorates diabetes
[59, 60]. Targeting ATM represents an important therapeutic
strategy for metabolic disease.
ATM are not the only cellular effectors of adipose tissue
inflammation. A pan-leukocyte infiltrate is present in obese
adipose tissue that includes T cells, B cells, NK cells, and
eosinophils, which potentiate ATM inflammatory responses
and regulate adipocyte metabolism. Cytotoxic T cells are
increased in number in adipose tissue in obese mice and
humans, while regulatory T cells, which attenuate macrophage inflammatory responses, are reduced. B cells, NK
cells, and eosinophils also regulate adipose tissue inflammation. In addition, adipocytes themselves express inflammatory cytokines and prime ATM inflammatory responses.
Finally, as inflammation persists, adipose tissue fibrosis
ensues, limiting adipocyte hypertrophic capacity and exacerbating adipocyte failure.
Model for Adipose Tissue Dysfunction
A
Obese adipose tissue manifests multiple signs of cell stress.
ER stress mediators are increased in adipose and other tissues from obese humans and reduced with weight loss,
including after bariatric surgery. Induction of ER stress in
mice induces systemic insulin resistance and steatosis, while
inhibition of ER stress has the opposite effect [61]. Increased
oxidative stress, ROS levels, and reduced mitochondrial
number, size, and function in serum, cells, and tissues from
obese humans have been demonstrated using HPLC, mass
spectrometry, and other assays [62]. Obese humans mount
increased peripheral blood monocyte ROS responses to a
meal, suggesting metabolic differences that predispose to
oxidative stress [63]. Chemical inducers of mitochondrial
uncoupling or ROS scavengers reverse insulin resistance in
obese mice, demonstrating the potential for therapy targeting
oxidative stress [64].
ER stress, oxidative stress, and inflammation are fundamental cellular processes that potentiate one another with
R. W. O’Rourke
Nutrient excess,
moderate adipocyte
hypertrophy
Early compensatory
ER stress
Continued
nutrient excess,
advanced adipocyte
hypertrophy
Hypoxia
Progressive ER stress,
oxidative stress
Inflammation
Fibrosis, limited adipocyte
hypertrophic capacity
Late ER stress, UPR,
advanced oxidative stress,
adipocyte necrosis, apoptosis
Failure of adipocyte nutrient
buffering capacity, systemic
overflow
Fig. 2.7 A model for adipose tissue failure in obesity: In early obesity,
adipocytes respond to nutrient excess with hypertrophy. As nutrient
excess persists, adipocyte hypertrophy continues, leading to hypoxia
and ER and oxidative stress responses, causing adipocyte apoptosis and
an inflammatory response. Hypoxia, ER and oxidative stresses, and
inflammation potentiate one another, inducing a vicious cycle. These
processes eventually lead to adipose tissue fibrosis, which further limits
adipocyte storage capacity exacerbating failure of adipose tissue nutrient buffering capacity. As adipose tissue failure proceeds, nonesterified
fatty acids, other nutrients, metabolites, and inflammatory cytokines
and adipokines overflow into the systemic circulation
intimate overlap in signaling pathways. While the exact
sequence, kinetics, and causal relationships of adipocyte
hypertrophy, nutrient excess, hypoxia, and cell stress
responses are not yet well defined, these events provide a
model for adipose tissue failure (Fig. 2.7). The end result of
these processes is impairment of adipose tissue’s nutrient
buffering capacity. As adipose tissue nutrient storage capacity is overwhelmed, nutrients “overflow” to peripheral tissues, and metabolic disease metastasizes.
2
The Pathophysiology of Obesity and Obesity-Related Disease
eyond Adipose Tissue: Systemic Metabolic
B
Disease
Adipose Tissue Overflow
In early obesity, nutrient excess, cell stress, and metabolic
dysfunction are confined to adipose tissue. Adipocytes are
exquisitely designed to store lipid and tolerate nutrient toxicity, but as nutrient excess persists, their storage capacity is
overwhelmed and nutrients overflow to peripheral tissues.
Nonesterified free fatty acids are released into the systemic
circulation and accumulate in peripheral tissues, and lipotoxicity contributes to peripheral organ dysfunction. Excess glucose and other simple carbohydrates induce formation of
advanced glycation end products in multiple tissues. ER
stress, oxidative stress, and inflammation unfold in peripheral tissues with mechanisms similar to those described in
adipose tissue (Fig. 2.8).
VAT drains its venous effluent to the liver via the portal
venous system, leading to portal overflow of excess nutrients
from VAT to the liver and establishing the liver as a dominant
secondary site of aberrant metabolism. Increased free fatty
acid delivery leads to hepatic steatosis, inflammation, and
insulin resistance. Aspects of the portal hypothesis are
debated. For example, isotope dilution techniques demonstrate that only 20% of free fatty acids delivered to the portal
circulation derive from VAT, with the majority from recirculation into the splanchnic bed from the systemic circulation,
calling into question the magnitude of the effect of VAT on
liver metabolism [65]. Nonetheless, the portal hypothesis
provides a coherent rationale for VAT’s role in the pathogenesis of liver disease in obesity. As obesity progresses, the
Excess caloric
intake
CNS:
Aberrant nutrient,
hormonal, neural afferent
inputs and efferent outputs
Adipose tissue:
Hypertrophy, ER, Ox
stress, inflammation,
overflow
Liver:
NAFLD, inflammation,
insulin resistance
Gut:
Microbiome
derangements
Peripheral tissues:
Lipotoxicity, inflammation,
ER, Ox stress, peripheral
insulin resistance
Fig. 2.8 Inter-organ communication and systemic metabolic disease:
A simplified model for systemic spread of metabolic disease. Excess
nutrient intake first affects adipose tissue, but evidence supports direct
effects on the CNS and the gut microbiome as well. As adipose tissue
dysfunction progresses, overflow to the liver and other peripheral
organs induces systemic metabolic disease. The progression of systemic metabolic disease in the liver and other peripheral tissues leads to
aberrant hormonal and neural communications between CNS and
peripheral organ systems as well as between peripheral organs. Not
shown are arrows representing direct communication between the CNS,
the gut, and all peripheral organ systems
29
byproducts of adipose tissue and liver metabolism and
inflammation overflow into the systemic circulation via
peripheral overflow, and all tissues suffer similar insults.
Lipotoxicity, ER and oxidative stress, and inflammation are
observed in the skeletal muscle, liver, vasculature, lung, and
other tissues.
The overflow concept underscores the importance of adipose tissue as a buffer for excess nutrients. Adipose tissue’s
ability to store large amounts of lipid and other nutrients protects other tissues not designed to tolerate lipotoxicity and
nutrient excess. This concept is reinforced by patients with
various forms of lipodystrophy who lack adipose tissue and
develop severe insulin resistance and hyperlipidemia, similar
to obese patients. Adipocyte hypertrophy is an adaptive
response which confines the stress induced by nutrient excess
in early obesity to adipose tissue. As obesity progresses,
however, adipose tissue storage capacity is overwhelmed,
and nutrient excess affects other tissues. Systemic metabolic
disease results from a complex communication between dysfunctional adipose tissue and all other organ systems.
entral Nervous System: Peripheral Organ
C
Communication
The complexities of central nervous system (CNS) regulation of energy homeostasis are beyond the scope of this
chapter, but in brief, the brain receives at least three primary
types of afferent signals regarding energy homeostasis:
dietary constituents, hormones, and neural afferents.
Neurons sensitive to dietary constituents, including glucose,
free fatty acids, amino acids, and their metabolites, reside
primarily in the ARCN and VMH of hypothalamus. Long-­
chain fatty acids (LCFA) are important stimuli: normal efferent signals from LCFA-sensitive neurons act to limit insulin
resistance and food intake. Chronic stimulation by saturated
LCFA leads to accommodation and exhaustion of LCFA-­
responding hypothalamic neurons, whereas polyunsaturated
fatty acids (PUFA) do not cause accommodation, thus
explaining the detrimental and beneficial health effects of
saturated LCFA and PUFA, respectively. Glucose- and
amino acid-sensitive neurons also exist in the hypothalamus
and other areas of the brain, and other metabolites also act as
afferent signals to the CNS. The brain also receives hormonal afferent signals. Leptin and insulin are dominant, but
multiple other hormonal mediators impact on hypothalamic
and other CNS networks, including glucagon, CCK, amylin,
ghrelin, and others. The hypothalamus also receives sympathetic and parasympathetic neural afferent inputs from multiple organs, including the liver, adipose tissue, gut, viscera,
and skeletal muscle. Gut afferents communicate short-term
food resource availability, while adipose tissue afferents signal the status of long-term energy resources. Hepatic afferents communicate the status of glucose and fatty acid level
resources, and all organs and tissues deliver afferent signals
30
to the brain that provide similar information regarding energy
stores. Efferent signals from the brain to the periphery are
complex, are poorly defined, and regulate diverse aspects of
food-related behavior and metabolism. The hypothalamus
generates anorexigenic and orexigenic programs in response
to multiple stimuli that involve not only satiety and hunger
but behavioral, emotional, physiologic, and reward responses
and are mediated by neural efferents to other areas of the
brain as well as to all peripheral organ systems.
Virtually all afferent CNS inputs are altered in obesity.
Hyperglycemia and hyperlipidemia contribute to the many
aberrations in metabolite input to the CNS, while hyperinsulinemia and hyperleptinemia, along with multiple other adipokine and gut hormones, alter hormonal inputs.
Hypothalamic resistance to leptin and insulin result, further
disrupting CNS regulation of energy balance. Peripheral
organ dysfunction contributes to aberrant neural afferent
inputs to the CNS. Research into central-peripheral neural
interactions is in early stages, but such communication is
clearly important: overexpression of the hepatic receptor for
the adipogenic mediator PPAR-γ2 in mice leads to steatosis
and obesity which is abrogated by transection of the hepatic
branch of the vagus nerve, demonstrating that afferent signals from liver to brain regulate food intake and
metabolism.
Inflammation contributes to CNS dysregulation. Obese
mice manifest increased hypothalamic levels of the inflammatory cytokines with a concomitant increase in inflammatory signaling. Nutrient excess contributes, as fatty acids
generate hypothalamic inflammation and ER stress [66].
Hypothalamic inflammation mediates resistance to leptin’s
and insulin’s anorexigenic effects, well-described phenomena in obesity, and blockade of hypothalamic ER stress or
inflammatory signaling ameliorates hypothalamic leptin and
insulin resistance and attenuates metabolic disease [61, 66].
Many questions remain: for example, direct blockade of
inflammatory cytokines within the hypothalamus paradoxically exacerbates rather than attenuates obesity and metabolic disease, suggesting some beneficial effects of
hypothalamic inflammation [66]. Nonetheless, this emerging
field of study demonstrates promise for manipulation of central mechanisms of metabolism.
he Gut Microbiome
T
The role of the gut microbiome in the pathogenesis of metabolic disease is an important emerging field. “Metagenomic”
sequencing of microbiome DNA, analysis of bacterial ribosomal RNA, and microbiota speciation are tools currently
used to interrogate the microbiome. Despite significant
variation between individuals, gut microbiota speciation
within individuals remains constant over time in the absence
of changes in energy homeostasis or physiology. Anywhere
from 1000 to 30,000 species of bacteria reside within the
R. W. O’Rourke
human gut, with total body bacterial number an order of
magnitude greater than total body cell number. Commensal
gut microbiota play an important role in metabolism, potentiating digestion and absorption of dietary constituents.
Animals raised in germ-free environments have 40–60%
lower body weight despite higher food intake relative to
those raised in standard conditions, and stool transfer from
mice with a normal complement of gut microbiota increases
body fat in recipient germ-free animals. Furthermore, stool
transfer from obese animals leads to greater weight gain
compared to stool from lean animals, suggesting that alterations in the microbiome contribute to obesity [67]. Indeed,
gut microbiota speciation is altered in obesity. Over 90% of
gut microbiota fall into the phyla Bacteroidetes or
Firmicutes; obesity in rodents and humans is associated
with an increased Firmicutes/Bacteroidetes ratio that is
reversed with weight loss, including after bariatric surgery,
and probiotics accelerate diet-induced and surgically
induced weight loss.
Gut microbiota regulate systemic metabolism and contribute to metabolic disease. Microbiota speciation patterns
correlate with metabolic disease in humans and mice. Fecal
transplant experiments in mice and humans demonstrate that
gut microbiota are capable of transferring obese, lean, and
metabolically diseased and healthy phenotypes. Underlying
mechanism is not well defined, but inflammation is implicated: commensal gut bacteria regulate immune function and
prevent colonization by pathogenic bacteria. Derangements
in microbiota induce inflammation through activation of pattern recognition receptors such as Toll-like receptors. Obesity
in mice and humans is associated with increased gram-­
negative gut bacteria and increased absorption of lipopolysaccharide [68], and antibiotic therapy directed towards
gram-negative bacteria decreases gut luminal lipopolysaccharide concentrations, systemic inflammation, and hepatic
steatosis in rats [69]. Manipulation of gut microbiota represents an important therapeutic frontier for metabolic
disease.
Specific Metabolic Diseases
Liver Disease
Nonalcoholic fatty liver disease (NAFLD) defines a range of
pathology that includes hepatic steatosis, steatohepatitis, and
cirrhosis. NAFLD is primarily a disease of obesity but may
exist in lean patients. Hepatic steatosis, defined as hepatic
lipid content >95th percentile for healthy lean subjects or
alternatively, as >5% of hepatocytes with cytoplasmic lipid,
is present in 15–30% of the general population depending on
diagnostic modality and in over 90% of patients with BMI
>40 [70]. Up to 30% of subjects with steatosis will progress
to steatohepatitis, a histologic diagnosis defined by hepato-
2
The Pathophysiology of Obesity and Obesity-Related Disease
cyte ballooning, apoptosis, inflammation, Mallory bodies,
and/or fibrosis. Of patients who develop steatohepatitis,
10–30% will progress to cirrhosis within a decade. Accurate
noninvasive predictors of disease progression remain elusive
and represent an active area of research. Liver biopsy is the
current gold standard for diagnosis.
Steatosis and steatohepatitis are influenced by genetics.
Ethnic subpopulations demonstrate variable propensity to
NAFLD, with Asians and Hispanics at highest risk,
Caucasians at intermediate risk, and African Americans at
lowest risk. Histology also varies among ethnicities:
Hispanics demonstrate increased Mallory bodies, while
hepatocyte ballooning predominates in Asians, suggesting
different mechanisms of pathogenesis [71]. NAFLD is highly
hereditable and NAFLD-associated polymorphisms are
identified in humans [72].
Steatosis results from an imbalance in hepatic lipid uptake
and release. Three primary sources of hepatic lipid include
(1) dietary lipid from the intestine as packaged as triglycerides in chylomicrons that are subsequently hydrolyzed into
nonesterified free fatty acids and delivered to the liver bound
to albumin; (2) de novo hepatic lipogenesis from glucose and
fructose substrates, regulated by PPAR-γ, C/EBPα, and
SREPB1, transcription factors that regulate cellular lipogenesis in adipocytes and hepatocytes; and (3) free fatty acid
delivery from adipose tissue. In obese subjects, isotope labeling studies demonstrate that approximately 60% of hepatic
lipid is derived from free fatty acids from adipose tissue,
25% from de novo lipogenesis, and 15% from diet [73].
Hepatic lipid uptake is balanced by lipid export via VLDL
synthesis. Obesity is associated with derangements in all
aspects of hepatic lipid flux. Increased dietary carbohydrates,
especially fructose, increase hepatic de novo lipogenesis via
activation of SREPB1. In addition, VLDL export is compromised in obesity in part secondary to decreased expression of
hepatic apolipoprotein B [74]. Nonetheless, increased free
fatty acid delivery from excess adipose tissue is the dominant
source of hepatic lipid in obesity. Steatosis correlates closely
with hepatic and systemic insulin resistance, both of which
are exacerbated due to the selective nature of insulin resistance in hepatocytes, which become resistant to insulin’s
normally suppressive effects on gluconeogenesis, while at
the same time remaining sensitive to insulin-mediated stimulation of de novo lipogenesis. Selective hepatic insulin resistance thus promotes both hyperglycemia and steatosis. As
steatosis progresses, excess free fatty acids and their derivatives, including ceramide and diacylglycerols, induce ER
and oxidative stress, and eventually apoptosis in hepatocytes,
generating an inflammatory response that contributes to
NAFLD. Expression of pro-inflammatory cytokines, including TNF-α and IL-6, is increased, inducing steatohepatitis.
Neutralization of TNF-α in obese mice reduces steatohepatitis, and anti-TNF-α antibody ameliorates steatosis in humans,
31
suggesting the possibility of cytokine-based therapy for
NAFLD [75]. Similar to adipose tissue, hepatic macrophage
(Kupffer cell) infiltration is increased, while anti-­
inflammatory NKT cells are reduced. The MAPK JNK is a
nexus for cell stress in hepatocytes, is activated by inflammation, free fatty acids, and ER and oxidative stress, and in turn
generates hepatic insulin resistance. Hepatic JNK activity is
increased in obese mice, while JNK knockout mice are protected from steatohepatitis and insulin resistance [76].
Finally, alterations in the microbiome, intestinal epithelial
integrity, and increased hepatic endotoxin exposure have
been implicated in NAFLD [77]. Current treatment for
NAFLD is limited to diabetes control, weight loss, and exercise. Bariatric surgery ameliorates steatosis and steatohepatitis. Thiazolidinediones and antioxidant therapy are emerging
treatment modalities, but long-term efficacy and safety are
not yet defined.
Diabetes
By 2050, it is estimated that a third of the US population will
be afflicted by type II diabetes [78]. Obesity is a strong risk
factor for diabetes, with odds ratios exceeding 5 [79].
Peripheral insulin resistance underlies the pathogenesis of
diabetes. Insulin binds its receptor on target cells and initiates an intracellular signaling cascade involving activation of
insulin receptor substrate-1 (IRS-1) and Akt, which in turn
mediate insulin’s effects on glucose homeostasis and in addition transmit parallel signals that induce cell proliferation
and inflammation. Skeletal muscle is responsible for 70–80%
of glucose utilization and is a dominant site of peripheral
insulin resistance. Increased lipid delivery to skeletal muscle
leads to downregulation of molecules involved in myocyte
glucose uptake as muscle shifts from glucose to lipid metabolism. This decrease in muscle glucose utilization contributes to hyperglycemia, which in turn induces a compensatory
increase in pancreatic beta-cell insulin secretion.
Hyperinsulinemia induces increased proliferation, increased
collagen synthesis, and activation of JNK in myocytes, all of
which potentiate skeletal muscle insulin resistance creating a
vicious cycle. Inflammation also contributes, with increased
skeletal muscle macrophage infiltration and inflammatory
cytokine expression [80]. The inflammatory cytokines
TNF-α and IL-6 promote skeletal muscle insulin resistance,
although IL-6 may have the opposite effect during exercise
[81]. The anti-inflammatory mediators IL-10 and adiponectin are decreased in obesity and attenuate skeletal muscle
insulin resistance [80]. In early insulin resistance, β-cell
mass and insulin secretion increase leading to compensatory
hyperinsulinemia which delays the onset of hyperglycemia.
As obesity and insulin resistance progress, ER and oxidative
stress and inflammation are triggered by free fatty acids and
glucotoxicity and cause beta-cell failure and eventually
death.
32
Salsalate, a modern anti-inflammatory salicylate derivative, is being studied in humans as treatment for diabetes
[82]. Initial trials of TNF-α antibody therapy in diabetic
humans did not demonstrate therapeutic efficacy, but recent
data from diabetic patients treated with long-term anti-­TNF-­α
therapy for autoimmune diseases demonstrate improved glucose homeostasis and have reinvigorated interest in TNF-α
blockade [83]. Anti-IL-1 antibody therapy also shows promise as treatment for diabetes in early human clinical trials
[84]. The importance of macrophages in insulin resistance
has prompted clinical trials in diabetic humans of drugs
designed to block macrophage homing to adipose tissue.
Vascular Disease
Risk ratios for atherosclerotic disease, hypertension, and dyslipidemia associated with obesity range from 1.5 to 3.0 [79].
Vascular disease is closely linked to obesity and type II diabetes and a dominant cause of mortality in diabetic patients.
The importance of insulin in the pathogenesis of atherosclerosis is demonstrated by experiments in animals in which
arterial infusion of insulin induces atherosclerosis in the
infused arteries [85]. Hyperinsulinemia stimulates proliferation and collagen synthesis in arterial smooth muscle cells via
Akt-mediated signaling pathways that are preserved in insulin resistance as discussed above. Insulin also increases LDL
transport into arterial smooth muscle cells, an early event in
atherosclerosis that causes lipotoxicity with resultant ER
stress, oxidative stress, and inflammation. Macrophages and
T cells infiltrate atheromas and contribute to plaque formation and progression. Saturated fatty acids and derivatives
directly activate TLR4 on these cells, exacerbating the inflammatory response. Nitric oxide (NO) plays a central role in
vascular disease in obesity. NO has vasorelaxant, anti-inflammatory, antioxidant, and antiproliferative action. Insulin’s
normal Akt-mediated stimulatory effect on endothelial NO
synthase is downregulated in insulin resistance, reducing NO
levels. Free fatty acids and ROS from oxidative stress also
directly inactivate NO. Insulin-resistant mice demonstrate
decreased NO and increased atherosclerosis. NO production
is decreased and abnormalities in NO-mediated vasodilation
correlate with coronary artery disease in diabetic humans
[86]. Multiple pharmacologic agents are used to treat vascular disease, many of which mediate their effects in part by
attenuating inflammation, most notably statins. Novel therapy for vascular disease directed towards inhibiting oxidative
stress, leukotriene synthesis, phospholipases, and inflammatory cytokines is in human clinical trials [87].
Cancer
Obesity is associated with an increased risk of cancer.
Inflammation promotes carcinogenesis, and the association
between cancer and inflammation independent of obesity is
well-established. Inflammation is generally associated with
catabolic states, such as sepsis, cachexia, and chronic illness.
R. W. O’Rourke
Obesity, in contrast, is one of the few inflammatory states
associated with anabolic signaling, which in the context of
chronic inflammation and increased cell stress and turnover
increases the opportunity for mutagenesis but in the absence
of the catabolic brake on proliferation that normally prevents
propagation of such damage. This combination of inflammation and anabolism is a perfect storm for carcinogenesis.
Diabetes is independently associated with increased cancer risk, including breast, pancreatic, hepatic, endometrial,
colorectal, and kidney. Insulin is a growth factor for multiple
cell types and binds not only the insulin receptor but also the
IGF-1 receptor to generate a pro-proliferative program.
Insulin receptor expression is upregulated in many cancers,
supporting a tropic role for insulin in tumor growth. Insulin
also induces hepatic growth hormone receptor expression,
which in turn increases growth hormone-mediated hepatic
IGF-1 expression. IGF-1 also acts as a growth factor for
many cells, including tumor cells, and increased IGF-1 levels
are associated with increased risk of cancer. Other adipokines
and cytokines also regulate tumor proliferation. Leptin has
growth-promoting effects on cancer cells in vitro, and hyperleptinemia is a risk factor for certain cancers [88]. Adiponectin,
levels of which are decreased in obesity, has a protective
effect, inhibiting tumor growth in vitro, while increased adiponectin levels have been linked to lower cancer risk in epidemiologic studies. Altered steroid metabolism provides
further proliferative stimulus. Estrogen receptor expression is
increased in multiple cancers, and obesity is associated with
increased estrogen levels as a result of peripheral conversion
of androgens to estrogens via aromatase expressed by adipose tissue. Furthermore, insulin and IGF-1, both increased
in obesity, inhibit sex hormone-­binding globulin expression,
increasing steroid bioavailability [89].
Hyperglycemia and lipotoxicity contribute to carcinogenesis. Tumor cells avidly take up glucose and are adapted to
anaerobic energy production (the Warburg effect), providing
a growth advantage but increasing oxidative stress. Saturated
free fatty acids promote tumor growth, as do adipocytes
themselves. Peri-tumor adipocytes are associated with worse
outcomes in multiple cancers, including the prostate, kidney,
colon, and breast. Peri-tumor adipocytes produce cytokines
and adipokines that upregulate proliferative genes and downregulate apoptotic programs in tumors, as well as matrix
metalloproteases implicated in metastasis. Adipocytes have
been shown to deliver metabolites, including fatty acids and
glutamine, to tumor cells, engaging in metabolic cross talk
that essentially “feeds” tumor cells and promotes tumor cell
proliferation.
The intracellular signaling kinase Akt provides an example of the overlap between metabolism and carcinogenesis.
Akt regulates multiple aspects of cell physiology and is one
of the most commonly mutated genes in cancer. Akt regulates glucose homeostasis and cell proliferation through distinct signaling pathways. Insulin activates Akt, and insulin
2
The Pathophysiology of Obesity and Obesity-Related Disease
resistance in obesity is selective with respect to Akt and characterized by resistance to insulin’s effects on glucose homeostasis but preservation of insulin-triggered Akt-mediated
activation of mitogenic and inflammatory signaling [90]. The
hypoglycemic agents metformin and thiazolidinediones
inhibit Akt’s proliferative effects while potentiating insulin
signaling activity, and long-term treatment with these drugs
in diabetic humans may be associated with decreased cancer
risk [91], suggesting the potential for cancer therapy by
exploiting metabolic drugs.
Conclusion
33
Question Section
Part I
1. The genetic contribution to the obesity phenotype based
on twin studies is estimated to be:
A. <1%
B. 10%
C. 50%
D. 70%
2. Thermogenesis:
A. Occurs when mitochondrial oxidative phosphorylation is completely coupled to electron transport
B. Is likely to be increased in obese subjects
C. Is increased with increased uncoupling protein
activity
D. Is decreased in response to a meal
3. Leptin:
A. Secretion is decreased in response to a meal
B. Is secreted by the hypothalamus and binds its receptors in the gut to induce satiety
C. Induces satiety and has primarily pro-inflammatory
effects
D. Induces endoplasmic reticulum stress
The above review of specific metabolic diseases is by necessity incomplete. Obesity is associated with kidney disease,
asthma, atopy, allergic disease, endocrine and cognitive disorders, and a range of other pathologies. The processes that
unfold in the tissues in which these diseases arise parallel
those discussed above in adipose tissue, liver, and skeletal
muscle. An understanding of this pathophysiology will lead
to therapy for metabolic disease. Conceptually, therapy may
be directed towards obesity itself or its metabolic sequelae.
Manipulation of satiety and hunger factors to prevent or
reverse obesity is a dominant effort and includes MC4R agonists and antagonists, cannabinoid antagonists, and anti-­
ghrelin “vaccines.” Drugs in various stages of research Part II
designed to increase energy expenditure regulate mediators
of cellular energy homeostasis, such as PPAR-δ, SIRT1, 4. Endoplasmic reticulum stress:
APMK, and dopamine receptors, among others. Methods to
A. Results from excess nutrient delivery to cells as well
manipulate adipocyte metabolism also hold promise.
as multiple other stimuli
Multiple agents that induce “browning” of WAT to a metaB. Is primarily mediated by reactive oxygen species
bolically favorable BAT phenotype are in human clinical triC. Occurs only in adipocytes
als. Manipulation of oxidative, stress, ER stress, and
D. Occurs in the hypothalamus in response to leptin
MAPK-related mediators are among the many avenues of
bonding its receptors
research towards this goal. Recent data demonstrating that 5. Insulin resistance:
hypothalamic leptin resistance may be ameliorated by agents
A. Is selective in the liver, leading to increased gluconeothat reduce ER stress has reinvigorated interest in leptin thergenesis and increased de novo lipogenesis
apy [61]. Inflammation-based therapies including salsalate,
B. Is selective in the liver, leading to decreased glucocytokine-directed therapies, and macrophage homing-­
neogenesis and decreased de novo lipogenesis
directed strategies are under active study in human trials.
C. Is characterized in early diabetes by pancreatic beta-­
Manipulation of macrophage phenotype and function and
cell failure and a defect in insulin secretion
targeting of specific pathogenic macrophage subpopulations
D. Is characterized by increased IRS-1 activity
represents an important avenue of research. Targeting other 6. Adipose tissue overflow:
cells involved in adipose tissue inflammation, such as regulaA. Is a normal response to a meal
tory T cells, NK cells, and NKT cells, has also shown potenB. Results from a failure of adipose tissue nutrient bufftial in animal models. Obesity-related metabolic disease
ering capacity and underlies systemic metabolic
exacts an enormous toll on public health, and an understanddisease
ing of its pathophysiology holds promise for novel pharmaC. Is characterized by reduced free fatty acid delivery to
cotherapy or genetic therapies for a wide range of diseases
the liver
with enormous impact on the human condition.
D. Leads to decreased systemic cellular stress
34
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3
History of the Development
of Metabolic/Bariatric Surgery
Elias Chousleb, Jaime A. Rodriguez, and J. Patrick O’Leary
Chapter Objectives
1. Review the history and evolution of bariatric and
metabolic surgery.
2. Learn from previous experiences in the development of bariatric and metabolic surgeries in order to
continue to improve safety and efficacy.
History of Bariatric Surgery
The odyssey of the surgical intervention for the treatment of
serious obesity began as all odysseys begin when a problem
was recognized and a prepared mind coupled divergent
observations and asked the question, “Why not?” In this
case, the problem was severe incapacitating obesity, and the
observation was that when individuals underwent resection
of the greater portion of their small intestine, weight loss
ensued even if the individual was of normal weight at the
outset.
As the world came out of the Second World War, farming
in many areas became more mechanized, manpower became
available, foodstuffs became extremely affordable, and the
fast-food industry emerged. The US agriculture thrived as
did the urbanization of not only the United States but also the
world. Preservatives were added to extend the shelf life of
food. The prevalence of obesity skyrocketed.
At this time young physicians who had their medical education interrupted by the call to military duty returned to
complete their specialty training. Several institutions, notably the University of Minnesota, shunted a substantial part of
E. Chousleb · J. A. Rodriguez · J. P. O’Leary (*)
Department of Surgery, Florida International University, Herbert
Wertheim College of Medicine, Miami, FL, USA
e-mail: olearyp@fiu.edu
this work force into research laboratories, many of which
were committed to unraveling the mystery of the gastrointestinal tract. Working in the environment nurtured by Owen
H. Wangensteen and under the direct tutelage of Richard
L. Varco, one such individual, John Linner, set about transposing segments of the small intestine to better understand
the physiologic role of the jejunum as compared to the ileum.
The job was arduous, the studies sophisticated, and the
research laboratory was not air-conditioned. The studies
were done in a canine model and were of such quality that
the work was selected for presentation at the American
Surgical Spring Meeting in 1954 [1]. As a part of the presentation, a comment was made about a young, seriously obese
woman with heart disease that had undergone an operation to
bypass the majority of her small intestine. She had lost
weight, and her cardiac disease had stabilized. In the discussion of this paper, Philip Sandblom from Sweden commented
that a Swedish surgeon, Viktor Henriksson, had performed a
similar procedure in a small number of patients, and although
they had experienced “some difficult situations of nutritional
balance,” they had experienced weight loss.
The patient described by Linner underwent a revision of
the primary bariatric procedure in 1981 and survived to age
61 when she died of a cardiac event (Linner JG, 1985, personal communication). Although still heavy, she had not
regained her original severely obese state. John Kral
researched the patients operated upon by Henriksson and
found they also experienced long-term control of their obesity (Kral J, 1985, personal communication).
Based in part on these results, Payne (a surgeon), DeWind
(a gastroenterologist), and Commons (a pathologist) as part
of a large study on “morbid” obesity (“morbid” a term coined
by Payne to encourage insurance companies to pay for these
procedures) performed an end-to-side jejunocolic shunt in
ten patients [2] (Fig. 3.1). This was a part of an experimental
study in which patients consented to a large number of baseline studies and to similar follow-up studies to characterize
the effects that the procedure produced. The results of these
studies were published in great detail and in a style that was
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_3
37
38
E. Chousleb et al.
Fig. 3.1 Jejunocolic bypass
Fig. 3.2 End-to-side jejunoileal bypass
popular at that time. Weight loss occurred in each of the
patients. One patient died 6 months after the procedure of a
pulmonary embolism. She had an antecedent history of pulmonary emboli. The protocol included the reestablishment
of continuity of the gastrointestinal tract when optimal
weight had been achieved. In the six patients in whom continuity of the gastrointestinal tract was restored, all regained
their previous obese state. The three remaining patients had
their jejunocolic shunt revised to an end-to-side jejunoileal
shunt (Fig. 3.2). One of these patients, in which a substantial
amount of jejunum was placed back in continuity, experienced weight regain to her preoperative level. The authors
observed that if a reasonable amount of jejunum (14 in.) and
a smaller portion of ileum (4 in.) were left in continuity with
the ingested food, weight loss could be maintained. In a later
publication, Payne and DeWind reported acceptable weight
loss results in a large number of patients [3].
By the late 1960s and early 1970s, there were a number of
reports of successful weight loss being produced by jejunoileal or jejunocolic shunts. Each of these studies identified
complications that were directly associated with the intestinal bypass procedure. As these reports became more numerous, it produced an extremely fertile field for a number of
researchers to investigate the various mechanisms of action
that produced the metabolic aberration. Perhaps, the most
interesting and best studied side effect of intestinal shunting
was the development of liver failure in certain patients. In
Payne’s original report, all of the patients had liver biopsies,
and the vast majority demonstrated steatosis of the liver.
Many surgeons paid little heed to this observation. After all,
the patient was fat and had fat everywhere else, why not in
the liver. If the excluded limb of the intestine was resected,
liver failure did not occur, although these patients did experience malabsorption and weight loss. When liver failure
3
History of the Development of Metabolic/Bariatric Surgery
39
occurred, biopsies of the liver looked identical to alcohol-­ Bariatric surgery was often looked upon as a nuisance that
induced cirrhosis, even to the point of including Mallory’s had a tendency to congest intensive care units with long-term
bodies. Many curmudgeons opined that these patients must stay patients. Academic advancement for young surgeons
be closet alcoholics. That was clearly not the case. Certain occurred in spite of their involvement in bariatric surgery not
investigators demonstrated bacterial overgrowth of gram-­ because of their achievements in this area. National meetings
negatives and anaerobic bacteria in the excluded limb of the rarely accepted papers about bariatric surgery, and when
intestine along with morphological changes in the intestinal papers were accepted, they almost always dealt with the
wall (separation of tight junctions between enterocytes) and management of complications that might be pertinent to simfelt that this played a role [4]. These investigators coined the ilar complications that occurred in normal weight individuterm “enterohepatic syndrome.” Other complications of als. The papers were always positioned at the worst spot on
intestinal shunting procedures included malnutrition, vita- the program.
min deficiencies (especially of fat-soluble vitamins), electroBy the early 1970s, certain surgeons became sensitized to
lyte abnormalities (especially of divalent cations), ketosis, the complications associated with malabsorptive procedures
iron malabsorption, hyperoxaluria, nephrolithiasis, migra- and looked for alternatives. From a simplistic standpoint, if
tory arthralgia, profound inflammation of synovial lined allowing patients to eat large volumes of food and then interspaces, and in some individuals weight regain. Although the rupting absorption by short-circuiting the intestine did not
benefits were profound, so were the complications. The work, perhaps limiting intake would.
second-­ever National Institutes of Health (NIH) Consensus
At the University of Iowa, there were strong connections
Development Conference was held in 1978 [5]. The focus to the University of Minnesota. Not only were they in relative
was the treatment of morbid obesity, including surgical inter- proximity, but many of the faculty at Iowa had been educated
vention. Although the recommendations were favorable for in part at the University of Minnesota. Edward E. Mason was
certain operative procedures in the treatment algorithm, it interested in the gastrointestinal tract and specifically in pepwas felt that the risk-benefit ratio for intestinal shunting pro- tic ulcer disease. Working with Chikashi “Chick” Ito, Mason
cedures was too high to recommend routine use.
performed a side-to-side anastomosis between the very upper
Up to this time, the academic surgical community had third of the divided stomach and a loop of the jejunum to
shown little interest in the development of bariatric surgery. treat duodenal ulcers disease (Fig. 3.3). A number of patients
The individuals doing bariatric surgery were felt to be some- were obese, and Mason observed that although the procedure
what of a renegade group of surgeons who were involved in did not control the ulcers, it was associated with weight loss.
the treatment of a “condition” that was simply the end result He reported this in a 1967 publication during the peak of
of gluttony and sloth. This prejudiced view augmented the
discrimination against the patients, their disease, and the surgeons and staff that treated them. It was a commonly held
belief that seriously obese individuals simply lacked willpower. Surgeons who lowered themselves to treat individuals that were affected by obesity, which was not a serious
disease (like cancer), deserved the headaches inherent in the
care of such patients. It was a waste of resources that could
have been used in the treatment of “real” surgical problems
such as duodenal ulcer disease.
There was little or no appreciation that obesity was a disease and intimately associated with other diseases such as
type II diabetes, hypertension, cardiovascular disease, and an
increased incident of certain malignancies. There was a failure to understand that the underlying inflammatory process
associated with severe obesity affected every system in the
body to a greater or lesser degree. It was not realized that
control of the obesity would be associated with increased
longevity and general health.
There was a real schism between believers that obesity
was a disease state and those that did not adhere to this premise. Department chairs grudgingly allowed young surgical
faculty to do bariatric surgery as it produced volume in the
operating room and technical experience for residents. Fig. 3.3 Side-to-side anastomosis
40
Fig. 3.4 Roux-en-Y limb for gastrojejunostomy
popularity for the jejunoileal bypass [6]. The paper was
somewhat confusing to the surgical community as it reported
results for patients with two different diseases. As these
patients were followed longer term, weight regain was
observed. Over the subsequent 8 years, Mason published
three more papers modifying the procedure by first making
the anastomosis between the stomach and the jejunum
smaller and then substantially decreasing the gastric pouch
size. The problems were multiple. The procedure was performed high in the abdomen and therefore was technically
demanding, and the enlarged left lobe of the liver was often
problematic. Staplers were not available in the early years.
Although early weight loss was obtained, weight regain
occurred in many patients by 6 months. Because the procedure involved a loop of jejunum, regurgitation of small bowel
content into the gastric pouch frequently occurred. Alden
solved some of the problems by doing away with the loop
and creating in Roux-en-Y limb for the gastrojejunostomy
[7] (Fig. 3.4).
Mason continued to modify his procedure and by the mid-­
1970s had first performed a gastric partition with the opening
on the greater curvature of the stomach. This was done only
in a small number of patients and did not seem to produce
long-term weight loss (Fig. 3.5). By 1975, Tretbar, Echout,
Fabito, Laws, O’Leary, and others had performed a vertical
gastric partition along the lesser curvature of the stomach
and controlled the outlet using a variety of devices from
chromic suture to a silicone ring [8] (Fig. 3.6). Staplers were
critical in the development of such a partition. Mason modified his approach by placing an end-to-end anastomosis
E. Chousleb et al.
Fig. 3.5 Gastric partition with the opening on the greater curvature of
the stomach
Fig. 3.6 Vertical gastric partition along the lesser curvature of the
stomach with the outlet controlled with a silicone ring
(EEA) stapler through the stomach at the distal end of the
lesser curvature cylindrical gastric tube and placing a piece
of Marlex® mesh through the hole and back up through an
aperture at the lesser curvature of the stomach sparing the
nerve of Latarjet [9] (Fig. 3.7). This vertical banded gastro-
3
History of the Development of Metabolic/Bariatric Surgery
Fig. 3.7 End-to-end anastomosis through the stomach at the distal end
of the lesser curvature cylindrical gastric tube with a piece of Marlex
mesh through the hole and back up through an aperture at the lesser
curvature of the stomach
plasty gained considerable popularity and for a period of
time in the early 1980s was probably the most commonly
performed bariatric operation in the United States.
The same NIH consensus conference that spelled the
demise of the jejunoileal bypass surgery opened an alternate
avenue for gastric restrictive procedures. A variety of different mechanisms had been explored to partition the stomach.
Various surgeon pioneers began to perfect the operative techniques surrounding gastric bypass procedures. Investigators
from the University of Kentucky and the University of North
Carolina published comparison studies between the intestinal bypass procedure and gastric bypass [10, 11].
Complications were clearly less in the gastric procedures,
and weight loss was equivalent. During the 1980s, Mason
continued to champion gastric restriction using the banded
gastroplasty. Various modifications of these procedures were
proposed.
In an ingenious modification of the silastic ring championed by Laws, L. Kuzmak invented a silastic ring with a
small balloon embedded on the inner aspect of the ring that
could be accessed from a subcutaneously placed reservoir
[12]. This allowed calibration of the outflow lumen (Fig. 3.8).
With this innovation, adjustable gastric banding was born.
At this phase in the development of bariatric surgery,
which occurred in the 1980s, a number of individuals adopted
the philosophy that gastric restrictive procedures—including
gastric bypass, which was thought at that time to be primarily a restrictive procedure—were associated with less in the
41
Fig. 3.8 Adjustable gastric banding. A silastic ring with a small balloon embedded on the inner aspect of the ring that could be accessed
from a subcutaneously placed reservoir
way of postoperative complications, produced satisfactory
weight loss, were associated with amelioration of the complications of obesity, and were technically reasonable to perform. Gastric restrictive procedures benefited enormously
from advances in technology, especially in the area of stapling devices. Surgeons also learned many invaluable lessons as to the management of obese individuals after other
intra-abdominal procedures. These lessons were accepted by
the general surgeons, who were not necessarily doing bariatric surgery but operating on seriously obese people for other
causes.
Not all of the advances in bariatric surgery were confined
to the North American continent. Bariatric surgery was
beginning to become recognized in Europe, South and
Central America, and to a lesser degree Asia. One of the most
prolific writers from the European continent was Nicola
Scopinaro, who in 1979 had devised an operation he termed
the biliopancreatic diversion (BPD) [13]. Scopinaro performed a generous gastrectomy, usually leaving a gastric
remnant about one-third the size of the original stomach. He
then divided the small intestine at about its midpoint and
brought the ileal end up to be anastomosed to the stomach
remnant. The other end of the intestine that carried the biliary
and pancreatic excretions was anastomosed to the side of the
ileum, approximately 120 cm from the ileocecal valve
(Fig. 3.9). This produced an abbreviated channel where the
digestive juices mixed with ingested food. Scopinaro reported
excellent weight loss results. His patients underwent a large
number of metabolic studies that demonstrated amelioration
of many of the comorbidities associated with morbid obesity.
42
E. Chousleb et al.
detailed physiology was at a much higher level than ever
before, although still quite incomplete. The vast majority of
procedures were gastric restrictive procedures, with the most
common operation performed being the gastric bypass. The
bariatric surgical community could now perform this type of
surgical intervention with an operative mortality of less than
1% and morbid complications occurring in less than 6% of
patients. The beneficial effects had now been clearly documented in certain areas. Although insurance coverage was
not widely available, certain payers were beginning to cover
the procedures. The field of surgery for morbid obesity was
poised at the precipice, awaiting the next great breakthrough.
These change agents came in two forms.
The first was a report by MacDonald and Pories published
in 1995 detailing the beneficial effect seen in obese individuals with adult-onset (type II) diabetes who had undergone a
Roux-en-Y gastric bypass [15]. It was known that diabetes
was ameliorated by weight loss. Previous studies, in the early
1980s, dealt with changes in insulin resistance and glucose
metabolism after intestinal shunting procedures [16]. Insulin
resistance improved, and hyperglycemia disappeared even
before weight loss had occurred. This report went virtually
unnoticed, in part because intestinal shunting procedures
were out of favor.
The Pories report about glucose metabolism and the amelioration of diabetes was well received in the bariatric surgical community but less well received in the general medical
community. The report showed that insulin levels plummeted, while glucose metabolism improved, suggesting a
change in insulin resistance.
Eight years later, in 2003, Schauer reported similar results
Fig. 3.9 A generous gastrectomy leaving a gastric remnant about one-­
third the size of the original stomach. The small intestine is divided at in a large cohort of patients who had either impaired testing
about its midpoint, and the ileal end is brought up to be anastomosed to glucose levels or type 2 diabetes mellitus (T2DM) [17].
the stomach remnant. The other end of the intestine that carried the bili- Shortly thereafter, prompted by these observations, a summit
ary and pancreatic excretions is anastomosed to the side of the ileum,
was convened in Rome by a diverse group of individuals
approximately 120 cm from the ileocecal valve
with an interest in T2DM. This summit was well attended by
a large number of scientific organizations. A consensus was
He did acknowledge many of the side effects seen in the pre- reached and published in 2010 [18].
viously discussed malabsorptive procedures, especially those
Perhaps the most important results of this meeting were
having to do with iron and divalent cation absorption as well the creation of a research agenda and the more widespread
as absorption of fat-soluble vitamins. From the literature, it understanding of some of the mechanisms by which diabetes
would appear that his patients required diligent and pro- was controlled with surgical intervention. It was understood
longed follow-up, but with this type of management, that something was happening to these patients that went far
Scopinaro reported excellent long-term results [14].
beyond simply rerouting the food flow in the intestines—
something metabolic. Although Wolfe had introduced the
term “metabolic intestinal surgery” in the mid-1970s, it was
Metabolic
only now as surgeons begin to truly appreciate the magnitude
of what was being accomplished that the name “metabolic”
As the decade of the 1980s drew to a close, the field of bar- resurfaced [19].
iatric surgery had stabilized. Much had been learned and
The third NIH consensus conference on obesity, in 1991,
applied over the preceding 25 years. The surgeon’s knowl- found that surgical intervention of morbid obesity amelioedge about the disease had improved substantially. The rated many of the comorbidities associated with obesity. In
understanding of complex hormonal mechanisms and 2008, the membership of the American Society of Bariatric
3
History of the Development of Metabolic/Bariatric Surgery
Surgery elected at the annual business meeting to change the
name of the society by adding “Metabolic” to the organization’s title. This seminal change refocused efforts on understanding how these procedures worked. In some ways, this
validated earlier bariatric surgeons who had demanded that
patients be followed long term and that their results be published using defined parameters of success. The conference
went on to conclude that the risk-benefit ratio in certain
patients favored surgical intervention [20].
Minimally Invasive Techniques
On the second front, in the early 1990s, there was a pivotal
technical revolution in general surgery. Surgeons had begun
to explore the laparoscopic approach to certain general surgical procedures. Obstetrics and gynecology physicians had
known for years that the abdominal cavity could be
approached by minimally invasive techniques. These techniques were usually limited to observation and, perhaps
through biopsy, diagnosis. Therapeutic interventions had not
been a part of their armamentarium. Advances in digital
imaging, light sources, miniaturization of cameras, and
advanced instrumentation would allow therapeutic intervention to become possible. With these advances, minimally
invasive surgery was spawned. As laparoscopic cholecystectomy became commonplace, the tsunami of minimally invasive operations followed. The first minimally invasive gastric
restrictive procedure was not far behind.
The first laparoscopic gastric bypass operation in the
United States was performed by Wittgrove and Clark in
October 1993, using a retrocolic limb with a circular stapler
anastomosis for the gastrojejunostomy [21]. Just as in the
open procedure, the three key components to the creation of
an effective gastric bypass were the creation of a small gastric pouch, a restrictive gastrojejunal anastomosis, and the
creation of a roux limb to promote malabsorption. Initially
technical constraints made this operation very difficult, but
as experience with laparoscopic surgery grew and as suturing, stapling, and electrocoagulation devices became readily
available, the popularity of laparoscopic gastric bypass
increased rapidly. By the late 1990s almost every academic
department of surgery had created a division that performed
minimally invasive bariatric procedures.
The era of minimally invasive surgery revolutionized the
surgical management of obesity. The number of bariatric
procedures multiplied exponentially allowing surgeons to
care for patients in a much safer and effective fashion.
Laparoscopy allowed surgeons to perform these complex
gastrointestinal operations with a level of safety that has
never before been seen. This improved morbidity and mortality profile made bariatric surgery increasingly more attractive to patients, surgeons, and referring physicians alike.
43
The landscape had truly changed – where operative mortality had been less than 1%, now the operative mortality
plummeted to less than 0.2%. The rate of complications fell
to a third of complication rate for open procedures [22].
Hospital stays went from 3 to 5 days down to 2 days. The use
of laparoscopy in bariatric surgery resulted in reduced
impairment of pulmonary function [23], less intraoperative
blood loss, shortened length of hospital stay, decreased rates
of wound infection, and incisional hernias becoming rare
[24]. Reduction in complication rates resulted in decreased
costs. Patients routinely returned to work in less than
2 weeks.
There was another innovation that affected the safety of
surgery for obesity and related disease. The first successful
laparoscopic banding procedure was published in 1993 by
Broadbent [25]. The authors reported the laparoscopic placement of a nonadjustable gastric band in a 16-year-old female
the year prior. Catona also published a series of patients who
underwent nonadjustable gastric banding using a laparoscopic approach in the same time frame [26]. These procedures were similar to the Laws procedure without the lesser
curvature partition. During the same time, Belachew
designed an adjustable gastric band that could be placed
using laparoscopic techniques. He described this procedure
in a porcine model [27]. This was similar to the band patented by Kuzmak a decade earlier. A large number of bands
were placed in Australia, Latin America, and Europe prior to
approval of the device in the United States. Subsequently,
O’Brien from Australia published a review of laparoscopic
adjustable gastric banding that showed durable weight loss
of 47% excess body weight (EBW) in patients followed up to
15 years [28].
In 1986, Hess and Hess performed an open procedure
adding a sleeve gastrectomy to the original biliopancreatic
bypass procedure and modified the anastomosis to a duodenojejunal (BPD-DS) configuration (Fig. 3.10) [29]. Some of
the advantages of BPD-DS included the avoidance of dumping syndrome and marginal ulceration by preserving the
innovated pylorus and creating the anastomosis between the
duodenum and the jejunum. A common channel of 100 cm
was created; therefore, malabsorption of protein and calories
were increased as compared to Roux-en-Y gastric bypass.
The first laparoscopic duodenal switch was performed by
Ren and Gagner in 1999, as a modification of the original
Scopinaro procedure [30]. Laparoscopic BPD-DS has been
associated with larger weight loss when compared to all
other bariatric procedures. It was reserved for patients with a
body mass index (BMI) of 60 or greater, but due to technical
difficulty as well as concerns for nutritional deficiency, the
procedure has not been widely adopted in the United States.
Throughout the history of bariatric surgery, there has been
avid interest in developing safer procedures with less complications and equivalent effectiveness in the short and long
44
E. Chousleb et al.
Fig. 3.10 An open procedure adding a sleeve gastrectomy to the original biliopancreatic bypass procedure and modifying the anastomosis to
a duodenojejunal (BPD-DS) configuration
Fig. 3.11 Sleeve gastrectomy
term. Johnston, in 1987, performed the first Magenstrasse
and Mill procedure [31]. The idea was to create a safe simple
alternative to the gastric bypass and the vertical banded gastroplasty. The Magenstrasse referred to a thin tube created
from the lesser curvature of the stomach and the Mill referred
to the antrum. The Magenstrasse and Mill procedure was
created by using a circular stapler to create a defect in the
antrum and then creating a narrow tube along the lesser curvature initially over a 40 Fr bougie. The diameter of the bougie was then reduced to a 32 Fr to optimize weight loss. The
technique was subsequently improved by simply resecting
the greater curvature of the stomach. The result was the
sleeve gastrectomy, which had previously been performed as
part of the restrictive component of the duodenal switch by
Hess and then Marceau [32].
Sleeve gastrectomy was initially used as part of a two-­
step procedure in high risk (BMI > 60) patients (Fig. 3.11).
Close follow-up of these patients revealed substantial weight
loss and resolution of comorbidities with the sleeve gastrectomy alone [33]. The indications for laparoscopic sleeve
gastrectomy (LSG) as a stand-alone procedure were published in 2008 [34]. The popularity of the LSG has grown
dramatically due to a perceived simplicity of the surgical
technique and adequate resolution of comorbidities.
However, long-­term studies on effectiveness and difficult to
treat complications, such as leak, require further evaluation.
Hormonal Weight Loss
As a better understanding of gut peptides emerged, innovative
procedures were developed to produce hormonally induced
weight loss. One such procedure targeted the gut neurohormonal activity by producing an ileal interposition in upper
intestines. Harkening back to the early work of Linner, Mason
in 1999 interposed the ileum to a position in the proximal
jejunum and produced weight loss [35]. A 170–200-cm-­long
portion of ileum was isolated leaving 30 cm of distal ileum.
This segment was relocated 50 cm distal to the ligament of
3
History of the Development of Metabolic/Bariatric Surgery
45
procedures. It seemed the complication rate was unacceptably high. The underlying bias and discrimination against
patients affected by obesity continued to create a public environment of blame for both the patient and the surgeons who
operated on them. The ASMBS moved not only to create
educational programs but also to establish accreditation for
surgeons and institutions that were performing bariatric surgical intervention.
Conclusion
Fig. 3.12 The ileum is interposed to a position in the proximal jejunum. A 170–200-cm-long portion of the ileum is isolated leaving 30 cm
of the distal ileum. This segment is relocated 50 cm distal to the ligament of Treitz utilizing two jejunoileal anastomoses. Bowel continuity
is restored with a third jejunoileal anastomosis
Treitz utilizing two jejunoileal anastomoses. Bowel continuity was restored with a third jejunoileal anastomosis
(Fig. 3.12). Multiple peptides have been studied, some of
which surely play a role in food intake and satiety. The most
fertile area of current research is in establishing the actual
mechanism of action by which metabolic procedures work
and relating that to the pathophysiology of obesity and related
disorders. It is through this path of investigation that future
innovation will improve the safety and effectiveness of these
procedures.
Accreditation
In 2004, an impending crisis loomed that centered in some
ways around ethics. Two separate factors contributed to the
conundrum; laparoscopic procedures were now performed
commonly by a markedly increased number of surgeons who
felt comfortable approaching the abdomen using a minimally
invasive approach. At the same time, more insurance coverage was available for patients needing surgical interventions
for their obesity. Although the operative procedure itself was
becoming better understood from a technical standpoint,
many surgeons, with only minimal skills, were operating on
patients who were at high risk. A few high-profile complications attracted attention both on television and in print media,
with challenging questions being asked about the level of
training of bariatric surgeons and about the necessity of these
At the close of the first decade of the twenty-first century,
several things would appear to be unequivocally true. Firstly,
surgical intervention in the treatment of morbid obesity has
an acceptable risk-benefit ratio and produces amelioration or
control of many of the diseases associated with serious obesity. Secondly, the minimally invasive approach has contributed remarkably to the improvement in the risk-benefit ratio.
Thirdly, although much remains to be understood, metabolic/
bariatric surgery has emerged from the shadows of charlatanism into the mainstream of general surgery. The baby was
not thrown out with the bathwater and has emerged on the
surgical stage as a vibrant, healthy adolescent.
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3. Payne JH, LT DW. Surgical treatment of obesity. Am J Surg.
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4. O’Leary JP. Historical perspective on intestinal bypass procedures.
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14. Scopinaro N, Adam GF, Marinari GM. Biliopancreatic diversion.
World J Surg. 1998;22:936–46.
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BM, et al. Who would have thought it? An operation proves to be
the most effective therapy for adult onset diabetes mellitus. Ann
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16. O’Leary JP, Duerson MC. Changes in glucose metabolism after
jejunoileal bypass. Surg Forum. 1980;31:87.
17. Schauer PR, Burguera B, Ikramuddin S, Cottam D, Gourash W,
Hamad G, et al. Effect of laparoscopic Roux-en-Y gastric bypass
on type 2 diabetes mellitus. Ann Surg. 2003;238(4):467–85.
18. Rubino F, Kaplan LM, Schauer PR, Cummings DE. Diabetes surgery summit delegates. The diabetes surgery summit consensus
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22. Miller MR, Choban PS. Surgical management of obesity: current
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et al. Comparisons of pulmonary function and postoperative pain
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4
The History of the American Society
for Metabolic and Bariatric Surgery
Robin P. Blackstone
Chapter Objectives
1. Review the history and evolution of the American
Society for Metabolic and Bariatric Surgery
(ASMBS).
2. Provide an overview of current programs and initiatives undertaken by the society.
3. Demonstrate the vision and leadership that led to
the current state of metabolic and bariatric surgery
within the United States.
Introduction
The history of the American Society for Metabolic and
Bariatric Surgery (ASMBS) parallels the development of
metabolic and bariatric surgery (MBS) closely. In studying
this history, three distinct periods emerge. The first, the Era
of Inquiry (1967–1988), established the initial scientific
foundation of MBS. The second is the Era of Rapid Growth
(1989–2004) during which the society supervised rapid
growth in the number of surgeons and programs and the
growth of integrated multidisciplinary teams. The number
of cases grew rapidly spurred on by laparoscopic access and
with increasing diversity in procedures performed and use
of devices. The third period, the Era of Quality and
Engagement (2004 to present), established the society’s
focus on safety and increasing engagement with other
stakeholders. These stakeholders include medical colleagues, international surgeons, the American College of
Surgeons, medical societies dedicated to the management
of obesity, and patient advocacy groups. Together we have
focused on building an infrastructure for the population
management of obesity in the United States and globally
R. P. Blackstone (*)
Metabolic and Bariatric Surgery, Banner University Medical
Center – Phoenix, Phoenix, AZ, USA
e-mail: robin.blackstone@bannerhealth.com
using a similar collaborative model that exits between surgery and medicine in other disciplines. Most patients with
obesity are treated in a community hospital setting. The
participation of surgeons and their integrated health partners in using high-quality data for ongoing quality improvement provides leadership to improve patient safety and
experience of care within the community. The ASMBS has
been successful in creating a high-value data-driven network of nationally accredited programs accepted as the
foundation of quality by payers. Over the last interval, the
network has been leveraged to address ongoing quality
issues for underperforming centers focused on readmissions and enhanced recovery protocols. These efforts are
transformational. MBS is conducted in the United States
within a learning and continuously improving culture. It is
the signal achievement of this era.
The Era of Inquiry 1967–1988
From the beginning, MBS developed through multidisciplinary collaboration with the focus located at the University
of Iowa (UI). At UI, a unique environment was created by the
collaboration of surgeons, physiologists, biochemists, and
integrated health professionals at the National Institutes of
Health (NIH) General Clinical Research Center (GCRC).
This Center, led by Edward Mason, MD (Fig. 4.1), presented
its multidisciplinary findings in collaborative discussions of
each other’s work. In 1967 in a symposium honoring Owen
H. Wangensteen, MD, Dr. Mason’s mentor, Dr. Mason, and
Chikashi Ito, PhD, presented the first case of gastric bypass.
These meetings became more formal and became known as
the Mason Surgical Treatment of Obesity Symposium
Workshop in 1976, attracting national and international scientists and surgeons interested in treating the disease of obesity. With NIH funding, the group continued to explore the
physiological and metabolic effect of gastric bypass and presented their findings at the American Surgical Association
Meeting in 1969.
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_4
47
48
Fig. 4.1 Edward Mason, MD
R. P. Blackstone
4
The History of the American Society for Metabolic and Bariatric Surgery
Edward Mason writes about those days:
The postgraduate course was started because of the increasing
number of surgeons performing obesity surgery, who were communicating and sharing experiences and ideas by phone. Nicola
Scopinaro, MD, from Genoa and surgeons from Sweden were
early attendees. In 1977, there were 28 presentations and symposia listed for the meeting, which was held April 28 and 29 and
called the Gastric Bypass Workshop. I found a copy of the bound
paperback of 187 pages recording transcript of the 1977 meeting,
which was distributed after the meeting. The last article is about
plans for a Gastric Bypass Registry. The Workshop transcript
was distributed a month after the meeting. It includes the presentations and discussion that were recorded and transcribed.
Long-term results and prospective and larger trials began
to contribute to the knowledge base, culminating in the first
NIH consensus conference on December 4, 1978. This conference was of pivotal importance. It was at this conference
that the jejunal-ileal bypass was shown to have substantial
problems, and restriction (gastric bypass and vertical banded
gastroplasty) was established as a credible procedure. The
society was formed on this strong scientific foundation.
John Kral writes:
Having attended the Iowa City colloquia, the academic surgeons
J D Halverson, J P O’Leary, H J Sugerman and myself, at the
colloquia in 1983, met in a pub during the lunch break to propose expanding the colloquia to the format of scientific meetings
with membership, program committees, minutes, abstract selection and “democratic” principles. That afternoon, June 3, 1983
at an impromptu business meeting of the attendees a proposal
for the formation of a society for the study of obesity surgery
was made and accepted.
The aims of the society were to “develop guidelines for
patient care, promote research into the outcomes and quality
of bariatric surgeries and encourage an exchange of ideas
among researchers and surgeons” [1]. In deference to Mason,
the term “bariatric”—a continuation of his tradition of the
colloquia—was adopted. In 1984, the first annual meeting of
the American Society for Bariatric Surgery (ASBS) was held
in Iowa City. The meeting attracted more than 150 participants and 36 oral presentations. After meeting again in
1985 in Iowa City, the society chose to rotate annually
between different venues.
The original officers were the following: Edward Mason,
MD, president; Boyd Terry, MD, secretary-treasurer; and
Patrick O’Leary, MD, program committee chair. Initially,
terms of office were 2 years in duration. However, as the
work of running the society increased, the term of office
decreased to 1 year in 1989 for the term of Cornelius Doherty.
In recognition of his leadership in bariatric surgery, the
Edward E. Mason Founders Lecture was established and
given for the first time on June 2, 1989, by H. William Scott
Jr., MD, from Vanderbilt.
In the early days of the academic effort to define the science of the surgical treatment of obesity, there was support
49
by the NIH in convening a consensus conference and presentations of critical data at the Society for Surgery of the
Alimentary Tract, the American Surgical Association, and
the Western Surgical Association meetings. Many of the
early surgeon scientists were also active in the American
College of Surgeons (Ward Griffen, MD, and Patrick
O’Leary, MD).
The majority of surgeon leaders from this era commented
on the serious barriers in trying to mainstream their research
and surgical treatment of obesity into their departments and
community hospitals. The formalization of the society served
to promote the ability to provide a forum for exchange of
ideas, research, and best practice and education of its members; however, it also established a political force within
American surgery and served to promote access to care for
the surgical treatment of obesity. The criticism and perception by the surgical establishment had a profound impact on
the character of the society and drove some decisions (both
good and bad) from a group that felt on the defensive.
Perhaps, in many ways, this reflects the very real discrimination and prejudice that patients who suffer from obesity also
feel. A fiercely independent and entrepreneurial character is
firmly entrenched in the society’s foundation. These echoes
of the underdog reappear throughout the 30+ year history of
the ASMBS and continue to contribute to the development of
our specialty and the identity of the society that serves to
forward its practice.
The nascent society continued to encounter a difficult
environment full of opportunity. Cornelius Doherty, a private
practice surgeon recruited to join Edward Mason in IU and
president of ASBS from 1989 to 1990, writes:
The early surgeons in our field operated at a time when the prejudice against surgical treatment of severe obesity was at its
zenith. Organized medicine had abandoned them with indifference. Third-party payers were denying patient access to surgery
arbitrarily. Professional liability carriers were stopping availability of coverage or charging exorbitant premiums. Plaintiff
attorneys were predatory about filing cases. My agenda during
my Presidency was to position the ASBS in the best possible
way to plea the case for acceptance of surgical treatment of
severe obesity at the National Consensus Development
Conference of 1991. I had early notice that this conference
would occur. I worked to that end tirelessly. I spearheaded the
appointment of Lars Sjostrom as an Honorary Life Time
Member of the ASBS. The team from ASBS effectively presented decisive data that advanced the recognition of the value of
bariatric surgery.
Twelve of the 14 surgeon speakers at the 1991 NIH
Consensus Development Conference, “Gastrointestinal
Surgery for Severe Obesity,” were ASBS members. In a
breakfast meeting at Brennan’s in New Orleans, Michael
Sarr, MD; Edward Mason, MD; John Kral, MD; Patrick
O’Leary, MD; Cornelius Doherty, MD; and Harvey
Sugerman, MD, set the agenda for the conference. These surgeons were able to present compelling data that influenced
50
R. P. Blackstone
the panel of nonsurgical experts to express a positive overall Table 4.1 Presidents of ASBS/ASMBS
position in the Consensus Conference Statement, which 1983–1985
Edward E. Mason, MD, PHD (A)
John D. Halverson, MD (A)
paved the way for improved acceptance of gastric restrictive 1985–1987
J. Patrick O’Leary, MD (A)
or bypass procedures for patients affected by severe obesity 1987–1989
1989–1990
Cornelius Doherty, MD (PP/A)
and influencing third-party payers. Thus, in many ways,
1990–1991
George S. M. Cowan Jr., MD (A)
advocacy for access to care was involved in the original man1991–1992
John H Linner, MD (PP)
date of the society. The society was focused during this time
1992–1993
Boyd E. Terry, MD (A)
on getting at least 200 surgeon members so that they could 1993–1994
Otto L. Willibanks, MD (PP)
qualify as a registered society with the American College of 1994–1995
Mervyn Deitel, MD (A)
Surgeons. There was significant growth in the specialty of 1995–1996
Alex M. C. MacGregor, MD (PP)
MBS, especially with the broader knowledge by patients that 1996–1997
Kenneth G. MacDonald (A)
S. Ross Fox, MD (PP)
there may be an effective treatment for this disease. The NIH 1997–1998
1998–1999
Henry Buchwald, MD, PhD (A)
consensus conference was the pivotal event of this time and
1999–2000
Latham Flanagan, Jr. MD (PP)
has stood the test of time. The 1991 guidelines still provide
2000–2001
Robert E. Brolin, MD (A)
the backdrop against which decisions are made about
2001–2002
Kenneth B. Jones, MD (PP)
whether a patient has access to surgery both in the United
2002–2003
Walter J. Pories, MD (A)
States and around the world.
2003–2004
Alan C. Wittgrove, MD (PP)
The society leadership reflects a strong commitment to 2004–2005
Harvey J. Sugerman, MD (A)
both private practice and academic practice. Although there 2005–2006
Neil Hutcher, MD (PP)
has never been a formal ratio established in the bylaws, tra- 2006–2007
Philip R. Schauer, MD (A)
ditionally one-half of the Executive Council has come from 2007–2008
Kelvin Higa, MD (PP), first president of ASMBS
Scott Shikora, MD (A)
private practice with a rotation of the presidency from 1 year 2008–2009
John Baker, MD (PP)
to the next between academic and private practice. As more 2009–2010
2010–2011
Bruce Wolfe, MD (A)
surgeons in private practice have been publishing peer-­
a
2011–2012
Robin Blackstone, MD (PP)
reviewed literature, serve to teach and train residents and fel2012–2013
Jaime Ponce, MD (PP)
lows, participate in the quality program, and serve on and
2013–2014
Ninh T. Nguyen, MD (A)
lead committees—along with the requirement by many aca2014–2015
John Morton, MD (A)
demic surgical departments for high-volume practice and the 2015–2016
Raul Rosenthal, MD (A)
employment by major hospital systems of physicians—the 2016–2017
Stacy Brethauer, MD (A)
lines delineating private practice from academic practice 2017–2018
Samer Mattar, MD (A)
have blurred. There remains, however, a very strong belief 2018–2019
Eric DeMaria, MD (A)
that both aspects of practice should be represented in the A academic, PP private practice
decisions of the society. Surgeons drove some of the pivotal aOnly woman to serve as president in the history of the society
developments in the specialty in private practice (Table 4.1).
of the data in bariatric surgery showed a lack of rigor; there
was a growing public awareness of the increase in the numbers of patients with obesity as well as the number of surgerThe Era of Rapid Growth 1989–2004
ies being done for obesity. These challenges foreshadowed
The original structure of the society was established in the the next era of the society’s growth.
bylaws and has evolved throughout time. Officers were nomAt the time Boyd Terry, MD, became president (1991–
inated by a nominating committee, and except for two elec- 1992), the society had just struggled through a major schism
tions, the slate of officers was unanimously selected. The of its membership because of problems regarding the use of
first occurred when Harvey Sugerman, MD, was nominated, dues for the journal and bylaw uncertainty. In addition, conbut George S. M. Cowan, MD, was elected in 1989.
troversy between biliopancreatic diversion and duodenal
This period of the society saw tremendous growth in the switch lent itself to spirited debate. Through Dr. Boyd’s leadnumbers of procedures and diversity of procedures including ership, the society emerged with more focus on representathe use of devices in large numbers of patients. Increasing tion from different regions of the country and an emphasis on
numbers of surgeons operating without a knowledge base or communication and well-focused objectives for committee
programmatic structure led to an increase in complications work. Surgeons within the society were concerned that their
with a rise in malpractice premiums. Many insurance com- success with gastric bypass would be eroded by the adoption
panies dropped benefits due to the sharp upturn in cost. This of untested “extreme” procedures that caused more harm than
was demonstrated starkly in 2005 when the State of Florida good. This theme, existing in 1991, has had an echo throughlost all access for bariatric surgery by any company. Scrutiny out the history of the society. Intense procedural controversy
4
The History of the American Society for Metabolic and Bariatric Surgery
erupted again when the Food and Drug Administration (FDA)
approved the first device to be used in the treatment of obesity: the adjustable gastric band (AGB). With the increase in
public scrutiny, surgeons who practiced unproven technology
outside of Institutional Review Board (IRB) guidance came
under increasing scrutiny and pressure not to offer unproven
and untested procedure variations. The tendency to develop
and use procedures without scientific support contributed to
uncertainty by medical and surgical colleagues and patients.
It hampers the advocacy by surgeons to garner support with
payers who may believe that we are advocating surgery in
order to line our own pockets. Even when we present valid
and strong evidence, we have trouble convincing payers and
others, in part because of this historical context. This tension
between commercialism and scientifically based procedure
indications continues to the modern era of the society including the omega-loop gastric bypass and one anastomosis duodenal switch. The society has taken a firm stand on these
issues, discouraging the use of procedures that do not have
sufficient evidence of safety and effectiveness from being
performed outside IRB guidance. The society, led by datadriven analysis through the clinical issues committee and
sanctioned by the Executive Council, developed and implemented a process for evaluating procedures and determining
when the evidence is sufficient for the society to place them
on the accepted procedures list. This encourages surgeons
and industry who contribute to the creation of new procedures to work through an IRB process and establish an evidence basis prior to widespread implementation.
ASBS began to achieve its political goals of formal participation in American surgery when it was voted a membership in the American College of Surgeons Board of Governors
1998. Patrick O’Leary, MD, had just joined the Executive
Council of the Board of Governors, and when the request by
Henry Buchwald, MD, came through, he was pivotal in getting it approved. Still, there were substantial barriers in the
academic world. Particularly harsh was some of the criticism
coming out of the surgical leadership of the University of
Louisville, Kentucky, where one prominent surgeon declared
bariatric surgery “charlatanism.” Within the academic establishment, surgeons who were involved in the surgical treatment of obesity were not well respected, their papers were
not given credibility or even published, and their careers
were at risk. Henry Buchwald, MD, recounts that when he
became the president of ASBS, his chairman commented,
“You have just killed your career.”
Integrated Health
Early on, awareness of the critical input and support of a
variety of professionals in addition to surgeons were recognized. This was followed by the formation of the Allied
51
Health Sciences Committee (AHSC) in June 1990 with
Georgeann Mallory, RD, as the first chair. The committee
included registered dietitians, exercise physiologists, bariatric physicians, psychologists, nurse practitioners, and physician assistants. The membership of this committee, which
elects its own president and council, has grown. Contributions
both to the peer-reviewed literature and to clinical pathways
of care as recognized in the accreditation standards have
emerged to enhance the management of patients before, during, and after surgery. With the growing needs of the society,
Georgeann Mallory, RD, who worked with Dr. Alex
Macgregor, the 10th president of the ASBS, was appointed
as executive director in 1993. She also served as the first
chair of the AHSC.
Mary Lou Walen was appointed the second chair of the
AHSC. She writes:
As Chair of the AHSC, it was important to me that all those
working with patients receive education and information about
the operations; complications; all aspects of care including
working with the hospital both clinical and administration;
learning about how to get paid for treating the patients; involving the primary care physicians and the specialists in becoming
members of the treatment team; keeping the patients motivated
and fully informed.
During Walen’s chairmanship, workshops were developed and included in the program on clinical issues, patient
education, insurance challenges, nutrition, psychology, and
other topics; an allied health keynote speaker was added to
the program; the AHSC chair was invited to all ASMBS
Executive Council meetings; the committee requested to
become a section and the Allied Health Sciences Committee
became the Allied Health Sciences Section; and the president of the section became an elected position serving a
2-year term (Table 4.2).
The AHSC chair became a voting member of the
Executive Council of ASBS in 2004. The Allied Health
Sciences Section became the Integrated Health Section in
2008. In the immediate perioperative period, the role of nursing in successful recovery and recognition of developing
complications was recognized, and a formal test and certification in bariatric nursing for RNs working for two or more
Table 4.2 Integrated health presidents of ASBS/ASMBS
1991–1996
1996–1999
1999–2004
2004–2006
2006–2008
2008–2010
2010–2012
2012–2014
2014–2016
2016–2019
Georgeann Mallory, RD
Mary Lou Walen
Tracy Martinez, BSN, RN, CBN
Deborah Cox, RN
Bobbie Lou Price, BSN, RN, CBN
William Gourash, MSN, CRNP
Laura Boyer, RN, CBN
Karen Schultz, NP
Christine Bauer, MSN, RN, CBN
Karen Flanders, MSN, ARNP, CBN
52
years in the field was established through the leadership of
Bill Gourash, PHD, MSN, CRNP, and a dedicated group of
item writers. For this work Dr. Gourash received the inaugural ASMBS Integrated Health Distinguished Advanced
Practice Provider Award.
The Allied Health Section also established the Circle of
Excellence Award, given annually to recognize outstanding
ASMBS members who made contributions to the Integrated
Health Section.
The Integrated Health Section has been integral to incorporating the role of a multidisciplinary team into the requirements for accreditation in metabolic and bariatric surgery.
The presidents of the Integrated Health and the integrated
health council have played a significant role in developing an
IH strategic plan. A focus over the last few years has been to
update the nutrition guidelines and begin to share best practice by publishing tool kits for integrated health teams across
the United States to use. They also have published a support
group manual. They participate in every committee of
ASMBS as well as having committees specifically for topics
pertinent to the integrated health team members. Since the
last publication of the history of ASBMS in the inaugural
textbook, the Integrated Health Leadership has the following
accomplishments:
• Micronutrient guidelines
• Support group manual
• Webinar offerings for IH members (to provide education
for all, but for those who cannot or do not attend OW)
• Established an Integrated Health Facebook group and
Twitter presence
• A new Certified Bariatric Nurse web-based platform for
renewals to simplify the process
• CBN working toward accreditation as a certification
program
• >1000 Certified Bariatric Nurses
• A task force exploring credentialing for advance practice
providers
• Tool kit on the ASMBS website with documents geared
toward helping new (and experienced) providers with
program start-up and development
• YouTube videos on the value of integrated health individuals in ASMBS membership
• Developed new categories of awards for recognition:
Distinguished Behavioral Health Provider, Distinguished
Advanced Practice Provider, IH Committee of the Year
• Change in leadership (IH President, IH President-elect,
and IH Secretary) terms from 2 to 1 year for each position, as well as change in process in which election is for
IH Secretary who then rotates to IH President-elect who
then rotates to IH President
R. P. Blackstone
Growth of the Society
The rapid growth in the society paralleled the growth in the
numbers of procedures and programs. This phenomenon was
promoted by an increase in the number of people experiencing obesity, a growing awareness of surgical treatment of
obesity, including the effect on type 2 diabetes; multiple stories began to be published including testimonials by celebrities like Carnie Wilson. The most significant factors in the
growth of MBS were the transition from open to laparoscopic access with a resulting marked decline of mortality
and morbidity and coverage by Medicare. Coupled with the
implementation of national accreditation in the field and a
strong access to care effort by the society, the numbers of
people accessing surgery began to number in the tens of
thousands. As the numbers of cases started to grow, the
strongest focus of the society during this era was in the education of the membership. Dr. Brolin, who was president
during the beginning of the “golden age” of laparoscopic
access to bariatric procedures, focused on the training of
general surgeons including a preceptorship committee
(formed in 1999), which has evolved into the Bariatric
Training Committee.
The “golden age” of laparoscopic approach to bariatric
surgery was born with controversy. By 2001–2002, during
the presidency of Ken Jones, MD, the surgeons supporting
open procedures and the surgeons who supported laparoscopic procedures were openly antagonistic to each other’s
approach. Surgeons who had been doing open procedures
were going to weekend courses sponsored by industry to
learn the laparoscopic approach and coming back to their
hospitals to do very complex laparoscopic gastric bypass
procedures (GBP) with serious complications. At this time
the delineation of privileges at many hospitals did not include
advanced vs. basic privileges in laparoscopy. Since that time
this has been corrected in part through the leadership of the
Society of American Gastrointestinal and Endoscopic
Surgeons (SAGES). This was a perfect storm for plaintiffs’
attorneys and the media, who regarded the surgery as unnecessary to treat obesity, a condition that they believed was
self-inflicted by an inability to control one’s desire to eat. All
of these aspects provided fertile ground for a malpractice crisis that almost brought down the society and the specialty.
Once again, the society found itself on the defensive. This
crisis was precipitated by a number of untrained general surgeons rushing into the then-fertile financial ground of providing bariatric procedures without appropriate training or
structure. Led by Samar Mattar, MD, this evolved into a certification of fellows in MBS including a didactic study program and test. This program has provided a strong scientific
and technical foundation for postgraduate practice of MBS.
4
The History of the American Society for Metabolic and Bariatric Surgery
Medical Liability
In the 1990s and into 2000, bariatric surgeons were making
“news,” not so much for the benefits in health and quality of
life for many but with not-so-back-page stories of procedures and outcomes gone awry for the few—especially for
those cases or patients with notoriety. For some liability
insurers, bariatric surgery outcomes were so uncertain that
risk stratification of bariatric procedures resulted in regions
where malpractice insurance for surgeons who practiced
MBS was unavailable (Florida) or, if so, at premium rates
that were increasingly higher than general surgery
coverage.
In 2005, with the support of our society, NOVUS
Insurance Company, a risk retention group, was founded,
with the expectation that with the guidance of a firm, expert
in medical malpractice defense, bariatric surgery could be
shown to be of actuarial risk similar almost to that of general
surgery. It was clear to the Board, which was made up of
regular members of the ASMBS that for any bariatric practice, careful attention to patient selection, education, evaluation, and operative preparation was critical. In addition, the
consent process, with expanded face-to-face explanation and
significantly improved documentation, was imperative.
However, the basis for most lawsuits had to be recognized
to have resulted not from technical operative error but a
breakdown in patient, sometimes family, and physician rapport and untimely or inappropriate response to indicators of
patient deterioration. In short, it is not that a leak occurred
that makes a claim likely, and perhaps difficult to defend, but
it is the “aggravating circumstances” together with an unanticipated outcome that make a claim virtually certain. Such
circumstances are many, including surgeon unavailability
when needed, inadequate surgeon empathy in a time of crisis, inexperienced “coverage” or poor “hand-off,” delay in or
failure to respond to calls, lack of communication between
all care providers, and inadequate initial risk disclosure
paired with undocumented patient understanding. In addition, there is a well-established and documented weight bias
among health-care providers and within the health-care
industry toward not only the patient with obesity but also the
surgeons or physicians who treat it. The society realized that
a strategy to establish a quality standard as well as share best
practice would be necessary and would be necessary to
underlie the overall increase in case volume.
In 2011, NOVUS was merged into NORCAL Mutual
Insurance Company. In 2011, the ASMBS “Professional
Liability” Committee became the “Patient Safety”
Committee. Increasingly, the committee recognized the
importance of closed claims as a significant resource in our
improving patient safety. In 2012, our monthly e-publication
(“Top 5 on the 5th”) vignettes, derived from closed claims,
met with broad society support. They are anticipated to
53
resume in a new format in the ASMBS new magazine
Connect. Investigation is ongoing as to whether we may
develop a closed claims database, similar to that of the
American Society of Anesthesiologists, which for more than
30+ years has resulted in material improvements in anesthesia services and a 30% average decline in anesthesiologists’
liability premiums. Over the past 5 years, more work has
done on evaluating closed claims, which were collected in
2016 and 2017.
he Era of Quality and Engagement
T
from 2004 to Present
Quality and Data Registries
One of the outgrowths of the period of crisis from 2001 to
2004 was an awareness that the image of the society needed
to change. Rather than allowing any surgeon with minimal
training, low volume, or no programmatic elements to participate, the society made a decision in its annual business
meeting to establish a national center of excellence program.
A minimum of 125 cases was required to qualify with the
result that the number of operating surgeons and programs
contracted sharply throughout the next few years. Surgeons
and programs that did not participate lost their ability to offer
MBS as the contraction in the market place occurred. As part
of that effort, the Bariatric Outcomes Longitudinal Database
(BOLD) was developed to support the accumulation of data
for both outcomes’ information and research. This was not,
however, the society’s first efforts at creating a registry.
Standardized data collection and analyses for surgical
treatment for obesity began in 1985 under the direction of
Edward Mason, Department of Surgery, University of Iowa
Hospitals and Clinics (UIHC). The National Bariatric
Surgery Registry’s (NBSR) goal was to meet a growing need
for quality control in reporting outcome results by assisting
surgeons in continuing improvement for patient care through
outcome analyses. The NBSR was run in the Department of
Surgery at UI and received full financial support from one
corporate sponsor during the first 2 years. Subsequent support came from surgeons who voluntarily participated
through membership fees, satellite data collection, and
submission.
The International Bariatric Surgery Registry (IBSR) provided software, training, and instruction manuals for collecting, storing, and preparing reports of local data for comparison
with the total data reported. Management of the system was
by Kathleen Rehnquist, BS, from 1986 to 2006. Dwight “Ike”
Barnes; John Raab, RN; and Mark Crooks provided personal
computer programming. Together they provided successful
software throughout ten updates/revisions. Graduate students
provided the integrated statistical analysis from the College
54
of Preventive Medicine, biostatistics division (Donald Jiang;
Elizabeth Ludington, PhD; Wei Zhang, PhD; and Shunghui
Tang, PhD). Professors mentoring the students included
Robert Woolson, PhD; Miriam B. Zimmerman, PhD; and
Michael P. Jones, PhD. The aggregate analyses were accomplished via SAS programming at the University Computer
Center on IBM mainframes until aggregate analysis and computers evolved to use PC SAS on a personal computer housed
in the IBSR office. In 2006, the final repository of the aggregate data represented 85 data collection sites for 45,294 subjects whose surgery was performed by 148 surgeons many of
whom were members of ASBS.
Newsletters, manuals, papers, and data for lectures or
publication could be prepared using the IBSR software or by
special reports of the aggregate data with assistance from
IBSR staff. Direct access to the registry data was never available, due to privacy policies of the UIHC, State of Iowa, and
Federal Regulations (HIPPA). Quarterly reports were provided to each satellite surgical practices with de-identified
results to help surgeons compare patient outcome with that
of the total IBSR experience. More than 70 newsletters were
published, with Dr. Mason soliciting a medical section for
surgeons and other IBSR staff writing articles of interest
regarding data collection and how data results were reported.
The ultimate closure of the IBSR resulted from inadequate
financing to support a Web-based data collection system and
incomplete follow-up methods for complete data analysis
and verification.
BOLD was the society’s second effort at a registry. In
2004 the ASBS established an independent not-for-profit
company, the Surgical Review Corporation (SRC), to oversee
the ASMBS Centers of Excellence quality program. The
BOLD registry was developed with input by ASMBS surgeons. A few years after the COE program was implemented,
participation in the registry became a requirement for accreditation. Requiring data entry of all bariatric cases began the
process of changing the surgical culture within community
hospitals where the majority of patients received MBS. This
second effort at a data registry was also problematic. These
include data not available reliably for use in continuous quality improvement; individual surgeon office, rather than hospitals, often paid registry fees and collected; poor definitions
and haphazard methods; and quality of data collection and
poor long-term follow-up. In addition, the registry was not
connected to the national data quality movement and began to
fall behind other efforts like the National Surgical Quality
Improvement Program (NSQIP). Despite the important
efforts of Deborah Winegar, PhD, the final database director
and surgeon members of the quality program who worked
tirelessly to try and improve the registry, a point was reached
which required a change in direction. A scientific project to
compare three data registry options was conducted, and with
input from the ASMBS Quality and Standards Committee,
R. P. Blackstone
the society decided to move away from BOLD. The aggregate
data from BOLD has not been lost; some publications have
resulted from this data.
Under the leadership of Robin Blackstone, MD, President
of the ASMBS, and David Hoyt, Executive Director of ACS,
ASMBS joined the Centers of Excellence program with the
American College of Surgeons Bariatric Surgery Network
on April 1, 2012. This established one authority for national
accreditation in the United States, the Metabolic and
Bariatric Surgery Accreditation and Quality Improvement
Program (MBSAQIP). The program established a registry
based on strong principles of data collection and integrity of
the data, including collection of 100% of cases performed at
the accredited center; defined data entry variables; and thirdparty data collection by certified of the clinical reviewers.
Each program receives two semiannual reports (SAR) that
allow comparison of their programs on key variables to
national benchmarking providing the high-quality data necessary for the use of outcomes to improve practice at the
local level with continuous quality improvement. In addition
to local efforts, the data is examined by the MBSAQIP
Quality Committee to identify areas where national improvement projects could take place. One project focused on programs with high emergency department readmission rates.
In this project, led by John Morton, MD, programs that were
high outliers in readmissions were identified and offered an
opportunity to participate in the DROP process (Decreasing
Readmissions through Opportunities Provided) [2]. The second project, led by Stacy Brethauer, MD, offered programs
with higher length of stay the opportunity to participate in
the use of a set of enhanced recovery protocols for metabolic
and bariatric surgery. In addition to prospective projects that
occur in the real-world setting of community practice as
demonstrated by these two national quality improvement
projects, the MBSAQIP registry accumulates high numbers
of patients annually. The quality of data collected and the
availability of public use files of the previous year’s data
allow retrospective review and study of even small effect
size complications. The data registry provides high-quality
data that offers a credible foundation for quality improvement and best practice at the community and university hospital level.
Strategic Plan Development
The society has successfully met many challenges during its
history. However, the world of medicine changes constantly,
and in order to respond, the society created a plan for its own
evolution. A formal strategic plan for the society—led by
Phil Schauer, MD, with input from the Executive Council—
was developed and embraced at the business meeting in
2008. As part of the evolution of the specialty, the society
4
The History of the American Society for Metabolic and Bariatric Surgery
elected to change its name from the American Society for
Bariatric Surgery (ASBS) to the American Society for
Metabolic and Bariatric Surgery (ASMBS) at the annual
business meeting on June 15, 2007.
The strategic plan was implemented fully during the presidency of Bruce Wolfe, MD, with a change in the structure of
the committees to align with the established mission, vision,
values, and goals of the society and direct alignment of the
committee projects with the overall budget of the society.
The strategic plan drove many of the expenditures of the
society, and all budget items are considered in light of the
overall mission and goals. The alignment of the committee
structure enabled a much higher productivity in the committees and drove improved communications and work product
of the committees. Every facet of the society from budget
decisions to the overall work plan of the committees was
aligned. Dr. Wolfe also created a Quality and Standards
Committee to assess the accreditation program and propose
an evolutionary process. These updates to the operating
structure of the ASMBS would transform the society into
one that had the engagement of a very large group of young
leaders and members of the society from both academic and
private practice. This current model has provided robust volunteerism and energized committees with emerging and
diverse merit-based leadership. Implementing a culture of
leadership development has been the ultimate guarantee of
continuation of new ideas and strategy to meet future challenges. The current committees report evolving goals/objective and accomplishments each year in the ASMBS Annual
Report (https://asmbs.org/about/annual-report).
The Journal
Obesity Surgery, the original journal of the ASBS, was
founded in 1990, adopted by the society in 1991 and achieved
Index Medicus status in 1995. Its birth was not without controversy. In 1989 at the annual meeting in Nashville,
Tennessee, the Executive Council, at its statutory meeting,
had prepared a nominating slate for consideration at the business meeting, including a proposal initiated by the president,
Patrick O’Leary, MD, for joining the North American
Association for the Study of Obesity (NAASO) and other
International Association for the Study of Obesity (IASO)
organizations in adopting the International Journal of
Obesity as the ASBS journal. As a guest at the council meeting, Dr. Mervyn Deitel presented his own proposal for a journal. The Executive Council supported Dr. Deitel’s proposal,
pending his providing a business plan and other details. At
the business meeting, however, following controversial presentations during the scientific meeting, which drew criticism for premature clinical use of novel operations without
adequate patient follow-up, the membership rejected the
55
nominating committee’s slate of candidates. At that same
meeting, the membership voted on, and accepted, the proposal to adopt IJO as its journal, affirming the possibility
that, at some later time, Dr. Deitel might provide a separate
proposal to be duly considered.
A few months later, Dr. Deitel (with support from some
newly elected council members) mailed selected members
requesting support for his journal. His rallying cry: “Pull out
all your rejected manuscripts and we will publish them!”
Through a closed ballot process, the leadership of ASBS nullified the 1989 business meetings’ decision, adopting
Dr. Deitel’s journal with mandatory subscription in 1990.
Dr. Deitel, who had sole ownership of the journal, later
decided to sell the journal. It came as a surprise to younger
members that the journal Obesity Surgery was actually privately owned; after considering the option to purchase it, the
ASBS decided to establish its own journal. Eventually,
Obesity Surgery was sold to a publisher and adopted as the
official journal of the International Federation for the Surgery
of Obesity and Metabolic Disorders (IFSO). It maintains the
tradition of publishing articles from the international community and—under the direction of Dr. Henry Buchwald and
Nicolas Scopinaro, MD, and the current editor, Scott Shikora,
MD—has made significant progress in improving its impact
factor.
In February 2004, the ASMBS established a new journal
Surgery for Obesity and Related Disease (SOARD) owned by
the society—with Harvey Sugerman, MD, as the first and
current editor. Dr. Sugerman is largely credited with developing an outstanding editorial board and with the high quality that the journal has achieved. The initial journal was
published in six issues during the year, increasing to monthly
publication in 2017. During the course of the journals’ history, the editorial board has made concerted efforts to standardize the reporting of key variable like total weight loss, in
order to produce articles with less heterogeneity. The impact
factor in 2017 was 4.5, placing it as number 11/165 surgical
journals. In 2017, the journal published 396 original manuscripts. The journal represents the readership with 44% of
manuscripts from North America, 34% from Europe, and
10% from Asia. A continuing medical education program
was implemented and led by Samar Mattar, MD, awarding
3671 h of CME to 278 readers and 472 h of CME to reviewers in 2017. Dr. Sugerman continues to lead the journal
effort. Raul Rosenthal, MD, was appointed coeditor. The
14-year history of the journal is a tribute to the men and
women who design, execute, and write about their research
and to those who guard the portals of good science in ensuring the journal reflects the highest values of inquiry. The
journal allows us to bring the light of scientific inquiry to
shine on our work in an environment without the bias that Dr.
Sugerman and many others, who struggled for recognition of
56
their work during their careers, faced. The journal is the
embodiment of how far the specialty has traveled.
Access to Care
Surgeons who treat other forms of disease have enjoyed wide
access to their procedures through coverage by insurance.
Patients who suffer from obesity, however, have long been
victims of a misperception of their role in being affected by
obesity (personal responsibility) and denied coverage based
on the perception of the “cosmetic” nature of surgical
treatment.
This quest to obtain wider access for patients has been
one of the critical driving forces behind the society’s growth.
These efforts have been ongoing since the earliest days of the
society but were formalized by the creation of the Access to
Care Committee on November 11, 2008. During the next
5 years, the work of the committee included partnering with
advocates outside ASMBS in the battle for access. This coincided with the vision the society had to create a population
management approach to the management and treatment of
obesity. Part of this strategy is to provide more balance in
reporting around obesity and to train advocates at many levels of leadership with ASMBS. The society engaged Roger
Kissin and Communications Partners in order to fulfill the
strategic goal of making the society the public voice of
authority in this field and add to the education of the media
about this subject.
This strategy has been extremely successful in changing
the dialogue. Currently, the president and senior leadership
give more than 300 interviews to major media outlets per
year with messaging that is developed and approved by the
Executive Council; media training is provided to all committee chairs and chapter presidents so that when we respond to
a query, we can do that with one consistent message. Another
successful strategy was to field a rapid response team
approach to changes in benefits. If any entity (company, government agency, state agency) tried to change or drop a benefit or began to consider implementing one, a group of
experts—including the surgeons from that area, industry
with lobbyists on the ground, and leadership from the
ASMBS Access to Care Committee as well as the Obesity
Action Coalition (OAC)—could convene to immediately
address the problem. This has been a very successful strategy
in maintaining and gaining new coverage. The most convincing argument, however, is the effectiveness of surgical therapy both on obesity itself and, perhaps even more profoundly,
for the effect on obesity-related diseases such as diabetes.
Even with all these efforts, which are intense and ongoing,
far less than 1% of the patients who have significant disease
that will limit their longevity have access to the most effective care. Although we often think of access as limited by
R. P. Blackstone
coverage, in fact it is just as limited by the available surgical
manpower, which at this time can provide only 1% of patients
with surgical treatment. It is also limited by reimbursement.
It takes many resources in structure, process, and personnel
to support patients through the entire course of care, and
reimbursement for all of this supportive care is lacking. In
this environment, the tricky questions of who should have
access to surgery and what the optimal procedure should be
persist despite efforts to define indications. Meanwhile the
scientific data on epigenetic transfer of obesity-promoting
genes and the differences in physiology in regard to hunger,
satiety, and metabolism of patients who suffer from obesity
are now widely documented. Support by the government for
treatment came with the announcement of the National
Coverage Decision by the Centers for Medicare and Medicaid
Services (CMS) providing access to surgical treatment for
Medicare and Medicaid beneficiaries as of February 21,
2006. It was expanded for the treatment of diabetes in 2009.
Although CMS continues to support access to surgery, they
dropped the requirement for accreditation of the program
providing the surgical care—a decision born in controversy
and of great concern to the society about the safety of the
decision. Currently the fight for access continues and has
come down to a state-by-state battle to establish bariatric surgery as an essential benefit in the Affordable Care Act.
Twenty-two states recognize bariatric surgery as an essential
health benefit. All these politics are local, and a local political force is needed. To meet this need, the ASMBS state
chapter program was established during the presidency of
Neil Hutcher, MD. The goals for the state chapters are to
advocate for increased access at the local level and to establish collaboration for best practice in the quality program.
Each state chapter has an elected State Advocacy
Representative. At the beginning of 2018, OMA and TOS
announced that their respective groups would be establishing
State Advocacy Representative (STAR) Programs—modeled
after the ASMBS STAR Program. Both TOS and OMA are
hopeful that they will have a STAR in every state by the end
of 2019. OAC is also formulating plans for regional
OACSTARs. At the time of this report, plans were underway
to establish an Obesity Care Continuum STAR Program to
link these programs across AND, TOS, OMA, OAC, and
ASMBS.
Obesity Action Coalition
In addition, a need for advocacy on the policy level was identified. Experts on public policy from Kellogg School of
Business at Northwestern were engaged to study the access
problem. Led by Dr. Daniel Diermeier, it was determined the
nature of the issues that led to the loss of insurance coverage
required a public policy approach. The Obesity Action
4
The History of the American Society for Metabolic and Bariatric Surgery
Coalition (OAC) was founded in 2005 by Robin Blackstone,
MD; Georgeann Mallory, RD; and Christopher D. Still, DO,
FACN, FACP, to fill the patient-advocacy gap for the disease
of obesity.
The Obesity Action Coalition (OAC) is a more than
60,000 member-strong 501(c) (3) national nonprofit organization dedicated to giving a voice to the individual affected
by the disease of obesity and helping individuals along their
journey toward better health through education, advocacy,
and support. The OAC’s core focuses are to raise awareness
and improve access to the prevention and treatment of obesity, provide science-based education on obesity and its
treatments, fight to eliminate weight bias and discrimination,
elevate the conversation of weight and its impact on health,
and offer a community of support for the individual affected.
The OAC is made up of a vibrant membership community
where individuals can find valuable information to help them
on their weight journey and connect with others who share
similar experiences. The OAC is also the founder of the
highly successful Your Weight Matters brand, which encompasses Weight Matters Magazine, the Your Weight Matters
National Convention, and the Your Weight Matters National
Campaign. The goal of the Your Weight Matters brand is to
deliver one clear, concise message: “Your Weight Matters –
For Your Health.”
Obesity Care Advocacy Network
The leading obesity advocate groups founded the Obesity
Care Continuum or “OCC” in 2010 to better influence the
health-care reform debate and its impact on those affected
by overweight and obesity. The OCC was composed of the
Obesity Action Coalition (OAC), the Obesity Society (TOS),
the Academy of Nutrition and Dietetics (AND), the
American Society for Metabolic and Bariatric Surgery
(ASMBS), and the American Society for Bariatric Physicians
(ASBP). The American College of Surgeons, although not a
member of the OCC, supports the work of the group by acting as an independent third-party advocate. The OCC
evolved into the Obesity Care Advocacy Network (OCAN)
with a mission to partner with medical societies and organizations to change how the nation perceives and approaches
the US obesity epidemic by educating and advocating for
public policies and increased funding for obesity education,
research, treatment, and care. Now with a membership of 19
organizations including the American Academy of Physician
Assistants; Academy of Nutrition and Dietetics; American
Association of Clinical Endocrinologists; American
Association of Nurse Practitioners; American Council on
Exercise; American Society for Metabolic and Bariatric
Surgery; AMGA; Black Women’s Health Imperative;
57
Healthcare Leadership Council; National Alliance for
Healthcare Purchaser Coalitions; Novo Nordisk, Inc.;
Obesity Action Coalition; Obesity Medicine Association;
SECA; the American Gastroenterological Association; the
Endocrine Society; The Obesity Society; Weight Watchers;
and the YMCA of the United States. The group has sponsored three workgroups centered around implementing the
provisions of TROA through the administrative mechanisms
as well as address military readiness on the impact of obesity on the national armed forces.
The Treat and Reduce Obesity Act (TROA)
In June of 2013, the ASBMS, as part of the OCC network,
endorsed the Treat and Reduce Obesity Act of 2013
(TROA)—a bipartisan, bicameral bill that has been introduced in the 113th Congress. The bill aims to effectively
treat and reduce obesity in older Americans by increasing
Medicare beneficiaries’ access to qualified practitioners who
can deliver intensive behavioral therapy for obesity and
allowing Medicare Part D to cover FDA-approved obesity
drugs. The initial efforts to enact the bill were not successful; however, it was reintroduced into congress in April of
2017 by Senators Bill Cassidy (R-LA) and Tom Carper
(D-DE) and Representatives Erik Paulsen (R-MN) and Ron
Kind (D-WI). TROA (Senate Bill 830/House of
Representatives Bill 1953) is strongly supported by OCAN
as well as the American College of Surgeons who joined the
advocacy effort in 2018. Specifically, TROA will provide the
Centers for Medicare and Medicaid Services (CMS) with
the authority to expand the Medicare benefit for intensive
behavioral counseling by allowing additional types of
health-care providers to offer these services. The legislation
would also allow CMS to expand Medicare Part D to provide coverage of FDA-approved prescription drugs for
chronic weight management. The budget impact analysis
paper developed by Wayne Su and IHS Markit has been useful in demonstrating the significant potential savings to the
Medicare program ($19–21 billion) over 10 years should
Congress pass TROA.
ational Obesity Care Week (NOCW) 2018
N
(October 7–13)
The Obesity Action Coalition (OAC), The Obesity Society
(TOS), the STOP Obesity Alliance, the Obesity Medicine
Association (OMA), and the American Society for Metabolic
and Bariatric Surgery (ASMBS) launched the first NOCW in
2018. The goal is to build within the public understanding of
obesity and value of science-based care. The ASMBS
58
R. P. Blackstone
believes that NOCW elevate awareness of the disease of obesity, create an understanding of the challenges people
affected by obesity endure, and promote the support of
treatment.
International Affiliations
Obesity is an epidemic affecting many countries outside the
United States. Our colleagues from around the world have
made exceptional contributions to the science and art of
MBS. In recognition of this, ASMBS became a founding
member of the International Federation for the Surgery of
Obesity (IFSO) formed in 1995 at a meeting in Stockholm.
IFSO currently has more than 50 member societies. There
are 3600 members of ASMBS that are also members of
IFSO.
The international committee was organized in 2009, and
Raul Rosenthal, MD, was the first chair. The first International
Congress was at the 2011 Annual Meeting: Bariatric Surgery
in Latin America. International interest and growth have
been strong and increasing annually (Fig. 4.2).
The ASMBS Foundation
The ASMBS Foundation is a 501(c) (3) nonprofit organization developed to raise funds for conducting research and
education, increasing public and scientific awareness and
understanding, and improving access to quality care and
treatment of obesity and severe obesity.
The ASMBS Foundation was established through the
efforts of the ASMBS Executive Council in 1997 spearheaded by S. Ross Fox, MD. The ASMBS Executive Council
and Dr. Fox recognized the need to provide fund-raising—
through charitable gifts and public and private donations—to
support their shared vision to improve public health and
well-being by lessening the burden of the disease of obesity
and related diseases throughout the world. The foundation
has continued to support the activities of the society centered
around access, education, and research. Currently the foundation is undergoing a strategic process to revitalize the
board, building a stronger foundation of philanthropy with a
new executive director, and continuing to build national presence to the Walk from Obesity.
Obesity Week
In fall 2013, the ASMBS and the Obesity Society (TOS)
held their annual meetings in conjunction with one another.
Surgeons, researchers, bariatric medicine specialists, and
ASMBS Historical Membership 2018
4500
4117 4065 4070
4000
4119
4247
3952
3800
3550
3500
3385
3059
3000
3198
2878
2697
2500
2407
2000
1500
1000
2385
1922
1511
1364
956 931
1619
1251
1078
1710
1833
1168 1226
1916
2055 2109
1282 1330
2576
2641
2180
1620
1441
2417 2462 2433
1732
1648 1608
1519 1543
1606
896
686 693
671
533 527
415
420
433
312 352 341
MD
IH
263
177 192 188 244 264 274 304
159
163 168 102 218 233
TOTAL
48 74 113
26 26 31
38
0 14 24
1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017 2018
500
Fig. 4.2 Growth of the ASMBS
4
The History of the American Society for Metabolic and Bariatric Surgery
integrated health professionals came together for one action-­
packed week. Each society maintained its own traditions and
meetings, but each member who attended was able to choose
from among a wide variety of educational options. Phil
Schauer, MD (ASMBS), and Gary Foster, MD (TOS),
forged the path to the first conference supported by the
ASMBS Executive Council and membership. The meeting
is designed to foster the understanding of the pathophysiology of obesity, the application of science to the clinical management of patents, and the mechanism of action of surgery
and pharmaceutical and behavioral management and to
establish collaboration in research. Obesity week has blossomed into one of the most well-attended scientific meetings
of the year with an expanded catalogue of course offerings
and sharing of dialogue among its many diverse members.
Attendance in 2018 included 5300 people, equally divided
between surgery and medicine physicians and integrated
health members.
Conclusion
The history of the ASMBS is one of the intense and focused
efforts by visionary leaders, but it is also the story of engagement of the members in the development of the specialty.
The foundation of the society is grounded in the efforts of
critical thinkers, scientists, and visionaries, but with the transition to the national accreditation system, all members of
the society have participated in one of the most important
and successful quality initiatives in American surgery. The
sense of having a special mission, of championing a group of
patients who face daily discrimination and prejudice, and of
being fierce advocates for a science that has delivered hope
to millions of patients affected by diabetes and obesity
defines members of the ASMBS. The surgeons and integrated health colleagues of ASMBS deliver on a daily basis
the most effective therapy in the history of medicine, with a
mortality that is less than a laparoscopic cholecystectomy.
The American Society for Metabolic and Bariatric
Surgery has matured throughout the 30+ years of its existence. The society has shown visionary leadership in educa-
59
tion, multidisciplinary care, access to care, accreditation,
and quality improvement. The ASMBS has responded to the
crises of its time with action and become part of the wider
society of physicians managing obesity. The society has
taken a leadership position in defining approved procedures,
providing guidance to the FDA in the approval of new
devices, providing guidance to members on a wide range of
topics, and establishing an ethics committee to hear grievances about advertising and practice issues. The twin drivers of access to care and quality have driven engagement of
the membership with their society. The strength of the society lies in the adherence to scientifically valid principles,
fairness, and increasing transparency of governance and in
the engagement of talented members who volunteer their
time to serve on committees. The dedication of our members to provide high-quality safe care continues to be our
most closely held goal. Although we may have been considered outsiders at one time, our experience in quality and
collaboration, access to care issues, and managing change
should propel us into the leadership of our hospitals and
American surgery.
Acknowledgments Written in collaboration with the following group
of contributors: Ed Mason, MD, FACS; Cornelius Doherty, MD; Patrick
O’Leary, MD; George S. M. Cowan Jr., MD; Boyd E. Terry, MD; Henry
Buchwald Jr., MD; Robert E. Brolin, MD; Kenneth B. Jones, MD;
Walter Pories, MD; Harvey Sugerman, MD; Neil Hutcher, MD; Kelvin
Higa, MD; Scott A. Shikora, MD; Karen Schultz; Laura Boyer, RN;
Mary Lou Walen; John Kral, MD, PhD; Mal Fobi, MD; William Sweet,
MD; George Blackburn, MD; James Zervios, OAC; Connie Stillwell,
ASMBS Foundation; Georgeann Mallory, RD; Joe Nadglowski; Chris
Gallagher; Kathleen E. Renquist; and Karen Flanders.
References
1. Blackburn GL, The Edward E. Mason founders lecture: interdisciplinary teams in the development of “best practice” obesity surgery.
Surg Obes Relat Dis. 2008;4:679–84.
2. Morton J. The first metabolic and bariatric surgery accreditation
quality improvement program quality national initiative: Decreasing
readmissions through opportunities provided. Surg Obes Relat Dis.
(SOARD May–June. 2014;10(3):377–8.
5
Physiological Mechanisms of Bariatric
Procedures
David Romero Funes, Emanuele Lo Menzo,
Samuel Szomstein, and Raul J. Rosenthal
Chapter Objectives
1. Describe some of the most commonly accepted
theories regarding the physiological mechanism of
bariatric procedures.
2. Address the potential physiological mechanisms
affecting both weight loss and resolution of
diabetes.
Introduction
In spite of the fact that obesity has reached pandemic proportions, it remains one of the most neglected public health
problems in the United States. This has awakened a growing
interest in placing obesity as a prime subject of many recent
public health campaigns. The need for these considerable
efforts derives from the alarming reports of the prevalence of
obesity in the US population. In 2015–2016, the prevalence
of obesity was 39.8% in adults and 18.5% in adolescents [1].
Despite the increased awareness of its severity, the linear
time trend forecasts suggest that by 2030, 51% of the US
population will be obese [2]. The progressive and continuous
rise in the prevalence of obesity have also determined a secondary epidemic of the related comorbidities, in particular
the risks of cancer, diabetes, and cardiovascular diseases.
Bariatric surgery is now considered the first management
option for failure of medical treatment in severely obese subjects and the most effective method for sustained long-term
weight loss. There is extensive evidence of the positive metabolic impact, remission, and resolution of most of the comorbidities associated with severe obesity, diabetes included [3].
Historically, bariatric procedures are thought to induce
D. R. Funes (*) · E. Lo Menzo · S. Szomstein · R. J. Rosenthal
Department of General Surgery, The Bariatric and Metabolic
Institute, Cleveland Clinic Florida, Weston, FL, USA
e-mail: funesd@ccf.org
weight loss by causing caloric restriction and/or malabsorption. However, newer mechanistic studies, in parallel with
the establishment of the gastrointestinal tract as a key regulator of energy and glucose homeostasis, have introduced the
hypothesis that alternative mechanisms mediate the weight-­
reducing and metabolic benefits of most bariatric/metabolic
operations. Furthermore, as the close interaction between
diet, gut, and brain hormones unwinds, the mechanisms of
action of these procedures, as well as their classification,
have significantly changed. In fact, the pathway describing
how the centrally regulated body weight homeostasis is profoundly influenced by hormones secreted in the intestinal
tract and adipose tissue is now well recognized [4]. The overall balance of these peripherally secreted hormones and their
interaction at the level of the hypothalamus would eventually
affect food intake and energy expenditure [5].
The mechanism of diabetes resolution after bariatric surgery is not entirely understood. Since insulin resistance is
one of the main etiologies, it seems obvious that weight loss,
although not the only component, continues to be an essential contributor. In fact, typically diabetes improvement or
resolution occurs within weeks after bariatric procedures.
Regardless if it is gastric bypass (GBP), sleeve gastrectomy
(SG), or biliopancreatic diversion (BPD), in all of these procedures, remission ensues from the preceding and expected
weight loss [6, 7]. Pories et al. were the first to suggest that
caloric restriction played a key role in the resolution of diabetes; following this historical finding, the important gluco-­
regulatory roles of the gastrointestinal (GI) tract were firmly
established. However, the physiological and molecular
mechanisms underlying the beneficial glycemic effects of
bariatric surgery remain incompletely understood. In addition to the mechanisms proposed by Pories et al., currently
other hypotheses involving changes in bile acid metabolism;
GI tract nutrient sensing and glucose utilization, incretins,
and possible anti-incretin(s); and the intestinal microbiome
have gained strength. According to recent studies, these
changes, acting through peripheral and/or central pathways,
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_5
61
62
D. R. Funes et al.
lead to reduced hepatic glucose production, increased tissue
glucose uptake, improved insulin sensitivity, and enhanced
ß(beta)-cell function. These findings suggest that a constellation of factors, rather than a single domineering mechanism,
likely mediates postoperative glycemic improvement, with
the contributing factors varying according to the surgical
procedure [8]. Nevertheless, all coincide in one common
positive effect resulting in the resolution of diabetes.
Here, we describe some of the most commonly accepted
theories regarding the mechanism of action of the most
widely accepted bariatric procedures.
Mechanism of Action
Caloric Restriction
The current understanding of different mechanisms of action
of these procedures, in particular the role of gut hormones,
has led to dispute the traditional classification of bariatric
procedures in the three main categories: restrictive, malabsorptive, and combined. Although a clear understanding of
all the mechanisms of action of bariatric procedures has not
been reached, multiple theories exist. It is likely that several
factors contribute to the final efficacy of the procedures.
Because of the overlap of effects, we will address the potential mechanisms of action affecting both weight loss and diabetes resolution. Potential contributors to weight loss and
diabetes resolution are outlined in Table 5.1.
Malabsorption
As previously mentioned, the surgically induced alterations
of the normal gastrointestinal absorption process lead to various degrees of weight loss. This is especially true in procedures such as the BPD and the BPD with duodenal switch
(BPD-DS) where long alimentary (250–300 cm) and biliopancreatic limbs leave a short (100 cm) common channel for
Table 5.1 Potential mechanisms of action of bariatric operations
Mechanism of action
Malabsorption
Caloric restriction
Energy expenditure
∆(Delta)-eating
behavior
Hormonal
Vagus nerve
Bile salts
Adipose tissue
Microbiota
ß(Beta)-cell function
Insulin sensitivity
Procedure
RYGB LSG
±
−
+
+
±
−
+
±
LAGB
−
±
−
−
BPD
+
+
+
?
BPD-DS
+
+
+
?
+
?/−
+
+
±
±
±
−
?/−
±
−
−
−
+a
+
?/−
+
+
±
±
++
+
?/−
+
+
±
±
++
Only related to weight loss
a
the absorption of nutrients. Even the more conservative alimentary limb lengths (100–150 cm) of the standard gastric
bypass have been shown to create a certain degree of fat malabsorption, as demonstrated by the increase in fecal fat at
6 months (126%) and 12 months (87%) [9]. Since there is no
significant alteration of the protein and carbohydrate absorption, the overall reduction of the combustible energy absorption has been shown to be only 6–11% [10]. While it is true
that the more malabsorptive procedures (BPD, BPD-DS)
result in a more impressive weight loss (excess weight loss
[EWL], 79%) and diabetes resolution (98.9%), it is unlikely
that the malabsorption by itself is solely responsible [11].
+
?/−
+
+a
?
?
+
Caloric restriction is one of the immediate effects of RYGB
and SG due to anatomical changes. The beneficial effect of
caloric restriction on the glycemic control has been previously demonstrated [12]. The carbohydrate-controlled
calorie-­restricted diet produces up to 40% improvement of
the insulin resistance and ß(beta)-cell function as measured
by the homeostatic model assessment (HOMA) method in
just 2 days [13]. If continued over a period of 11 weeks, the
diet can improve the peripheral insulin resistance, even if the
hepatic insulin sensitivity remains unchanged [13]. In the
perioperative period of bariatric surgeries, the caloric intake
is dramatically reduced to 200–300 kcal/day. This factor
undoubtedly contributes to the immediate weight loss experienced by these patients postoperatively. In fact, some
authors were able to demonstrate similar weight loss results
in non-operated obese subject after 4 days of post-Roux-en­Y gastric bypass (RYGB) diets [14]. The rate of secretion of
gastrointestinal hormones, however, was altered in the
RYGB group [14]. These findings were replicated by other
authors who found similar results in weight loss at short-­
term follow-up comparing RYGB and low-calorie diet, but
only RYGB patients determined improvements of insulin
resistance, insulin secretion, and insulin-stimulating gut hormones, such as GLP-1 [15]. This is obviously true only for
the first few weeks. In fact, there is a significant difference in
the rate of weight loss, as demonstrated by the time needed
to lose 10 kg between RYGB (30 days) and caloric restriction (55 days) [16]. Also, if the caloric restriction was the
only responsible mechanism for glucose control, the
improvement of this parameter should be uniform between
the different bariatric operations. It has been clearly demonstrated how BPD ± DS, RYGB, and laparoscopic sleeve gastrectomy (LSG) provide a quicker improvement of diabetes
as compared to laparoscopic adjustable gastric banding
(LAGB) [11, 17]. This is also demonstrated by the change in
the profiles of the glucose and insulin curves between LAGB,
low-calorie diets, and RYGB. In fact, if LAGB and a low-­
5
Physiological Mechanisms of Bariatric Procedures
calorie diet produce a downward shift of such curves, RYGB
determines shortened times to peak glucose and insulin with
a leftward shift of the curves [18].
It is reasonable to conclude that, although caloric restriction is an important factor contributing to the improvement
in hepatic insulin sensitivity, it likely plays a role only in the
immediate postoperative period, and other factors are
involved in the long-term weight loss and glycemic control
improvement.
Energy Expenditure
Under normal circumstances, the energy expenditure
decreases consequently to caloric restriction and the resulting weight loss [19]. This adaptive mechanism on one hand
is meant to preserve the individual and on the other hand
could be responsible in part for the long-term failure of the
caloric restrictive diets. The data on energy expenditure after
bariatric surgery is somewhat conflicting. In fact, if some
investigators found a decrease in energy expenditure secondary to the weight loss after RYGB, others were able to demonstrate its increase in both RYGB and BPD, but not after
vertical banded gastroplasty (VBG) [15, 20–22]. There is
data that shows evidence of significant reduction of resting
energy expenditure and a significant degree of metabolic
adaptation both occur after sleeve gastrectomy. The hypothesis is that a greater metabolic adaptation could be partly
responsible for a lower weight loss after surgery. Furthermore,
there is recent evidence that suppression in resting energy
expenditure after sleeve gastrectomy and RYGB remained
up to 2 years, even after weight loss had plateaued. This
study suggests that energy adaptation is not a contributing
mechanism to medium-term weight maintenance after SG
and RYGB bariatric surgeries. No definite conclusions on
the role of energy expenditure can be drawn at this time, and
additional mechanisms should be sought to explain the metabolic improvements after bariatric surgery.
Changes in Eating Behavior
The consumption of diets high in fat has been associated
with the development and maintenance of obesity in both
humans and rodents [23, 24]. Also obese individuals have a
greater propensity to choose high-fat foods, as compared to
lean ones [25]. On the other hand, it is known how the eating
behaviors change after bariatric surgery.
In fact several studies have shown the predilection of
lower-fat foods after RYGB [26, 27]. More recently, food
choices after SG have been studied in rats [28]. Similarly to
what is found after RYGB, in spite of the different anatomic
alterations, post-SG rats preferentially choose low-fat and
63
avoid calorie-dense diets [28]. These findings cannot only be
explained by the mechanical restriction, as a compensatory
choice of more calorie-dense foods to maximize caloric
intake would have occurred.
Other options to explain such behaviors include postoperative changes of the taste acuity and neural responses to
food cues. Two studies have shown enhanced taste acuity
and altered hedonic craves for food in post-RYGB patients
[29–31]. This has been validated by functional magnetic
resonance imaging (fMRI) studies of RYGB patients who
presented reduced activation of the mesolimbic reward areas,
especially after high-calorie foods [32].
Other possible mechanisms include the aversive symptoms proper of some of the bariatric operations derived by
improper food choices. In particular, the development of the
uncomfortable symptoms of the dumping syndrome might
steer patients away from high caloric carbohydrates.
Unfortunately, no scientific evidence on the impact of aversive symptoms and weight loss exists. Occasionally, the
aversion to certain foods promotes the development of maladaptive eating behaviors, which ultimately affect the weight
loss process. The underlying behavioral and physiological
mechanisms of the described phenomenon seem to be complex. However, results from animal models of bariatric surgery indicate that learning processes may play a role as
changes in diet selection progress with time in rats after
RYGB.
ntero-Hormones, Incretins, and Intestinal
E
Adaptation
Gut hormones play a crucial role in regulating appetite, satiety, food intake, systemic metabolism, and insulin secretion.
Different degrees of evidence support the physiological roles
for ghrelin, CCK, GLP-1, and PYY in GI motility [8]. An
important feature of these relationships is that gastric volume, gastric emptying, intestinal-nutrient sensing, and the
secretion of these four hormones are linked in negative-­
feedback loops. Changes in GI hormone secretion provide
plausible mechanisms for the remarkable therapeutic efficacy of bariatric surgery. Interestingly, similar changes have
been seen between patients who have undergone SG and
those who have undergone RYGB [8]. After RYGB, the alimentary limb undergoes hyperplasia and hypertrophy,
together with increased expression of glucose transporters,
increased uptake of glucose into intestinal epithelial cells,
and reprogramming of intestinal glucose metabolism to support tissue growth and increased bioenergetic demands. The
number of cells producing GLP-1 and GIP within the alimentary limb also increases. Analysis using 2-deoxy-2-[18F]
fluoro-D-glucose in rodents and humans show that the alimentary limb becomes a major site for glucose disposal.
64
These changes are likely to contribute to improved glycemic
control. In contrast, there is no evidence of GI tract hyperplasia after SG. However, the number and density of cells containing GLP-1 reportedly increase after SG in rodents.
Moreover, SG reduces intestinal glucose absorption, potentially contributing to improved glucose tolerance [8]. These
findings yet again highlight that RYGB and SG improve glucose homeostasis by different as well as overlapping
mechanisms.
Entero-Hormones
The ingestion of food determines alterations of the gastrointestinal, endocrine, and pancreatic secretions, known as the
enteroinsular axis. The main modulators of such mechanism,
including GLP-1, GIP, peptide YY, oxyntomodulin, cholecystokinin, and ghrelin, have been found altered after some
bariatric surgery procedures (RYGB, BPD-DS, VSG)
(Table 5.2).
Glucagon-Like Peptide-1 (GLP-1)
This is a peptide released by the L cells of the ileum and
colon in response to the ingestion of meals. Overall, it is an
insulinotropic hormone, and as such, it is responsible for the
increase of insulin secretion in response to oral glucose
(incretin effect). Additionally it has been linked to stimulate
ß(beta)-cell growth, decreasing their apoptosis and, ultimately, increasing their mass in rats [33]. The modulating
effect of GLP-1 on postprandial glycemia is also achieved by
suppression of glucagon secretion, decreased gastric emptying, and intestinal motility (ileal brake), as well as central
nervous system pathways to induce satiety [33, 34]. Overall
GLP-1 enhances satiety and reduces food intake. Normally
GLP-1 secretion is stimulated by the presence of nutrients in
the distal ileum. This is one of the theories to explain the
rapid (within days post-procedure) and durable hormonal
increase demonstrated after the metabolic procedures with
intestinal bypass (RYGB, BPD, BPD-DS) [35–37]. Bypass
of a proximal gut (“foregut”) and the increased distal gut
(“hindgut”) L-cell nutrient exposure are two potential explanations for the altered gut hormone profile observed after
RYGBP. However, the burden of evidence is in favor of the
latter. Enhanced GLP-1 responses are also observed after
SG, despite the absence of alteration in the route of nutrient
delivery.
In RYGBP, nutrients rapidly pass through the small gastric pouch, bypassing the majority of the stomach and upper
small bowel and directly entering the mid-jejunum. In SG,
the removal of the gastric fundus and body results in an unaltered route of nutrient passage through the GI tract [38, 39].
D. R. Funes et al.
Both procedures result in accelerated gastric emptying and a
rapid entry of undigested food into the jejunum. Consequently,
there is enhanced direct contact of nutrients with the apical
surface of L cells, interspersed among intestinal epithelial
cells, resulting in Ca2-dependent stimulation of GLP-1
secretion into intestinal small blood vessels [40, 41].
Additional mechanisms to explain the GLP-1 increase are
related to the inhibition of the GLP-1 degrading enzyme
dipeptidyl peptidase-IV (DDP-IV) demonstrated after RYGB
and not in type II DM [42]. Once again the evidence is discordant as increased levels of DDP-IV have been reported
after BPD [43].
Finally, the role of the GLP-1-induced hunger modulation and decrease in food intake on the weight loss after bariatric operations remain controversial. Evidence for a link
between GLP-1 response and weight loss is at best correlative, and a causal relationship has not yet been established.
In fact, although the procedures that present the more pronounced weight loss are also the ones determining the highest levels of GLP-1, the increased satiety does not correlate
with a significant increase of GLP-1 on longer follow-up
studies [44, 45].
We can conclude that although GLP-1 is not the main
direct responsible for the weight loss after bariatric operations, it contributes to some weight loss, and it is likely a key
contributor to the glycemic homeostasis proper to these
procedures.
Glucose-Dependent Insulinotropic
Polypeptide (GIP)
The K cells of the duodenum and proximal jejunum mainly
secrete this hormone. Its secretion is enhanced by the presence of nutrients (especially carbohydrates and lipids) in this
portion of the intestine. As the name indicates, this is an insulinotropic hormone, although less powerful than GLP-1,
determining increased postprandial insulin secretion and
pancreatic ß(beta)-cell augmentation [46]. Contrary to GLP-­
1, GIP has no effect on the intestinal and gastric motility.
GIP also affects lipid metabolism by increasing lipogenesis
and promoting fat deposition [33]. The function of GIP in
diabetic patients is less clear, although consistently demonstrated to be impaired [47]. Due to its site of secretion, GIP
has been regarded as one of the hormones possibly involved
in the foregut theory. The changes seen in this hormone in
animal models of bariatric surgery have not been consistent.
Most human studies have reported a decrease in this hormone post-malabsorptive surgery. The effects of bariatric
surgery on GIP are discordant, although in general more evidence exists on the decreased levels of this hormone after
RYGB and BPD, likely from bypassing the proximal intestine, than the contrary [38, 48]. In contrast, no changes in
GLP-1
GIP
PYY
Oxyntomodulin
CCK
Ghrelin
Origin
L cells
K cells
L cells
L cells
I cells
Oxyntic
Satiety
↑
No Δ(delta)
↑
↑
↑
↓
Glycemic control
↑
↑
↑ or no Δ(delta)
↑
No Δ
No Δ
Table 5.2 Characteristics of entero-hormones after bariatric operations
GI motility
↓
No Δ(delta)
↓
↓
↑
No Δ
RYGB
↑
↓
↑
↑
?
↓
LSG
↑
Unknown
↑ or no Δ(delta)
↑
↑ or no Δ(delta)
↓↓
LAGB
No Δ(delta)
No Δ(delta)
No Δ(delta)
No Δ(delta)
Unknown
No Δ(delta)
BPD
↑
↓
↑
↑
Unknown
No Δ(delta)
BPD-DS
↑
↓
↑
↑
Unknown
↓↓
5
Physiological Mechanisms of Bariatric Procedures
65
66
D. R. Funes et al.
GIP levels are reported after LAGB [38]. The changes of GIP
after LSG remain undetermined. Overall the role of GIP in
the mechanism of action of bariatric procedures remains
elusive.
levels increase after RYGB, but not after LAGB [59].
Because of the overlap in secretion and function, it is difficult to attribute the true value of each one of them in postsurgical weight loss.
Peptide Tyrosine Tyrosine (PYY)
Cholecystokinin (CCK)
PYY is also expressed in the endocrine pancreas, where
PYY may have paracrine intraislet actions. Also, PYY is
expressed by neurons in the gigantocellular reticular nucleus
of the rostral medulla, which have widespread central projections. PYY activates several neuropeptide Y-family receptors
(NPYR), including NPY1R (or Y1R), NPY2R, NPY4R, and
NPY5R, whereas PYY is selective for NPY2R. NPY2R are
expressed throughout the body, including in several brain
regions, the GI tract, and vagal afferents [49–51].
PYY may contribute to gastric emptying via the ileal
brake mechanism, to the inhibition of eating, and to the control of meal-related glycemia, but the evidence that these are
physiological actions remains scarce. Similarly, PYY role in
RYGB remains unclear. This modest progress may be due in
part to the difficulties of PYY research, including the low
threshold for eliciting illness with PYY infusions, the lack of
NPY2R antagonists for human use, and the possibility of
neuropod PYY signaling. After RYGB, plasma levels of
PYY increase modestly (20%) in the fasting state and by 3.5-­
fold in the postprandial state [51].
Similarly, postprandial levels of PYY increase 1 year following VSG. Animal studies support a prominent role for
PYY in mediating bariatric weight loss, as postsurgical
weight loss is lower in PYY gene knockout as compared
with wild-type mice, and infusion of anti-PYY antibodies
increases food intake in postbypass rats. Thus, enhanced
PYY secretion may contribute to weight loss after RYGB
[52–55].
The key role of PYY in the post-bariatric surgery weight
loss is supported by encouraging evidence in animal models
but needs further dislucidation in human studies which present a challenge given to the current limitations previously
discussed.
CCK is normally secreted from the duodenum and proximal
jejunum in response to nutrients. CCK has been clearly
established as a satiation signal in humans and may contribute to the control of meal-related glycemia both indirectly,
via its effect on gastric emptying, and directly via control of
hepatic glucose production. Pathophysiology of CCK signaling may contribute to overeating, to obesity and T2DM in
some patients, and to early satiation after RYGB. Additionally,
CCK plays a key role in gallbladder and gastric emptying
and exocrine pancreatic secretion. Preclinical studies indicate that CCK is a candidate for obesity pharmacotherapy,
especially in combination with other endocrine-based therapies. However, evidence is still unclear on the changes of this
hormone after bariatric surgery. Some have shown an
increase after LSG, but its overall role in the mechanism of
action of these procedures remains undefined [58].
Oxyntomodulin
Since its polypeptide structure is similar to GLP-1, oxyntomodulin’s metabolic pathways present several resemblances
both in its food-related secretion and degradation process via
the enzyme dipeptidyl peptidase-IV (DDP-IV) [56–58].
Similarly to GLP-1, oxyntomodulin reduces gastrointestinal
motility and participates in the regulatory mechanism of glucose homeostasis. As seen for the other two hormones
secreted by the L cells—GLP-1 and PYY—oxyntomodulin
Ghrelin
Ghrelin (growth hormone-releasing peptide) is a hormone
secreted mainly by the oxyntic glands of the fundus of the
stomach and in smaller amounts in the rest of the small
bowel. As its name implies, it is involved in the secretion of
the growth hormone. This is primarily an orexigenic hormone stimulating directly the hypothalamus. Obese individuals present a decreased suppression of ghrelin after a meal
[56, 59, 60]. In addition, ghrelin inhibits insulin secretion by
an unknown pathway [61]. It seems that, thanks to this latter
property, ghrelin suppresses the insulin-sensitizing hormone
adiponectin, negatively affecting the glucose metabolism
[62]. Because of these negative effects on the glucose homeostasis, the reduction of ghrelin seen after certain bariatric
operations could be beneficial for overall glycemic control
[62]. Although most of the biological effects of ghrelin are
due to its acylated form, the non-acylated equivalent seems
biologically active as well [33]. The challenge in identifying
the two forms with different assays might explain some of
the discordant findings of ghrelin variation after bariatric
operations. In general, although it would be reasonable to
speculate that bariatric procedures that do not alter the contact of food with the fundic glands (LAGB, BPD) do not
determine significant alteration of ghrelin levels, evidence of
the opposite exists [63, 64]. However, if some reports have
shown the reduction of ghrelin levels after RYGB, others
5
Physiological Mechanisms of Bariatric Procedures
found no changes or even increases of such levels [57, 65,
66]. In randomized trials, ghrelin levels have been found to
be permanently lower after LSG than RYGB, likely due to
the complete removal of gastric fundus [67]. Also vagal stimulation might affect ghrelin secretion, and vagotomy has
been associated with decreased levels [68], although the role
of the vagus nerve on the secretion of ghrelin has been disputed by others [69]. Overall, contradicting evidence exists
on the role of ghrelin on the weight loss after bariatric surgery, and this hormone likely plays only a marginal role.
Mechanisms of Diabetes Resolution
The existence of an entero-hormonal mechanism to explain
diabetes resolution has been postulated for several years [7].
This is also indirectly proven by the pattern of diabetes resolution after gastric banding that follows the weight loss curve
and by the multiple hormonal changes described after gastric
bypass [70, 71]. In particular, insulin and leptin levels
decrease, whereas GLP-1, GIP, PYY, and ACTH increase
even before any significant weight loss [71, 72]. Currently,
two main theories exist on the mechanism of diabetes resolution after bariatric surgery: the “foregut” and “hindgut.”
Foregut Hypothesis
According to this theory, the exclusion of the duodenum
from the pathway of the nutrients will prevent the secretion
of an unidentified “anti-incretin” substance. In fact, diabetes
mellitus (DM) could be due to the overproduction of an
“anti-incretin” that determines decreased insulin secretion,
insulin resistance, and depletion of the β(beta)-cell mass.
When the food bypasses the duodenum, this “anti-incretin”
is inhibited. Among the advocates for this theory, Rubino
et al. have elegantly demonstrated the resolution of diabetes
in rats in which the duodenum was surgically bypassed and
excluded [73]. The restoration of duodenal passage in the
same group of animals resulted in recurrence of the impaired
glucose tolerance state. Others believe that the glucose
absorption changes after duodenal bypass. In fact, it has
been previously described in a rodent model that both the
intestinal morphology and the Na+/glucose cotransporter 1
(SGLT1) function are altered after gastric bypass [74]. In
particular, the villous height and crypt depth of the intestinal
segments exposed to nutrients are increased, but, unexpectedly, the glucose transport activity is decreased. According
to the authors, this could be one of the mechanisms involved
in the improvement or resolution of diabetes after duodenal
exclusion procedures, such as gastric bypass. Although the
process by which duodenal exclusion leads to decreased glucose transport is unclear, some authors have speculated that
67
the interruption of the proximal intestinal regulation of
SGLT1 via the sweet taste receptors T1R2 and T1R3 is
responsible [74].
Hindgut Hypothesis
Additional and/or alternative theories of glucose homeostasis entail the secretions of putative peptides determined by
the increase glucose load in the hindgut (“hindgut theory”).
According to this second theory, the early presence of undigested food in the distal small bowel stimulates the secretion
of “incretin” substances, which, in turn, determines normalization of the glycemia, increases insulin production, and
decreases insulin resistance. Although, once again, a single
substance has not been identified, GIP and GLP-1 remain the
most promising putative candidates. Initially increased
GLP-1 and GIP cannot account for improved glucose tolerance, but as glucose normalizes, the action of especially GIP
on insulin secretion might be restored [8].
Neuroendocrine Mechanism
Experimental models highlight a complex interplay of hormonal and neural pathways that converge and possibly interact at various levels of the gut-brain axis to regulate energy
balance. Bariatric surgery procedures, including Roux-en-Y
gastric bypass (RYGB) and sleeve gastrectomy (SG), influence body weight and glucose regulation via central neural
circuits that are recruited by vagally mediated pathways following activation of stretch or chemoreceptors in the stomach. Gut hormones are able to exert their effects on central
pathways by either acting locally on vagal endings or via the
circulation [75].
Vagus Nerve
The activation of central neural circuits, downstream of vagal
afferent signaling, was recently suggested to be involved in
mediating satiety and glycemic control in a mouse model of
RYGB. These data implicates vagal endings in sensing the
elevation in gastric distension and nutrients in the roux limb
to activate an anorexigenic pathway involving the nucleus
tractus solitarius (NTS), lateral parabrachial nucleus, and
central nucleus of the amygdala [75]. The activation of this
pathway in the immediate period following RYGB is likely
to be responsible for the dramatic reduction in food intake
after RYGB and may also contribute to the consumption of
smaller and slower meals. In addition, there is evidence supporting the reorganization of hindbrain feeding circuits following RYGB and SG. Experimental models of SG indicate
68
that vagal mechanisms contribute to the efficacy of the procedure and that there is a lower threshold for activation of
neurons in the NTS in response to a nutrient stimulus, as
demonstrated by elevated levels of Fos protein. We have also
recently generated data showing increased neural activation,
under fasting conditions, within the same vagal circuits.
Furthermore, the extent to which vagal mechanisms are central to the reduction in appetite (and weight loss) induced by
SG also remains unclear. There is no evidence of the benefits
of vagotomy on the postsurgical weight loss. Several trials
on LAGB and RYGB have shown no benefits on weight loss
by adding a vagotomy [69, 76–79]. Nevertheless, vagally
mediated mechanisms seem to have a crucial role in the neuroendocrine mechanisms of RYGB and SG.
Bile Acids (BA)
Bile acids are synthesized from cholesterol in the liver.
Ingestion of food causes bile acid secretion from the gallbladder through the common bile duct to the duodenum.
Upon reaching the ileum, bile acids are transported by specific transport proteins to the portal circulation for recycling
back to the liver.
The two primary bile acids produced by the liver in
humans are cholic acid (CA) and chenodeoxycholic acid
(CDCA). Bile acids undergo chemical modification through
conjugation in the liver and dehydroxylation by gut bacteria
[80]. Bile acids also function as a ligand for a specific nuclear
transcription factor, the farnesoid X receptor (FXR), which
forms a heterodimeric complex with retinoic X receptor-𝛼
(RXR-𝛼) that binds to an inverted repeat sequence in gene
promoters. Bile acids not only function in lipid absorption in
the gut but also appear to be part of a broader physiological
response to ingested nutrients that also involves glucose
metabolism [81]. This is consistent with the anabolic need to
store fatty acids as triglycerides, which requires a glycerol-­3-­
phosphate backbone that is derived from glucose. The effects
of bile acids on the glucose metabolism might be mediated
by the activation of the L cells via bile acid-TGR5 (G protein-­
coupled bile acid receptor) and FXR signaling [86]. When
recognized by TGR5 and FXR-α receptor in the liver, bile
acid induces liver glycogen synthesis, inhibits gluconeogenesis, ameliorates body’s insulin sensitivity, and controls glucose metabolism. FXR−/− mice exhibit peripheral insulin
resistance, reduced glucose disposal, and decreased adipose
tissue and skeletal muscle insulin signaling, and, conversely,
activation of FXR by the agonist GW4064 in insulin-­resistant
ob/ob mice reduced hyperinsulinemia and improved glucose
tolerance. The hindgut hypothesis is based on the premise
that inappropriate delivery of ingested nutrients and/or digestive juices to more distal regions of the small intestine
induces a putative molecular mediator that ameliorates T2D
D. R. Funes et al.
[82]. Bile acids have been implicated as key molecules in
this hypothesis. Recent work in both clinical studies and animal models supports a key role for bile acids. Systemic BA
levels are elevated in patients following RYGB, suggesting
an increase in BA signaling after RYGB. SG has been shown
to modify the expression of certain hepatic genes involved in
the metabolism of bile acid [83–85]. Furthermore, recently
FXR has been shown to be required for the antidiabetic effect
of SG in mice [28]. Also SG resulting in resolution of T2D
seems to contradict the hindgut hypothesis, inappropriate
delivery of nutrients and digestive components to the distal
intestine hypothesis. However, gastric transit is substantially
increased in SG, expediting delivery through the duodenum
into the distal intestine. The binding of bile acids with the
nuclear receptor FXR (farnesoid X receptor) has been associated with positive alterations of the feeding behavior
(repression of rebound hyperphagia), improved glucose tolerance, and likely alteration of the gut flora in post-vertical
sleeve gastrectomy mice, as opposed to post-VSG FXR
knockout counterpart [87]. Further delineation of the molecular mechanisms underlying these beneficial effects could
provide target for novel, less invasive, and efficient
treatments.
Gastrointestinal Microflora
The composition of the gastrointestinal microflora established during the first year of life influenced by a variety of
environmental and metabolic factors is relatively stable
during adulthood. However, the adult colon has rich microbial diversity resulting from the estimated 1000–36,000
different bacterial species contained within its lumen
[103]. This diverse bacterial population contains perhaps
100 times more genes than the human genome [104]. The
coexistence of the intestinal microbiota is essential for
several host functions, such as vitamin synthesis. Recently
additional links between gut flora and the metabolism have
been discovered. Instrumental in this process is the fact
that both mouse and human microbiota are prevalently
populated by the same bacterial species: Bacteroidetes and
Firmicutes. Comparisons of the distal gut microbiota in
genetically obese mice and their lean littermates have
revealed that changes in the relative abundance of the two
dominant bacterial divisions, the Bacteroidetes and
Firmicutes, are associated with the level of adiposity
[105–107]. Specifically, obese mice have a significantly
higher level of Firmicutes and lower levels of Bacteroidetes
compared with their lean counterparts [108]. Similar
results have been established in humans [107]. Furthermore,
biochemical analyses have indicated that such shifts in
microbial community structure are associated with an
increased efficiency in energy harvest in obese individuals
5
Physiological Mechanisms of Bariatric Procedures
from a given caloric load; these findings suggest that the
gut microbiota may be a significant contributor to an individual’s energy balance.
It has been well documented that weight loss is of great
benefit in obese patients with type II diabetes mellitus
(T2DM), often eliminating the need for pharmacologic intervention to treat insulin resistance [109, 110]. It has also been
established that diet-induced weight loss in humans has a
marked effect on gut microbial ecology—shifting the gut
microbial community composition toward that seen in lean
individuals [107]. Intriguingly, experimental alteration of
intestinal flora in genetically obese mice results in weight
loss independent of improvement of glycemia [111]. The
division-wide change in microbial ecology that has been
associated with obesity suggests that the obese gut microbiota may play an important role in the morbidity associated
with obesity, and its modification might be responsible for
the resolution of some comorbidities.
Changes in the composition of the gut microflora after
RYGB are a potential contributor to both weight loss and
comorbidity resolution. However, this mechanism has
received little attention. Zhang et al. demonstrated that the
Firmicutes were decreased in three gastric bypass patients
compared to normal-weight and obese individuals [112].
Meanwhile, Woodard et al. directly manipulated the gastrointestinal microbiota using a Lactobacillus probiotic agent following gastric bypass [113]. They showed that the probiotic
group had greater weight loss than matched controls. In a
mouse model, SG is associated with changes in the gut microbiome at 1 week and persists 1 month following surgery. The
identified increases in members of the Enterobacteriaceae,
Enterococcaceae, and Porphyromonadaceae families correlate with reduced weight. Enterobacteriaceae, within
Proteobacteria, has been observed to increase following SG
and RYGB in mice by others as well. This parallels observations in humans following RYGB. These experiments suggest
that the gastrointestinal microbiota may play a significant role
in human energy homeostasis. Although it is clear that microbiota play important roles in many aspects of energy metabolism, further work is needed to characterize and identify the
metabolic contribution of gut microbial changes associated
with SG.
Adipose Tissue
The excessive peripheral deposition of fat has been associated with peripheral and hepatic insulin resistance [88].
Furthermore, it is well known how the visceral fat constitutes
a true hormone-producing substrate. Consequently, obese
patients present increased levels of pro-inflammatory cytokines such as TNF, interleukin-6, and leptin and reduced levels of anti-inflammatory hormones such as adiponectin [89].
69
The impact of bariatric surgery on the inflammatory
markers, specifically which inflammatory markers are
closely associated with changes in obesity and improvements in insulin sensitivity, needs further delineation. The
endocrine role of the adipose fat has been well established
[90]. Among the multiple adipokines described, omentin-1
has been more recently described as an important modulator
of insulin sensitivity [91, 92]. Plasma omentin-1 levels and
its adipose tissue gene expression are markedly decreased in
obese individuals [92]. Plasma omentin-1 levels are positively correlated with both adiponectin and HDL levels and
negatively with insulin resistance [92]. The omentin genes
are located in the same chromosomal region associated with
the development of type II diabetes [93, 94].
Leptin
A paramount contribution for the comprehension of the regulatory mechanisms between food intake and energy regulation has been the discovery of the adipokine leptin. As it
stands now, levels of circulating leptin result from the contribution of two major organs, the white adipose tissue and the
gastric mucosa. This hormone crosses the blood-brain barrier, and its main sites of action are the hypothalamic cells
where it plays fundamental roles in the control of appetite
and in the regulation of energy expenditure. At first it was
considered a hormone specific to the white adipose tissue;
however, recently it was found expressed by other tissues.
Among these, the gastric mucosa has been demonstrated to
secrete large amounts of leptin. Secretion of leptin by the
gastric chief cells was found to be an exocrine secretion.
While secretion of leptin by the white adipose tissue is constitutive, secretion by the gastric cells is a regulated one
responding very rapidly to secretory stimuli such as food
intake [95]. In general, decreased levels of leptin have been
associated with increased hunger [96]. Some authors suggested a direct link between leptin and inhibition of lipogenesis and increased lipolysis. In fact, obese individuals have
an increased baseline concentration of leptin, and the levels
decrease after weight loss [97].
Since the reduction of leptin also leads to a reduction in
energy expenditure, the maintenance of weight loss simply
through diet becomes challenging [51]. The reduction of
leptin has been reported in all the bariatric procedures
(RYGB, LSG, LAGB), and it has been linked directly with
weight loss [52]. Interestingly, post-RYGB patients who
remain obese present a decreased level of leptin, suggesting
mechanisms other than weight loss to explain the postoperative changes [98]. Further studies regarding the effects of
bariatric surgery in the gastric mucosal leptin secretion are
needed to determine the extent of its contribution to the well-­
established physiological mechanisms of bariatric surgery.
70
D. R. Funes et al.
Table 5.3 Changes of adipocytokine after bariatric operations
Obese
Post RYGB
Leptin
↑
↓
Adiponectin
↓
↑
Omentin
↓
↑
Adiponectin
Adiponectin is also produced by the adipose tissue, and it is
related to insulin sensitivity and fatty acid oxidation [99].
Contrary to leptin, adiponectin levels are decreased in obese
patients and increase with weight loss [100]. Low adiponectin levels are associated with insulin resistance and coronary
artery disease [101]. After RYGB, the levels of adiponectin
increase and correlate with the improved insulin sensitivity
measured by HOMA-IR [98]. Furthermore, lower
­preoperative levels of adiponectin have been linked to greater
increase in postoperative levels and increased weight loss,
maybe because of enhanced fatty acid oxidation into the
muscle [98]. The adiponectin-related decrease in TNFα(alpha) has been advocated as a potential mechanism to
decrease monocyte adhesion to the endothelial cells [102].
The reason for the changes of the mentioned cytokines
after RYGB seems to be related mainly, but not exclusively,
to the weight loss, as it has been similar for other bariatric
procedures and for calorie-controlled diets [51] (Table 5.3).
β(Beta)-Cell Changes
Besides the previously mentioned gastrointestinal hormones,
residual ß(beta)-cell function has been implicated as a determinant in the glycemic control after bariatric operations
[114]. In fact, the rate of remission of diabetes has been
linked to the patient-specific characteristics of the diabetes
itself. Shorter diabetes duration, lesser degree of β(beta)-cell
dysfunction (C-peptide positive), and lesser or no insulin
requirements have been linked to higher chance of diabetes
remission after surgery [114, 115]. Also it has been shown
how, on one hand, RYGB results in an improvement of insulin sensitivity proportionally to the weight loss, but on the
other hand, β(beta)-cell glucose sensitivity increases independently from it [116]. To further validate the importance of
the residual ß(beta)-cell function for the remission of diabetes, some studies have shown the lack of significant benefit
of RYGB in glycemic control of type I DM, in spite of similar changes of GLP-1 and weight loss as in type II DM
patients [114]. It is important to note that some, and probably
less convincing, evidence exists of type I DM amelioration
after RYGB. In fact, in a small series of three patients, a significant and durable (8 years) improvement in glycemic control was demonstrated, suggesting other mechanism other
than residual β(beta)-cell function [117]. However, the
increase of GLP-1 after type I DM, although comparable
with a similar increase in type II DM patients, does not determine suppression of glucagon secretion, but rather an
increase [114]. This unexplained phenomenon, once again,
suggests additional factors responsible for glycemic control
after bariatric operations besides the degree of β(beta)-cell
function. However, more recent animal studies have demonstrated pancreatic islet cell histopathological changes following RYGB showing reduced islets interstitial fibrosis, as
well as regeneration and hypertrophy of beta cell mass.
These findings suggest that RYGB may have a role in promoting islet regeneration. Notch signaling is an evolutionary
conserved pathway of cell-cell communication and cell-fate
determination during embryonic development and tissue
homeostasis. The results from previously mentioned animal
studies indicate a potential role of this signaling pathway in
regulating the pancreatic islet regeneration following RYGB.
End-Organ Changes
Increased Insulin Sensitivity
The beneficiary effects of bariatric surgery are evident on
both the insulin secretion and the improvement of insulin
sensitivity. In general, weight loss determines increases in
peripheral insulin sensitivity, but this is not the only mechanism after bariatric surgery.
The most convincing evidence of increased peripheral
insulin sensitivity derives from the studies on BPD. Mari
et al., in fact, using the hyperinsulinemic-euglycemic clamp
methodology, demonstrated significant improvement of the
insulin sensitivity within the day of the procedure [118]. The
data for RYGB is, instead, discordant [119–123]. No significant changes have been shown in the LAGB and LSG studies
[120].
ardiac Response to Obesity and Bariatric
C
Surgery
The “thrifty gene hypothesis” of James Neel postulates that
obesity and type 2 diabetes were an evolutionary advantage
in times of starvation [124]. In modern times, the ability to
continually store energy has become a major disadvantage.
Obesity and the development of associated complications are
multifactorial and dictated by the individual exposures which
include the ones that enter the body from the environment as
well as those generated in excess within the body by inflammation, oxidative stress, and metabolic dysregulation. There
are specific mechanisms that the body uses in an attempt to
reestablish homeostasis [125]. In obesity, the body’s initial
response to excess energy is to partition it into adipose tissue
5
Physiological Mechanisms of Bariatric Procedures
to reduce the metabolic burden on its major organs such as
the heart. However, when the storage capacity of adipose tissue is exceeded, energy is stored ectopically as fat in vital
organs creating a lipotoxic environment in non-adipose tissue. In obesity, through environmental and subsequently
intrinsic factors, there is an increased hemodynamic, neurohormonal, and metabolic load.
There is strong evidence that the deposition and also the
utilization of fatty acids as source of energy by the cardiac
tissue are associated with increased myocardial oxygen
consumption and decreased mechanical efficiency. Such
­
studies have helped to establish obesity as an independent
predictor of increased myocardia oxygen consumption and
increased cardiovascular risk [125, 126]. Just until recently it
is widely recognized that bariatric surgery improves cardiac
function in obese patients and also reduces the risk of cardiovascular disease. The principal mechanisms involved in the
benefits of bariatric surgery, predominantly RYGB and SG,
occur at a micro cellular level in the endoplasmic reticulum
(ER). The ER is responsible for balancing the nutritional status of the cell, homeostasis that is vital for protein synthesis,
energy storage, and continued nutrient sensing. When supplied with excess substrate, ER undergoes stress, widely
associated with cardiac dysfunction and disease. In bariatric
surgery, the most studied procedure in this regard is RYGB,
which has shown to reduce the metabolic load and stress to
the heart making it plausible that the beneficial cardiovascular effects may be mediated by the reduction of cardiac ER
stress or load [127].
Gastrointestinal-Renal Axis
There is growing evidence strengthening the rationale to further explore the hypothesis of the existence of a direct communication between the gastrointestinal (GI) tract and the
kidneys. This theory is based on the fact that GI hormones
and peptides have shown to regulate the autocrine function
of renal hormones, affecting renal function and including
sodium excretion. GLP-1 is the GI hormone that has been
most widely studied in this regard, demonstrating a direct
and indirect natriuretic effect by targeting early tubular
sodium reabsorption [128]. Moreover, along with reference
to emerging data demonstrating that GLP-1 can exert direct
anti-inflammatory and antioxidant effects in the kidney, we
can now explain the link between the beneficial effects of
bariatric surgery on hypertension resolution and kidney
function improvement. Animal models provide one of the
most important pieces of evidence linking the physiological
mechanisms of bariatric surgery and the GI-renal axis; these
are the effects of glucagon-like peptide 1 (GLP-1) and GLP-1
receptor agonists (GLP-1RAs) on renal hemodynamics.
Several vascular and tubular factors result in a net reduction
71
in afferent renal arteriolar resistance, a net increase in efferent renal arteriolar resistance and/or a reduction in hydraulic
pressure in Bowman space, and thereby an increase in glomerular hydraulic pressure and single-nephron glomerular
filtration rate [128, 129]. GLP-1RAs are associated with
direct GLP-1R-mediated and, at least in part, nitric oxide-­
dependent vasodilation of the afferent renal arteriole, as well
as indirect inhibition of vascular and tubular factors that are
putative mediators of glomerular hyperfiltration, which is
well known to be the primary event resulting in chronic kidney injury [128, 130].
In an experimental model, the integrated effect of incretin-­
based therapy on renal hemodynamics seems to be the result
of direct vasodilative actions and inhibition of pathways of
glomerular hyperfiltration, which may lead us to believe that
the changes in GLP-1 following bariatric surgery may result
in a similar effect on renal hemodynamics [128].
ariatric Surgery and the Control of Blood
B
Pressure Through the GI-Renal Axis
The kidney plays a vital role in the regulation of sodium balance and blood pressure. However, the gastrointestinal (GI)
tract, which is the organ first exposed to components of
food, has taste receptors and sensors for electrolytes including sodium [130]. Therefore, in addition to the kidney, there
is increasing realization of the importance of the GI tract in
the regulation of sodium balance and consequently on blood
pressure level. Excessive sodium in the body, as a consequence of increased dietary intake and/or impaired excretion, is the most common risk factor for hypertension. In
addition to renal regulation of sodium homeostasis, which
has been widely described, gastrointestinal absorption and
its control via GI hormones play a critical role in the control
of blood pressure. Most of the electrolytes including sodium
are absorbed in the small (95%) and large (4%) intestine.
The intestinal absorption of fluid by GI epithelial cells
occurs via active transport of (NaCl) sodium chloride. NaCl
absorption occurs from the small intestine to the distal colon.
The GI-derived hormones can be grouped into three classes:
GI hormones, pancreatic hormones, and GI neuropeptides.
According to their ability to affect sodium excretion, we can
further classify these hormones and neuropeptides into two
groups: a group that increases and another group that
decreases sodium excretion. Of these hormones, ghrelin and
GLP-1 have the strongest evidence implicating them with
the beneficial effects of bariatric surgery [130, 131]. In animal models, ghrelin exerts its effect on distal nephron-promoting diuresis and renal nitric oxide production.
Additionally, ghrelin also stimulates nephron-dependent
sodium reabsorption. Ghrelin’s direct effect in the function
of renal cells consists in the reduction of mitochondrial
72
membrane potential, and mitochondrial-derived reactive
oxygen species (ROS) ameliorates angiotensin II-induced
cell senescent in the renal proximal tubule cells. GLP-1
inhibits sodium uptake and facilitates natriuresis, and an animal model demonstrates the effect of GLP-1 in the brush
border of proximal tubules inhibiting the sodium-hydrogen
antiporter 3 (NHE3) activity and sodium reabsorption in
RPT cells. Both long-term and short-term studies have
shown that the blood pressure decreases in adults who
underwent RYGB and SG. Compared with RYGB, sleeve
gastrectomy is associated with better early remission rates
for hypertension. Overall evidence suggest that this may be
related to the ability of bariatric surgery to increase the
plasma levels of natriuretic enterokines such as GLP-1
[130–132].
Conclusion
Although the mechanism of action of the different bariatric
operations is not completely understood, multiple factors
seem to play a role.
The weight loss seems only in part due to purely restrictive mechanisms. Hormonal changes stimulate anorexigenic
pathways in the brain. Furthermore, the role of bile salts and
the gastrointestinal microflora needs further elucidation.
Similarly the resolution of diabetes appears to be a multifactorial process. It is likely that two of the major early contributors are the increased hepatic insulin sensitivity due to
caloric restriction and the improved ß(beta)-cell function
secondary to increased entero-hormones caused by altered
exposure of the distal small intestine to nutrients. Later
changes of the glucose homeostasis are likely due to weight
loss-induced improvement of peripheral skeletal muscle
insulin sensitivity.
Question Section
1. Which one of the following gut hormones increases after
RYGB?
A. GLP-1
B. Ghrelin
C. GIP
D. A + C
E. A + B
2. Which one of the following statements is/are TRUE about
leptin?
A. Leptin is inversely associated with hunger.
B. Leptin increases lipolysis and decreases lipogenesis.
C. Leptin decreases after bariatric surgery.
D. Leptin is directly related to energy expenditure.
E. All of the above.
D. R. Funes et al.
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6
Indications and Contraindications
for Bariatric Surgery
Christopher DuCoin, Rachel L. Moore,
and David A. Provost
Chapter Objectives
1. To assess the risk-benefit ratio and indications of
bariatric surgery
2. To discuss contraindications to bariatric surgery
Introduction
Metabolic and bariatric surgery is a proven therapy for the
treatment of obesity and obesity-related comorbidities.
Available evidence, as detailed elsewhere in the text, strongly
suggests that metabolic and bariatric surgery produces weight
loss that is significantly greater and more durable than that
achieved with the best nonsurgical therapies. This was validated with the 1991 National Institutes of Health (NIH)
Consensus Development Conference Statement which set
the eligibility criteria for bariatric surgery. To qualify individuals should have a BMI ≥ 40 kg/m2 or a BMI between 35
and 40 kg/m2 if they also have high-risk comorbidities such
as severe type 2 diabetes or cardiovascular risk factors [1]. At
that time, all of bariatric surgery was being performed via on
open laparotomy. Since 1991, bariatric surgery has also been
shown to result in resolution or improvement of associated
diseases or conditions including, but not limited to, hyperlipidemia, obstructive sleep apnea, polycystic ovarian syndrome, gout, nonalcoholic fatty liver disease, gastroesophageal
C. DuCoin (*)
Division of Bariatric & General Surgery, University of South
Florida, Tampa, FL, USA
e-mail: cducoin@health.usf.edu
R. L. Moore
Moore Metabolics & Tulane University Department of Surgery,
New Orleans, LA, USA
D. A. Provost
Division of General and Bariatric Surgery, Baylor Scott & White
Medical Center, Temple, TX, USA
reflux, and pseudotumor cerebri. Reductions in the development of cancers, particularly gynecological, breast, and colon
cancers, have been demonstrated. Several case-controlled
studies have demonstrated improvements in long-term survival. A major benefit of metabolic and bariatric surgery,
though not often considered when defining the indications
for surgery, is the improvement in overall quality of life.
When selecting appropriate candidates for surgery, these
benefits must be carefully weighed against the potential perioperative and long-term risks of the procedures.
I ndications for Metabolic and Bariatric
Surgery
Although almost 30 years old, the 1991 National Institutes of
Health (NIH) Consensus Development Conference Statement
on Gastrointestinal Surgery for Severe Obesity [2] continues
to be the most frequently referenced guideline and gold standard when determining the body mass index (BMI) indications for metabolic and bariatric surgery. The statement notes
that patients must be acceptable of the operative risks, motivated, well-informed, and able to participate in treatment and
follow-up. Patients judged to have a low probability of success with nonsurgical methods of weight loss may be considered for surgery. Assessment of risk-benefit ratio should be
performed for each case. Potential candidates include:
• Patients whose body mass index (BMI) exceeds 40 kg/m2
• Patients with BMIs between 35 and 40 kg/m2 who also
have high-risk comorbid conditions or lifestyle-limiting
obesity-induced physical conditions
Examples of associated comorbid conditions to be considered in patients with a BMI less than 40 kg/m2 include
common conditions such as hypertension, diabetes mellitus, and obstructive sleep apnea to life-threatening cardiopulmonary problems such as obesity-hypoventilation and
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_6
77
78
obesity-­related cardiomyopathy. Physical conditions to be
considered include joint disease and gout. The conditions
listed were examples and not meant to be all-inclusive.
Other obesity-­related comorbidities often considered when
determining the appropriateness of surgery in patients with
a BMI less than 40 kg/m2 include hyperlipidemia, nonalcoholic fatty liver disease, gastroesophageal reflux, pseudotumor cerebri, asthma, venous stasis disease, and urinary
incontinence [3]. Many subspecialty surgeons such as neurosurgeons and orthopedic surgeons will refer their patients
for weight loss surgery prior to their definitive procedure.
The NIH Consensus Conference Statement noted that surgical candidates should be evaluated by a “multidisciplinary
team with access to medical, surgical, psychiatric, and nutritional expertise” [2]. The pros and cons of various treatment
options, both surgical and nonsurgical, should be discussed
with the patient. Metabolic and bariatric surgery should be
performed by a surgeon experienced with the appropriate
procedure, working in a program with adequate support for
all aspects of perioperative and postoperative care.
Postoperative surveillance should continue indefinitely.
No upper age limit for bariatric surgery was recommended by the consensus panel. At the time of publication, it
was felt that insufficient data was available to make a recommendation for or against surgery in the adolescent population. However, multiple studies have now shown bariatric
surgery to be safe in both extremes of age.
Defining the indications for metabolic and bariatric surgery begins with an assessment of the risk-benefit ratio of a
given procedure. Significant advances in surgical techniques,
reductions in operative risk, and greater knowledge of the
potential risk of untreated obesity have greatly altered the
risk-benefit ratio of surgery since 1991. Many of these
changes were summarized in the 2004 American Society for
Bariatric Surgery (ASBS) Consensus Conference Statement
on Bariatric Surgery for Morbid Obesity [4] and include:
1. The marked increase in the incidence of obesity
2. Expansion of available operative procedures (e.g., vertical sleeve gastrectomy and laparoscopic adjustable gastric banding)
3. Significant reductions in perioperative mortality and
morbidity
4. The introduction of laparoscopic techniques
5. Increased experience with a team management approach
6. Increased experience with metabolic and bariatric surgery
in adolescents and the elderly
7. Greater demonstration of the effect of surgery in improving or reversing obesity-related comorbidities
8. Demonstration that metabolic and bariatric surgery
improves life expectancy
The 1991 NIH guidelines currently preclude individuals
with a BMI between 35 and 40 kg/m2 without comorbidities
C. DuCoin et al.
or with a BMI < 35 kg/m2 from bariatric surgery. With the
development of “accredited” bariatric programs and surgeons with focused bariatric training, there has been a large
reduction in the morbidity and mortality associated with
these procedures. The health and mortality risk of untreated
obesity is better defined and greater than was appreciated in
1991. The result is a shift in the risk-benefit ratio, again,
favoring surgery and leading to the consideration of lowering
the BMI indications for metabolic and bariatric surgery. The
American Society for Metabolic and Bariatric Surgery
(ASMBS), the Obesity Society, the American Association of
Clinical Endocrinologists (AACE) [2], the International
Diabetes Federation (IDF), and the American Diabetes
Association (ADA) [5] have endorsed guidelines recommending consideration of metabolic and bariatric surgery in
patients with a BMI of 30–34.9 kg/m2 with diabetes or metabolic syndrome. The IDF position statement from March
2011 recommends that surgery should be considered as an
alternative treatment option in patients with a BMI between
30 and 35 kg/m2 when the diabetes cannot be adequately
controlled with an optimal medical regimen, especially in
the presence of other major cardiovascular disease risk factors [5].
Multiple studies also support that BMI alone is not the
perfect predictor for severity of obesity. Recently waist circumference has been used as both a surrogate and in conjunction with BMI. Values used for waist circumference
include 40 in. (102 cm) for men and 35 in. (88 cm) for
women. When BMI and waist circumference are used
together, it has been found that those with more central obesity have a higher risk of disease and death.
Recently, a variety of weight loss devices have been introduced to the market, each with their own criteria for use. In
2001 the US Food and Drug Administration (FDA) approved
the Lap-Band™ laparoscopic adjustable gastric band for
patients with a BMI between 30 and 34.9 kg/m2 and an
obesity-­
related comorbidity. In 2015 the FDA approved
three intragastric balloon systems for patients with a BMI
ranging between 30 and 40 kg/m2. Although the FDA took
steps to lower the BMI criteria for these implantable devices,
the organization did not do so for all implantable weight loss
devices. The vagal nerve blocking therapy (VBLOC) was
approved in 2015, and the BMI requirements were identical
to the 1991 NIH guidelines. Approved in 2016, the
AspireAssist system, a gastric-emptying device, was
approved for a BMI range between 35 and 55 kg/m2.
ontraindications to Metabolic and Bariatric
C
Surgery
While there are few absolute contraindications to bariatric
and metabolic surgery, there are no absolute contraindications specific to bariatric surgery [6]. Most would be included
6
Indications and Contraindications for Bariatric Surgery
in lists of contraindications to any elective surgical procedure. Relative contraindications to surgery may include
severe heart failure, unstable coronary artery disease, end-­
stage lung disease, active cancer diagnosis or treatment, cirrhosis with portal hypertension, uncontrolled drug or alcohol
dependency, and severely impaired intellectual capacity [6].
Crohn’s disease may be a relative contraindication to RYGB
[7] and BPD [8]. Poor results following a variety of bariatric
surgical procedures have been reported in patients with lower
levels of mental capacity. This inability to comprehend the
treatment process is considered a contraindication by most
surgeons.
Patients deemed a prohibitive operative risk should not be
offered surgery including those with contraindications to
general anesthesia or uncorrectable coagulopathy. Bariatric
surgery should not be performed on patients with limited life
expectancy. Metabolic and bariatric surgery should be postponed in patients with active peptic ulcer disease until successful treatment has been confirmed. Patients who are
pregnant or who expect to be pregnant within 12–18 months
of surgery should be deferred. Patients who are on the transplant list or who have received transplants are candidates for
bariatric surgery [9]. In addition, patients must be able, willing, and motivated to comply with postoperative lifestyle
changes, dietary supplementation, and follow-up.
Specific Considerations
Extremes of Age
The 1991 NIH Consensus Conference Statement did not
include an upper age limit for surgery for obesity although
many programs and authors have restricted metabolic and
bariatric surgery to patients less than 65 years of age. While
a few publications have noted increasing age to be a risk factor for postoperative complications, both ASMBS & SAGES,
along with numerous publications, have demonstrated that
surgery can be performed safely and effectively in the older
patient population [10, 11]. A review of perioperative outcomes following bariatric surgery in nearly 50,000 patients
in the American College of Surgeons (ACS) National
Surgical Quality Improvement Program database demonstrated no significant increase in mortality in elderly patients
[10]. While improvements in longevity resulting from surgery are difficult to demonstrate, improvements in obesity-­
related comorbidities and quality of life justify performing
metabolic and bariatric surgery in appropriately selected
patients aged 65 and older.
Sufficient evidence has accumulated to consider surgery
for severe obesity an appropriate therapeutic option in properly selected adolescents [12]. Selection criteria and specific
79
considerations in the preoperative evaluation and postoperative management are addressed in greater detail in Chap. 7.
As the effects on maturation and growth are unknown,
metabolic and bariatric surgery in the preadolescent is considered experimental and is not recommended.
Psychiatric Illness
Patients referred for bariatric surgery have a higher incidence
of obsessive-compulsive disorder, substance abuse/dependency, binge eating disorder, post-traumatic stress disorder,
generalized anxiety disorder, depression, and schizophrenia
when compared to the general population [13]. Patients with
poorly managed psychiatric disorders may have a suboptimal outcome after bariatric surgery [13]. However, no consensus recommendations exist regarding preoperative
psychological evaluation [14, 15]. A diagnosis of psychopathology, including eating disorders, does not preclude metabolic and bariatric surgery [16]. Successful outcomes have
been demonstrated in patients with major depressive disorder, bipolar disorder, stable schizophrenia, and binge eating.
A preoperative psychological evaluation in patients with a
history of psychiatric illness or a positive screening is beneficial in assessing the patient’s emotional stability at the time
of surgery and ensuring adequate support during the preoperative and postoperative phases of surgery [17].
Patients with active psychosis or recent hospitalization
for psychosis, as well as patients with suicidal ideation or
recent suicidal attempts, should have surgery delayed or
postponed and treatment initiated. However, this does not
preclude a patient from becoming a surgical candidate once
the disease process is stable. Ongoing therapy for these
patients is essential in the postoperative period if deemed
appropriate for surgery.
Cirrhosis
Nonalcoholic fatty liver disease is common in severe obesity,
with histologic evidence of steatosis present in nearly 90%
of patients undergoing metabolic and bariatric surgery and
unexpected cirrhosis identified in 2% of patients [18]. Weight
loss following surgery has been demonstrated to improve the
histologic findings of steatosis and steatohepatitis. Bariatric
surgery has also shown potential to halt and even reverse
liver damage, while liver functions largely remained stable
[19]. Surgery may be safely performed in patients with stable
cirrhosis [20]. When cirrhosis is an incidental finding at surgery, it is recommended to proceed in the absence of findings
of significant portal hypertension including severe ascites
and perigastric varices. If evidence of portal hypertension is
encountered unexpectedly, the procedure should be aborted.
Essentially, patients with decompensated cirrhosis are far
80
C. DuCoin et al.
more likely to suffer adverse outcome than those with compensated disease after bariatric surgery [21].
Bariatric surgery has been reported in highly selected
patients with advanced cirrhosis in preparation for liver
transplantation. Reported cases are few and should only be
performed in tertiary centers in partnership with a liver transplant service.
Question Section
Nonambulators
References
Nonambulatory status is considered a relative contraindication to bariatric surgery by some programs. Although nonambulatory status and poor functional capacity have been
demonstrated to increase perioperative morbidity and reduce
postoperative weight loss, this increased risk does not exceed
the potential benefit in properly selected, motivated patients.
1. Gastrointestinal surgery for severe obesity: National Institutes of
Health Consensus Development Conference Statement. Am J Clin
Nutr. 1992; 55(2 Suppl):615S–9S.
2. NIH conference. Gastrointestinal surgery for severe obesity.
Consensus development conference panel. Ann Intern Med.
1991;115:956–61.
3. Mechanick JI, Youdim A, Jones DB, Garvey WT, Hurley DL,
McMahon MM, et al. Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient – 2013 update: cosponsored by American
Association of Clinical Endocrinologists, The Obesity Society, and
American Society for Metabolic & Bariatric Surgery. Surg Obes
Relat Dis. 2013;9:159–91.
4. Buchwald H. 2004 ASBS consensus conference: consensus conference statement – bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payors.
Surg Obes Relat Dis. 2005;1:371–81.
5. Dixon JB, Zimmet P, Alberti KG, Rubino F. Bariatric surgery:
an IDF statement for type 2 diabetes. Surg Obes Relat Dis.
2011;7:433–47.
1. The following should all be considered contraindications
for bariatric surgery except:
A. Inability to undergo general anesthesia
B. Limited life expectancy due to irreversible cardiopulmonary disease or inoperable malignancy
C. Inability to comprehend the risks and benefits of the
planned procedure and comply with postoperative
HIV Infection
lifestyle and dietary modifications and follow-up
D. HIV positivity
Patients with human immunodeficiency virus (HIV) infec- 2. Which of the following psychiatric conditions is a contration were once considered inappropriate candidates for metindication for bariatric surgery?
abolic and bariatric surgery due to the expected progression
A. Bipolar disorder
to acquired immunodeficiency syndrome (AIDS) and AIDS-­
B. Active psychosis or recent suicidal ideation
associated cachexia. Modern antiretroviral therapies have
C. Stable schizophrenia
dramatically reduced disease progression, extending life
D. Binge eating disorder
expectancy, often with nearly undetectable viral loads. 3. Which age, comorbid condition, and BMI is a contraindiAntiretroviral-induced lipodystrophy has contributed to the
cation to surgery?
incidence of obesity in the HIV population, with 20% of
A. 56-year-old with steatohepatitis and a BMI of 41 kg/
patients progressing from normal/overweight to obesity
m2
within 2 years of starting antiretroviral therapy.
B. 67-year-old with HTN and a BMI of 36 kg/m2
Reported case series have demonstrated the safety and
C. 47-year-old with perigastric varices and a BMI of
efficacy of metabolic and bariatric surgery in patients with
67 kg/m2
well-controlled HIV infection [22, 23]. Patients with HIV
D. 19-year-old with OSA and a BMI of 41 kg/m2
infection considered for surgery should demonstrate a stable, 4. Which procedure is approved for a BMI < 35 kg/m2?
appropriate response to antiretroviral therapy as determined
A. Sleeve gastrectomy
by CD4 counts. Preoperative and postoperative consultation
B. Intragastric balloon
with an HIV infectious disease specialist is mandatory. HIV
C. Roux-en-Y gastric bypass
and AIDS is not a contraindication to surgery.
D. AspireAssist
Conclusion
Metabolic and bariatric surgery produces durable weight
loss well beyond that achieved with medical and behavioral
therapies, with resultant improvement in obesity-related
comorbidities and quality of life. Advances in the field have
led to an expansion of the indications for surgery. Appropriate
patient selection is mandatory to ensure optimal results while
minimizing perioperative risks.
6
Indications and Contraindications for Bariatric Surgery
6. SAGES Guidelines Committee endorsed by ASMBS, Guideline
for the Clinical Application of Laparoscopic Bariatric Surgery, 25
March 2008. https://www.sages.org/publications/guidelines/guidelines-for-clinical-application-of-laparoscopic-bariatric-surgery/.
7. Pretolesi F, Camerini G, Marinari GM, et al. Crohn disease obstruction of the biliopancreatic limb in a patient operated for biliopancreatic diversion for morbid obesity. Emerg Radiol. 2006;12(3):116–8.
8. Parikh M, Duncombe J, Fielding GA. Laparoscopic adjustable gastric banding for patients with body mass index of ≤ 35 kg/m2. Surg
Obes Relat Dis. 2006;2(5):518–22.
9. Gheith O, Al-Otaibi T, Halim MA, et al. Bariatric surgery in renal
transplant patients. Exp Clin Transplant. 2017;15(Suppl 1):164–9.
10. Dorman RB, Abraham AA, Al-Refaie WB. Bariatric surgery outcomes in the elderly: an ACS NSQIP study. J Gastrointest Surg.
2012;16:35–44.
11. Lainas P, Dammaro C, Gaillard M, et al. Safety and shortterm outcomes of laparoscopic sleeve gastrectomy for patients
over 65 years old with severe obesity. Surg Obes Relat Dis.
2018. pii: S1550-­
7289(18)30122-9; https://doi.org/10.1016/j.
soard.2018.03.002.. [Epub ahead of print].
12. Michalsky M, Reichard K, Inge T, Pratt J, Lenders C. Update:
ASMBS pediatric committee best practice guidelines. Surg Obes
Relat Dis. 2012;8:1–7.
13. Kinzl JF, Schrattenecker M, Traweger C, et al. Psychosocial
predictors of weight loss after bariatric surgery. Obes Surg.
2006;16(12):1609–14.
14. Bauchowitz AU, Gonder-Frederick LA, Olbrisch ME, et al.
Psychosocial evaluation of bariatric surgery candidates: a survey of
present practices. Psychosom Med. 2005;67:825–32.
81
15. Van Hout GC, Verschure SK, van Heck GL. Psychosocial predictors
of success following bariatric surgery. Obes Surg. 2005;15:552–60.
16. LeMont D, Moorehead MK, Parish MS, Reto CS, Ritz
SJ. Suggestions for the pre-surgical psychological assessment
of bariatric surgery candidates. ASMBS 2004.; http://asmbs.
org/2012/06/pre-surgical-psychological-assessment/.
17. Pull CB. Current psychological assessment practices in obesity
surgery programs: what to assess and why. Curr Opin Psychiatry.
2010;23:30–6.
18. Marceau P, Biron S, Hould FS, Marceau S, Simard S, Thung SN,
Kral JG. Liver pathology and the metabolic syndrome X in severe
obesity. J Clin Endocrinol Metab. 1999;84:1513–7.
19. Jan A, Narwaria M, Mahawa K. A systematic review of bariatric surgery in patients with liver cirrhosis. Obes Surg.
2015;25(8):1518–26.
20. Shimizu H, Phuong V, Maia M, Kroh M, Chand B, Schauer PR,
et al. Bariatric surgery in patients with liver cirrhosis. Surg Obes
Relat Dis. 2013;9:1–6.
21. Mosko JD, Nguyen GC. Increased perioperative mortality following
bariatric surgery among patients with cirrhosis. Clin Gastroenterol
Hepatol. 2011;9(10):897–901.
22. Flancbaum L. Initial experience with bariatric surgery in asymptomatic human immunodeficiency virus-infected patients. Surg
Obes Relat Dis. 2005;1:73–6.
23. Selke S, Norris S, Osterholzer D, Fife KH, DeRose B, Gupta
SK. Bariatric surgery outcomes in HIV-infected subjects: a case
series. AIDS Patient Care STDs. 2010;24:545–50.
7
Preoperative Care of the Bariatric
Patient
Renée M. Tholey and David S. Tichansky
Chapter Objectives
1. Describe evidence-based preoperative evaluation of
the bariatric patient.
2. Discuss risk assessment to optimize patient
selection.
3. Discuss informed consent.
4. Explain the establishment of preoperative care
pathways.
Introduction
Preoperative care of the bariatric patient starts before the
patient arrives. Establishment of data-driven patient selection protocols and preoperative evaluation pathways not
only streamlines practice but also improves patient safety.
Both evaluation and individualized risk assessment are
essential for achieving best outcomes and allowing the
patient to give a truly informed consent. Ideally, comprehensive informed consent would include specific outcome
assessments based on the patient’s own metabolic acuity and
known outcomes for weight loss and comorbidity resolution. Best preoperative care will yield a comprehensive
understanding of a patient’s medical history as it pertains to
predicted outcomes, cardiac health, venous thromboembolism risk, sleep architecture and pulmonary function, gastroesophageal anatomy and Helicobacter pylori status, and
psychological ability to comply with required postoperative
recommendations. Regardless of whether a specific evaluation in question is subjective or objective, it should be standardized in an evidence-­based protocol. This chapter will
R. M. Tholey (*) ∙ D. S. Tichansky
Department of Surgery, Thomas Jefferson University Hospital,
Philadelphia, PA, USA
e-mail: Renee.Tholey@jefferson.edu
describe evidence-­based comprehensive preoperative evaluation of the bariatric patient, discuss risk assessment to optimize patient selection and informed consent, and explain
establishment of preoperative pathways.
Patient Selection
Perhaps the most important part of the preoperative evaluation is patient selection. Ideally, patient selection is a dynamic
process, rather than a single point-in-time decision. During
the initial consultation, the surgeon and care team should
take a thorough history and physical and determine if there
are any immediate contraindications to surgery. If the patient
is acceptable at that point, it only means they are acceptable
to continue the preoperative evaluation. This workup should
be conservative and data informed. Ultimately, the increase
in the acceptance of weight loss surgery by the medical community and the public is likely based on improved outcomes.
These outcomes are partially based on improved understanding of the risk and benefits of weight loss surgery.
Bariatric surgery patient selection is still based on the
National Institute of Health Consensus Statement on
Gastrointestinal Surgery for Severe Obesity. This states that
patients with a body mass index (BMI) of 40 kg/m2 or
greater, or patients with a BMI of 35 kg/m2 or greater with an
obesity-related comorbidity, will likely benefit from weight
loss surgery [1]. Please keep in mind this consensus was
reflective of a time when open surgery was prevalent and different bariatric procedures were being performed, versus the
more commonly done sleeve gastrectomy today. However,
the consensus provides a good starting point, and other organizations have elected to follow these guidelines. For example, the International Diabetes Federation Taskforce in 2011
concordantly recommended bariatric surgery be considered
for adults with a BMI ≥ 35 and Type 2 diabetes [2]. BMI
cutoffs aid in selection criteria and have been largely adopted
by insurance companies, but what about the postoperative
risks as BMI increases? Multiple studies have documented
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_7
83
84
that as the BMI increases so do the postoperative complications, especially as those BMIs became more extreme, for
example, greater than 70 kg/m2 [3]. While it seems nonintuitive to consider extreme weight an exclusion criterion for
weight loss surgery, it should raise concern that these patients
are not average-risk and require more extensive preoperative
evaluation. Several studies have also shown that male gender
and hypertension have been associated with increased
­mortality [4].
There are many more data points to examine beyond
BMI, gender, and hypertension. For example, the patient’s
age and mobility should be taken into account. Finks et al.
demonstrated that age greater than 50 and mobility limitations both independently increased the risk of a p­ ostoperative
complication in a large study of 2075 patients undergoing
gastric bypass [5]. A more recent study used the Metabolic
and Bariatric Surgery Accreditation and Quality Improvement
Program (MBSAQIP) data set and again found that immobile patients had a greater risk of mortality and multiple
complications regardless of procedure type, including both
the gastric bypass and the sleeve gastrectomy [6]. Conversely,
another study did not find any difference in perioperative
mortality in immobile patients undergoing bariatric surgery
but did find statistically significant less improvement in diabetes, hypertension, and obstructive sleep apnea in the
wheelchair bound group [7]. The question of age and mobility limitations can be determined at the programmatic level.
Should there be an age cutoff in your practice? Should you
refuse to even consider surgery on a patient who cannot
ambulate? The literature appears to mostly support an affirmative answer should you choose that path or at least an
informed discussion for the patient regarding these issues
should you choose not to enforce cutoffs.
There are other issues that predispose the patient to
increased risk. For example, venous thromboembolism
(VTE) risk must be evaluated, as well as cardiac risk and
obstructive sleep apnea. These disease processes and how
they affect the bariatric patient are discussed in depth in the
next few sections.
Cardiac Evaluation
Evaluation of cardiac status and cardiac risk preoperatively is
one of the essential elements in promoting safety in any surgical patient, but especially in morbidly obese patients. Obesity
is associated with multiple comorbidities including diabetes,
obstructive sleep apnea, dyslipidemia, and hypertension. All
of these conditions can potentially contribute to severe cardiovascular events such as heart failure, arrhythmias, and sudden cardiac death. Excessive adipose accumulation increases
cardiac workload by increasing sympathetic tone and heart
rate as well as filling pressure leading to cardiac failure [8].
R. M. Tholey and D. S. Tichansky
There is evidence that obesity has a paradoxical (protective)
effect on mortality in patients presenting with STEMI, as a
normal BMI is actually a predictor of inducible-VT [9]; however, increased BMI is also shown to predict increased cardiovascular mortality sometimes two to four times higher than
normal weight individuals [10]. Rates of cardiac arrest and
annualized mortality were found to be substantially higher in
those undergoing bariatric surgery when compared with other
forms of general surgery [11].
Preoperative workup should include history of coronary
artery disease, coronary symptoms, and risk factors (diabetes,
smoking, hypertension, etc.). Anyone over the age of 50 certainly requires cardiac evaluation. A physical and electrocardiogram (ECG) are then performed. If the patient’s age is less
than 50 with a normal ECG and no cardiac risk factors other
than obesity, they fall into the low-risk stratification for a perioperative cardiac event. Regarding ECG interpretation, bariatric patients are more likely to have an increased QT interval
which could degenerate into torsade de pointes [12]. This is
important to recognize as several drugs used perioperatively
in gastrointestinal surgery can produce prolonged QT.
Patients who have a history of heart failure, cerebrovascular disease, renal insufficiency, diabetes, or compensated
ischemic heart disease will likely require stress testing to
accurately evaluate left ventricular function according to the
American College of Cardiology (ACC) and American Heart
Association (AHA) Guidelines. Should the patient have had
a recent intervention requiring a drug-eluting stent, it would
be prudent to wait 6 months before attempting an elective
procedure to decrease the risk of stent thrombosis and a cardiac event [13]. Aspirin should be continued perioperatively
[14]. If the patient is on antiplatelet therapy, then the ACC/
AHA 2014 guidelines recommend that the management of
discontinuing antiplatelet therapies is at the discretion of the
surgeon and cardiologist and to continue aspirin if possible.
We recommend that cardiac risk assessment be left to the
expertise of a board-certified cardiologist. Bariatric surgeons
should collaborate with cardiologists using evidence-based
risk stratification. Test results should be available to anesthesia and the cardiology team chosen should be available postoperatively should the need arise.
Preoperative VTE Evaluation
The second leading cause of death after leaks in bariatric
surgery patients is pulmonary embolism (PE) and is responsible for 40–50% of fatalities. Venous thromboembolism
(VTE) rates, which include both PE and deep venous thrombosis (DVT), are reported to be between 0.25% and 3.5%.
The majority of patients, approximately 97%, have a predicted risk of less than 1% of developing VTE, but identifying the other 2.5% of patients is critical. Among 45 examined
7
Preoperative Care of the Bariatric Patient
variables, a final risk-assessment model contained 10 variables that were predictive of post-discharge VTE including
congestive heart failure, paraplegia, reoperation, dyspnea at
rest, nongastric band surgery, age ≥60, male sex, BMI
≥50 kg/m2, hospital stay ≥3 days, and operative time ≥3 h
[15]. This study utilized a risk calculator and suggested that
a calculated 0.4% risk should translate to 2 weeks of postdischarge prophylaxis, and this incorporated approximately
20% of patients. Very high risk was considered to be a calculated risk of >1% and would mandate 4 weeks of anticoagulation. The risk calculator can be found here http://
www.r-calc.com under the formulas tab. Another scoring
system, the Michigan Bariatric Surgery Collaborative,
divides patients into low (<1%), moderate (1–4%), and high
risk (>4%) and provides guidelines for chemical thromboprophylaxis based on this stratification [16].
Another recent study found that the major risk factors for
VTE included a prior history of VTE, heart failure, postoperative complications, and open surgery with VTE rates at 30
and 90 days equaling 0.34% and 0.51% [17]. They found
that no use of postoperative chemoprophylaxis was an independent predictive factor of VTE. None of these studies provide specific dosing strategies.
An even more rare concern is porto-mesenteric venous
thrombosis with median development being 14 days post-op
[18]. The most common cause of coagulopathy disorders
was protein C and/or S deficiency followed by prothrombin
gene mutation. It is therefore important to remember to take
a thorough history. Any patient with a past history of VTE or
a personal family history of the relatively uncommon hypercoagulable states such as factor V Leiden, protein C and S
deficiency, and protein C resistance also increases the risk
for VTE.
Lastly the use of inferior vena cava filters for prevention
has largely fallen out of favor at most institutions. Several
studies have demonstrated that there is no evidence to suggest that the benefits of the filter outweigh the risks [19, 20].
In addition to anticoagulants, the risk of VTE can be
decreased further by smoking cessation, increasing ambulation, and use of thromboembolism-deterrent (TED) hose and
sequential
compression
devices
perioperatively.
Anticoagulation can be proved to all patients postoperatively
for a duration of at least 14, if not 30, days or can be more
specifically individualized to each patient using the risk calculators cited above.
leep Apnea and Obesity Hypoventilation
S
Evaluation
The incidence of obstructive sleep apnea (OSA) in the morbidly obese population is quoted at anywhere from 71% to
95% depending on the patient’s BMI [21]. This places bariatric
85
patients at significant risk for ischemic heart disease, hypertension, cerebrovascular accidents, and cardiac arrhythmias. Of
particular interest to surgeons is the potential for postoperative
respiratory issues including hypoxia, hypercapnia, and bronchospasm and the need for reintubation. This risk is exacerbated by the use of anesthetics and narcotic medications in the
postoperative period. Hypercapnia as a component of obesity
hypoventilation syndrome (OHS) puts patients with this syndrome at particular risk for becoming hyper-somnolent due to
carbon dioxide narcosis.
The gold standard for evaluation is nocturnal polysomnography (PSG). During PSG, the number of apneic episodes can be quantitated. The apnea-hypopnea index (AHI)
indicates the abscess of sleep apnea if less than 5, mild OSA
for 5–15, moderate OSA for >15, and severe OSA if >30.
However, ordering PSG routinely for every bariatric patient
is not cost-effective or appropriate.
A consensus panel was formed to specifically address this
issue. The panel provided 58 statements as recommendations
for the guideline [22]. They determined that the Epworth
Sleepiness Score (ESS) should not be used as a screening
tool. They instead proposed that the STOP-Bang score be
used to stratify high-risk OSA [23]. The STOP-Bang score
includes risk factors for OSA such as snoring, daytime sleepiness, observed apnea, hypertension, age >50, neck circumference, and male gender. A score ≥3 indicates a moderate
risk of OSA. The panel also recommended venous HCO3 be
used as part of the routine screening tool for coexistence of
OHS and that OHS should be screened for in bariatric
patients with OSA (coexistence 20%). Patients with neuromuscular disorders or obstructive lung disease should be
considered as this may increase perioperative hypoventilation risk. Lastly, they stated that the oxygen desaturation
index, which is the number of times per hour of sleep that the
blood oxygen level drops below baseline, is reliable for
detection of OSA.
If sleep apnea is diagnosed, a titration study is indicated
to determine the appropriate setting of a continuous positive
airway pressure (CPAP) device that can help maintain an
open airway when the patient is asleep. Patients should be
encouraged to bring this mask with them for use in the hospital after their surgery. Another set of guidelines from May
2012 can be found on the American Society for Metabolic
and Bariatric Surgery (ASMBS) website.
Obesity hypoventilation syndrome (OHS) as mentioned
above is present in a subset of patients with OSA. The diagnosis is made in obese patients with a pCO2 >45 in the
absence of other respiratory or neuromuscular disorders. A
serum bicarbonate level of >27 is sensitive but not specific
for elevated carbon dioxide. These patients suffer more profound hypoxemia when asleep. Selected patients such as
those on home oxygen or those who have severe COPD may
need formal pulmonary function testing prior to surgery.
86
Patients with severe pulmonary dysfunction are at risk for
prolonged mechanical ventilation, tracheostomy, and higher
mortality. A good understanding of the patient’s preoperative
pulmonary function is necessary to adequately assess this
subset of patients for surgery.
valuation of Upper Gastrointestinal
E
Anatomy
The decision on whether to evaluate patients preoperatively
with an esophagogastroduodenoscopy (EGD) or an upper
gastrointestinal series (UGI) is still controversial and varies
between bariatric centers. Certainly patients undergoing
revision surgery will need both an UGI and EGD to define
the anatomy and evaluate for reflux or ulcers. If there is
severe reflux or dysmotility suspected, then, rarely, manometry and pH studies may be needed.
The controversy comes in for patients undergoing a primary bariatric procedure. Some studies suggest a preoperative EGD in all patients. An analysis of 801 patients found
abnormal EGD findings in 65% of patients, most commonly
gastritis (32%) and gastroesophageal reflux (24%) [24].
Malignancies were observed in 0.5% of patients. Helicobacter
pylori were diagnosed in 3.7%. Other studies suggest EGD
be performed only in those patients with symptoms as the
EGD is more likely to yield pathology [25].
Conversely, some studies recommend against EGD especially in patients undergoing a sleeve gastrectomy. One such
study found that 89% of scopes were completely normal, and
no cancers were found [26]. Another study evaluated the use
of a preoperative swallow and recommends against it [27].
The researchers found that the preoperative swallow does not
offer any advantage over selective intraoperative hiatal
exploration in the discovery of a hiatal hernia. In fact they
found that when there is a false positive result the surgery is
slightly prolonged.
A meta-analysis identified 532 citations and included 48
studies to reveal that the proportion of EGDs resulting in a
change in surgical management was 7.8% [28]. After removing benign findings with a controversial impact on management (hiatal hernia, gastritis, peptic ulcer), this was found to
be 0.4%. Changes in medical management were seen in
27.5%, but after eliminating Helicobacter pylori infection,
these were found to be 2.5%.
Based on the aforementioned data the following recommendations are reasonable. For symptomatic patients, EGD
is recommended. EGD is preferable to UGI and can in addition allow a biopsy for Helicobacter pylori. For asymptomatic patients undergoing a sleeve gastrectomy, an EGD is not
required. For operations in which the intestinal anatomy is
excluded, such as a RYGB or biliopancreatic diversion with
R. M. Tholey and D. S. Tichansky
duodenal switch, an EGD is recommended. All patients
undergoing revision should have evaluation of the anatomy
using EGD, UGI, or both.
Regarding Helicobacter pylori infection, an EGD is not
warranted solely for this reason as breath tests or stool antigens are available. Routine screening for Helicobacter pylori
is recommended for high-prevalence areas. When performing an EGD, it is important to keep in mind that undiagnosed
OSA may be observed when the patient undergoes conscious
sedation.
Psychological Evaluation
All patients should undergo a preoperative psychological
evaluation prior to bariatric surgery. This accomplishes several things. First, it screens for the few patients for whom
surgery is contraindicated whether due to severe psychiatric
disease such as schizophrenia or due to an inability to understand and adhere to the postoperative instructions. Second, it
identifies those patients that may have a temporary contraindication such as undertreated depression, psychosis, or bipolar disorder. These patients may require several weeks to
months of therapy to eventually proceed to surgery and reach
the best postoperative outcome.
Psychiatric screening also evaluates for those patients that
meet criteria for food addiction. One study found that 16.9%
of patients met criteria for food addiction and 15–40%
endorsed emotional eating [29]. Emotional eating may affect
outcomes although further research needs to be done in this
area. A second study found food addiction is present in 25%
of patients and that these patients had a significantly higher
prevalence of mood and anxiety disorders as well as suicidality [30]. The study did not find a link between food addiction
and current alcohol addiction. Of note psychological screening also delves into present or past alcohol or drug abuse.
Bariatric patients are at high risk of “addiction transfer” substituting food for a new addiction such as alcohol or drugs
following surgery [31].
Often patients want to use their own psychologist, and
this should be discouraged for two reasons. First, many therapists do not know how to perform a comprehensive bariatric
evaluation and may not be familiar with how to counsel our
particular patient population postoperatively. Second, if
there is a failure of therapy, therapists may be reluctant to
highlight that by rejecting someone for surgery.
We therefore recommend that a psychologist that can perform a high-quality pre-bariatric assessment be mandated
and the resulting assessment be communicated with the surgical team in a multidisciplinary fashion or via a medical
letter that summarizes the main conclusions of the
evaluation.
7
Preoperative Care of the Bariatric Patient
Informed Consent
Truly informed consent requires a consent that is individualized to each patient. Upon completion of the preoperative
workup, the benefit-risk ratio that was discussed at the
patient’s initial evaluation may have changed. If so, these
findings must be discussed with the patient to obtain fully
informed consent. Of note, Madan et al. showed that patients
often forget significant elements of their preoperative teaching and education including the most common postoperative
complications [32]. Thus, the consent process should ideally
be another full discussion of the potential risks, including
any extra risks those individualized to the patient, at their
preoperative visit. It is a physician’s legal obligation that the
patient has all of the information required to make an
informed decision.
Many institutions, and some states through legislation,
are now requiring the physician, rather than another licensed
healthcare provider such as a nurse practitioner, obtain surgical consent from the patient. Physicians should present their
outcomes in the context of the national outcomes as well as
risks and alternatives being offered to the patient. The provider obtaining consent should be familiar with the content
of the forms and should review the forms with the patient. An
individualized form specific to the procedure is preferred
over the institution’s generic consent form. The language in
the consent form should be in simple terms. As lack of patient
memory or understanding of the content of a consent form
can sometimes discredit the multiple releases theoretically
provided on signed standardized consent forms, it is essential the patient convey an understanding of what they are
signing. The patient should be given a last chance to ask any
and all questions prior to consenting. The surgeon should
perform documentation of the specifics of this discussion.
The ultimate consent privilege lies with the patient alone.
Once consent is obtained, the patient still retains the legal
and ethical right to revoke the consent as well as ask additional questions to reinforce it. It is prudent for patients to be
educated and express understanding for truly informed
consent.
Conclusion: Standardized Care Pathways
In summary, it is essential to set up practice standards such
that each patient can be approached in a standardized,
evidence-­
based fashion preoperatively to optimize care.
Recent literature reviews imply a decrease in hospital complications associated with care pathways. In one recent
comparison of 65 patients who were treated in a care pathway versus 64 patients who were not, the pathway group
had Foley catheters removed earlier, were mobilized on the
surgery day more often, used spirometers more often, and
87
had nutrition conducted in a better fashion [33]. While clinical pathways are typically used in the in-hospital setting,
they can also enhance care in the preoperative setting. It is
likely the surgeon’s data review involved in setting up these
pathways is at least partially what improves care by better
informing the surgeon’s practice. Also a comprehensive
data review followed by standardized preoperative protocols will limit errors of omission and inappropriate offerings of surgery, ensuring no patient gets left behind or falls
through the cracks while increasing efficiency and avoiding
unnecessary testing. In this manner, risk of process failure is
minimized and patient risk is reduced resulting in improved
quality of care.
Hence, this chapter recommends that the surgeon who
has not yet developed a formal preoperative pathway should
perform a focused examination of their practice patterns,
processes, and outcomes. These elements should then be
compared to what is data driven in the literature.
Discrepancies between the two should be corrected by
changes in practice or justified objectively by variations
in local standards of care. Once done, the final resolutions
should be written down and followed as a formal standardized protocol for patient selection, a multisystem preoperative evaluation, and informed consent. Gaining acceptance
by staff and collaborating physicians is often straightforward
when offered in the context of education. Lastly, these standards have to be “living” documents and periodically
reviewed to ensure that they evolve as new data emerges. As
these pathways were recommended in previous “excellence”
initiatives, they will likely be present in the new era of quality assessment and improvement.
Question Section
1. All of the following patient characteristics have been
shown to increase the risk of perioperative complications
except:
A. Male gender
B. Age >50
C. Hypertension
D. Black race
E. Inability to walk 200 ft
2. Most current data support the following except:
A. Prophylactic IVC filter in someone with a history of
DVT
B. Cardiac stress test in someone with a history of heart
failure
C. Preoperative and postoperative use of CPAP in a
patient with an AHI >15
D. Not offering surgery to someone with undertreated
bipolar disease
E. Obtaining a sleep study with a STOP-Bang score ≥3
88
3. A preoperative EGD is recommended for the following
patients:
A. Patients undergoing revision surgery
B. Patients with a history of reflux
C. Patients undergoing procedures that exclude the
stomach
D. Patients with a history of ulcer disease
E. All of the above
4. Truly informed consent involves all of the following
except:
A. Explanation of risks and benefits
B. Discussion of the patient’s individualized risk profile
C. Demonstrated fifth-grade reading level by the patient
D. Expressed understanding by the patient
E. The consent form written in simple terms
References
1. Gastrointestinal Surgery for Severe Obesity. NIH Consensus
Statement 1991. Accessed July 2018; Available from: http://consensus.nih.gov/1991/1991GISurgeryObesity084html.htm.
2. Dixon JB, et al. Bariatric surgery: an IDF statement for obese type
2 diabetes. Diabet Med. 2011;28(6):628–42.
3. Longitudinal Assessment of Bariatric Surgery, C, et al. Perioperative
safety in the longitudinal assessment of bariatric surgery. N Engl J
Med. 2009;361(5):445–54.
4. DeMaria EJ, Portenier D, Wolfe L. Obesity surgery mortality risk
score: proposal for a clinically useful score to predict mortality
risk in patients undergoing gastric bypass. Surg Obes Relat Dis.
2007;3(2):134–40.
5. Finks JF, et al. Predicting risk for serious complications with bariatric surgery: results from the Michigan bariatric surgery collaborative. Ann Surg. 2011;254(4):633–40.
6. Higgins RM, et al. Preoperative immobility significantly impacts
the risk of postoperative complications in bariatric surgery patients.
Surg Obes Relat Dis. 2018;14(6):842–8.
7. Sharma G, et al. Comparative outcomes of bariatric surgery in
patients with impaired mobility and ambulatory population. Obes
Surg. 2018;28(7):2014–24.
8. Lavie CJ, Milani RV, Ventura HO. Obesity and cardiovascular disease: risk factor, paradox, and impact of weight loss. J Am Coll
Cardiol. 2009;53(21):1925–32.
9. Samanta R, et al. Influence of BMI on inducible ventricular tachycardia and mortality in patients with myocardial infarction and
left ventricular dysfunction: the obesity paradox. Int J Cardiol.
2018;265:148–54.
10. Litwin SE. Which measures of obesity best predict cardiovascular
risk? J Am Coll Cardiol. 2008;52(8):616–9.
11. Poirier P, et al. Cardiovascular evaluation and management of
severely obese patients undergoing surgery: a science advisory from
the American Heart Association. Circulation. 2009;120(1):86–95.
12. Grandinetti A, et al. Association of increased QTc interval with
the cardiometabolic syndrome. J Clin Hypertens (Greenwich).
2010;12(4):315–20.
13. Wijeysundera DN, et al. Risk of elective major noncardiac surgery
after coronary stent insertion: a population-based study. Circulation.
2012;126(11):1355–62.
14. Oscarsson A, et al. To continue or discontinue aspirin in the perioperative period: a randomized, controlled clinical trial. Br J Anaesth.
2010;104(3):305–12.
R. M. Tholey and D. S. Tichansky
15. Aminian A, et al. Who should get extended thromboprophylaxis after bariatric surgery?: a risk assessment tool to guide
indications for post-discharge pharmacoprophylaxis. Ann Surg.
2017;265(1):143–50.
16. Finks JF, et al. Predicting risk for venous thromboembolism with
bariatric surgery: results from the Michigan bariatric surgery collaborative. Ann Surg. 2012;255(6):1100–4.
17. Thereaux J, et al. To what extent does posthospital discharge chemoprophylaxis prevent venous thromboembolism after bariatric
surgery?: results from a nationwide cohort of more than 110,000
patients. Ann Surg. 2018;267(4):727–33.
18. Karaman K, et al. Porto-mesenteric venous thrombosis after laparoscopic sleeve gastrectomy: a case report and systematic review of
the 104 cases. Obes Res Clin Pract. 2018;12(3):317–25.
19. Birkmeyer NJ, et al. Preoperative placement of inferior vena
cava filters and outcomes after gastric bypass surgery. Ann Surg.
2010;252(2):313–8.
20. Rowland SP, et al. Inferior vena cava filters for prevention of venous
thromboembolism in obese patients undergoing bariatric surgery: a
systematic review. Ann Surg. 2015;261(1):35–45.
21. Lopez PP, et al. Prevalence of sleep apnea in morbidly obese
patients who presented for weight loss surgery evaluation: more
evidence for routine screening for obstructive sleep apnea before
weight loss surgery. Am Surg. 2008;74(9):834–8.
22. de Raaff CAL, et al. Perioperative management of obstructive sleep
apnea in bariatric surgery: a consensus guideline. Surg Obes Relat
Dis. 2017;13(7):1095–109.
23. Chung F, Abdullah HR, Liao P. STOP-bang questionnaire: a
practical approach to screen for obstructive sleep apnea. Chest.
2016;149(3):631–8.
24. Wolter S, et al. Upper gastrointestinal endoscopy prior to bariatric
surgery-mandatory or expendable? An analysis of 801 cases. Obes
Surg. 2017;27(8):1938–43.
25. Abd Ellatif ME, et al. Place of upper endoscopy before and after
bariatric surgery: a multicenter experience with 3219 patients.
World J Gastrointest Endosc. 2016;8(10):409–17.
26. Salama A, et al. Is routine preoperative esophagogastroduodenoscopy screening necessary prior to laparoscopic sleeve gastrectomy?
Review of 1555 cases and comparison with current literature. Obes
Surg. 2018;28(1):52–60.
27. Goitein D, et al. Barium swallow for hiatal hernia detection is
unnecessary prior to primary sleeve gastrectomy. Surg Obes Relat
Dis. 2017;13(2):138–42.
28. Bennett S, et al. The role of routine preoperative upper endoscopy
in bariatric surgery: a systematic review and meta-analysis. Surg
Obes Relat Dis. 2016;12(5):1116–25.
29. Miller-Matero LR, et al. To eat or not to eat; is that really the question? An evaluation of problematic eating behaviors and mental
health among bariatric surgery candidates. Eat Weight Disord.
2014;19(3):377–82.
30. Benzerouk F, et al. Food addiction, in obese patients seeking bariatric surgery, is associated with higher prevalence of current mood
and anxiety disorders and past mood disorders. Psychiatry Res.
2018;267:473–9.
31. Steffen KJ, et al. Alcohol and other addictive disorders following
bariatric surgery: prevalence, risk factors and possible etiologies.
Eur Eat Disord Rev. 2015;23(6):442–50.
32. Madan AK, Tichansky DS, Taddeucci RJ. Postoperative laparoscopic bariatric surgery patients do not remember potential complications. Obes Surg. 2007;17(7):885–8.
33. Ronellenfitsch U, et al. The effect of clinical pathways for bariatric surgery on perioperative quality of care. Obes Surg.
2012;22(5):732–9.
8
Anesthetic Considerations
Hendrikus J. M. Lemmens, John M. Morton, Cindy M. Ku,
and Stephanie B. Jones
Chapter Objectives
1. Provide the anesthesiologist with a practical
approach to the problems that require special consideration in patients with severe obesity.
2. Identify comorbidities that require preoperative
evaluation.
3. Evaluate anesthetic and analgesic options.
4. Discuss how obesity affects airway management
and how bariatric surgery affects fluid
management.
5. Review postoperative considerations.
Introduction
Anesthetic management of the patient with severe obesity
(SO) presenting for bariatric surgery differs significantly
from that of the normal-weight patient undergoing similar
procedures. Well-planned and rational management of
patients undergoing bariatric surgery requires detailed
knowledge of how severe obesity affects anesthesia care.
The mechanical effects of increased body mass index (BMI)
as well as the physiological changes and associated comorbidities all impact safe management and decision-making by
the anesthesiologist. The aim of this chapter is to provide a
practical approach to the problems that require special consideration in patients with severe obesity.
H. J. M. Lemmens
Multispecialty Division, Department of Anesthesia, Stanford
University School of Medicine, Stanford, CA, USA
J. M. Morton
Bariatric and Minimally Invasive Surgery Division, Yale School of
Medicine, New Haven, CT, USA
C. M. Ku · S. B. Jones (*)
Department of Anesthesia, Critical Care and Pain Medicine, Beth
Israel Deaconess Medical Center, Boston, MA, USA
e-mail: sbjones@bidmc.harvard.edu
Preoperative Evaluation
A full assessment for medical conditions that can affect perioperative complications must be performed. Preoperative
“clearance” by a primary care physician or allied health professional and surgical consultation notes may not include
information pertinent to anesthesia care, and while electronic
health records can be helpful in information sharing, errors
and gaps in information may be perpetuated. Organ dysfunction identified in the preoperative evaluation should be thoroughly evaluated and optimized before proceeding with this
elective surgery.
espiratory Issues Relevant to Anesthesia
R
Management
The effect of obesity on the respiratory system decreases the
margin of safety of anesthetic agents and increases the risk of
respiratory failure in the perioperative period [1]. Respiratory
failure is a life-threatening complication after bariatric surgery, with a reported incidence of 1.35–8% [2, 3]. Risk factors that increase the likelihood of respiratory failure are
congestive heart failure, open surgery, chronic renal failure,
peripheral vascular disease, male gender, age >50 years,
alcohol abuse, chronic lung disease, diabetes, and smoking
[2]. The presence of metabolic syndrome significantly
increases the odds of postoperative pulmonary adverse
events [4, 5].
At baseline, subjects with severe obesity may be mildly
hypoxemic, with higher respiratory rates and lower tidal volumes. The compliance of the respiratory system is reduced
and work of breathing increased. Functional residual capacity (FRC) and expiratory reserve volume (ERV) decrease
exponentially with increasing BMI, with the greatest rate of
change in the overweight (BMI 25.0–29.9 kg/m2) and mildly
obese (BMI 30.0–34.9 kg/m2). In sitting subjects with a BMI
of 30 kg/m2, FRC and ERV are 75 and 47%, respectively, of
the values for a person with a BMI of 20 kg/m2 [6]. In anes-
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_8
89
90
will assist in that regard. Strategies such as reverse
Trendelenburg positioning (when appropriate for the surgical
procedure), periodic intraoperative lung recruitment, avoiding reabsorption atelectasis by keeping FiO2 <0.8, using less
than 8 ml/kg of LBW for volume-controlled mechanical ventilation to avoid volutrauma, and utilizing incentive spirometry and noninvasive ventilation in the PACU may help prevent
respiratory complications in the patient with obesity.
ardiovascular Issues Relevant to Anesthesia
C
Management
80
70
60
50
Blood Volume (mL/kg)
90
100
The increased tissue mass of the patient with severe obesity
needs to be perfused, leading to an increased total blood volume. While the total blood volume is increased, on a per kg
total body weight basis, blood volume is decreased. Blood
volume per kg total body weight (TBW) decreases exponentially from 70 ml/kg TBW at a BMI of 22 kg/m2 to 40 ml/kg
TBW at a BMI of 65 kg/m2 (Fig. 8.1) [16]. If 70 ml/kg TBW
is used for blood volume calculation, blood volume is overestimated, and under-transfusion of blood products may
occur when significant blood loss during surgery is encountered. The increased total blood volume of the patient with
SO results in an increased cardiac output (CO). CO increases
from 4 L/min at a BMI of 20 kg/m2 to more than 6 L/min at
BMIs greater than 40 kg/m2. CO affects early pharmacokinetics, the front-end kinetics of drug distribution, and dilution in the first minutes after administration. An increased
CO decreases the fraction of drug distributed to the brain and
increases the rate of redistribution, which will result in lower
40
thetized supine patients, the effect of BMI on FRC is more
pronounced, and tidal volume is more likely to fall within
closing capacity, promoting shunting [7]. In addition to the
changes in respiratory mechanics and lung volumes, the
prevalence of obstructive sleep apnea (OSA) in bariatric
patients can be as high as 75% [8]. Of those with OSA and
severe obesity, up to 20% may have obesity hypoventilation
syndrome (OHS), which is characterized by daytime awake
hypercapnia, hypoxemia, and elevated HCO3− [9]. It is
important for anesthesiologists to recognize patients with
OHS since it is associated with severe upper airway obstruction, restrictive lung disease, blunted central respiratory
drive, pulmonary hypertension, and increased mortality.
Before bariatric surgery, these patients should be referred to
sleep medicine for polysomnography and positive airway
pressure (PAP) titration. An echocardiogram should be performed to assess right ventricular function and pulmonary
hypertension. Poor right ventricular function and high mean
pulmonary artery pressures (>35 mmHg) are associated with
an unacceptable anesthesia-related perioperative mortality
risk. Perioperative precautions for OHS include prudent airway management, rapid emergence, monitoring for ventilatory impairment, and early resumption of PAP therapy.
The compromised respiratory status of the patient with
obesity requires special precautions to prevent oxygen desaturation at induction of anesthesia, during surgery, and in the
postoperative phase. After preoxygenation with 100% oxygen and complete denitrogenation, an anesthetized supine
paralyzed SO patient’s oxygen saturation decreases from
100% to 90% in about 2.5 min [10]. Premedication with anxiolytics or opioids depresses spontaneous ventilation and
should be minimized. Preoxygenation techniques delaying
the onset of hypoxia should be used: the 25° head-up position may add a minute to the safe apnea time [11], the use of
supplemental oxygen or high flow oxygen decreases the rate
of desaturation [12], and application of noninvasive positive
airway pressure during induction of anesthesia can increase
safe apnea time by 50% [13] while improving oxygenation
during maintenance of anesthesia [14].
Immediately after induction of anesthesia, atelectasis
develops mainly in the dependent areas of the lung. Atelectasis
results in pulmonary shunting and hypoxemia. Release of
inflammatory cytokines associated with atelectasis may contribute to postoperative ventilator-associated lung injury such
as pneumonia and respiratory failure. In the patient with
severe obesity, ventilatory strategies to prevent atelectasis
may require recruitment maneuvers and positive end-expiratory pressure (PEEP) values higher than 10 cm H2O. Although
high PEEP levels combined with pneumoperitoneum will
decrease venous return and can induce hypotension, PEEP
levels up to 20 cm H2O are generally tolerated in wellhydrated patients [15]. The trend toward maintaining preoperative normovolemia as part of enhanced recovery protocols
H. J. M. Lemmens et al.
20
30
40
50
Body Mass Index (kg/m2)
60
70
Fig. 8.1 Effect of BMI on blood volume in mL per kg TBW. Blood
volume (mL per kg TBW) for a patient with a given BMI (BMIp) can be
calculated using the equation:
70
BMIp
22
Pharmacological Considerations
Until recently, obese subjects have been routinely excluded
from clinical trials to obtain regulatory approval for investigational drugs. This has resulted in package insert dosage
recommendations based on total body weight, valid for
normal-­weight patients but not for the obese. Severe obesity
alters the pharmacokinetics and drug response of anesthetic
agents. In addition, the decreased pulmonary and cardiac
reserve of the patient with SO significantly decreases the
margin of safety of anesthetic agents. Incorrect dosing can
increase the rate of perioperative complications.
Obesity is not only associated with an increase in tissue
mass but also changes in body composition and tissue perfusion. Fat mass and lean body mass both increase, but the
increase is not proportional. The percentage of lean body
mass as a percentage of total body weight decreases as BMI
increases (Fig. 8.2). The different ratio of lean body weight
(LBW) to fat weight at different BMIs has a significant
impact on drug distribution. Fat perfusion is also altered at
different BMIs. At low BMIs, fat is relatively well perfused;
at high BMIs fat is poorly perfused. Because of the different
ratio of fat to lean body weight at different BMIs and changes
in fat perfusion, the effect of obesity on drug distribution into
the different tissues is poorly understood.
The increased CO of the patient with SO increases the dose
requirements of induction agents, but not to the level of total
body weight. In patients with normal cardiac function, CO is
Kg
100
150
Total Body Weight
Lean Body Weight
50
concentrations, faster awakening, and increased dose requirement. This phenomenon has important implications for the
induction dose of intravenous anesthetic agents.
The most prevalent comorbidity in bariatric patients is
hypertension. Obesity may lead to abnormal cardiac function
through pathways that are associated with or independent of
hypertension. The mechanisms of decreased cardiac contractility associated with obesity independent of hypertension
are related to metabolic dysregulation, but not completely
understood. The increased body mass, metabolic syndrome,
insulin resistance, type 2 diabetes, and physical inactivity all
contribute to systolic and diastolic dysfunction even in otherwise healthy young obese subjects. This may eventually
progress to left and/or right heart failure. The combination of
super obesity (BMI > 50 kg/m2) with hypertension and diabetes is associated with a twofold increased risk of death and
adverse cardiac events in the perioperative phase [5].
Congestive heart failure, peripheral vascular disease, and
chronic renal failure are predictive factors of increased in-­
hospital mortality after surgery. Obesity is also associated
with an increased risk of atrial fibrillation and ventricular
ectopy. Cardiac events can be a significant cause of 30-day
mortality after bariatric surgery.
91
200
Anesthetic Considerations
0
8
Fat Weight
20
30
40
50
60
70
BMI (kg/m2)
Fig. 8.2 Changes in body composition for a typical frame 160-cm-tall
female who increases her BMI. Lean body weight was calculated using
the equations published by Janmahasatian et al. [17]. Fat weight was
calculated by subtracting lean body weight from total body weight
highly correlated to lean body weight, more so than total body
weight or other variables. Therefore, lean body weight and CO
are more appropriate dosing scalars than total body weight.
Total body weight dosing of induction agents will result in
overdosing and side effects such as hypotension.
Numerous pharmacokinetic studies have shown that
clearance, the most relevant pharmacokinetic parameter for
maintenance dosing, is linearly related to lean body weight
but not total body weight. This implies that lean body weight
is the appropriate dosing scalar, not only for determining
induction and loading doses but also for maintenance doses.
Recommended dosing scalars for several anesthetic agents
are summarized in Table 8.1.
Induction Agents
Thiopental
Although thiopental is part of the World Health Organi­
zation’s “Essential Drugs List,” it is currently unavailable in
the United States. Nevertheless, thiopental is an ideal anesthetic induction agent with arguably less side effects than
propofol. Immediately after intravenous (IV) administration,
thiopental distributes to highly perfused tissues such as the
brain, lung, liver, heart, kidney, gut, and pancreas. After an
anesthetic induction dose, redistribution into the muscle
depletes thiopental from the brain and terminates the anesthetic effect within 5–10 min. The increased CO associated
with severe obesity has a significant effect on the thiopental
dose requirement. After a thiopental induction dose of
250 mg, the higher CO of a patient with severe obesity results
in peak arterial concentrations up to 50% lower than those of
92
H. J. M. Lemmens et al.
Table 8.1 Recommended dosing scalars for morbidly obese patients
Dosing
scalar
Induction agents
Thiopental
LBW
Propofol
LBW
Etomidate
LBW
Opioids
Fentanyl
Alfentanil
Sufentanil
Remifentanil
LBW
LBW
LBW
LBW
Muscle relaxants
Succinylcholine TBW
Rocuronium
Vecuronium
Cisatracurium
Atracurium
LBW/
IBW
LBW/
IBW
LBW/
IBW
LBW/
IBW
Comments
For continuous infusion or
maintenance dosing TBW
Use in septic patients is controversial;
may cause adrenal suppression
Titrate to effect
TBW dosing may result in significant
hypotension and/or bradycardia
The incidence of myalgia is low in
morbidly obese patients
IBW dosing results in shorter duration
of action
Fast administration may result in
histamine release
LBW lean body weight, TBW total body weight, IBW ideal body weight
a lean subject. Thiopental dose adjusted according to lean
body mass or increased CO results in the same peak plasma
concentration as for a normal size person.
Propofol
In current practice, propofol is the induction agent of choice
for obese patients. CO has a significant effect on peak plasma
concentration and duration of effect. After a bolus dose for
induction of anesthesia, propofol’s peak plasma concentration is inversely related to CO. In addition, a higher CO is
associated with a faster wake-up time. For COs of 8.5, 5.5,
and 2.5 L/min, recovery of consciousness is predicted to
occur at 2.9, 8.6, and 18.7 min, respectively. CO does not
affect onset time. LBW is a more appropriate weight-based
scalar than TBW for propofol induction of general anesthesia in patients with SO [18]. Patients in whom anesthesia was
induced with propofol dose based on LBW required similar
doses of propofol and had similar times to loss of consciousness compared to nonobese control patients given propofol
based on TBW.
Etomidate
Etomidate is less likely to cause a significant decrease in
blood pressure than thiopental or propofol. Thus, in patients
with significant heart disease or hemodynamically unstable
patients, anesthetic induction with etomidate may be a better
choice. The pharmacology of etomidate in obese patients has
not been studied, but an induction dose based on lean body
mass and CO can be justified given the pharmacokinetic and
pharmacodynamic similarities of etomidate, thiopental, and
propofol.
Etomidate transiently suppresses corticosteroid synthesis
in the adrenal cortex by reversibly inhibiting 11-beta-­
hydroxylase. This suppressant effect on steroid synthesis is
probably clinically insignificant after a single dose used for
induction of anesthesia. However, in patients with sepsis, the
use of etomidate for induction of anesthesia is controversial.
Other side effects are pain at injection, myoclonus, and a
high incidence of postoperative nausea and vomiting.
Dexmedetomidine
Dexmedetomidine is used as a sedative agent with both anxiolytic and analgesic effects. Dexmedetomidine is a selective
alpha-2 adrenergic receptor agonist. Respiratory depression
is minimal, but dexmedetomidine potentiates the respiratory
depressant effect of opioids and benzodiazepines. The short
distribution half-life (8 min) and relatively short elimination
half-life (2 h) make it suitable for titration by continuous
infusion. The sympatholytic effect of dexmedetomidine
decreases norepinephrine release and will decrease arterial
blood pressure and heart rate. This may result in severe
hypotension in hypovolemic patients and severe bradycardia
in patients with heart block. Another side effect is dry mouth,
which when used during fiber-optic intubation is an advantage. Postoperatively, dexmedetomidine reduces shivering.
During open gastric bypass surgery when used instead of
fentanyl to supplement desflurane, a loading dose of dexmedetomidine, 0.5 mcg/kg, given over 10 min followed by an
infusion of 0.4 mcg/kg/h, resulted in significantly lower arterial blood pressure and heart rate, shorter time to tracheal
extubation, lower pain scores, and less use of morphine and
antiemetics in the postanesthesia care unit (PACU). A
­systematic review of 30 studies with intraoperative use of
dexmedetomidine showed a decrease in morphine consumption, lower pain scores, and lower rates of PONV [19]. For
adjunctive use during laparoscopic bariatric surgery, a lower
infusion rate (0.2 mcg/kg/min) is recommended to reduce
the risk of cardiovascular side effects.
Opioids
Compared to fentanyl and its analogues alfentanil, sufentanil, and remifentanil, the longer-acting opioids morphine
and hydromorphone are not potent enough to effectively
8
Anesthetic Considerations
block somatic and autonomic responses during surgery. In
addition, the drowsiness and sleepiness at emergence associated with morphine and hydromorphone administration are
unwanted in the morbidly obese. Therefore, their use during
surgery is best avoided. If necessary, morphine should be
dosed with IBW [20] and titrated to effect with close respiratory monitoring, as opioid-related adverse events remain a
significant complication in SO patients [21].
Fentanyl
Fentanyl has a fast onset of effect (5 min) and effectively
blocks somatic and autonomic responses during surgery.
Fentanyl is probably the most commonly used opioid during
bariatric surgery. The higher CO in patients with obesity will
result in significantly lower fentanyl concentrations in the
early phase of distribution. Pharmacokinetic parameters of
normal size persons will overpredict measured fentanyl concentrations in patients with obesity. The clearance of fentanyl is higher in patients with obesity and increases
nonlinearly with increasing TBW, but linearly with lean
body weight (LBW). These data suggest loading and maintenance doses of fentanyl should be based on LBW. However,
obesity increases the probability of respiratory depression in
the perioperative period, and fentanyl and other opioid
administration should be carefully titrated according to individual patient’s need.
Sufentanil
Sufentanil is highly lipophilic and has an onset time of
approximately 5 min. Like fentanyl, pharmacokinetic parameters of normal size persons will overpredict measured sufentanil concentrations in patients with severe obesity.
Alfentanil
Alfentanil has a fast-onset time of approximately 1 min. The
higher CO in patients with obesity will result in significantly
lower alfentanil concentrations in the early phase of distribution. Alfentanil is less lipid soluble than fentanyl or sufentanil and has a smaller volume of distribution. No data on the
effects of obesity on the pharmacokinetics of alfentanil have
been published.
Remifentanil
Remifentanil’s physicochemical properties result in a
rapid-­onset time of approximately 1 min. Bolus admin-
93
istration in awake patients may result in severe bradycardia, hypotension, and muscle rigidity. Plasma and
tissue esterases rapidly hydrolyze remifentanil, resulting
in an extraordinary high clearance (3 L/min) unaffected by
hepatic or renal insufficiency. The fast-onset time and high
clearance make remifentanil especially suitable for administration by continuous infusion. Volumes and clearances
not normalized for weight are similar in obese and nonobese patients and do not correlate with TBW, but correlate significantly with LBW. Therefore, in the patient with
obesity, dosing of remifentanil based on TBW will result
in concentrations higher than those needed for clinical purposes and an increased incidence of side effects such as
hypotension and bradycardia. Remifentanil dosing based
on LBW will result in plasma concentrations similar to
those in normal-weight subjects when dosed according to
TBW. After discontinuation of administration, drug effects
terminate rapidly, within 5–10 min. Therefore, when postoperative pain is anticipated, alternative analgesics should
be administered prior to remifentanil’s discontinuation.
Remifentanil may also induce postoperative hyperalgesia, requiring higher than normal dosages of longer-acting
opioids to effectively treat pain, putting the patient with
severe obesity at higher risk of opioid complications such
as respiratory depression.
Inhaled Anesthetics
Isoflurane
The solubility of inhaled anesthetic agents in fat and the
increased fat mass of the patient with obesity would theoretically result in an increased anesthetic uptake, especially with
more fat-soluble anesthetics such as isoflurane. However,
blood flow per kg of fat tissue decreases significantly with
increasing BMI, therefore limiting uptake. In addition, the
time constants (the time to reach 63% of equilibrium) for
equilibrium with fat are long (2110 and 1350 min for
­isoflurane and desflurane, respectively). The decreased fat
perfusion and relatively long time constants will diminish
the effect of the increased fat mass on the uptake of inhalational agents. During routine clinical practice, the effect of
BMI on the uptake of desflurane and the more lipid-soluble
isoflurane is clinically insignificant.
The concern that isoflurane prolongs emergence from
anesthesia in patients with obesity due to its lipid solubility
could also not be substantiated. Obese and nonobese patients
emerged from anesthesia at similar times (7 min) after 0.6
MAC isoflurane administration for procedures lasting 2–4 h.
After termination of isoflurane administration, the time to
extubation can be decreased significantly by increasing alveolar ventilation using an isocapnic hyperpnea method [22].
94
Desflurane
The effect of BMI on desflurane uptake is insignificant, and
obese and nonobese patients emerge from anesthesia equally
rapidly (4 min) after 0.6 MAC desflurane administration for
procedures lasting 2–4 h. Several studies in patients with
obesity have compared desflurane and sevoflurane with variable results, finding either a faster awakening with desflurane
or no difference [23, 24].
Sevoflurane
Sevoflurane appears to provide a slightly more rapid uptake
and elimination of anesthetic in patients with severe obesity
than does isoflurane. Fluoride, a metabolite of sevoflurane, in
concentrations greater than 50 mmol/L, can be nephrotoxic.
In addition, sevoflurane is degraded to compound A by carbon dioxide absorbers containing a strong base such as barium hydroxide lime or to a lesser extent by soda lime.
Reductions in fresh gas flow as well as an increase in temperature in the gas mixture will increase compound A concentrations. Albuminuria, glycosuria, and enzymuria are
associated with inhaled doses of compound A greater than
160 ppm/h. In the few studies in patients with renal impairment, no evidence of further worsening of renal function
could be demonstrated after sevoflurane administration.
However, the safety of sevoflurane in patients with impaired
renal function is unclear.
Neuromuscular Blocking Agents
Succinylcholine
Succinylcholine is a depolarizing muscle relaxant. It is a
nicotinic acetylcholine receptor agonist causing fasciculations followed by flaccid paralysis via depolarization of
the motor end plate. Succinylcholine has the fastest onset
and shortest duration of action of all muscle relaxants—
excellent properties to achieve intubation of the trachea
rapidly. If difficulty is encountered managing the airway of
the patient, return of neuromuscular function and spontaneous ventilation will occur within 5–7 min. Maximum
effect and duration of action are determined by the extracellular fluid volume and elimination by the plasma
enzyme butyrylcholinesterase (also known as pseudocholinesterase). Extracellular fluid volume and activity of
butyrylcholinesterase both increase with increasing
BMI. Therefore, patients with severe obesity have larger
succinylcholine requirements than normal size patients.
Succinylcholine, 1 mg/kg total body weight, will result in
complete neuromuscular blockade and excellent intuba-
H. J. M. Lemmens et al.
tion conditions in the obese. Lower doses are associated
with poor intubating conditions due to incomplete neuromuscular block. Succinylcholine use is associated with
increases in potassium and myalgia. The incidence of succinylcholine-induced myalgia is low in morbidly obese
patients.
Rocuronium
Rocuronium is a nondepolarizing muscle relaxant that can
be used as an alternative to succinylcholine for rapid
sequence intubation. A dose of 1.2 mg/kg ideal body weight
(IBW) provides excellent or good intubating conditions 60 s
after administration. However, the time to reappearance of
T1 is 52 min. Rocuronium maintenance dosing based on lean
body weight has not been studied, but dosing on the basis of
ideal body weight is appropriate. Maximum effect and recovery times of rocuronium and all other muscle relaxants are
highly variable; therefore, continuous monitoring of the
degree of neuromuscular blockade is recommended. The use
of rocuronium for rapid sequence intubation has become
more common with the wider availability of sugammadex
(below) for urgent reversal, if needed.
Vecuronium
The pharmacokinetic parameters uncorrected for weight are
similar between obese and nonobese subjects. In obese subjects receiving 0.1 mg/kg vecuronium based on TBW, recovery times from neuromuscular blockade were approximately
60% longer than in normal-weight control subjects. The prolonged recovery from neuromuscular blockade in the obese
patients can be explained by the larger dose of vecuronium.
The similar pharmacokinetics will result in higher
vecuronium plasma concentration in the patient with obesity.
With higher doses and higher plasma concentrations,
­recovery from neuromuscular blockade will occur at a time
when plasma concentration decreases more slowly, instead
of the more rapid decline after a smaller dose when recovery
occurs earlier during the distribution phase. To avoid overdose in the patient with obesity, administering vecuronium
on the basis of IBW is recommended.
Cisatracurium
Cisatracurium is eliminated via Hoffman degradation, a
pathway independent from kidney or liver function. As
expected, TBW dosing results in a prolonged duration of
action when compared with a control group of normal body
weight patients. When administered to patients with severe
8
Anesthetic Considerations
obesity based on IBW, the duration of action of cisatracurium was decreased when compared to normal size patients.
95
Monitoring
In the relatively healthy patient undergoing bariatric surgery,
noninvasive monitoring during anesthesia will suffice. There
Reversal Agents of Neuromuscular Blockade
are no data showing that invasive monitoring improves outcome in patients with severe obesity without advanced carRapid and complete recovery from neuromuscular blockade diac or pulmonary disease [28].
is particularly important in the morbidly obese patient.
During surgery, a combination of lead II and lead V5 elecResidual neuromuscular blockade will further compromise trocardiographic monitoring has a sensitivity of 80% to
respiratory function in the immediate postoperative phase. detect myocardial ischemia. Lead V4 and V5 monitoring has
Obesity is a risk factor for residual blockade [25]. a sensitivity of 90%. The best combination is lead V4, V5,
Acceleromyography should be used preferentially over tra- and II monitoring, resulting in a sensitivity of 98%. Cardiac
ditional twitch monitoring when monitoring and reversing abnormalities such as rhythm and conduction problems
neuromuscular blockade [26] and has been shown to signifi- occur frequently in the patient with severe obesity. Atrial
cantly reduce the incidence of residual block.
fibrillation is the most commonly occurring abnormal
rhythm, especially in patients with OSA. If during surgery or
in the postoperative phase atrial fibrillation develops, atrial
Neostigmine
distension due to fluid overload can be the causative factor.
Prolonged QT interval syndrome is a precursor of torsades
The dose-response relationship of neostigmine for neuro- de pointes, which can result in sudden cardiac death. Many
muscular blockade reversal in morbidly obese patients has drugs used in the perioperative phase such as ondansetron,
been poorly studied. When vecuronium is reversed with neo- sevoflurane, and methadone prolong the QT interval and
stigmine at 25% recovery of twitch height, there is no differ- should not be used in patients with prolonged QT interval
ence between normal size and morbidly obese patients in syndrome.
A well-fitting blood pressure cuff encircling at least 75%
time to a recovery of train-of-four (TOF) ratio to 0.7 (3.8–
4.8 min). However, recovery time to adequate reversal (a of the arm should be used to obtain reliable blood pressure
train-of-four ratio of 0.9) is four times slower in morbidly measurements. A blood pressure cuff that is too large will
obese patients (25.9 versus 6.9 min). The recommended dose underestimate blood pressure. A cuff that is too small will
of neostigmine is 0.04–0.08 mg/kg, not to exceed a total dose overestimate blood pressure. Special conical-shaped cuffs
of 5 mg. A deep neuromuscular block (TOF ratio of 0) can- for morbidly obese patients are available. If a blood pressure
cuff cannot be fitted on the upper arm, a standard blood presnot be reversed with neostigmine.
sure cuff placed on the forearm is a useful alternative. Lower
arm measurements overestimate blood pressure. The threshold to place an intra-arterial catheter should be low since
Sugammadex
invasive blood pressure measurement is accurate and comSugammadex is the first selective relaxant-binding agent plications of radial arterial line placement are rare.
The recommendation that a central venous line be inserted
specifically designed to bind and encapsulate rocuronium
and vecuronium. It can provide immediate reversal of an routinely in obese patients is not valid. Peripheral venous
intubating dose of rocuronium at 16 mg/kg. The muscle access can be more difficult, but this is not a definitive indirelaxant is bound with high affinity within sugammadex’s cation for a central line. If placement of a peripheral venous
core and cannot bind to the acetylcholine receptor at the neu- catheter is problematic, ultrasound can be used to locate a
romuscular junction. The bound complex is excreted by the peripheral vein. Central venous access via the internal jugukidneys at a rate equal to the glomerular filtration rate. Unlike lar vein is associated with a lower complication rate than
the acetylcholinesterase inhibitor neostigmine, sugammadex subclavian vein puncture. Positioning the patient on a ramp
has no effect at the receptor level, and there is no need to similar to the positioning used for tracheal intubation with a
coadminister antimuscarinic agents such as atropine or gly- roll under the shoulders will maximize neck exposure and
copyrrolate. Deep neuromuscular blockade (TOF =0, post-­ facilitate placement. Thereafter, the patient can be placed in
tetanic count of 1–2) can be reversed with 4 mg/kg Trendelenburg position as tolerated. Insertion of a central
sugammadex at IBW [27], and at a moderate level of block- venous catheter under ultrasound guidance facilitates correct
placement and is currently the recommended approach [29].
ade (TOF = 2), 2 mg/kg is recommended.
The value of the central venous pressure (CVP) measureSugammadex was approved for use in the European
Union in 2008 and subsequently approved by the US Food ment does not necessarily reflect adequacy of circulating
blood volume or response to fluid loading. A decreased CVP
and Drug Administration (FDA) in 2015.
96
can reflect venodilation or hypovolemia. An increased CVP
can reflect decreased cardiac pump function, increase in thoracic pressure and/or pericardial pressure, or increased pulmonary artery resistance. In contrast to the CVP pressure
readings, the shape of the CVP waveform can be highly diagnostic. For example, the presence of large v waves, which are
diagnostic for tricuspid regurgitation, may indicate the presence of pulmonary hypertension and right heart failure.
Intravascular volume status is difficult to assess in obese
patients. Pulse pressure variation, the decrease in arterial
pulse pressure with positive pressure ventilation, is a more
reliable indicator of hypovolemia than CVP. During inspiration of controlled ventilation, the great veins entering the
heart are compressed, resulting in a reduction of right ventricle preload and an increase in afterload. The decreased
preload and increased afterload decrease the stroke volume
of the left ventricle at the end of the expiration cycle. When
this is exaggerated, the blood volume of the patient is contracted, and a fluid bolus will improve CO. Commercial
devices are being marketed that provide real-time changes in
pulse pressure variation. However, these devices typically
require positive pressure ventilation and higher tidal volumes, which may be contrary to the goals of lung protective
ventilation strategies.
Pulmonary artery pressure monitoring has fallen into disfavor because it is a poor indicator of left ventricle preload or
circulating blood volume, but it is still being used to assess
pulmonary hypertension.
Transesophageal echocardiography (TEE) is an invaluable tool to assess the possible cause of sudden intraoperative cardiac or hemodynamic instability such as myocardial
ischemia associated with wall motion abnormalities,
emboli, and hypovolemia. TEE cannot be used routinely
during bariatric surgery because the ultrasound probe is in
the surgical field.
The degree of neuromuscular blockade should be monitored during surgery. During surgery, train-of-four monitoring (TOF) monitoring is used to guide the administration of
neuromuscular blocking agents. Acceleromyography should
be utilized over traditional qualitative twitch monitors, if
available. At the end of surgery, the TOF ratio is used to
guide administration of reversal agents. A deep neuromuscular block (TOF ratio of 0) cannot be reversed with neostigmine, and reversal should be delayed until a TOF count
of 2 is observed. The administered dose of neostigmine
should not exceed 5 mg, and the trachea should not be extubated with a TOF ratio of <0.9. As noted above, deep neuromuscular blockade can be reversed with sugammadex at
4 mg/kg IBW.
Electroencephalographic-based brain function monitors
are being used to guide administration of anesthetic agents
and to prevent awareness. The efficacy of these monitors is
H. J. M. Lemmens et al.
controversial, and routine use of brain function monitoring
during surgery is not supported by data. However, its use is
recommended in cases where a high risk for awareness may
be suspected. Administration of nitrous oxide, ketamine, isoflurane, or halothane can be associated with a paradoxical
increase in BIS.
A Foley urinary catheter may be placed before any
major surgery, but not required if the surgery is anticipated
to be of short duration and routine. A low urine output
may be encountered during laparoscopic bariatric surgery.
Pneumoperitoneum decreases urine output by increasing
ADH, aldosterone, and plasma renin activity.
Preoperative Sedation
For most patients, premedication with sedatives should be
used with caution. Respiratory depression caused by benzodiazepines and opioids is pronounced in patients with severe
obesity, especially in those with OSA. The upper airway collapsibility of the patient with severe obesity combined with
the decreased arousal response to airway occlusion makes
these patients particularly sensitive to drug-induced respiratory depression. Benzodiazepines decrease upper airway
muscle activity with consequent obstruction and cause central apnea during the initial post-administration minutes. If
very anxious patients need premedication, small doses of
midazolam can be administered upon transport to the operating room under continued visual monitoring and verbal communication during transport. Administration of oxygen
during transport is recommended.
In the operating room, it is practical to have unpremedicated patients climb off the gurney and then position themselves on the operating room table.
Airway Management
According to recent data from the American Society of
Anesthesiologists Closed Claim Database, almost 40% of
adverse airway events during induction of anesthesia
occurred in obese patients, with a significant proportion
resulting in permanent brain damage or death [30]. This is
not surprising since inability to mask ventilate and intubate
the morbidly obese patient will result in rapid development
of hypoxemia. An understanding of the different requirements for airway management and adequate preparation is
vital to avoid untoward events.
The supine position, routinely used for induction of anesthesia in nonobese patients, is not appropriate for the patient
with severe obesity. The supine position will decrease the
FRC further and will increase the intra-abdominal pressure,
8
Anesthetic Considerations
resulting in restriction of diaphragmatic movement with respiration. The torso of the morbidly obese should be elevated
25–30° prior to induction of anesthesia in reverse
Trendelenburg position. Offsetting the mass loading of the
abdomen and chest will increase the FRC, decrease the
restrictive component of the lung function, and increase
compliance. Therefore, reverse Trendelenburg positioning
will not only improve the ability to ventilate the lungs by bag
and mask but also will increase the time before desaturation
starts to occur when there is an inability to manage the
airway.
The standard “sniffing position” for tracheal intubation,
which results in optimal alignment of axes of the head and
neck in the nonobese, is inadequate for the patient with
severe obesity. A “ramped” position, with the patient’s upper
body, head, and neck elevated until the external acoustic
meatus and the sternal notch are in horizontal alignment,
results in optimal position for tracheal intubation (Fig. 8.3).
It also provides increased submandibular space facilitating
manipulating the laryngoscope handle and laryngoscopy.
Obesity itself is not an independent risk factor for difficult
tracheal intubation, but patients with obesity plus a large
neck circumference, excessive pretracheal adipose tissue,
and high Mallampati classification do have a higher probability of difficult intubation. Obesity and OSA are independent risk factors for difficult mask ventilation. Since facial
hair can make ventilation of the lungs by bag and mask ineffective, it is appropriate to ask patients to shave beards
preoperatively.
When very difficult mask ventilation and/or tracheal intubation is suspected, awake fiber-optic intubation (FOI) is the
technique of choice. Spontaneous ventilation and airway
patency will be maintained in the awake patient, assuming
sedatives are carefully titrated—keeping in mind that even
small amounts may result in airway obstruction. Adequate
topical anesthesia of the larynx and pharynx and gentle technique will result in intubation with minimal discomfort for
the patient. Visualization of the larynx may be difficult due to
97
airway narrowing by redundant folds of fat tissue. In a sitting
patient, the pharyngeal space will be increased, and instructing the patient to protrude the tongue will further increase
the diameter of the airway. Several reports have described
the use of a laryngeal mask airway in an awake patient to
open the surrounding tissues permitting easier visualization
of the vocal cords and passage of the fiberscope. Video laryngoscopy, with multiple models available on the market, has
become a ubiquitous and invaluable alternative to FOI and
DL in the patient with severe obesity. The video laryngoscope allows for indirect visualization of the vocal cords and
rapid intubation in the anesthetized patient. However, due to
the indirect visualization, the tonsillar pillars and soft tissue
in the pharynx and hypopharynx are not visualized well and
are at risk for traumatic injury [31] during intubation; substantial training is required [32].
Aspiration Risk
The traditional belief that patients with obesity are at higher
risk for aspiration at induction of anesthesia is unfounded.
The volume of gastric contents is not greater in fasted patient
with obesity when compared to normal-weight subjects, and
gastric emptying is not delayed, except in the setting of
obesity-­related disease as noted below. In fact, the proportion of high-volume low pH gastric content in obese unpremedicated subjects is lower (26.6%) when compared to
normal-weight patients (42%).
Patients with comorbid conditions such as symptomatic
gastroesophageal reflux disease, diabetes mellitus, and gastroparesis are at increased risk for gastric acid aspiration. A
rapid sequence induction with cricoid pressure should be
performed in these patients as well as in all patients with a
prior gastric banding procedure. There are, however, emerging studies using biomarkers suggesting that cricoid pressure
does not necessarily lead to decreased aspiration in these
patients.
Pneumoperitoneum: Implications
for Ventilation, Hemodynamics, and Urine
Output
Fig. 8.3 Ramped position for tracheal intubation
After insufflation of the abdomen, the increased intra-­
abdominal pressure and absorption of CO2 account for the
majority of physiologic alterations. The diaphragm moves in
the cephalad direction, which may result in migration of the
endotracheal tube into the right main stem bronchus. High
peak inspiratory pressures followed by hypoxemia and hypotension will result if this phenomenon is not recognized and
corrected in a timely fashion. Appropriate ventilatory adjust-
98
H. J. M. Lemmens et al.
ments can eliminate most of the absorbed CO2 and prevent
Maintenance with balanced salt solutions such as lacacid-base disturbances. Reverse Trendelenburg position, tated Ringers is preferred, with boluses as needed when
>10 cm PEEP, and recruitment maneuvers can dramatically signs and symptoms of hypovolemia present. Under anesimprove oxygenation in the morbidly obese in both open and thesia, use of a vasopressor such as phenylephrine may be a
laparoscopic cases [33].
better choice than repeated fluid boluses, as decreased blood
Upon insufflation, heart rate and blood pressure typically pressure is more likely due to decreased vascular tone rather
increase; however, some patients may experience vagal-­ than hypovolemia. It is important to realize that heart rate,
mediated bradycardia due to peritoneal stretching—a phe- blood pressure, urine output, and central venous pressure
nomenon typically short-lived and relieved with peritoneal are not particularly accurate measures of volume status,
desufflation and administration of IV atropine or glycopyrro- especially during laparoscopic procedures. Variations in
late. In patients with severe obesity, CO decreases with insuf- stroke volume or pulse pressure can be utilized for goalflation, while systemic vascular resistance, pulmonary vascular directed fluid therapy, but these measurements are less accuresistance, mean arterial pressure, right atrial pressure, and rate in the presence of pneumoperitoneum and lower tidal
pulmonary capillary wedge pressure increase. In general, the volume ventilation. In addition, benefits of goal-directed
impact of pneumoperitoneum on the cardiovascular system of fluid therapy have not been as evident when the patient is
the patient with severe obesity is well tolerated.
euvolemic, as is more commonly the case for enhanced
A decrease in renal perfusion occurs with pneumoperito- recovery pathways [35].
neum as well as increased release of antidiuretic hormone,
plasma renin activity, and serum aldosterone, resulting in
water retention and a rapidly decreasing urine output. The Postoperative Considerations
extent of intraoperative oliguria is directly related to the
extent of increased intra-abdominal pressure. Despite the In laparoscopic bariatric surgery, a deep neuromuscular
hormonal changes and transient oliguria, clinically signifi- block is needed to ensure an adequate surgical field. After
cant renal impairment as measured by serum creatinine does completion of surgery, before tracheal extubation is
not occur after laparoscopic gastric bypass with insufflation attempted, it is imperative to completely reverse the neuropressures not exceeding 15 mmHg. However, in patients muscular block. Even minimal residual paralysis causes retwith preexisting renal impairment, minimal insufflation roglossal and retropalatal narrowing during inspiration,
pressure and adequate IV hydration should be instituted to which may result in upper airway collapse.
avoid further exacerbation of renal insufficiency.
Use of continuous positive airway pressure (CPAP)
Effects of pneumoperitoneum on hepatic blood flow and reduces the risk for atelectasis, and noninvasive ventilafunction are similar to those of the kidneys, and transaminase tion can be used as a prophylactic and/or therapeutic tool
levels may rise as much as sixfold 24 h after surgery. These to improve gas exchange postoperatively. There is coneffects may be enhanced in morbidly obese patients because cern CPAP may increase the likelihood of an anastomotic
many have underlying hepatic disease due to fatty leak by air forced into the gastric pouch. However, it has
infiltration.
been demonstrated that changes in transmural gastric
Use of sequential compression devices (SCDs) in combi- pouch pressure with the application of CPAP do not occur
nation with pneumoperitoneum is associated with a signifi- [36].
cant improvement in CO, stroke volume, portal venous and
The American Society of Anesthesiologists (ASA) prachepatic arterial blood flow, and marked improvement in renal tice guidelines for the perioperative management of patients
perfusion, urine output, and systemic vascular resistance.
with OSA recommended that patients with OSA treated with
CPAP should continue CPAP as soon as feasible after surgery [37]. The same guideline recommends that patients
Fluid Management
with OSA be monitored for 3 h longer than their non-OSA
counterparts before discharge from the PACU. The recomGoals for fluid management should center around mainte- mendations for increased monitoring are based on expert
nance of euvolemia, when possible. Extended fasting is opinion and not scientific evidence. The same guidelines
avoided, and oral intake is resumed as soon as possible post- caution performing upper abdominal laparoscopic surgery in
operatively [34]. The concept of the “third space” has been an outpatient setting for patients with known or suspected
shown to be false; administered fluid either remains intravas- OSA. In a series of 746 patients with obstructive sleep apnea
cular or distributes to the interstitial space. The increase in after ambulatory laparoscopic gastric banding, 40% did have
hydrostatic pressure damages the endothelial glycocalyx and an incidence of hypoxia in either the OR or PACU [38].
alters vascular permeability, leading to gut wall edema and However, there were no episodes of respiratory failure or traileus.
cheal reintubation.
8
Anesthetic Considerations
Postoperative Nausea and Vomiting
99
sion. The laparoscopic approach provides substantial benefit
with less postoperative pain and medication use.
Bariatric surgery is associated with a high incidence of postPostoperative oral administration of analgesics can be utioperative nausea and vomiting (PONV). Besides the surgery lized in the ambulatory surgery setting, and oral absorption
itself, female sex, a history of PONV, and motion sickness of drugs is essentially unchanged in obese patients, with liqare known risk factors. Opioids, volatile anesthetics, and uid preparation being best tolerated. The most common analnitrous oxide all have dose-related emetogenic effects. The gesic drugs given orally are nonsteroidal anti-inflammatory
most commonly used antiemetic agent for the prevention of drugs (NSAIDs), acetaminophen, and opioids. NSAIDs are
PONV is the serotonin antagonist ondansetron, with a half-­ not generally given due to potential risk of bleeding, particulife of 4 h. This short half-life makes the efficacy of ondanse- larly for surgical staple lines.
tron for longer-lasting prophylaxis, such as in the ambulatory
Patient-controlled analgesia (PCA) was developed to
surgery setting, questionable. The incidence of post-­ allow intravenous administration of analgesics in an incredischarge nausea and vomiting (PDNV) after ambulatory mental fashion, so that respiratory depression and heavy
surgery is higher than PONV and has been reported to be as sedation could be avoided. PCA use is highly recommended
high as 50% in patients who did not experience for the severely obese patient, compared to intermittent
PONV. Laparoscopic sleeve gastrectomy, currently the most bolus dosing [43]. Bupivacaine infusion devices for concommonly performed bariatric procedure, is particularly tinuous postoperative infiltration of the surgical wound
emetogenic. One Polish study demonstrated an 8.2% inci- have been developed to avoid the risk of respiratory depresdence for LSG, compared to 1.4% for laparoscopic Roux-­ sion associated with opioids. Mixed results have been seen
en-­
Y gastric bypass, with the use of enhanced recovery for potential benefits of heating and humidifying carbon
pathways [39]. Aggressive antiemetic protocols using multi- dioxide (CO2) insufflation for postoperative pain relief in
ple agents, and sparing opioids as able, seem to be the key to laparoscopic surgery. The European Association for
reducing this rate.
Endoscopic Surgery practice guidelines state that “the clinBesides adequate hydration with intravenous fluids, anti- ical benefits of warmed, humidified insufflation gas are
emetic strategies covering a longer duration should be minor and contradictory” [44]. Theoretically, intraperitoemployed [40]. Multiple agents with different mechanisms neal (IP) administration of local anesthetics can provide
of action (multimodal therapy) are more effective than a sin- analgesia without opioid-­related complications. A single
gle agent. Dexamethasone, 8 mg, intravenously administered randomized clinical trial examined the use of continuous IP
at the beginning of surgery combined with the transdermal infusion in laparoscopic adjustable gastric banding [45]. A
cholinergic antagonist scopolamine is an effective longer-­ statistically significant decrease in VAS was noted in the IP
lasting strategy. For patients with several risk factors, addi- infusion group with no differences in shoulder pain and
tional medications such as haloperidol (0.5–1 mg) or additional medication use.
promethazine (12.5 mg) can be added. Both can result in
Obese patients with obstructive sleep apnea syndrome
oversedation and should be administered with caution in (OSAS) appear to be more sensitized to sedation than normal
patients with significant OSA. For patients with a history of individuals. Mortality may occur in OSAS patients after
intractable nausea and vomiting, the neurokinin-1 receptor minimal doses of anesthetics or sedatives due to a change in
antagonist aprepitant, 40 mg p.o., administered before sur- airway tone resulting in obstruction [46].
gery could be added and continued in the postoperative
The ASA Guideline for Patients with Obstructive Sleep
period. Opioid-sparing analgesia, beginning in the preopera- Apnea Syndrome (OSAS) is intended to improve perioperative period and continued throughout the intraoperative tive care and reduce the risk of adverse outcomes in patients
period, and utilization of total intravenous anesthesia (TIVA) with OSAS who receive sedation, analgesia, or anesthesia.
can help to decrease the rate of PONV in these patients [41, During preoperative evaluation, the severity of the patient’s
42]. Non-pharmacological methods such as acupuncture and OSAS, the type of surgery and anesthesia, and the requireacupressure have limited efficacy, but may be worthwhile ment for postoperative opioid analgesics should be considadjuncts.
ered [37]. There is tremendous interest in establishing
enhanced recovery after surgery (ERAS) guidelines that utilize opioid-sparing strategies for analgesia [42, 47], includPostoperative Analgesia
ing the use of preoperative acetaminophen and
gabapentinoids, and intraoperative dexmedetomidine, transAdequate postoperative pain relief is critical for patient com- versus abdominis plane or rectus sheath blocks [48], ketfort, pulmonary toilet, and early ambulation. Postoperative amine, esmolol infusion and lidocaine infusion with the
analgesia must be balanced to avoid opioid-related compli- goals of decreased opioid-related adverse events, rates of
cations like PONV, sedation, ileus, and respiratory depres- PONV [49], and shortened time to discharge or even same-­
100
day laparoscopic sleeve gastrectomy [50]. However, there is
significant heterogeneity among published reports of ERAS
[51], and further work is needed in this area.
Question Section
1. The obese patient is at increased risk for respiratory complications due to:
A. Hypoxemia
B. Higher respiratory rates
C. Lower tidal volumes
D. Decreased functional residual capacity
E. Obstructive sleep apnea
F. All of the above
2. The “sniffing” position of an obese patient during anesthesia induction is preferred to the supine position.
A. True
B. False
3. At the end of a laparoscopic sleeve gastrectomy, a 64-inchtall, 120-kg anesthetized patient is noted to have zero train-offour twitch and 1 post-tetanic count. The rocuronium-induced
neuromuscular blockade should be reversed with:
A. Neostigmine 0.08 mg/kg with glycopyrrolate
B. Sugammadex 2 mg/kg at ideal body weight
C. Sugammadex 4 mg/kg at total body weight
D. Sugammadex 4 mg/kg at ideal body weight
4. A 60-inch-tall, 100-kg woman presents for bariatric surgery. Any of the following dosing would be appropriate
except:
A. Succinylcholine 50 mg for intubation
B. Rocuronium 54 mg for intubation
C. Propofol 140 mg for induction
D. Succinylcholine 100 kg for intubation
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9
Components of a Metabolic
and Bariatric Surgery Center
Wayne J. English, D. Brandon Williams, and Aaron Bolduc
Chapter Objectives
After reading this chapter, the reader will have a better
understanding of the:
1. Essential components necessary to operate a successful, high-quality metabolic and bariatric surgery center
2. Requirements to achieve national accreditation
3. Most common deficiencies encountered during an
accreditation site survey
Introduction
The incidence of morbid obesity is increasing in epidemic
proportions [1]. This alarming trend is being accentuated by
frequent media-driven highlights and periodic calls for
action from government officials. General surgeons are coming under increasing market pressures to provide surgical
solutions for patients who seek significant and durable
weight loss. Patients with class II and III obesity often carry
multiple diagnoses, and many surgeons who had embarked
on this specialty rapidly realized that the safest and most
effective approach to managing these patients successfully is
through a comprehensive management program [2].
There has been a 44.31% increase in the number of metabolic and bariatric procedures performed in the United States
from 2011 through 2017 [3]. As the number of procedures
being performed annually continues to increase, there is an
even greater need for performing metabolic and bariatric sur-
W. J. English (*) · D. B. Williams
Department of Surgery, Vanderbilt University Medical Center,
Nashville, TN, USA
e-mail: wayne.english@vumc.org
A. Bolduc
Department of Surgery, Augusta University Medical Center,
Augusta, GA, USA
gery with rigorous organizational and operational standards
to ensure patients receive safe care.
In this chapter, we will describe the essential components
of a successful, comprehensive bariatric center including
essential staff, ancillary personnel, material infrastructure,
and educational and patient support strategies based on the
Metabolic and Bariatric Surgery Accreditation and Quality
Improvement Program (MBSAQIP) manual “Optimal
Resources for Metabolic and Bariatric Surgery: 2019
Standards.” We will also briefly describe some tips to prepare
for an MBSAQIP site survey and outline the most common
deficiencies encountered during site surveys.
he Metabolic and Bariatric Surgery
T
Accreditation and Quality
Improvement Program
In 2012, the American Society for Metabolic and Bariatric
Surgery (ASMBS) and the American College of Surgeons
(ACS) jointly developed the MBSAQIP standards to improve
quality and facilitate access to care for patients. The decision
to recommend surgery for obese patients requires multidisciplinary input to evaluate the indications for operation and to
define and manage comorbidities properly. Institutions performing metabolic and bariatric surgery must have absolute
commitment, organization, leadership, human resources, and
physical resources to provide optimal care. Surgeons must
demonstrate the necessary training, skills, and experience.
Furthermore, high-quality surgical care requires data collection with reliable risk-adjusted measurements of outcomes.
For metabolic and bariatric surgery centers to improve,
surgeons require feedback, which is dependent on accurate
data collection [4]. MBSAQIP semiannual data reports provide feedback for surgeons and their centers to help improve
quality of care. Capturing uniform data elements for all participating MBSAQIP centers allows equal comparison of
centers, which provides an opportunity for centers to continuously evolve and improve.
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_9
103
104
W. J. English et al.
Metabolic and bariatric surgery procedure estimates in Periodic interrogation of the non-risk-­adjusted data provided
2016 demonstrate that approximately 92% of centers per- by MBSAQIP allows an intelligent and critical analysis of
forming metabolic and bariatric surgery are MBSAQIP-­ patient outcomes, thereby indicating center components that
accredited centers [5]. Ideally, all metabolic and bariatric may require special attention, and will allow centers to
surgery centers in the United States will participate in the develop individualized quality improvement plans.
MBSAQIP and assemble the essential components at the
center to meet the required standards to achieve nationally
recognized accreditation.
MBS Committee
ssential Components of a Metabolic
E
and Bariatric Surgery (MBS) Center
The essential components of an MBS center include commitment to quality care, data collection with continuous
quality improvement efforts, and designated leadership with
the appropriate committee structure, surgical experience,
critical care support, appropriate equipment and instruments,
qualified call coverage, continuity of care pathways including long-term follow-up care and support groups structure.
Leadership at the surgeon, integrated health and administrative levels are essential in developing a high-quality bariatric surgery center. A surgeon and integrated health partner
would not be expected to completely understand the nuances
of running the business aspect of a practice, nor should an
administrator be expected to completely understand the clinical and technical aspects of surgery. Once the center has
established a firm commitment for administrative support to
develop and maintain a program, it is essential to assemble
the “Leadership Trifecta,” a dedicated team comprised of the
MBS Director (the leader of this elite group), MBS
Coordinator, and Clinical Reviewer. The center should then
reference the MBSAQIP standards as a guide to achieve their
goals of developing and maintaining a high-quality MBS
center.
ata Collection and the Bariatric Surgery
D
Database
An important requirement for any bariatric center is the ability to maintain a repository of information that includes
patient demographics, comorbid factors, operative characteristics, and follow-up. Such a database will prove to be an
invaluable resource for both clinical and research purposes.
Ideally, patients will be followed for life, and there will occasionally be the need for rapid access to patient information.
By collating and sorting data, a well-maintained database will
demonstrate past performance and help direct future trends.
For example, MBSAQIP focuses on perioperative safety and
continuous quality improvement for all bariatric surgery centers. MBSAQIP provides semiannual risk-­adjusted reports
(SAR) to determine how a center compares to other centers.
The structure of a metabolic and bariatric center must consist
of an MBS Committee that involves, at a minimum, the MBS
Director, all surgeons performing metabolic and bariatric
surgery at the center, the MBS Coordinator, the MBS Clinical
Reviewer, and institutional administration representatives
involved in the care of metabolic and bariatric surgical
patients. The center must have a clearly defined mission,
vision, goals, and objectives, which are discussed, and agreed
upon, within the MBS Committee.
The MBS Committee provides a setting for sharing best
practices, reducing practice variation, responding to adverse
events, and fostering a culture to improve patient care.
Balanced representation is essential, and all surgical practices performing bariatric surgery at the center must participate in a collaborative manner focused on improving quality
of care. The responsibility is upon the center, the metabolic
and bariatric surgeon and, ultimately, the MBS Committee
and MBS Director, to appropriately select patients and
develop selection guidelines for the center relative to the
center’s available resources and experience.
The MBS Director and other team members of the MBS
Committee at each center must embrace a culture of camaraderie and collaboration in order to report and analyze data,
identify gaps of care, and implement strategies resulting in
continuous quality improvement. Such efforts must be readily identified through the center’s MBS Committee.
Major quality improvement projects that can result in
decreasing rates of readmissions, reoperations, emergency
department visits, length of stays, surgical site infections,
leaks, or venous thromboembolism are extremely important
in achieving safety and effectiveness of the procedures performed at a high-quality metabolic and bariatric surgery center. However, equally as important is the examination of
clinical pathways of care to maximize the patient experience
and improving overall patient satisfaction.
The MBS Committee can also be considered a training
ground for emerging and future leaders to refine their skills
and abilities.
Preparation for the center’s initial or the triennial site survey requires thorough documentation, within the meeting
minutes, of the three meetings required, including at least
one comprehensive review meeting annually. The comprehensive review meeting must be attended by all surgeons and
proceduralists at the center.
9
Components of a Metabolic and Bariatric Surgery Center
The center is required to review the two semiannual
reports (SAR). For the third required meeting, the center is
required to review the raw data available from the MBSAQIP
data registry. Documentation of the review can be listed in
generic terms and does not require patient-specific details.
MBS Director
The MBS Director, in collaboration with the MBS
Committee, and the administration of the institution, organizes, integrates, and leads all metabolic and bariatric
surgery-­related services throughout the accredited center.
The Director is responsible for standardizing and integrating metabolic and bariatric patient care throughout the center
and maintaining continuous compliance with accreditation
standards. Continuous review of the standards will allow
centers to identify, if present, any areas where there are gaps
in compliance.
All relevant staff must be educated on patient safety and
complication recognition. An important goal would be to
prevent “failure to rescue” situations, in which differences in
mortality are proposed to result from the failure to timely
recognize, and effectively manage, a postoperative complication. Additional training for the surgical teams and the
integrated health personnel in postoperative complication
recognition and management may improve outcomes [6].
The MBS Director is responsible for supervising all surgeons and proceduralists performing metabolic and bariatric
procedures at the center and is obligated to report any significant ethical and/or quality deviations by surgeons and proceduralists to the appropriate institutional entities (e.g., chief of
surgery, credentialing committee, medical staff, risk management, etc.). The MBS Director should have the authority
to recommend plans for remediation or make formal recommendations to limit or redact privileges to the appropriate
administrative or credentialing body at the center.
MBS Coordinator
Metabolic and bariatric surgery centers must have a designated MBS Coordinator who reports to and assists the MBS
Director. The MBS Coordinator assists in center development, managing the accreditation process and ensuring continuous compliance with accreditation bodies, maintaining
relevant policies and procedures, patient education, outcomes data collection, quality improvement efforts, and education of relevant institution staff in the various aspects of
the metabolic and bariatric surgery patient with a focus on
patient safety.
It is essential for the MBS Coordinator to coordinate all
services involved with the care of a metabolic and bariatric
105
patient. It is recommended that representatives for these services meet on a regularly scheduled manner to maintain
compliance with the standards and address any issues that
may arise with patient care. Services represented at these
meetings could include, but are not limited to, designated
bariatric floor, emergency department, radiology, lab, central
supply, supply chain, bed control, and patient
transportation.
The MBS Coordinator supports the development of written protocols and education of nurses detailing the rapid
communication and basic response to critical vital signs that
is specifically required to minimize delays in the diagnosis
and treatment of serious adverse events.
One of the most important functions of the MBS
Coordinator is to ensure all practicing surgeons and proceduralists are actively involved with the MBS Committee
activity and process and quality improvement efforts. This
can become very complicated if multiple surgical practices
are involved at the center. The MBS Coordinator serves as
the liaison between the institution and all surgeons performing metabolic and bariatric surgery at the center and, if applicable, all general surgeons providing call coverage. The
MBS Coordinator will assist in coordinating and maintaining documentation of the call schedule provided by all covering surgeons.
The MBS Coordinator must also work closely with the
MBS Clinical Reviewer to assure timely submission of outcomes data.
MBS Clinical Reviewer
Managing data is a critical component of optimizing performance and quality of care. The center must designate a person, or department, that is accountable for gathering and
entering data in a timely and accurate manner and providing
outcomes reports when necessary.
In an effort to eliminate any data collection bias, the designated MBS Clinical Reviewer should not be actively participating in a metabolic and bariatric surgery patient’s care
(e.g., a surgeon, physician assistant, or advanced practice
nurse).
The MBS Clinical Reviewer will also fulfill ongoing
training and recertification requirements, retrieve and enter
long-term follow-up data on a compounding number of
patients over time, and fulfill requests for patient data and
reports to the MBS Coordinator and hospital quality improvement staff for analysis. The MBS Clinical Reviewer should
work closely with the institution and clinicians to ensure that
appropriate short-term and long-term data points are available in the medical records.
It is critical that there is continuous communication
between MBSCR and all surgeons performing MBS at the
106
center. It is imperative that the MBSCR has access to records
from surgeons whose records are not integrated with the hospital electronic medical record system. This typically
involves surgeons located off of the hospital grounds. A
common site survey deficiency involves surgeons not allowing access to the records. Forms filled out by the surgeon or
office staff containing specific data elements that can be
biased are not considered appropriate for entry into the
MBSAQIP data registry. The MBSCR must have full access
to the records to ensure uniformity of the data collected in an
unbiased manner. The MBSCR can contact the patient to collect data elements but cannot participate in direct patient
care.
Off-site third-party MBSCR services are available that
can prepare your meeting agendas, reports, and meeting
minutes.
Healthcare Facility Accreditation
Simply stated, hospitals pursue accreditation because it is
required to receive payment from federally funded Medicare
and Medicaid programs. However, there is consistent evidence that shows that accreditation programs improve the
process of care provided by healthcare services and improve
clinical outcomes of a wide spectrum of clinical conditions
[7]. The accreditation process has the potential to significantly influence quality through a series of three mechanisms: coherence, organizational buy-in, and collective
quality improvement action [8].
Healthcare facility accreditation ensures that the facility
performed a comprehensive assessment of processes, policies, and procedures to provide safe care for all patients,
including metabolic and bariatric surgery patients.
The facility must be licensed by state or nationally recognized licensing authorities, if required by state law. Examples
of licensing agencies include, but are not limited to, the Joint
Commission, state health department, Det Norske Veritas,
the American Osteopathic Association, the American
Association for Accreditation of Ambulatory Surgery
Facilities (AAAASF), the Accreditation Association for
Ambulatory Health Care (AAAHC), or the Institute for
Medical Quality (IMQ).
Metabolic and Bariatric Surgeon “Verification”
It is important that centers have at least one surgeon who
dedicates a significant portion of their practice to metabolic
and bariatric surgery. MBSAQIP requires that a center must
have at least one “Verified” surgeon performing metabolic
and bariatric surgery. Surgeon “Verification” recognizes the
specialized skills of the dedicated metabolic and bariatric
W. J. English et al.
surgeon and is based on lifetime procedure volume of over
100 stapling procedures and a volume of at least 25 stapling
procedures annually.
It is essential for the “Verified” surgeon to document 24 h
of bariatric-specific CME credits per triennial cycle. CME
credits will not count unless the certificate specifically states
the activity was bariatric-specific. Generic certificates without CME credit itemization will not apply to the total number of credits required for “Verification.” In addition to
attending conferences related to obesity medicine and surgery to fulfill this requirement, there are a number of online
opportunities to meet compliance with the “Verified” CME
requirements through journal article reviews (Surgery for
Obesity and Related Diseases, Journal of the American
College of Surgeons), societies (ASMBS, The Obesity
Society, Obesity Medicine Association), and the American
Board of Obesity Medicine.
I nstitutional Requirements for Metabolic
and Bariatric Surgeon Credentialing
Well-trained surgeons are vital in delivering high-quality
care to metabolic and bariatric surgery patients in a consistent manner. Centers performing metabolic and bariatric surgery should be committed to improving outcomes and
require surgeons to obtain the skills necessary to achieve
optimal outcomes.
The institution’s credentialing body should follow nationally recognized credentialing guideline regarding surgeon
experience and training for surgeons seeking metabolic and
bariatric surgery privileges which are separate from general
surgery guidelines. Credentialing guidelines, such as that collectively produced by the joint task force involving the ASMBS,
the Society of American Gastrointestinal and Endoscopic
Surgeons (SAGES), ACS, and the Society for Surgery of the
Alimentary Tract (SSAT), aim to ensure that bariatric surgeons
have undergone appropriate training and have achieved a certain minimum level of skill to safely perform bariatric surgery
and to recognize and treat complications [9–12].
ualified Metabolic and Bariatric Surgery Call
Q
Coverage
All surgeons performing metabolic and bariatric surgery at a
center must have qualified coverage at all times by a colleague who is responsible for the emergency care of a metabolic and bariatric surgery patient. Call coverage may involve
one or more general surgeons who are not privileged to perform metabolic and bariatric surgery. The covering general
surgeon must have general surgery privileges at the facility
and must have completed formal education and training
9
Components of a Metabolic and Bariatric Surgery Center
regarding a basic understanding of the (1) metabolic and bariatric procedures commonly performed at the center, (2)
signs and symptoms of postoperative complications, and (3)
management and care of the patient by a review of the center’s clinical pathways and protocols. Centers may elect to
require general surgeons to perform as a first assistant for a
designated number of procedures to become better acquainted
with anatomy and potential complications.
MBSAQIP participating centers are required to document
a care pathway for metabolic and bariatric surgery patients
who have had surgery elsewhere. Examples to address this
issue include having complete coverage by the center’s credentialed metabolic and bariatric surgeons or general surgeons covering unassigned patients with metabolic and
bariatric surgeon being available when needed. Smaller or
solo surgeon centers may opt to obtain locum tenens bariatric surgery coverage.
esignated Area for Metabolic and Bariatric
D
Surgery Patients
It is important to standardize care with personnel that routinely have contact with metabolic and bariatric surgery
patients. The center must have a dedicated metabolic and
bariatric surgery floor, or designated group of beds, maintained in a consistent area of the facility.
Designated Personnel
The center must involve an integrated health approach to the
metabolic and bariatric surgery patient. The optimal care of
the metabolic and bariatric surgery patient requires specialized training, education, and experience, such as that
obtained with Certified Bariatric Nurse (CBN®) certification. It is essential that a consistent operating room team is
assigned to optimize patient safety and the flow of the procedure. As needed, the center must provide access or referral to
registered nurses, advanced practice nurses, or other physician extenders, registered dietitians, psychologist, psychiatrist, social worker, or other licensed behavioral healthcare
provider, and physical/exercise therapists.
egistered Dietitians and the Dietary Evaluation
R
Registered dietitians (RD) are essential for the success of
any bariatric center and especially the success of the patient
undergoing bariatric surgery. They provide nutritional counseling for patients preparing for surgery and assist patients
with postoperative nutritional counseling and maintenance.
Dietitians have been shown to improve outcomes in the postoperative bariatric surgery patient. A retrospective analysis
of a prospective database was performed on bariatric surgery
107
patients who were followed up by either a surgeon alone or
by a surgeon and RD for initial postoperative visit. Patients
in the RD follow-up group had significantly fewer readmissions due to dietary-related problems and more favorable
3-month change in serum thiamine, high-density lipoprotein,
and triglycerides. Additionally, patients trended toward a
lower number of minor complications [13].
An additional important role for nutritional counselors is
the assessment of a candidate’s ability to comply with the
required dietary modifications imposed by bariatric surgery.
Patients should have an appreciable degree of motivation to
accept and reliably follow dietary guidelines and should have
a minimum level of understanding of the potential repercussions of nonadherence. Dietitians are in an ideal position to
gauge patients’ eligibility and compliance from a cognitive
and motivational perspective [14, 15].
Of all the dietary macronutrients, proteins are the most
valuable and essential. Patients’ dietary regimens must meet
their daily requirements for these nutrients. Nutritional
counselors are trained to deliver advice on the proper identification of protein sources and the preparation of foodstuffs
to render them more palatable. They will also advise patients
on proper chewing and swallowing techniques and give tips
on how to avoid consuming liquids concomitantly with solids. Patients are required to know the hazards of insufficient
fluid intake and are counseled to imbibe through the day,
pausing before meals. The daily administration of vitamins
and supplements is a critical requisite for postoperative
patients, and it is incumbent on surgeons to ensure that
patients are meeting their nutritional needs. Surgeons have
been held liable for complications of vitamin deficiencies,
particularly neurological manifestations that may result
from inadequate intake. The provision of appropriate access
to nutritional counselors and opportunities for periodic laboratory assessment of nutritional parameters may reduce the
occurrence of these indefensible and undesirable outcomes.
sychologist and the Psychological Evaluation
P
The primary objective for the psychosocial evaluation for
patients with Class II and III severe obesity interested in
undergoing metabolic and bariatric surgery is to screen for
risk factors and identify potential challenges that may contribute to a poor postoperative outcome.
Patients with Class II and III obesity often carry a diagnosis of depression, anxiety, and other stress-related conditions. There are often problems with body image and with
low and demoralized self-esteem. Psychologists offer invaluable support in assessing patients’ mental conditions and
counsel the patient to withstand the lifelong changes imposed
by bariatric surgery. Several instruments for psychological
assessment of morbidly obese patients in the preoperative
and postoperative periods have been developed and validated
and are in wide use.
108
Pre- and postoperative education of patients presenting
for weight loss surgery is more critical as compared to that of
patients preparing for non-bariatric surgery. For example,
knowledge of the “rules of eating” and the “rules of vomiting” is essential for the positive outcome of gastric restrictive
surgery. Discrepancies between patients’ weight goals,
“ideal” or healthy weight for post-obese individuals and
­realistic weight loss based on body composition and energy
balance, contribute to subjective assessment of quality of life
after bariatric surgery.
It is common for bariatric patients to experience postoperative nausea, depression, and possibly remorse for several
months following surgery. Many patients who successfully
lose weight may experience jealousy from close friends and
relatives. Difficulty exists for the surgeon in delineating the
physical from the psychological etiologies of many postoperative symptoms that afflict patients. Stress factors may significantly influence a patient’s ability to achieve maximum
and durable benefit or may even predispose to deviations and
weight regain. Preoperative education, evaluation, and preparation, although essential, will not identify nor eliminate all
the potential problems.
Psychological intervention is sometimes useful in achieving overall patient stability and emotional well-being,
thereby underscoring its important role throughout the entire
preoperative and postoperative course of a patient’s treatment experience [16, 17]. To further emphasize the importance of having continued behavioral health services
available in the postoperative period, a review of patients
undergoing bariatric surgery in Pennsylvania, patients with a
diagnosed mental health disorder had 34% greater odds of
30-day readmission relative to patients with no diagnosed
mental health disorder. Patients with major depressive disorder/bipolar disorder had 46% greater odds of 30-day readmission compared with patients with no major depressive
disorder/bipolar disorder diagnosis [18].
Addiction transfer is an issue that should be monitored in
the postoperative metabolic and bariatric surgery patient. It
has been theorized that obesity-induced dysregulation of the
dopamine reward processing can result in compensatory
overeating, which may be reversed after RYGB. After surgery, patients may seek alternative means, such as alcohol
and illicit substances, to obtain the dopaminergic reward previously obtained with food [19].
Many factors may significantly influence a patient’s ability to achieve maximum and durable benefit or may even predispose to deviations and weight regain. Preoperative
education, evaluation, and preparation is essential, although
it is likely that it will not identify, nor eliminate, all potential
issues that may arise after surgery.
A systematic review revealed an increased risk, with an
odds ratio of 3.8, for self-harm and suicide attempt in patients
undergoing bariatric surgery compared to matched control
W. J. English et al.
subjects. A study in Sweden looked at patients who underwent primary RYGB between 2001 and 2010 found that
patients were nearly 2.85 times more likely to make a suicide
attempt than the general population reference group. A number of psychosocial issues that can potentially be attributed
to suicide must be considered in the metabolic and bariatric
surgery patient, including lack of improvement in quality of
life after surgery, continued or recurrent physical mobility
restrictions, persistence or recurrence of sexual dysfunction
and relationship problems, low self-esteem, a history of child
maltreatment, inadequate weight loss, or weight regain
[20–22].
Appropriate Equipment and Instruments
For optimal safety and excellent outcomes, a successful bariatric surgery center requires the facility have appropriate
furniture and equipment to accommodate patients within the
weight limits established by the program. Patients with morbid obesity should feel welcome and safe upon entering any
part of the center where they might receive care as an outpatient or inpatient (e.g., clinic, lab, endoscopy suite, radiology
department, hospital admitting, and emergency department).
At a minimum, they must be accommodated with appropriate weight capacity furniture, exam tables, wheelchairs, and
toilet facilities in the waiting areas and examination rooms in
all such areas. Often, wall-mounted toilets may not have a
sufficient weight capacity. Installing a floor support is a simple solution to this problem (Fig. 9.1).
The same considerations apply to weight scales and
sphygmomanometer cuffs. All inpatient units of the hospital
that the bariatric patient might encounter (e.g., pre-op holding, operating rooms, PACU, surgical ward, radiology,
endoscopy, and ICU) must have all of the above in addition
to appropriate clothing, sequential compression device
sleeves, stretchers, operating room tables, hospital beds,
shower rooms, doorways, walkers, and transfer equipment.
Particular consideration must be given to having immediate
access to equipment that may be rarely used, but can be
indispensable in a crisis, such as extra-long surgical instruments (open and laparoscopic), difficult airway devices, and
a lift for a patient who has collapsed in a chair or on the floor
and cannot get up. Centers must have a thorough written system of documenting the weight capacity of all relevant
equipment according to the manufacturer. Most importantly,
this information must be easily accessible to all staff members caring for the bariatric patient. Centers may opt to have
rental agreements for equipment that is not available on-site,
but such agreements must have guaranteed delivery
timeframes.
Should a program choose to care for patients who exceed
the weight capacity of any key equipment, such as the CT
9
Components of a Metabolic and Bariatric Surgery Center
109
Fig. 9.1 Examples of floor supports. Courtesy of Big John Products Inc.
scanner or fluoroscopy tables, then there must be a documented care pathway for such patients with specific attention
to the preoperative patient counseling and consent regarding
this limitation and how it will be handled.
Bariatric surgery centers must have a dedicated metabolic
and bariatric surgery unit or designated group of beds maintained in a consistent area. There must be well established,
properly managed, and ongoing in-service education programs for all the nurses and staff caring for the bariatric
patients. The educational programs must ensure maintenance
of competency in at least the following areas:
1. Recognizing the signs and symptoms of postoperative
complications. All nurses and staff must be able to quickly
recognize evidence of complications (e.g., pulmonary
embolus, respiratory distress or hypoventilation, anastomotic leak, infection, or bowel obstruction) to facilitate
timely intervention and help prevent failure to rescue.
2. Understanding the treatment of obesity as a disease, as
endorsed by the American Medical Association [23].
Patients with obesity have likely long suffered from pejorative language and attitudes associated with the social
stigma of obesity. Unfortunately, much of the contempt
and criticism may have come from healthcare professionals [24]. Therefore, it is essential that the entire patient
care team receive sensitivity training to ensure provision
of compassionate and supportive care for bariatric
patients. This training should emphasize the burden of
obesity, its detrimental impact on health and quality of
life, and include an appreciation for the necessary role of
metabolic and bariatric surgery.
3. Safe patient transfer and mobilization. The staff should be
well educated in fundamental transfer techniques, as well
as where to obtain relevant equipment and how to properly use it to avoid injury to themselves or to bariatric
patients when assisting with transfer or mobilization.
Critical Care Support
Bariatric centers, namely, the bariatric surgery committee
and medical director, must develop patient selection protocols and guidelines relative to the available resources and
experience level of the center. For example, patients at risk
110
for major organ failure should only be treated in centers with
immediate access to all the medical resources that such
patients might require. On occasion, however, metabolic and
bariatric surgery patients will require unexpected critical
care, and centers must ensure that patients receive appropriate care. At all times, centers must have immediate, on-site
availability of personnel capable of administering advanced
cardiac life support. Also, centers must have the ability to
stabilize critically ill bariatric patients with resources such as
difficult airway equipment, ventilator support, and hemodynamic monitors.
If a facility is unable to manage on-site all aspects of critical care, namely, pulmonology/critical care, cardiology, and
nephrology, the center must have the ability to transfer
patients to a higher level of care. In this situation, the center
must have a signed written transfer agreement that details the
transfer plan of patients to other facilities capable of managing the full spectrum of complications.
Anesthesiology for Bariatric Surgery
Just as pediatric patients are not merely “little people,”
patients with morbid obesity are not typical patients who
happen to be very large. Failure to appreciate the sequelae of
morbid obesity fully will result in unacceptable morbidity
and mortality.
Anesthesiologists, certified registered nurse anesthetists (CRNAs), and anesthesiologist assistants (AAs) who
are charged with managing bariatric patients undergoing
major surgery should be experienced in diagnosing and
treating immediate or imminent life-threatening ­conditions,
such as a difficult airway, hypoventilation syndrome, sleep
apnea, congestive heart failure, renal insufficiency, and
venous thromboembolism, to name a few. Anesthesiologists,
CRNAs, and AAs who will manage bariatric patients
undergoing laparoscopic operations must be cognizant of
the pulmonary and hemodynamic changes that occur upon
establishing and maintaining prolonged pneumoperitoneum. These cases are not to be taken lightly and certainly
not to be delegated to inexperienced staff. There should, at
all times, be more than one experienced anesthesiology
staff member or qualified, similarly experienced, anesthesia nursing personnel available who can provide care in
accordance with state laws governing their scope of
­practice [25].
The collaboration between experienced bariatric surgeons, anesthesiologists, and the OR staff represents a powerful intellectual combination that greatly benefits patients.
Perioperative recommendations by “bariatric” anesthesiologists are invaluable in promoting favorable outcomes in
patient safety and comfort.
W. J. English et al.
Continuum of Care
Although bariatric surgery has been practiced for several
decades, it remains an evolving discipline. Many biological
features of the metabolic, endocrine, nutritional, and psychological manifestations of morbid obesity are just now being
revealed. Patients undergo dramatic physical, metabolic,
physiological, and psychological changes in many aspects,
often by unclear mechanisms. There is, however, a constant
accrual of voluminous information as more research is
expended on this growing field. Understandably, morbidly
obese patients considering weight loss surgery, or who are
recovering from these operations, often possess insatiable
appetites for information. Although all members of a bariatric surgery center should be reasonably abreast of established
and emerging knowledge, it is incumbent on the physicians
to assume the role of experts in the scientific aspects of bariatric medicine. Physicians, and their physician assistants
and nurses, represent an invaluable reference source to
patients. Their information is best delivered to patients in the
way they learn best, both in one on one patient interaction
and in a group setting where discussion can flow freely
between inquisitive patients (and their family members) and
bariatric center personnel. Informal group settings may provide the most efficient method of disseminating information.
Two examples of effective group activities are the preoperative educational workshops and the support groups.
he Preoperative Educational Workshop
T
Educational seminars, or workshops, represent the gateway
into most metabolic and bariatric surgery centers. The primary purpose of these sessions is to educate the patient and
gain critical information to ensure safety for the patient.
Evidence shows that teaching about the specific risks and
benefits and how each procedure may fit a different person
has the effect of providing informed consent. Some patients
will choose to change their procedure (15%), and some will
choose not to undergo surgery (9%) [26].
This is a mutually beneficial exercise between prospective patients and bariatric center health providers. Patients
gain acquaintance, in a broad sense, with the scheme of the
center, the pathway they will follow in their preoperative
evaluation, the inherent features that pertain to different laparoscopic and possibly open operations, the risks and benefits of each procedure, and the importance of adhering to
feeding and exercise guidelines. Particular emphasis is
placed on the need for lifelong follow-up and periodic
assessment of nutritional parameters. The center’s health
providers, on the other hand, may perform initial evaluations
of the patients, review their nutritional and medical backgrounds, and consider patients’ eligibility for surgery.
Patients who are deemed to require specialist work-ups are
9
Components of a Metabolic and Bariatric Surgery Center
appropriately referred. The duration of these workshops varies from center to center but includes informative presentations by the center’s staff with audiovisual aids and printed
material for future review. Family members should be
encouraged to attend. Patients and their family members
should be given ample opportunity to participate in a dedicated free-flowing discussion.
Support Groups
Support groups are designed for patients who are in the
recovery phase of their operations. Although prospective
patients are encouraged to attend, these sessions should be
primarily targeted to addressing medical, nutritional, psychological, and social issues experienced by postoperative
patients. Patients undergo dramatic changes that affect every
sphere of life, some of which may be difficult to accept.
Patients greatly benefit from the tips and advice delivered by
more experienced patients and from the center staff.
Additional gain may be achieved by holding informal educational lectures, in lay terms, by a variety of invited speakers.
It is important that staff members of the bariatric center consistently attend support group sessions, moderating and
monitoring the discussion to ensure that false information or
misconceptions are not disseminated [27]. Currently, many
centers have online support groups/blogs and use other forms
of social media to keep in touch with patients and make them
feel connected to the center.
Following bariatric surgery, the inclusion of a support
group as part of the treatment plan makes aftercare easier and
more efficient for the patients, as well as for the physicians.
The MBSAQIP accreditation requires that centers provide
regularly scheduled organized and supervised support groups
to metabolic and bariatric surgery patients.
It is therefore obvious that institutions must ensure the
availability of enough space to accommodate educational
seminars and support group sessions. Moreover, such dedicated space should be furnished according to the needs of the
bariatric patients and their families. Such a dedicated environment will clearly reassure patients that they are welcomed
and will be a strong encouraging factor in optimizing their
attendance and participation.
Goals of Preoperative Patient Education and Teaching
• Establishment of a process of informed consent that
can be documented
• Encouragement for compliance and praise
• Education about life after surgery, including nutrition, exercise, and dieting techniques
• Identification of problems
• Identification and development of new kinds of
self-nurturing
111
• Participation in a forum where others really “understand” the challenges and difficulties associated
with “change,” even when the change is for the
better
• Creation of a friendly, safe atmosphere where
patients can bring spouses, parents, and significant
others so that they may also understand, encourage
continuing success, and recognize their own personal issues related to major changes that they are
experiencing with their loved one
• Opportunity for curious potential patients in the
community to come and learn from the “experts” in
an environment of true caring and concern
pecialty Consultants and Preoperative
S
Clearances
Morbidly obese patients often have associated comorbid factors that negatively affect quality of life and often pose a significant risk on a day-to-day basis. Additionally, if
unrecognized or inappropriately managed, these factors may
be a cause of perioperative complications. Serious medical
conditions associated with morbid obesity include cardiovascular, pulmonary, endocrine, metabolic, hematological,
and many other diseases. The availability of consultants and
experts in these fields is critical. Specialty physicians should
be familiar with the particular pathophysiologic consequences of morbid obesity and should be able to ascertain
with a certain degree of confidence the eligibility of candidates to withstand the rigors of major surgery and the
required physical demands on patients in the postoperative
period. Such consultants should be proficient in adequately
preparing patients for general anesthesia, particularly regarding cardiac and pulmonary reserve, and the implementation
of special preoperative patient respiratory training.
All patients should undergo extensive evaluation prior to
weight loss surgery. Careful initial history taking and clinical
examinations will guide clinicians to diagnose previously
unrecognized diseases. Risk factors associated with increased
complication rates after surgery were identified in a number
of published studies [28–31]. These risk factors include
increasing age, male gender, increasing body mass index,
mobility limitations, hypertension, prior history of a venous
thromboembolism, coronary artery disease, myocardial
infarction within the previous 6 months, angina, prior history
of coronary intervention, congestive heart failure, history of
stroke, bleeding disorder, smoking history, procedure type,
procedure time greater than 3 h, obstructive sleep apnea, dyspnea, corticosteroid use, peripheral vascular disease, and
liver disease. A center can consider utilizing one or more risk
112
prediction models established to assess the patient’s overall
risk associated with metabolic and bariatric surgery. By following appropriate algorithms and considering particular
risk factors, many known and undiagnosed conditions can be
evaluated, not in an attempt to discourage or prevent operations, but with the goal of fully optimizing surgical outcomes
by taking special perioperative precautions and additional
supportive measures.
W. J. English et al.
As more patients participate in social networking platforms like Facebook, Twitter, and YouTube, there is an
emerging trend in using social media within bariatric surgery
centers. A University of Florida study suggested there might
be a sixfold increase in the number of social media users in
the next generation of physicians. The study found that only
13% of physician residents compared to 64% of medical students had Facebook profiles [32]. More healthcare professionals are using LinkedIn to keep in contact with other
professionals as well. Sharing knowledge and informing
Electronic and Remote Access
patients using the social network can be of great benefit to
your patients and for your center as it allows your profesto the Metabolic and Bariatric
sional identity to develop. However, it is important to emphaSurgery Center
size that if a center decides to integrate social media into
The ability to obtain information instantly on any topic is the their practice, protecting the rights of patients and exhibiting
results of the tremendous advancements made in the field of online professionalism are paramount.
cyber technology, which includes access to the Internet,
To guide physicians through the complex nature of social
Telehealth, and social media. The positive benefits obtained media interaction with patients, the American College of
through this achievement, however, present as a double-­ Physicians and the Federation of State Medical Boards pubedged sword. Internet and social media content is not regu- lished a position paper with recommendations about the
lated or controlled. For the most part, metabolic and bariatric influence of social media on the patient–physician relationsurgery and obesity-related websites provide valuable infor- ship, the role of these media in public perception of physimation, but there are sites that do disseminate erroneous and cian behaviors, and strategies for physician–physician
false information.
communication that preserve confidentiality while best using
For this reason, it is highly advisable to invest in creating these technologies (Table 9.1) [33].
electronic on-site resources that accurately reflects the mission and purpose of the bariatric surgery center. A website
should contain, in lay terms, an explanation of the problems Metabolic and Bariatric Surgery
of obesity and the available medical and surgical solutions. It in Adolescents
should describe the physical and personal setup of the center,
and the preoperative and postoperative patients will follow. The prevalence of childhood obesity and numerous obesity-­
Additionally, it would be of great benefit for the website to related comorbidities has risen exponentially over the past
possess the ability to accept initial patient application forms several decades. In addition, a mounting body of scientific
electronically, to be used as a basic screening tool prior to evidence demonstrating a high propensity for severely obese
inviting the patient for the educational workshop. A chat adolescents to become severely obese adults has led to an
room for patients and/or a social media platform where increase in the consideration and utilization of surgical
patients could directly contact the surgery center personnel weight reduction procedures in this emerging population.
may result in a modality that is more efficient and practical Adolescent bariatric surgery is safe and effective in treating
than relying on conventional telephonic arrangements.
patients with obesity. In addition to weight loss and comorEstablishing a HIPAA-compliant Telehealth network can bidity resolution, adolescents also benefit from prevention of
allow better access to your center and may help improve many other conditions. The 2018 ASMBS pediatric metaoverall long-term follow-up with your patients. For many bolic and bariatric surgery guidelines recommend early
rural bariatric centers, patients may need to travel many intervention to reduce progression of end-organ damage
hours to attend preoperative seminars, educational sessions, [34]. This is further outlined and supported by data derived
support groups, and routine postoperative visits. Patients can from Teen-Longitudinal Assessment of Bariatric Surgery
simply travel to their local clinic or physician’s office, sign (Teen-LABS) and Treatment Options of Type 2 Diabetes in
into the Telehealth network, and engage in a routine patient– Adolescents and Youth (TODAY) [35, 36].
physician encounter with their bariatric surgeon remotely,
Metabolic and bariatric surgery should only be performed
thus reducing some of the financial burden associated with on adolescent patients at an adolescent center accredited by
high costs of fuel and lodging. Avoiding lengthy trips in the MBSAQIP. Essential personnel, trained in evaluating and
dreaded weather conditions is an unequivocal benefit of caring for adolescent patients, must be available to ensure
Telehealth as well, especially in the wintertime when road safe care for the adolescent patient and to optimize long-term
conditions may be dangerous and not readily accessible.
success after surgery.
9
Components of a Metabolic and Bariatric Surgery Center
113
Table 9.1 Activities of physicians online. The pros, the cons, and recommended conduct
Online physician behavior
Type of online activity
Communicating with patients
via email, text, and instant
messaging
Using social media to gather
information about patients
Referring patients to online
educational resources and
related information
Physician blogging,
microblogging, and physician
postings of comments by
others
Physician posting of their
own personal information on
public social media sites
Physician using electronic
venues (e.g., text and Web) to
discuss patient care with
colleagues
Pros
Greater accessibility to
patients and vice versa
Cons
Possible security breaches in
confidentiality
Can provide and receive
immediate answers
regarding nonurgent issues
Absent or reduced face-to-face or
telephone interactions
Possible ambiguity or misinterpretation
of information provided
Sensitivity to source of information
Allows observation of
patients engaged in any
risk-taking or health-averse
behaviors
Counsel patients or even
intervene in an emergency
Encourages patient
empowerment through
self-education
Supplements resource-poor
environments
Allows advocacy and public
health enhancement
Introduces a physician
“voice” into online medical
conversations
Can improve networking and
communications
Allows easy communication
with colleagues
Can create trust problems in the patient–
physician relationship
Patients may be unable to differentiate
between good information sources and
non-peer-reviewed materials that may
provide inaccurate information
Scam “patient” sites that misrepresent
therapies and outcomes
Allows for negative online comments
that disparages patients and colleagues
Can blur professional and personal
boundaries
Can have negative impact on how the
individual and the profession are
represented to the public
Raises patient confidentiality concerns
Possible unsecured networks and
accessibility of what should be protected
health information
Recommended conduct
Establish guidelines for the types
of issues that are appropriate for
online communication
Reserve digital communication
only for patients who maintain
face-to-face follow-up
Consider the intent of observing
patients via their social media
activities and how to address
adverse findings
Consider the impact on ongoing
care
Physician should review the
information patients find in order
to ensure the accuracy of the
content
Refer patients only to reputable
websites and sources
“Pause before posting”
Consider the content of
comments and the message it
sends about a physician as an
individual and the profession
Physicians should maintain
separate personas for their
personal and professional online
behavior
Physicians should scrutinize
what material they make
available for public consumption
Implement health information
technology solutions for secure
messaging and information
sharing
Follow institutional practice and
policy for remote and mobile
access of protected health
information
Adapted from Farnan et al. [33]
Pediatric Medical Advisor (PMA)
Every adolescent patient requires a pediatrician or equivalent
provider who will participate in the preoperative and postoperative care of the adolescent patient and provide ongoing general pediatric medical oversight. In addition, the PMA can
assist in the utilization of adolescent-specific s­ ubspecialty consultation when needed (i.e., sleep medicine, gastroenterology,
endocrinology, hematology, nephrology, behavioral health,
etc.). This individual should possess the necessary training and
be credentialed in general pediatrics and/or pediatric subspecialty training (i.e., endocrinology, cardiology, gastroenterology, adolescent medicine). Responsibilities should also
include assisting in the development of comorbid-specific
treatment plans in conjunction with the patient’s primary care
provider in order to optimize perioperative health.
Adolescent Behavioral Specialist
In order to achieve successful outcomes in adolescents, there
must be assurances that patients and their families have the
ability and the motivation to comply with recommended
treatments preoperatively and postoperatively, including
consistent use of recommended nutritional supplements. A
history of reliable attendance at office visits for weight management and compliance with other medical needs is critical
in determining compliance.
114
W. J. English et al.
The adolescent patient and family must be able to demonstrate awareness of the general risks and benefits of metabolic and bariatric surgery as well as the dietary and physical
activity requirements following a metabolic and bariatric
procedure [37].
A psychologist, psychiatrist, or other qualified and
independently licensed provider with specific training and
credentialing in pediatric and adolescent care must perform this assessment. The practitioner must have experience in treating obesity and eating disorders as well as
experience evaluating adolescent patients and families.
The elements of behavioral assessment should include evidence for mature decision-making and awareness of potential risks and benefits of the proposed operation,
documentation of the adolescent’s ability to provide surgical assent, evidence of appropriate family and social support mechanisms (i.e., engaged and supportive family
members, caretakers, etc.), and clinically stable behavioral
disorders (i.e., depression, anxiety, etc.) that have been satisfactorily treated.
ommon Deficiencies Encountered During
C
the MBSAQIP Site Survey
1. Data entry of all procedures: In most cases, this involves
incomplete entry of procedures due to having no
MBSCR available or unavailability of medical records
from surgeon office records. In some cases, deficiencies
are cited because centers are performing investigational
procedures without Institutional Review Board approval.
Table 9.2 Top ten deficiencies encountered during a site survey
The MBSAQIP accreditation process is laborious and
involves triennial site visits by a surgeon surveyor. The site
survey assesses whether the center is in compliance with the
standards, including Case Volume, Commitment to Quality
Care, Appropriate Equipment and Instruments, Critical Care
Support, Continuum of Care, Data Collection, and
Continuous Quality Improvement Processes. Additional
requirements are necessary for stand-alone Children’s
Hospitals and Ambulatory Surgery Centers. Each standard is
comprised of various elements, and accreditation is only
achieved if compliance is met with all components for each
standard.
Standard
6.1
7.1
6.2
% of sites with
deficiency
5.98
5.01
4.85
Requirement
Data entry of all procedures
Institutional collaborative
Data reports, quality metrics, and
quality monitoring
Process improvement initiatives
Credentialing guidelines
MBSCR
Monitoring of safety culture
Qualified call coverage
Surgeon verification
Facilities, equipment, and
instruments
7.2
2.6
2.4
7.3
2.8
2.7
3.1
3.88
3.72
3.39
3.32
3.07
2.91
2.42
# of Deficiencies per Standard
140
120
100
80
60
40
20
0
123
75
67
9
DA
R
ST
AN
D
DA
R
D
8
7
ST
AN
DA
R
D
6
D
# of Deficiencies
ST
AN
DA
R
ST
AN
D
DA
R
5
0
5
4
DA
R
D
3
D
DA
R
ST
AN
D
DA
R
ST
AN
2
1
D
ST
AN
24
18
15
ST
AN
7
DA
R
ST
AN
Fig. 9.2 Number of
deficiencies per standard
found on MBSAQIP site
surveys
In a review of 619 site surveys performed between
September 2014 and August 2016, nearly one-quarter of
MBSAQIP applicants had at least one deficiency. The
Standards categories most often cited were related to quality
and data, indicating opportunities for improvement (Fig. 9.2).
98.9% of centers with deficiencies were able to gain or maintain accreditation through corrective or remedial actions,
demonstrating the effectiveness and potential developmental
prospect of the accreditation process [38].
Understanding which standards are most commonly deficient following MBSAQIP site surveys allows centers to
become better prepared for their accreditation or reaccreditation process. Table 9.2 describes the most common deficiencies found during site surveys.
9
Components of a Metabolic and Bariatric Surgery Center
115
2. Institutional collaborative: Many centers will review and effectively will strengthen accordingly. Because morbid
their adverse events and its semiannual risk-adjusted obesity is a disease that globally affects patients, it can only
report (SAR), but deficiencies are cited when there is no be managed by a diverse group of skilled individuals, all of
documentation of such a review in the meeting whom are united in the common purpose of its eradication.
minutes.
The aim of surgical solutions should be permanent weight
3. Data reports, quality metrics, and quality monitoring: loss, and this will require the prolonged services of bariatriSimilar to #2, centers will typically review their out- cians, nutritionists, physical therapists, perhaps even spiritual
comes, but deficiencies are cited when the center does healers, and marriage counselors. The fact is that there must
not document in the MBS Committee meeting minutes be a comprehensive program in place, with the ability to evalthat this was reviewed at least three times annually.
uate prospective patients in a comprehensive manner, and to
4. Process improvement initiatives: Most commonly, cen- prepare them mentally and physically for the rigors of surters will fail to document at least one quality, or process, gery and permanent lifestyle changes they will need to adopt.
improvement project annually. Most importantly, defiThe most important element in the bariatric surgery cencient centers fail to address high outlier status on their ter is leadership from the surgeons and integrated health
SARs.
staff. Such a comprehensive center requires dedicated per5. Credentialing guidelines for metabolic and bariatric sonnel, a strong fundamental infrastructure, and total institusurgeons: Centers that are deficient in this standard most tional commitment. Most important of all, there needs to be
commonly lack credentialing guidelines that are sepa- a pervasive philosophy that stretches across all institutional
rate from general surgery credentialing guidelines. The departments and that accepts morbid obesity as a disease
standards require centers to adhere to nationally recog- process, the management of which is a noble and dramatinized credentialing guidelines [9].
cally rewarding mission.
6. MBSCR: The most common reason for deficiencies in
this standard is the MBSCR cannot enter data from all
procedures and follow-up due to lack of access to office Question Section
records from surgeon offices. All surgeons participating
at the center must provide access to remain compliant 1. The Metabolic and Bariatric Committee must include all
with this standard.
of the following personnel except for:
7. Ongoing monitoring of safety culture: Centers that
A. Surgeon Director who is actively performing metareceived a deficiency with this standard failed to review
bolic and bariatric surgery
all mortalities by the MBS Committee within the
B. Bariatric coordinator
required 60-day time limit from the time of discovery.
C. All surgeons performing metabolic and bariatric sur8. Qualified metabolic and bariatric surgeon call covergery at the center
age: Centers received deficiencies because they failed to
D. Operating room nursing representative
provide documentation of a bariatric surgery-specific 2. The most common MBSAQIP site survey deficiency is
call schedule. Some centers did not provide protocols
associated with:
outlining the care of an unaffiliated metabolic and barA. Credentialing
iatric surgery patient presenting at the center.
B. Data entry
9. Metabolic and bariatric surgeon verification: In almost
C. Joint Commission accreditation
all cases, deficiencies were issued because there was
D. Furniture
insufficient documentation of the required bariatric-­ 3. The MBSAQIP standard found to have the highest numspecific CME credits.
ber of deficiencies is:
10. Facilities, equipment, and instruments: The three most
A. Standard 2 – Commitment to Quality Care
common deficiencies listed with this standard include
B. Standard 3 – Facilities, Equipment, and Instruments
absence of appropriate furniture in the waiting areas,
C. Standard 6 – Data Collection
lack of toilet supports, and the inability of centers to
D. Standard 7 – Continuous Quality Improvement
document equipment weight limits.
4. What is the estimated number of metabolic and bariatric
surgery centers participating in a nationally recognized
accreditation program?
Conclusion
A. 63%
B. 74%
As the worldwide epidemic of obesity continues its exponenC. 85%
tial growth, the demand on surgeons to treat patients safely
D. 92%
116
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CL. Trends in obesity and severe obesity prevalence in US youth
and adults by sex and age, 2007-2008 to 2015-2016. JAMA. United
States. 2018:1723–5.
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Evaluation of Preoperative Weight Loss
10
Hussna Wakily and Aurora D. Pryor
programs to decrease body mass index (BMI) would theoretically result in decreased perioperative and postoperative
complications such as bleeding, wound infection, etc. In
1. To explain the principles of preoperative weight
addition, shorter operative times and hospital stays could
loss
occur. In addition to the hypothetical risk improvement with
2. To review the data supporting and refuting the benpreoperative weight loss, many medical providers theorized
efits of preoperative weight loss
that patients who are able to demonstrate PWL are more
motivated and serious about adhering to postoperative diet
and exercise recommendations. Based on these theoretical
advantages, many physicians have supported PWL [4]. In
Introduction
addition, over the last several years, many insurance compaObesity has become an epidemic in the USA and around the nies added attempted PWL as a prerequisite for surgery [1].
world, leading to increased interest in bariatric surgery as a Many surgeons have questioned, however, if it is truly approtreatment option. Many bariatric patients have had multiple priate to exclude patients from definitive therapy if they
failed attempts at weight loss and are looking for longer-­ prove that medical management is ineffective [5].
Most PWL programs include several meetings with nutrilasting results. Although there is consensus for many surgical
procedures, optimal preoperative management is more tionists and physicians, as well as psychiatric assessments
debated. Preoperative weight loss (PWL) has been proposed and weigh-ins at these appointments. If the patients are
as a screening tool for predicting success in surgical candi- unable to show adequate weight loss or if they miss appointdates. It has also been mandated by many surgeons and ments, they are forced to start over or are even refused surinsurers [1]. This chapter will discuss the strategy of PWL gery. The guidelines used by some surgeons and insurance
carriers originated with the National Institutes of Health
and review the available evidence.
(NIH)
Consensus
Development
Conference
on
Gastrointestinal Surgery for Severe Obesity [6] convened in
1995 and published in 1998 [7]. This consensus group based
Principle Behind the Support of Preoperative
the recommendation for attempted weight loss on a review of
Weight Loss
Medline queryable published reports. They supported
It is an accepted concept that patients who weigh less have attempted medical weight loss as some patients may be sucdecreased risk with surgery and less weight-related comor- cessful with diet and exercise alone; however, no data was
bidity. Thinner patients generally require less rigorous pre- presented to demonstrate differences with outcomes after
operative clearance than their heavier counterparts due to a weight loss surgery with or without pre-op diet attempts. In
lower burden of obesity-related disease [2]. In addition, it is fact, the NIH panel concluded that less than 20% of patients
technically easier to operate on someone who is thinner due have long-term success with diet and exercise alone, bringto improved exposure and accessibility [3]. Preoperative ing into question the legitimacy of the proposed 6-month
PWL requirement.
Since the NIH consensus panel, many authors have studH. Wakily
ied the impact of mandated PWL on eventual surgery. Jamal
Division of General Surgery, Department of Surgery, NY and NJ
Surgical Associates, Queens, NY, USA
and colleagues compared two groups of patients: 72 undergoing a mandated 13-week dietary counseling program and
A. D. Pryor (*)
Department of Surgery, Stony Brook Medicine,
252 without this requirement. Both groups were similar preStony Brook, NY, USA
operatively except for a slight difference in sleep apnea. The
Chapter Objectives
e-mail: aurora.pryor@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_10
117
118
PWL group had a 50% higher dropout rate before surgery
(28% versus 19%), lower percentage of excess weight loss
(%EWL), and higher BMI and weight following surgery.
Other tracked outcomes were equivalent [8].
Sadhasivam and colleagues performed a retrospective
review of their bariatric surgery candidates from 2001 to
2005 and looked at reasons patients did not undergo surgery.
They reviewed 1054 patients and found that only 519 (49%)
underwent bariatric surgery and that 29.7% were denied due
to insurance denial. Major denial reasons were that patients
could not meet the strict preoperative prerequisites established, such as 5–10% reduction in BMI, documented prior
weight loss attempts, multiple meetings with nutritionist,
etc. Other reasons patients did not undergo surgery were
because of frustration with the rigorous requirements and
long waiting time. From 2001 to 2005, the authors demonstrated an increase in insurance denials from 9.9% to 19.9%
[9]. This study is important in showing that insurance company mandates are resulting in increasing denials for bariatric surgery coverage.
eview of the Data Supporting and Refuting
R
the Benefit of Preoperative Weight Loss
Postoperative Weight Loss
The Obesity Surgery Mortality Risk Score has been used
as a strategy to predict perioperative mortality risk [2]. It
is a multivariable analysis used to identify BMI >50,
hypertension (HTN), male gender, elevated pulmonary
embolism risk, and age >45 years as independent risk variables for bariatric surgery [2]. Among those variables,
BMI is the only one that can be modified preoperatively,
potentially supporting mandated PWL for higher-risk
patients. However, several studies addressing PWL as a
means for risk reduction have failed to demonstrate a benefit. Harnisch and colleagues compared two groups of
patients undergoing Roux-en-Y gastric bypass (RYGB),
those achieving greater than 10 lbs. weight loss (88
patients) before surgery and those that instead gained at
least 10 lb. (115 patients). The authors failed to find a difference in perioperative complications, comorbidity resolution, or weight loss at 12 months compared to the
immediate preoperative weight [10]. Alami and colleagues
completed a rare randomized controlled trial study comparing 26 patients completing the required PWL versus 35
with no preoperative diet requirements [11]. Although
excess weight loss was noted to be greater in the PWL
group compared to the non-PWL at 6 weeks and 3 months,
there was no change in 6-month follow-up visit and 1-year
H. Wakily and A. D. Pryor
postoperative weight loss. In addition, the groups showed
no difference in intraoperative complications or conversions, complication rates, blood loss, or hospital stay. In
the 12-month follow-up reported by Solomon, there was
also no difference in BMI or comorbidity resolution at
1 year in the population as a whole. A small benefit in
%EWL at 1 year was seen, however, in the subgroup able
to lose more than 5%EWL preoperatively [12].
In 2011, Cassie, Menezes, and Birch reviewed 17 studies,
including 4611 patients that showed PWL beneficial, and 20
studies with 2075 patients showing no benefits to PWL [13].
This analysis includes the studies previously discussed in
this chapter (Table 10.1). Most reviewed analyses focused on
the 12-month follow-up point. Combining all studies reporting 12-month data, the non-preoperative weight loss groups
had an estimated weight loss of 70.7 ± 5.7% versus the preoperative weight loss group of 69.0 ± 7.1%. At 2 years, there
was still no significant difference in both weight groups with
the PWL showing 66.7 ± 2.7% estimated weight loss and the
non-preoperative weight loss group at 72 ± 6.3%. The authors
concluded that there was inadequate data to support mandated PWL based on the outcome of postoperative weight
loss [1, 2].
Livhits and colleagues performed a meta-analysis of 15
articles including 3404 patients. Only two of the included
cohorts were excluded from the Cassie review. Not surprisingly, the authors drew similar conclusions. Of the 15 articles
analyzed, 5 studies had positive effects for PWL, 2 studies
showed positive short-term effects, 5 studies showed no difference, and 1 study showed a negative effect. Overall no
significant heterogeneity was seen among the studies with
results of postoperative weight loss [3].
Operative Time
One of the hypothesized benefits of PWL includes shorter
operative times, so looking at the studies that analyzed, this
is important in determining if PWL is needed. In the Alami
study, total operating time was greater in the non-­preoperative
weight loss group (257.6 ± 27.8 min versus 220.2 ± 31.5 min)
as compared with the preoperative weight loss group [4].
Harnisch and colleagues also found a slight benefit in OR
time with PWL (119.7 versus 104.9 min, P = 0.02) [5]. The
savings of 12.5–23 min with PWL are consistent in other
studies as well [1, 3]. The problem with these papers is that
it is not properly distinguished how operating time is measured, so there could be a discrepancy in what is a standardized operating time. Also, there is no study so far that has
demonstrated that the time saved has contributed to improved
patient safety and outcomes.
10 Evaluation of Preoperative Weight Loss
119
Table 10.1 Studies comparing effectiveness of preoperative weight loss
Study inclusion
Investigator
Year
2007 Alami
2008
2007
2005
2010
2009
2007
2008
2008
Study type
RCT
Patients
(n)
61
Procedure
LRYGB
Alger-Mayer
Ali
Alvarado
Becouarn
Benotti
Broderick-­Villa
Carlin
Conlee
Prospective
Retrospective
Retrospective
Retrospective
Retrospective
Retrospective
Retrospective
Retrospective
150
351
90
507
881
353
295
105
RYGB
LRYGB
LRYGB
RYGB/LAGB/SG
LRYGB/RYGB
RYGB
LRYGB
RYGB
2010
1997
2008
2008
2008
Eisenberg
Finigan
Fujioka
Gallo
Harnisch
Retrospective
Prospective
Retrospective
Retrospective
Retrospective
256
31
121
494
203
LRYGB
LAGB
LRYGB/RYGB
LAGB
LRYGB
2005
2008
Hong
Huerta
Retrospective
Retrospective
100
40
LAGB
RYGB
2009
2005
1995
2007
2008
Jantz
Liu
Martin
Micucci
Mrad
Retrospective
Retrospective
Prospective
Retrospective
Retrospective
384
95
100
NR
146
2005
2008
Phan
Reiss
Retrospective
Retrospective
364
262
LRYGB
LRYGB
RYGB
RYGB
LRYGB/RYGB/
LAGB/VGB
LRYGB/RYGB/LAGB
LRYGB
2009
2009
2007
1999
Segaran
Solomon
Still
Van de Weijgert
Prospective
RCT
Prospective
Retrospective
37
44
884
153
RYGB/LAGB/SG
LRYGB
LRYGB/RYGB
RYGB/VGB
Variables assessed
Postoperative EWL, operating room time, complication
rate, comorbidity resolution
Postoperative EWL
Postoperative EWL
Postoperative EWL, operating time, comorbidity resolution
Postoperative EWL
Complication rate
Postoperative EWL
Postoperative EWL
Postoperative EWL, operating time, complication rate,
length of stay
Postoperative EWL
Postoperative EWL
Postoperative EWL, complication rate
Postoperative EWL, operating time
Postoperative EWL, operating time, complication rate,
comorbidity resolution
Postoperative EWL
Postoperative EWL, operating time, complication rate,
length of stay
Postoperative EWL
Operating time, complication rate, length of stay
Postoperative EWL, complication rate
Postoperative EWL
Postoperative EWL
Postoperative EWL
Postoperative EWL, operating time, complication rate,
length of stay
Complication rate
Postoperative EWL, conversion rate, complication rate
Postoperative weight loss, length of stay
Postoperative EWL
Adapted from Cassie et al. [1]
RCT randomized controlled trial, LRYGB laparoscopic Roux-en-Y gastric bypass, EWL excess weight loss, RYGB Roux-en-Y gastric bypass,
LAGB laparoscopic adjustable gastric banding, SG sleeve gastrectomy, VGB vertical gastric banding
Operative Complications
Livhits and colleagues proposed that meta-analysis of complications is difficult due to the lack of consistency in definition.
However, they concluded that there was no significant difference between groups [3]. Cassie noted decreased complications with PWL in 2 of 11 studies. However, when the data
from the reviewed papers were pooled, the complication rates
for the preoperative weight loss group were 18.8 ± 10.6% versus 21.4 ± 13.1% in the non-preoperative weight loss group
showing that there was no real difference in the two groups [1].
Hospital Stay
Decreased length of stay is one benefit that would also result
in cost-reducing measures, but again there are inadequate
data to support a length of stay benefit with PWL. Cassie
reported on five studies with the length of stay ranging from
2.2 to 4.3 days for the PWL versus 2.3–6.0 days for the non-­
preoperative weight loss group. The mean from pooled studies was 3.34 ± 0.83 for the PWL versus 3.98 ± 1.49 days for
the non-preoperative weight loss group [1]. Although there
was a trend in support of PWL, the data are inconclusive.
Liver Reduction and VLED
Many bariatric surgeons have recognized variability in fatty
liver intraoperatively and attribute reduced liver size to preoperative weight loss. Some surgeons have specifically
implemented a very-low-energy diet (VLED) for weight loss
and liver volume reduction. Colles investigated the actual
changes in liver volume and the pattern of this change with
120
H. Wakily and A. D. Pryor
Baseline
Week 12
Fig. 10.1 Single cross-sectional images of the liver performed by
computed tomography at baseline and week 12 of a very-low-energy
diet. The images, taken from within a series of contiguous 8-mm slices
used to calculate total liver volume, illustrate the extent of the change in
liver volume with weight loss in a 35-year-old man with an initial liver
volume of 3.7 L and final liver volume of 2.4 L. A 35% reduction in
liver size and a weight loss of 18 kg were observed
VLED, the relative change in liver volume, body weight and
visceral and subcutaneous adipose tissue (VAT/SAT) areas,
the clinical and biochemical risk factors that may predict an
enlarged pretreatment liver or predict the total change in liver
volume after treatment, patient acceptability and compliance, and treatment side effects. Patients with BMI between
40 and 50 were chosen based on the fact that surgeons find
that patients in this range posed the greatest surgical difficultly. The diet itself consisted of three shakes/day providing
456 kcal, 52 g protein, 7 g fat, and 45 g carbohydrate plus the
recommended daily allowance of vitamins, minerals, and
trace elements. This diet took place over 12 weeks. The
changes in the liver were assessed by computed tomography
(CT) scan and magnetic resonance imaging (MRI) during
the 12-week interval (Fig. 10.1). At the end of the diet, the
average decrease in liver size was 18.7%. Also, this study
showed that the larger the initial liver volume, the better the
decrease in liver volume. The authors reported no hepatomegaly in the study patients and a low perioperative risk,
although the study was not powered for complications. The
most important pattern noted is that the majority of the volume reduction occurred within the first 2 weeks [6]. This
data supports potential benefit with PWL; however, a short
2-week time course may be adequate.
Healthcare System became a great source for evaluating this
specific type of population. Collins and colleagues looked at
changes in liver volume and adipose tissue in patients with
BMI >50 [7]. The authors felt these patients in theory would
benefit most from a reduction in liver volume and adipose
tissue to facilitate surgery and decrease complication rates.
The comorbidities with increased prevalence in the super
obese include all those associated with obesity: type II diabetes mellitus, hypertension, obstructive sleep apnea, congestive heart failure, and so on. The technical difficulties related
to this population of patients include thick abdominal wall,
excess visceral adipose tissue, a relatively short mesentery,
and an enlarged fatty liver. Altering these characteristics
should in theory decrease complication rates and shorten
operative times.
To achieve acute preoperative weight loss, Collins
employed a liquid low-calorie diet consisting of 800 kcal/
day, nutritional and behavioral counseling, and education
with the goal of a 10% weight loss reduction. The goal of this
study was to evaluate change in obesity-related comorbidities, liver volume, and subcutaneous adipose tissue over several weeks. Since the weight loss and methods were drastic,
the patients were required to have multiple assessments during their preoperative course. The authors also tracked
changes in mediations, weekly laboratory tests, and weekly
physical exams because of the aggressive nature of the
weight loss. At baseline and after the completion of the diet
program, computed tomography (CT) scans of the abdomen
were compared. A total of 30 patients underwent the program with a mean BMI at baseline of 56, mean age 53. The
program lasted a total of 9 weeks, and the patients had an
Super Obese
Characteristics that put patients at a higher level of risk for
bariatric surgery include BMI >50, male gender, and a lower
socioeconomic status. The Veterans Affairs Pittsburgh
10 Evaluation of Preoperative Weight Loss
average body weight loss of 12.1%. After the low-calorie
diet was completed, the mean BMI decreased to 49. They
recognized an 18% decrease in liver volume over 9 weeks in
patients enrolled in the study. They did not, however,
­compare complications or outcomes to patients not completing the diet. Their final conclusion is that a preoperative diet
is safe to decrease liver volume for bariatric surgery in an
effort to improve perioperative and postoperative course,
especially for those with a BMI >50. As with Colles and
Collins, other studies have supported this finding as well [8].
Additional Considerations with PWL
121
scored greater in the dietary adherence experienced a weight
loss that was 2.4% points greater at postoperative week 40
and 3.8% points greater at week 66 compared to those
patients with a lower score on the dietary adherence. By
week 92, both groups had regained some of their weight, but
the group that scored in the high adherence group still had
achieved a weight loss that was 4.5% points greater than
those in the low adherence group, representing a 28% greater
weight loss. This study was able to demonstrate improvements in psychosocial status postoperatively. They had
improved self-esteem, increased positive affect, and
decreased negative affect and depressive symptoms, as well
as had changes in their eating habits [13]. These results suggest that there is a positive psychosocial benefit to nutritional
and behavioral education, although not necessarily
PWL. Teaching better eating habits not only helps the
patients maintain postoperative weight loss but also improves
their self-esteem. All these translate to patients who participate in a preoperative educational program and may be better
equipped to help keep off weight postoperatively. As a result,
Sarwer supports that PWL should be encouraged but not
used as a way to screen for surgical candidates who would
obtain the most from bariatric surgery.
Most bariatric patients gain some portion of their weight
back after their postoperative nadir. It is supported by most
surgeons that weight regain and weight loss failure are
largely tied to behavioral and psychosocial causes, although
recent research suggests that the root cause of weight regain
may be due to the genetic predisposition [9] or from alteration of the physiological mechanisms by which metabolic
operations appear to work [10–12].
The psychosocial benefit of PWL may have the most dramatic results on maintaining postoperative weight loss in the
long term. Sarwer analyzed the relationship between preoperative eating behavior and postoperative dietary adherence Study Limitations
[13]. The goal of this study was to look at the relationship of
postoperative weight loss to preoperative psychosocial vari- The studies reviewed in this chapter have some limitations to
ables such as self-esteem and mood, as well as preoperative address. Only one study is available with a prospective, raneating behaviors, dietary intake, and patients’ self-reported domized study design [4]; however, even in this analysis,
adherence to the postoperative diet over a 92-week period. fewer than 100 patients were available. The other studies are
Approximately 200 patients participated in the study, with primarily retrospective studies with significant variability in
the initial evaluation at 4 weeks before surgery. The partici- data collection. Larger-scale, prospective randomized trials
pants completed a psychosocial/behavioral evaluation to would need to support a benefit in PWL before this should be
assess their appropriateness for surgery followed by a packet mandated. The Sarwer study was limited due to the high
of questionnaires. They were again asked to fill out the ques- number of attrition, which is typical for these types of studtionnaires at 20, 40, 66, and 92 weeks after surgery. The ies, and only a 2-week educational period prior to surgery.
packet included the following measures: Rosenberg Self-­ Only 56% of the patients completed the study, impacting the
Esteem Scale, Beck Depression Inventory-II, Positive and significance of the paper by decreasing the population size.
Negative Affect Scale, Eating Inventory, Block 98 Food Another limitation to this paper was that the data was based
Frequency Questionnaire, dietary adherence, and weight. on self-analysis, which is difficult to interpret [13].
Approximately 2 weeks prior to surgery, the participants met
with a dietician and were instructed on dietary and behavioral changes that the authors felt would give them the best ASMBS Position Statement
postoperative outcome, followed by dietary instructions
postoperatively to help maintain the weight loss. From the The American Society for Metabolic and Bariatric Surgery
variables that were looked at, the ones that were significant (ASMBS) issued a position statement due to questions raised
predictors for success (measured by percentage of weight to the society by physicians, hospitals, patients, and insurloss over time) included gender, baseline cognitive restraint, ance companies regarding preoperative weight loss [14].
and self-reported dietary adherence. Those patients who (This statement is reviewed in Chap. 11.) The final summary
were able to show cognitive restraint preoperatively also did and recommendations, as also demonstrated by the studies
well at 20 weeks postoperatively, when the patients were reviewed here, are that there is a low level of evidence supadvanced back to a regular diet. Those individuals who porting the need for preoperative weight loss. Class I or
122
evidence-­based studies currently are not available to support
the request for mandated PWL. Lower levels of evidence do
exist, but the data and results are not consistent. Although
there is some evidence in the Class II–IV range for acute
preoperative weight loss, the studies are not consistent, and
some are conflicting, leaving us with no clear answers. There
is some low level of evidence to suggest that preoperative
weight loss can help with evaluating a patient’s adherence to
the new lifestyle, but this should be judged by each individual situation. The studies so far have shown no difference in
comorbidity improvement, postoperative complications, or
postoperative weight loss to justify the need for PWL. The
current recommendation is that insurance companies and
physicians should reevaluate the need for PWL. Thus far, it
contributes to higher attrition rates, increases frustration
among patients, and blocks certain patients from obtaining a
life-altering and beneficial surgery.
Conclusion
The only evidence-based support for preoperative education
and encouraging PWL is that these tools may help patients
prepare for surgery and understand techniques to maintain a
healthier lifestyle postoperatively. The data so far is inconsistent and inconclusive with regard to the benefits of PWL,
but the majority of the studies show no difference in complication rates or morbidities in patients undergoing PWL versus no PWL. If considering PWL, the data supports the
notion that shorter-term preoperative diets (i.e., 2 weeks)
may also reduce liver volume and reduce operative time,
without significant reduction in risk. Mandated programs in
excess of this are a barrier to our patients and without supportive evidence.
Question Section
1. Studies have shown that a very-low-energy diet has been
beneficial and should be started preoperatively. What is
the optimal timing for starting the diet?
A. 2 weeks
B. 6 weeks
C. 8 weeks
D. 12 weeks
2. The ASMBS position statement was issued to clarify the
validity of PWL by reviewing the current literature and
evidence. The statement’s final conclusion is that there is
a strong level of evidence to justify the use of PWL.
A. True
B. False
H. Wakily and A. D. Pryor
References
1. Cassie S, Menezes C, Birch DW, Shi X, Karmali S. Effect of preoperative weight loss in bariatric surgical patients: a systematic
review. Surg Obes Relat Dis. 2011;7(6):760–7.
2. Ray EC, Nickels MW, Sayeed S, Sax HC. Predicting success after
gastric bypass: the role of psychosocial and behavioral factors.
Surgery. 2003;134(4):555–63.. discussion 563–4
3. Livhits M, Mercado C, Yermilov I, Parikh JA, Dutson E, Mehran
A, et al. Does weight loss immediately before bariatric surgery
improve surgical outcomes: a systematic review. Surg Obes Relat
Dis. 2009;5(6):713–21.
4. Alami RS, Morton JM, Schuster R, Lie J, Sanchez BR, Peters A,
et al. Is there a benefit to preoperative weight loss in gastric bypass
patients? A prospective randomized trial. Surg Obes Relat Dis.
2007;3(2):141–5.. discussion 145–6
5. Harnisch MC, Portenier DD, Pryor AD, Prince-Petersen R, Grant
JP, DeMaria EJ. Preoperative weight gain does not predict failure
of weight loss or co-morbidity resolution of laparoscopic roux-­
en-­
y gastric bypass for morbid obesity. Surg Obes Relat Dis.
2008;4(3):445–50.
6. Colles SL, Dixon JB, Marks P, Strauss BJ, O’Brien PE. Preoperative
weight loss with a very-low-energy diet: quantitation of changes
in liver and abdominal fat by serial imaging. Am J Clin Nutr.
2006;84(2):304–11.
7. Collins J, McCloskey C, Titchner R, Goodpaster B, Hoffman M,
Hauser D, et al. Preoperative weight loss in high-risk superobese
bariatric patients: a computed tomography-based analysis. Surg
Obes Relat Dis. 2011;7(4):480–5.
8. Fris RJ. Preoperative low energy diet diminishes liver size. Obes
Surg. 2004;14(9):1165–70.
9. Matzko ME, Argyropoulos G, Wood GC, Chu X, McCarter RJ,
Still CD, et al. Association of ghrelin receptor promoter polymorphisms with weight loss following Roux-en-Y gastric bypass surgery. Obes Surg. 2012;22(5):783–90.
10. Liou AP, Paziuk M, Luevano JM Jr, Machineni S, Turnbaugh PJ,
Kaplan LM. Conserved shifts in the gut microbiota due to gastric bypass reduce host weight and adiposity. Sci Transl Med.
2013;5(178):178ra41.
11. Angelakis E, Armougom F, Million M, Raoult D. The relationship between gut microbiota and weight gain in humans. Future
Microbiol. 2012;7(1):91–109.
12. Frazier TH, DiBaise JK, McClain CJ. Gut microbiota, intestinal
permeability, obesity-induced inflammation, and liver injury. JPEN
J Parenter Enteral Nutr. 2011;35(5 Suppl):14S–20.
13. Sarwer DB, Wadden TA, Moore RH, Baker AW, Gibbons LM,
Raper SE, et al. Preoperative eating behavior, postoperative dietary
adherence and weight loss after gastric bypass surgery. Surg Obes
Relat Dis. 2008;4(5):640–6.
14. Brethauer S. ASMBS position statement on preoperative
supervised weight loss requirements. Surg Obes Relat Dis.
2011;7(3):257–60.
ASMBS Position Statements
11
Stacy A. Brethauer and Xiaoxi (Chelsea) Feng
Chapter Objectives
1. Review bariatric surgery recommendations based
on current knowledge, expert opinion, and published peer-reviewed scientific evidence.
2. Summarize current position statements of the
ASMBS for the care and treatment of bariatric
patients.
Introduction
Why Have Position Statements?
Most large medical and surgical societies publish position
statements and guidelines for their membership. The majority of these position statements are evidence-based documents that provide a comprehensive summary of the available
data on a topic that is of particular interest to the membership. The intent of publishing these statements in many cases
is to clarify a controversial issue, to provide guidance for
healthcare leaders and payers, and to provide support for
clinical decisions made by the membership.
The American Society for Metabolic and Bariatric
Surgery (ASMBS) publishes position statements in response
to numerous inquiries made to the society by patients, physicians, society members, hospitals, and others regarding a
particular topic relevant to the field. In these statements,
available data are summarized, and recommendations for
treatment are made based on current knowledge, expert opinion, and published peer-reviewed scientific evidence available at the time. The ASMBS leadership also collaborates
S. A. Brethauer (*)
Department of Surgery, The Ohio State University,
Columbus, OH, USA
e-mail: Stacy.Brethauer@osumc.edu
with other medical societies to develop and publish practice
guidelines that are relevant to the care of the bariatric surgery
patient [1].
How Are Statements Developed?
ASMBS statements can be generated within the Clinical
Issues Committee (CIC) or within other committees as the
need arises. The Executive Council can also task the CIC to
generate position statements based on the need to clarify the
society’s stance on a particular topic. The Clinical Issues
Committee has formalized the processes for statement development and approval to ensure that these documents are
developed, published, and revised in the appropriate time
frame. The development and vetting process for position
statements are summarized in Fig. 11.1.
Summary of Current Position Statements
Access to Care for Obesity Treatment
1. Obesity is a medical condition that meets all criteria as a
disease, including a genetic predisposition and personal,
societal, and environmental factors that contribute to
expression of the disease [2].
2. Obesity is an independent risk factor for heart disease and
is predominant in patients with hypertension, high cholesterol, and type 2 diabetes.
3. People who suffer from the disease of obesity should be
free from prejudice and discrimination in accessing care
for obesity.
4. People who suffer from the chronic disease of obesity
should have access to evidence-based medical, pharmaceutical, behavioral, and surgical care similar to the
access provided for the evaluation and management of
other chronic disease.
X. (C.) Feng
Department of General Surgery, Cleveland Clinic,
Cleveland, OH, USA
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_11
123
124
S. A. Brethauer and X. (C.) Feng
5. Prevention of obesity through new strategies of healthy
lifestyles should complement the commitment to treat
those currently suffering from the metabolic consequences of the disease.
6. Weight loss surgery is effective, durable, and increases
quality and quantity of life. Obesity should be treated.
reoperative Supervised Weight Loss
P
Requirements
1. There are no data from any randomized controlled trial,
large prospective study, or meta-analysis to support the
practice of insurance-mandated preoperative weight loss.
The discriminatory, arbitrary, and scientifically unfounded
practice of insurance-mandated preoperative weight loss
contributes to patient attrition, causes unnecessary delay
of lifesaving treatment, leads to the progression of life-­
threatening comorbid conditions, is unethical, and should
be abandoned [3].
2. There is no level 1 data in the surgical literature or consensus in the medical literature (based on over 40 published RCTs) that has clearly identified any 1 dietary
regimen, duration, or type of weight loss program that is
optimal for patients with clinically severe obesity [3].
3. Patients seeking surgical treatment for clinically severe
obesity should be evaluated based on their initial BMI
and comorbid conditions. The provider is best able to
determine what constitutes failed weight loss efforts for
their patient [3].
Fig. 11.1 (a, b) The general
algorithm for statement
development within the
ASMBS
a
I mpact of Obesity and Obesity Treatment
on Fertility and Fertility Therapy
There is a very high prevalence of obesity among women of
childbearing age. Obesity in women is associated with an
increased risk of infertility and an increased rate of complications during every stage of pregnancy. Obesity is associated with PCOS and IR, which also negatively impact
fertility. Overall, however, there is a paucity of high-level
evidence regarding the impact of obesity and obesity treatment on fertility and infertility treatment. Ongoing investigation and randomized controlled trials are necessary to fully
understand the role of obesity and the impact of medical and
surgical treatments for obesity on male and female fertility
and infertility treatment outcomes [4].
1. Obesity is associated with a significant delay in conception that is partly, but not entirely, due to an impact on
normal ovulation.
2. Obesity reduces male fertility parameters and should be
considered in the evaluation of a couple presenting with
infertility.
3. The symptoms of PCOS, particularly with respect to fertility and metabolic disturbance, are exacerbated in the
presence of obesity.
4. Weight loss can improve weight-associated causes for
infertility such as PCOS and IR.
5. For some overweight and obese women, particularly with
PCOS, weight loss may improve ovulatory function,
leading to improved fertility.
11
ASMBS Position Statements
b
125
Alcohol Use Before and After Bariatric Surgery
There is conflicting data as to the lifetime and current prevalence of alcohol use disorder (AUD) in patients seeking
weight loss surgery. Most studies indicate that AUD affects a
minority of bariatric surgery patients. Studies have shown
that some individuals are at risk for AUD relapse or for
developing new-onset AUD after weight loss surgery, especially after gastric bypass. Other studies have shown a
decrease in high-risk drinking after surgery compared with
baseline [5].
Based on current studies, gastric bypass surgery is associated with:
1. Accelerated alcohol absorption (shorter time to reach
maximum concentration)
2. Higher maximum alcohol concentration
3. Longer time to eliminate alcohol in both men and women
4. Increased risk for development of AUD
Fig. 11.1 (continued)
6. Obese women have a lower probability of achieving live
birth after in vitro fertilization.
7. Bariatric surgery is effective in achieving significant and
sustained weight loss in morbidly obese women and has
been shown in case-control studies to improve fertility.
8. Pregnancy is not recommended during the rapid weight
loss phase after bariatric surgery; therefore, counseling
and follow-up regarding contraception during this period
are important.
9. The specific impact of either medical weight loss treatments or bariatric surgery on the responsiveness to subsequent treatments for infertility in both men and women is
not clearly understood at this time.
This position statement has been endorsed by the
American College of Obstetricians and Gynecologists, May
2017, and should be construed as its clinical guidance.
The data are less clear regarding altered pharmacokinetics
after sleeve gastrectomy, and there is no evidence that alcohol absorption is affected by gastric banding. Given the
recent increase in popularity of sleeve gastrectomy, more
studies regarding the pharmacokinetic effects of sleeve gastrectomy on alcohol metabolism are needed.
Patients undergoing bariatric surgery should be screened
and educated regarding alcohol intake both before and after
surgery. Active AUD is considered a contraindication by
most programs and in published guidelines [1]. Adequate
screening, assessment, and preoperative preparation may
help decrease the risk of AUD in bariatric surgery patients
[6]. A period of sustained abstinence with treatment is indicated before weight loss surgery. A history of AUD is not a
contraindication to bariatric surgery. However, patients
should be made aware that AUD can occur in the long term
after bariatric surgery.
ariatric/Metabolic Surgery in Class I Obesity
B
(BMI 30–35kg/m2)
There is a growing body of literature supporting the use of
metabolic surgery for patients with lower BMIs, particularly
for patient with type 2 diabetes mellitus (T2DM). The current ASMBS position statement provides a summary and
recommendations based on the available evidence [7]:
1. Class I obesity (BMI 30–35 kg/m2) causes or exacerbates
multiple other diseases, decreases longevity, and impairs
quality of life. Patients with class I obesity require durable treatment for their disease.
2. Current nonsurgical treatments for class I obesity are
often ineffective at achieving major, long-term weight
reduction and resolution of comorbidities.
126
S. A. Brethauer and X. (C.) Feng
3. The existing BMI inclusion criterion of ≥35 kg/m2 as a 3. Patients who have documented moderate to severe OSA
prerequisite for bariatric and metabolic surgery—excludshould be strongly encouraged to accept treatment preoping individuals with class I obesity—was established
eratively with CPAP and to use it postoperatively until
arbitrarily more than a quarter century ago, in the era of
clinical evaluation demonstrates resolution of OSA.
open surgery when morbidity and mortality of surgery 4. These patients should also bring their CPAP machines, or
were significantly higher than today. There is no current
at least their masks, with them at the time of surgery and
evidence of clinical efficacy, cost-effectiveness, ethics, or
use them following bariatric surgery at the discretion of
equity that justifies this group being excluded from lifethe surgeon.
saving surgical treatment. Access to bariatric and meta- 5. All commonly performed bariatric operations that have
bolic surgery should not be denied solely based on this
been assessed for impact on OSA have shown evidence
outdated threshold.
for significant relief of subjective symptoms of OSA and
4. For patients with BMI 30–35 kg/m2 and obesity-related
improvement of objective parameters of OSA that may
comorbidities who do not achieve substantial, durable
not always correlate with amount of weight lost.
weight loss, and comorbidity improvement with reason- 6. Since bariatric surgery produces many improvements in
able nonsurgical methods, bariatric surgery should be
the quality of life and other coexisting medical conditions
offered as an option for suitable individuals. In this popufor severely obese patients with OSA, it should be considlation, surgical intervention should be considered after
ered as the initial treatment of choice for OSA in this
failure of nonsurgical treatments.
patient population as opposed to surgical procedures
5. Particularly given the presence of high-quality data in
directed at the mandible or tissues of the palate.
patients with type 2 diabetes, bariatric and metabolic sur- 7. Routine pulse oximetry or capnography for postoperative
gery should be strongly considered for patients with BMI
monitoring of patients with OSA after bariatric surgery
30–35 kg/m2 and type 2 diabetes.
should be utilized, but the majority of these patients do
not routinely require an ICU setting.
6. AGB, SG, and RYGB have been shown to be well-­
tolerated and effective treatments for patients with BMI 8. No clear guidelines exist upon which to base recommendations for retesting for OSA following bariatric surgery.
30–35 kg/m2. Safety and efficacy of these procedures in
However, strong consideration should be given to retestlow-BMI patients appear to be similar to results in patients
ing patients who present years after bariatric surgery with
with severe obesity.
regain of weight, a history of previous OSA, and who are
7. Perioperative and long-term nutritional, metabolic, and
being reevaluated for appropriate medical and potential
nonsurgical support must be provided to patients after
preoperative surgical therapy.
surgery according to established standards, including the
ASMBS Clinical Practice Guidelines.
8. Currently, the best evidence for bariatric and metabolic
surgery for patients with class I obesity and comorbid VTE Prophylaxis
conditions exists for patients in the 18–65 age group.
There is no class I evidence to provide guidance regarding
the type, dose, or duration of VTE prophylaxis in the bariatObstructive Sleep Apnea
ric surgery patient. Based on current evidence available, the
following recommendations are made [9]:
Based on the evidence in the literature to date, the following
guidelines regarding OSA in the bariatric surgery patient and 1. All bariatric surgery patients are at moderate to high risk
its perioperative management are recommended [8]:
for VTE events, and VTE prophylaxis should be used.
2. Factors that place patients into a high-risk category for
1. OSA is highly prevalent in the bariatric patient populaVTE after bariatric surgery may include high BMI,
tion. The high prevalence demonstrated in some studies
advanced age, immobility, prior VTE, known hypercoagsuggests that consideration be given to testing all patients
ulable condition, obesity hypoventilation syndrome, puland especially those with any preoperative symptoms
monary hypertension, venous stasis disease, hormonal
suggesting obstructive sleep apnea.
therapy, expected long operative time or open approach,
2. Untreated OSA is yet another comorbidity observed with
and male gender.
high prevalence in the bariatric patient population that leads 3. Individual practices should develop and adhere to a prototo increased mortality and increased medical disability from
col for VTE prevention. Available evidence suggests that
several cardiovascular diseases. These observations further
adherence to any specific practice for VTE prevention
emphasize the value of bariatric surgery as a potentially
will reduce but not eliminate VTE as a complication of
definitive treatment for OSA in severely obese patients.
bariatric surgery.
11
ASMBS Position Statements
127
4. Mechanical prophylaxis is recommended for all bariatric
weight loss than is seen after the adjustable gastric band
surgery patients. There may be individual circumstances
(AGB) or nonsurgical interventions. There is no consis(severe lymphedema) when lower extremity compression
tent conclusion on which procedure produces greater
devices are not practical and alternative strategies may be
weight loss early after surgery. However, most current
needed.
evidence seems to demonstrate that RYGB produces
5. Early ambulation is recommended for all bariatric surgreater EWL compared to SG beyond the 1st year [13].
gery patients.
2. The effect of SG on GERD is less clear, because GERD
6. The combination of mechanical prophylaxis and chemoimprovement is less predictable and GERD may worsen
prophylaxis should be considered based on clinical judgor develop de novo. Preoperative counseling specific to
ment and risk of bleeding. Although there is some
GERD-related outcomes is recommended for all patients
low-level evidence that mechanical prophylaxis alone in
undergoing SG.
low-risk patient results in low VTE rates (o.4%), the pre- 3. The ASMBS recognizes SG as an acceptable option for a
ponderance of bariatric data supports using a combination
primary bariatric procedure or as a first-stage procedure
of chemoprophylaxis and mechanical prophylaxis with
in high-risk patients as part of a planned, staged approach.
overall VTE rates o.5%.
4. As with any bariatric procedure, long-term weight regain
7. There are conflicting data in the literature regarding the
can occur after SG and may require one or more of a varitype of chemoprophylaxis to use, but the highest-quality
ety of re-interventions.
data currently available suggest that LMWH offers better 5. Informed consent for SG as a primary procedure should
VTE prophylaxis than UFH without increasing the bleedbe consistent with the consent provided for other bariatric
ing risk.
procedures and, as such, should include the risk of long-­
8. Most post-discharge VTE events occur within the first
term weight regain. In addition, as with all currently rec30 days after surgery. Extended VTE prophylaxis should
ognized bariatric procedures, surgeons performing SG are
be considered, but there are insufficient data to recomencouraged to prospectively collect, analyze, and report
mend a specific dose or duration of extended post-­
their outcome data in peer-reviewed scientific forums.
discharge VTE prophylaxis for patients deemed to be at
high risk for VTE.
9. The use of IVC filters as the only method of prophylaxis Single-Anastomosis Duodenal Switch
before bariatric surgery is not recommended. Filter placement may be considered in combination with chemical The following recommendations are currently endorsed by
and mechanical prophylaxis for selected high-risk patient the ASMBS regarding single-anastomosis duodenal switch
in whom the risks of VTE are determined to be greater (SADS) for the primary treatment of obesity or metabolic
than the risks of filter-related complications.
disease [14]:
1. Single-anastomosis duodenal switch procedures are considered investigational at present. The procedure should
be performed under a study protocol with third-party
There have been three previously published statements by
oversight (local or regional ethics committee, institutional
the American Society for Metabolic and Bariatric Surgery
review board, data monitoring and safety board, clinical(ASMBS) on the use of sleeve gastrectomy (SG) as a bariattrials.gov, or equivalent authority) to ensure continuous
ric procedure [10–12]. With the emergence of this procedure
evaluation of patient safety and to review adverse events
as the most commonly performed, bariatric procedure today
and outcomes.
prompts a review of the current evidence. Substantial long-­ 2. Publication of short- and long-term safety and efficacy
term outcome data published in the peer-reviewed literature,
outcomes is strongly encouraged.
including studies comparing outcomes of various surgical 3. Data for these procedures from accredited centers should
procedures, confirm that SG provides significant and durable
be reported to the Metabolic and Bariatric Surgery
weight loss, improvements in medical comorbidities,
Accreditation and Quality Improvement Program dataimproved quality of life, and low complication and mortality
base and separately recorded as single-anastomosis DS
rates for obesity treatment [13].
procedures to allow accurate data collection.
Sleeve Gastrectomy as a Bariatric Procedure
1. In terms of initial early weight loss and improvement of
most weight-related comorbid conditions, SG and RYGB
appear similar. Studies demonstrate that SG and Rouen-­Y gastric bypass (RYGB) provide more comparable
These recommendations are not intended to impede innovation within our field. The ASMBS understands and supports the need for new and innovative procedures that can
further benefit our patient population. The single-­anastomosis
128
modification of the DS procedure, however, represents a significant change to a procedure that is historically rarely performed. In addition to potential unique long-term risks
without clear benefit, there are nutritional concerns that will
require further evaluation and study to ensure the safety of
both our patients and our members and to protect them from
undue harm.
Gastric Plication
Gastric plication is a new bariatric procedure that involves
imbricating the anterior or greater curvature of the stomach
to reduce gastric volume without placement of a device or
gastric resection. This emerging procedure has been performed as a stand-alone procedure as well as a combination
procedure with a laparoscopic adjustable gastric band [15].
The ASMBS currently supports the following recommendations regarding gastric plication alone or in combination
with adjustable gastric band placement for the treatment of
obesity:
1. Gastric plication procedures should be considered investigational at this time. This procedure should be performed under a study protocol with a third-party oversight
(local or regional ethics committee, institutional review
board [IRB], data monitoring and safety board, or equivalent authority) to ensure continuous evaluation of patient
safety and to review adverse events and outcomes.
2. Reporting of short- and long-term safety and efficacy outcomes in the medical literature and scientific meetings is
strongly encouraged. Data for these procedures should
also be reported to a program’s center of excellence
database.
3. Any marketing or advertisement for this procedure should
include a statement to the effect that this is an investigational procedure.
4. The ASMBS supports research conducted under an IRB
protocol as it pertains to investigational procedures and
devices. Investigator meetings held to facilitate research
are necessary and supported, as is the reporting of all data
through a bariatric quality improvement program or a
specific research database. The ASMBS does not support
continuing medical education (CME) courses on investigational procedures and devices held for bariatric surgeons for the purpose of use of investigational procedures
outside an IRB research protocol.
Prevention and Detection
of Gastrointestinal Leak
There has been a decrease in the incidence of GI leaks after
primary stapled open and laparoscopic bariatric procedures
S. A. Brethauer and X. (C.) Feng
(GB and SG) over time. Despite this decline, a GI leak
remains a significant cause of morbidity and mortality and
remains a potential complication of these procedures. Early
detection and treatment remain pivotal principles in the management of GI leaks and may play a role in reducing subsequent morbidity and mortality. Some of the factors promoting
leak may be different between GB and SG procedures. This
may be related to the technical differences between the two
procedures, as well as the distinct anatomic and physical
properties that exist between the sleeve conduit versus the
gastric pouch, which are helpful when considering some of
the qualitative and temporal dissimilarities reported in the
clinical manifestation of GI leaks after these procedures.
Despite the advent of new technologies, the management of
GI leaks after GB and SG procedures can be extremely complex and involve multiple and/or multimodal treatment
options [16].
1. Intraoperative leak tests (air, dye, endoscopy) are
described for both GB and SG. Although widely used,
they have not been found to reduce the incidence of leak
after GB and SG procedures.
2. Intraoperative leak prevention interventions described for
both GB and SG procedures include oversewing, SLR,
tissue sealants, and glue. There is still considerable debate
over the utility or superiority of any of these interventions. Mandated use of any of these leak prevention interventions was not indicated by the data.
3. Radiographic studies after GB and SG procedures have
varying sensitivity and specificity that is affected by study
choice, patient factors, facility factors, and reviewer
factors.
• There is no high-quality evidence available to mandate
the routine postoperative use of UGI contrast studies
after GB or SG procedures, particularly for SG given
the greater likelihood of leaks presenting in a delayed
fashion. Routine or selective UGI studies may, however, identify other technical or anatomic problems
after GB or SG procedures. Based on current evidence,
the decision to perform routine versus selective UGI
contrast studies should be left to the discretion of the
surgeon, based on factors related to the system of care
in place and on other characteristics of the patient and
the population being treated.
4. Radiographic evaluation versus surgical exploration for
suspected leak after GB and SG.
• Clinically unstable patients suspected of having a leak
may not be appropriate candidates for radiographic
evaluation. Re-exploration through a laparoscopic or
open approach should be considered.
• In the clinically stable patient with a suspected leak,
CT of the abdomen and pelvis with oral and IV contrast
may have higher sensitivity and specificity than UGI
contrast studies, with the added utility of identifying
11
ASMBS Position Statements
129
associated intra-abdominal abscesses, hernias, or other not provide traditional durable benefits comparable to curpathologic conditions after GB or SG. Addition of the rently accepted bariatric procedures [18].
chest component to the abdominal CT to rule out disHowever, it has become clear that clinical trials can be,
tinct or concomitant pulmonary pathologic conditions and have been, manipulated by for-profit entities, including
may be considered.
medical device companies, and that this influence on clinical
• Given the high mortality from untreated GI leaks, it is trial results can misrepresent the outcomes of the clinical
understood that re-exploration, open or laparoscopic, trial. It is therefore essential to ensure the integrity of clinical
is an appropriate and acceptable treatment modality trials by recommending the following actions by physicians
when a GI leak is suspected and remains the diagnostic involved in clinical trials, as recommended by DeAngelis
test with the highest sensitivity and specificity after and Fontanarosa [19] and supported in full by the ASMBS in
GB and SG.
this Position Statement: “For-profit companies that sponsor
5. Operative management (open or laparoscopic) for acute biomedical research studies should not be solely or primarily
GI leaks after GB or SG follows the goals of drainage, involved in collecting and monitoring of data, in conducting
placement of drains to create controlled fistulas, use of the data analysis, and in preparing the manuscript reporting
antimicrobial agents, and nutrition considerations.
study results. These responsibilities should primarily or
• Chronic fistulas are described after SG with long clo- solely be performed by academic investigators who are not
sure times (≥1–3 months). Definitive surgical manage- employed by the company sponsoring the research.”
ment of nonhealing fistulas is technically challenging, Furthermore, the society supports the registration of all cliniand current available data do not favor one procedure cal research trials and mandatory reporting of outcomes,
over another.
whether favorable or not.
6. Nonoperative management may be an appropriate treatment option for GI leaks after GB or SG in stable patients.
• Nonoperative methods of GI leak treatment after both Intragastric Balloon Therapy Endorsed by
GB and SG include endoscopic endoluminal self-­ the Society of American Gastrointestinal
expandable stents, clips, endoscopic and percutane- and Endoscopic Surgeons
ously placed drains, and biologic glue/tissue sealants.
Multiple endoscopies and multimodality treatments 1. Level 1 data regarding the clinical utility, efficacy, and
may be required to achieve full healing of a chronic
safety of intragastric balloon therapy for obesity are
fistula. The available data do not favor one treatment
derived from randomized clinical studies [20].
over another.
2. Implantation of intragastric balloons can result in notable
weight loss during treatment. A few studies, representing
lower-level evidence, have suggested that the weight loss
Endosurgical Intervention
effect can be maintained after balloon retrieval for some
for Treatment of Obesity
finite time into the future.
3. Although utilization of intragastric balloons results in
Currently, a number of endoluminal innovations and novel
notable weight loss, separating the effect of the balloon
devices and technologies are in various stages of developalone from those of supervised diet and lifestyle changes
ment or application to the elective treatment of obesity,
may be challenging. Of note, recent FDA pivotal trials
including revisional interventions. The theoretical goals of
demonstrated a benefit to balloon use compared with diet
these therapies include decreasing the invasiveness, risk, and
alone in their study populations. In general, any obesity
barriers to acceptance of effective treatment of obesity; howtreatment, including intragastric balloon therapy, would
ever, these outcomes cannot be assumed and must be proven.
benefit from a multidisciplinary team that is skilled and
Therefore, the use of novel technologies should be limited to
experienced in providing in-person medical, nutritional,
clinical trials done in accordance with the ethical guidelines
psychological, and exercise counseling.
of the ASMBS and designed to evaluate the risk and efficacy 4. The safety profiles for intragastric balloons indicate a safe
of the intervention. The results of appropriate trials should
intervention, with serious complications being rare. Early
include the generation of data for risk-benefit analysis,
postoperative tolerance challenges can be significant but
assessments of disability, durability, and the resource use
can be controlled with pharmacotherapy in the majority
associated with the intervention. An intervention undergoing
of patients, thereby minimizing voluntary balloon removevaluation should not be judged favorably if the risk/benefit
als. These early symptoms should be discussed with the
ratio is increased compared with the spectrum of currently
patient before the procedure.
accepted surgical procedures [17]. A dramatic reduction in 5. Although therapy with prolonged balloon in situ time and
risk might allow for the acceptance of interventions that do
the use of sequential treatments with multiple balloons
130
have been studied, awareness and adherence to absolute
and relative contraindications of use and timely removal
optimize device safety. Based on current evidence, balloon therapy is FDA approved as an endoscopic, temporary (maximum 6 months) tool for the management of
obesity. Further review will evaluate the impact of diet,
lifestyle changes, and pharmacotherapy during and after
balloon removal.
6. The ability to perform appropriate follow-up is essential
when intragastric balloons are used for weight loss to
enhance their safety and avoid complications related to
spontaneous deflation and bowel obstruction.
Vagal Blocking Therapy for Obesity
The American Society for Metabolic and Bariatric Surgery
currently supports the following regarding vagal blocking
therapy for obesity (VBLOC) for the treatment of obesity
and encourages members to participate in post-FDA approval
studies [21]:
1. Reversible vagal nerve blockade has been shown to result
in statistically significant EWL at 1 year compared with a
control group in one of two prospective randomized trials.
2. Reversible vagal nerve blockage has been shown to have
a reasonable safety profile with a low incidence of severe
adverse events and a low revisional rate in the short term.
More studies are needed to determine long-term reoperation and explantation rates.
3. The prospective collection of VBLOC outcomes as part
of the national center of excellence databases is encouraged to establish the long-term efficacy of this new
technology.
ostprandial Hyperinsulinemic Hypoglycemia
P
After Bariatric Surgery
Based on the available evidence to date, the following recommendations are made in the patient with postprandial
hyperinsulinemic hypoglycemia after bariatric surgery [22].
1. Postprandial hyperinsulinemic hypoglycemia after bariatric surgery is rare and most commonly associated with
RYGB. Nonetheless, patients should be screened for,
educated, and counseled to recognize the signs and symptoms of hypoglycemia.
2. Extreme, progressive, and unrecognized neuroglycopenic
symptoms of postprandial hyperinsulinemic hypoglycemia can result in cognitive and neurologic impairment
with risk of seizures and loss of consciousness posing risk
to both patient and others.
S. A. Brethauer and X. (C.) Feng
3. Insulinoma must be ruled out in patients with confirmed
fasting hypoglycemia.
4. Diagnosis of postprandial hyperinsulinemic hypoglycemia requires a dietary journal, along with confirmatory
laboratory and provocative testing, in the setting of
symptoms presenting more than 1 year after surgery.
Treatment with dietary modification in mild cases is
often implemented successfully without a definitive
diagnosis.
5. Postprandial hyperinsulinemic hypoglycemia can be
effectively treated in the majority of cases with dietary
modification alone. A dietitian should be an integral part
of the treatment team and an endocrinologist consulted in
cases not responding to initial treatment.
6. Pharmacotherapy produces variable results but should be
attempted before surgical intervention. A gastrostomy
tube with feeding into the remnant stomach provides
nutritional support and in some cases symptomatic relief
and should be considered in patients not responding to
nonoperative treatment. Partial pancreatectomy is not
recommended.
Metabolic Bone Changes After Surgery
Obesity appears to be independently associated with vitamin and mineral deficiencies involved in bone homeostasis
affected by race and potentially affected by gender. These
pre-existing vitamin and mineral deficiencies may compound postoperative absorption of bone homeostatic
micronutrients depending on the type of weight loss surgery and degree of weight loss. Patients preparing for bariatric surgery should be screened for the presence of
vitamin D deficiency and hyperparathyroidism with treatment initiated [23].
Cross-sectional, retrospective, and prospective studies do
not conclusively support any increased incidence of osteoporosis or increased fracture risk after bariatric surgery.
Accuracy of current methods of assessing bone mineral density (BMD) (DXA) in patients who have extreme obesity as
well as after extreme weight loss should be evaluated with
further research. The use of one third distal forearm to measure BMD can be considered in situations of extreme weight
that exceeds the limits of conventional DXA tables as well as
in cases of secondary hyperparathyroidism related to malabsorption of vitamin D and calcium.
The degree of bone turnover and BMD loss after bariatric
surgery is related to the type of procedure performed, the
amount and rate of weight loss, and the degree of malabsorption of other micronutrients and protein. Long-term followup monitoring and supplementation should be provided
­
according the type of procedure and the individual patient’s
risk for bone loss.
11
ASMBS Position Statements
1. Preoperative assessment:
(a) The high prevalence of vitamin D deficiency and secondary hyperparathyroidism in the obese population
supports routine laboratory testing of 25-OHD and
intact PTH levels before bariatric surgery, with initiation of treatment for deficiencies and documentation
of improvement before surgery when possible.
(b) Preoperative DXA can be performed in estrogen-­
deficient women and in premenopausal women and
men who have conditions associated with bone loss
or low bone mass to establish a baseline before bariatric surgery. There is, however, no compelling data
to support routine DXA for all obese adolescents,
men or premenopausal women undergoing bariatric
surgery. If low bone mass is diagnosed preoperatively, a thorough evaluation should be undertaken to
identify secondary causes. This laboratory testing can
include thyroid-stimulating hormone and testosterone levels in men.
(c) A baseline DXA is recommended by the National
Osteoporosis Foundation 2013 (http://www.nof.org/
hcp/practice/practice-and-clinical-guidelines/cliniciansguide) for all women 65 years and older and for
younger postmenopausal women and men 70 years or
older and men age 50–69 about whom you have concern based on their clinical risk factor profile patients
such as those undergoing a malabsorptive procedure.
(d) The US Preventative Services Task Force recommends a bone density test at least once for all women
age 65 and older. This recommendation can be made
in consideration with general medical optimization as
indicated.
2. Procedure-specific recommendations for monitoring
bone loss are made below. The doses of recommended
calcium supplementation and vitamin D supplementation
are consistent with previously published 2013 AACE/
TOS/ASMBS Guidelines for the Perioperative Nutritional,
Metabolic, and Nonsurgical Support of the Bariatric
Surgery Patient [1, 24].
(a) LAGB:
• Calcium supplementation after LAGB should
include 1200–1500 mg/d, which can be taken in
two to three split doses, 4–5 h apart for optimal
absorption [25]. In the early postoperative period,
minimum vitamin D of at least 3000 IU/d, titrate
to 430 ng/mL. Minimum vitamin D maintenance
after LAGB should be consistent with established
age-specific recommendations for patients at risk
for vitamin D deficiency until non-­
obese. The
Endocrine Society Clinical Practice Guideline
currently recommends a minimum of 600 IU/d of
vitamin D from age 19 to 70 years and 800 IU/d of
vitamin D after 70þ years [24, 26].
131
• Bone loss monitoring should include annual albumin, calcium, PTH, and 25-OHD levels.
• DXA should be used after LAGB according to the
most recent established guidelines for the general
patient population that a particular patient belongs
to, based on age, gender, and associated risk factors.
(b) Gastric bypass and malabsorptive procedures (BPD
and BPD/DS):
• Supplementation after gastric bypass should
include calcium citrate 1200–1500 mg/d, which
can be taken in two to three split doses, 4–5 h
apart for optimal absorption [27]. Minimum vitamin D intake of 3000 IU/d, titrate to 430 nl/
mL. Calcium citrate is preferable to calcium carbonate due to better ­absorption in the absence or
reduction of gastric acid. Supplementation after
BPD and BPD/DS should include calcium of
1800–2400 mg/d and minimum vitamin D
3000 IU/d, titrate to 430 nl/mL [1, 24].
• Based on the most recent Endocrine Society
Clinical Practice Guidelines, vitamin D deficiencies should be treated with 50,000 IU of vitamin
D2 or vitamin D3 once a week for 8 weeks or its
equivalent of 6000 IU of vitamin D2 or vitamin
D3, daily to achieve a blood level of 25 (OH)D
above 30 ng/mL, followed by maintenance therapy of 1500–2000 IU/d. Severe deficiencies can be
treated with higher doses up to 50,000 IU three
times a day. Intramuscular injections of ergocalciferol 100,000 IU once a week can be used but are
rarely necessary [26].
• Bone loss monitoring should include a minimum
of annual albumin, calcium, PTH, and 25-OHD
levels. 1,25-OH2 D should be monitored in
patients with renal compromise.
• Bone loss monitoring can also include markers for
altered bone turnover. Monitoring to include bone
alkaline
phosphatase,
osteocalcin,
serum
C-­telopeptide, serum propeptide of type I collagen, and urine N-telopeptides can be considered.
The appropriate use of biochemical markers as a
screening tool, however, has not been established
and warrants additional investigation.
• Routine DXA scan after RYGB is not supported by
current data. A baseline DXA is recommended by
the National Osteoporosis Foundation 2013 (http://
www.nof.org/hcp/practice/practice-and-clinicalguidelines/clinicians-guide) for all women 65 years
and older and for younger postmenopausal women
and men 70 years and older and men age 50–69
about whom you have concern based on their clinical risk factor profile patients such as those undergoing a malabsorptive procedure.
132
S. A. Brethauer and X. (C.) Feng
(c) SG:
• Given the current lack of procedure specific data,
recommendations regarding supplementation and
bone monitoring should at a minimum be consistent with that recommended for the LAGB
although it is unlikely that recommendations for
the gastric bypass would be harmful.
mergency Care of Patients
E
with Complications After Bariatric Surgery
The ASMBS recommends the following guidelines for hospitals and physicians regarding the emergency care of
patients with complications related to bariatric surgery procedures [28]:
1. Hospitals are called on to recognize bariatric surgery as a
surgical subspecialty, and, similar to the emergency coverage arrangements hospitals provide for other surgical
subspecialties, hospitals are required to recognize that a
patient with bariatric surgery-related complications
should ideally be treated by an appropriately qualified
bariatric surgical specialist. Such treatment can be provided by an appropriately qualified and credentialed
member of the medical staff in hospitals performing bariatric surgery procedures or by transfer to another facility.
Life-threatening conditions that require immediate intervention are appropriately treated by an available general
surgeon at hospitals that do not provide bariatric surgery
services (see No. 3 below).
2. All hospitals in which elective bariatric surgery procedures are performed are called on to provide care to
patients experiencing bariatric surgery-related complications. This is essential to provide a safe system of care,
because issues such as relocation, insurance coverage
changes, patient access issues, or the nature of an emergency situation can interfere with the provision of care by
the primary bariatric surgeon who performed the procedure, their surgical practice, or hospital, as outlined
above. Hospitals that provide emergency services to the
community and perform bariatric surgical procedures
should provide 24-h emergency access to evaluation and
treatment (e.g., by way of emergency room coverage) by
qualified surgical specialists for all bariatric surgical
patients. Hospitals that perform bariatric surgical procedures should also accept the transfer of patients with bariatric surgery-related emergencies from hospitals that do
not provide bariatric surgery services.
3. Hospitals that do not perform bariatric surgery might not
be equipped to take care of bariatric surgical emergencies and might need to transfer such patients to appropriately equipped centers with qualified bariatric surgical
specialists who can treat bariatric surgery-related complications. However, this should only occur if the condition of the patient and specifics of the transfer arrangement
will allow safe transfer. Bariatric patients who present
with life-threatening surgical problems, whether related
to the bariatric surgery or not, should not have their
health jeopardized by efforts to arrange such a transfer if
it is clear that urgent surgical intervention is indicated. In
such circumstances (e.g., closed-loop bowel obstruction
threatening perforation or infarction), a general surgeon
should perform the lifesaving surgical intervention and
avoid the delays inherent in transferring the patient.
4. Bariatric surgeons, as recognized surgical subspecialists,
have an obligation to maintain their familiarity with the
various bariatric surgical procedures and inherent complications of these procedures as a part of their obligation to
provide care to all patients requiring emergency treatment
of bariatric surgery-related complications.
5. Bariatric surgeons have an obligation to provide both
emergency and elective care to their own postoperative
patients, to educate their patients that they are available to
provide such care, and to inform their patients how to
access this care.
6. Bariatric surgeons must maintain privileges at a hospital
with appropriate facilities for bariatric patients that also
provide emergency services accessible 24 h daily to care
for their bariatric surgery patients who develop complications. Bariatric surgeons who practice exclusively in an
outpatient-only facility will not be able to satisfy this
obligation and must, therefore, satisfy one of the following criteria:
(a) Have in place an approved transfer acceptance emergency care agreement with an appropriate hospital
that performs bariatric surgery with emergency services accessible 24 h daily with a qualified bariatric
surgeon or surgeons practicing at that facility who
will accept their patients and provide emergency care
to them.
(b) Join the medical staff of an appropriate hospital that
performs bariatric surgery and provides emergency
services accessible 24 h daily to provide emergency
care to their patients who develop bariatric surgery-­
related complications.
Global Bariatric Healthcare (Medical Tourism)
Based on the limited available data, guidelines published by
other medical societies, expert opinion, and a primary concern for patient safety, the American Society for Metabolic
and Bariatric Surgery supports the following statements and
guidelines regarding bariatric surgical procedures and global
bariatric healthcare [29]:
11
ASMBS Position Statements
1. Based on the unique characteristics of the bariatric patient,
the potential for major early and late complications after
bariatric procedures, the specific follow-up requirements
for different bariatric procedures, and the nature of treating the chronic disease of obesity, extensive travel to
undergo bariatric surgery should be discouraged unless
appropriate follow-up and continuity of care are arranged
and transfer of medical information is adequate.
2. The ASMBS opposes mandatory referral across international borders or long distances by insurance companies
for patients requesting bariatric surgery if a high-quality
bariatric program is available locally.
3. The ASMBS opposes the creation of financial incentives
or disincentives by insurance companies or employers
that limit patients’ choices of bariatric surgery location or
surgical options and, in effect, make medical tourism the
only financially viable option for patients.
4. The ASMBS recognizes the right of individuals to pursue
medical care at the facility of their choice. Should they
choose to undergo bariatric surgery as part of a medical
tourism package or pursue bariatric surgery at a facility a
long distance from their home, the following guidelines
are recommended:
• Patients should undergo procedures at an accredited JCI
institution or preferably a bariatric center of excellence.
• Patients should investigate the surgeon’s credentials to
ensure that the surgeon is board eligible or board certified by a national board or credentialing body.
Individual surgeon outcomes for the desired procedure
should be made available as part of the informed consent process whenever possible.
• Patients and their providers should ensure that a follow-­up care, including the management of short- and
long-term complications, is covered by the insurance
payer or purchased as a supplemental program prior to
traveling abroad.
• Surgical providers should ensure that all medical
records and documentation are provided and returned
with the patient to their local area. This includes the
type of band placed and any adjustments performed in
the case of laparoscopic adjustable gastric banding, as
well as any postoperative imaging performed.
• Prior to undergoing surgery, the patient should establish a plan for postoperative follow-up with a qualified
local bariatric surgery program to monitor for nutritional deficiencies and long-term complications and to
provide ongoing medical, psychological, and dietary
supervision.
• Patients should recognize that prolonged traveling
after bariatric surgery may increase the risk of deep
venous thrombosis, pulmonary embolism, and other
perioperative complications.
133
• Patients should recognize that there are risks of contracting infectious diseases while traveling abroad that
are unique to different endemic regions.
• Patients should recognize that travel over long distances in a short period of time for bariatric surgery
may limit appropriate preoperative education and
counseling regarding the risks, benefits, and alternatives for bariatric operations. This also significantly
limits the bariatric surgery program’s ability to medically optimize the patient prior to surgery.
• Patients should understand that compensation for
complications may be difficult or impossible to
obtain.
• Patients should understand that legal redress for medical errors for procedures performed across international boundaries is difficult.
5. When a patient who has had a bariatric procedure at a
distant facility presents with an emergent life-threatening
postoperative complication, the local bariatric surgeon on
call should provide appropriate care to the patient consistent with the established standard of care and in keeping
with ethical guidelines of the ASMBS. This care should
be provided without risk of litigation for complications or
long-term sequelae resulting from the initial procedure
performed abroad. Routine or non-emergent care for
patients who have had bariatric surgery elsewhere should
be provided at the discretion of the local bariatric
surgeon.
Question Section
1. The purpose of an ASMBS position statement is to:
A. Clarify a controversial issue
B. Provide guidance for healthcare leaders and payers
C. Provide support for clinical decisions made by the
membership
D. All of the above
2. The conclusions in the “Preoperative Weight Loss
Requirement” position statement include:
A. Every patient, regardless of BMI, should undergo at
least 6 months of supervised dieting before surgery.
B. There is no level 1 evidence to support mandatory
preoperative weight loss, and this policy often delays
care.
C. The policy of mandatory supervised diet policies for
every patient is acceptable because bariatric patients
need to demonstrate the willpower needed to be successful after surgery.
D. The ASMBS supports insurance-mandated preoperative weight loss policies for all patients seeking bariatric surgery.
134
3. Based on current studies, which of the following statements regarding alcohol use after gastric bypass are false?
A. RYGB results in accelerated alcohol absorption
(shorter time to reach maximum concentration).
B. RYGB causes higher maximum alcohol concentration.
C. After RYGB, it takes a longer time to eliminate alcohol in men but not in women.
D. RYGB poses an increased risk for development of
alcohol use disorder.
4. Position statements and guidelines published by the
ASMBS:
A. Are written by the Clinical Issues Committee, sometimes in collaboration with another ASMBS committee or another professional society
B. Undergo a thorough vetting and revision process
C. Are sent to the membership for comment before final
approval
D. Are reviewed every 3 years to determine if updates are
needed
E. All of the above
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6. Heinberg LJ, Ashton K, Coughlin J. Alcohol and bariatric surgery: review and suggested recommendations for assessment and
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S. A. Brethauer and X. (C.) Feng
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11. Clinical Issues Committee of the American Society for Metabolic
and Bariatric Surgery. Updated position statement on sleeve gastrectomy as a bariatric procedure. Surg Obes Relat Dis Off J Am
Soc Bariatr Surg. 2010;6:1–5.
12. ASMBS Clinical Issues Committee. Updated position statement on
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13. Ali M, El Chaar M, Ghiassi S, et al. American Society for Metabolic
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Part II
Primary Bariatric Surgery and Management of
Complications
Laparoscopic Gastric Bypass: Technique
and Outcomes
12
Kelvin D. Higa and Pearl K. Ma
Chapter Objectives
1. Discuss the basic construct and operative techniques used in laparoscopic gastric bypass.
2. Discuss patient preparation.
3. Review long-term outcomes.
Introduction
Historically, the first laparoscopic gastric bypass performed
by Wittgrove and Clark in 1994 was a remarkable achievement [1]. Their pioneering work accelerated public acceptance and industry interest in bariatric surgery that led to
further innovation and helped define this specialty. Variations
of this original technique exist, but the basic tenets of the
procedure remain the same: small, isolated gastric pouch,
limited diversion of bilioenteric secretions, and reproducible, safe anastomotic methods.
During this time period, the vertical banded gastroplasty
was declining in popularity, giving way to the open gastric
bypass as it evolved into a more standardized operation. The
original gastric bypass described by Mason in 1966 [2] has
little similarity to operations performed today, so it is unfair
to compare earlier outcomes to current procedures. However,
it was because of this early experience and subsequent modifications adopted in order to avoid complications that our
present laparoscopic procedures owe their lineage.
Our current understanding of the physiologic effects of
the gastric bypass is as naïve as our understanding of the
disease for which we are treating: morbid obesity. Early constructs were based on the anatomic “restrictive” or “malabsorptive” concepts that did not correlate well with our
observation of patient behavior. Why was there such a proK. D. Higa (*) · P. K. Ma
Department of Surgery, Minimally Invasive and Bariatric Surgery,
Fresno Heart and Surgical Hospital, University of California San
Francisco, Fresno, CA, USA
nounced effect on metabolic syndrome prior to weight loss,
and how did our patients maintain “satiety” without a seemingly “restrictive” component?
With the discovery and further understanding of enteric
hormones, such as gastrin, GLP-1, and PYY, the hypothesized mechanism(s) of action of the gastric bypass fits better
with our long-standing clinical observations [3]. The effect
on the individual patient, by whatever means, is reproducible—but these proposed mechanisms also explain the variability of the response of each individual as well as consistent
response of the group given the wide range of anatomic variability in the anatomic construct.
In other words, a pouch that varies in volume of 10 cc
compared to one of 30 cc, a 200% difference, has not been
shown to increase weight loss or improve outcomes.
Likewise, creating a Roux limb of 150 cm does not impart
greater effect than one of 75 cm. Although there are studies
that have shown short-term benefit of pouch and/or stoma
reduction and lengthening of the Roux limb to enhance
weight loss, results have been inconsistent and without long-­
term benefit.
The best predictor of success seems to be genetic similarity among related individuals, rather than environmental factors [4]. The performance of the gastric bypass may not be
influenced as strongly by compliance of the patient as it
seems to be with the adjustable gastric band and may be predetermined by the genetic and biologic nature of each individual patient.
Operative strategy, therefore, is the same as it was in
1966: to achieve the anatomic effect of proximal alimentary
diversion, with the least side effects and complications with
long-term control of weight and medical comorbidities—
safely and cost-effectively.
The laparoscopic gastric bypass was once considered to
be one of the most challenging minimally invasive operations. It is now the most common foregut operation and,
despite its complexity and learning curve, has been shown to
be safer and more cost-effective than its open predecessor.
The operation has evolved to include a variety of anasto-
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_12
139
140
motic techniques and trocar placements, giving individual
surgeons the latitude to adopt or modify the procedure based
on their own preference and experience.
This chapter will discuss the basic construct and operative
techniques in use today. There is no one method that is the
“gold standard.” Comparative studies are few, and those that
exist only reinforce that there are subtleties to operative technique that defy observation. For example, gastrojejunal stricture rate may be influenced more by preservation of blood
supply and operative technique rather than the diameter of
the circular stapler. It would be naïve to expect every surgeon
to achieve the same results, given the same basic technique;
it is up to each individual to modify, adapt, and improve
through his or her own experience.
K. D. Higa and P. K. Ma
Trocar placement is a highly variable and yet critical step
toward a safe and successful operation. Most authors describe
external landmarks such as the umbilicus or xiphoid to determine placement. However, obese patients have a high degree
of abdominal wall thickness with corresponding varying
degrees of rigidity. Also, the size of the liver and presence of
previous operations and their associated internal adhesions
will determine initial and subsequent trocar placement. One
must recognize that placement of the trocars needs to accommodate manipulation and construction of both the small
bowel and hiatus, often challenging with the larger patients.
Therefore, we feel it better to place the trocars based on
internal anatomy, rather than external landmarks. In this way,
triangulation and visualization will be preserved, accommodating for variations in the size of the liver or length of the
patient’s torso.
Preparation of the Patient
Attention must be given not only to individual trocar
placement but also to the angle in which the trocar enters the
Psychosocial and nutritional education is paramount to long-­ skin. Some individuals’ thick, muscular abdominal wall does
term success with any bariatric/metabolic operation and is not allow for the range of motion necessary to achieve the
covered in detail in other chapters and in volume 2 (The objective, forcing redirection of the trocar internally, through
ASMBS Textbook of Bariatric Surgery, Volume II: Integrated the same skin incision, but different fascial opening, or by
Health). In general, most patients fail to appreciate the life- placement of another trocar. In general, the optimal placestyle changes experienced after surgery despite a high degree ment is to orient all trocars toward the midline, pointing to
of preparation; postoperative support and education are nec- the base of the mesocolon.
Extra-long trocars may be necessary. Although some suressary requirements and should be made available lifelong.
Concurrent health-care maintenance with evaluation and geons prefer to limit the number of 12 mm trocars (necessary
optimization of cardiovascular and pulmonary risks is appro- to accommodate stapling devices), this may limit proper stapriate for all elective procedures. Mandatory preoperative pler orientation and compromise the anatomic construct. The
weight loss can be effective in decreasing the size of the liver hernia risk is minimized by either closing the trocar defects
but has not been shown to improve outcomes or diminish or, preferably, using non-bladed trocars without fascial
closure.
rates of complication or open conversion.
An example of a trocar placement scheme is as follows:
Thromboembolism prophylaxis and perioperative antibiits purpose is only to illustrate the rationale necessary for
otics are currently the standard of care.
consistency of this important and underappreciated first step
in performing the laparoscopic gastric bypass. Variations,
depending on experience, technique, and judgment, are necPositioning and Trocar Placement
essary for evolution to occur and should be encouraged:
Positioning of the patient is by surgeon preference and
should take into consideration patient habitus and avoidance 1. Initial trocar (12 mm)—left, upper quadrant, subcostal,
of pressure points (Fig. 12.1). Many surgeons prefer the
and midclavicular line. This is often an optical entry
lithotomy or “French” position, standing between the
without prior insufflation. The rationale is that many
patient’s legs in steep reverse Trendelenburg, while others
patients have had previous procedures; pelvic or otherwill operate from the side, with the legs together. Either
wise—this area is rarely affected with intra-abdominal
way, one must consider the weight capacity of the operating
adhesions from common open procedures. This allows
table along with adequate securing measures when the need
dissection of midline adhesions, inspection of the size
for lateral extension in extreme cases should arise. One must
of the liver, and determination of the best level for the
also consider ergonomics of the operative surgeon and assisprimary optical port. This will also be the primary port
tant personnel. The surgeon and supportive staff are obliged
for vertical stapling of the gastric pouch. Once adheto operate in a safe and comfortable environment so as to
sions are mobilized, then the optical port can be
avoid back and neck injury or carpal tunnel syndrome from
thoughtfully placed as to see the ligament of Treitz as
suboptimal positioning or unavoidable repetitive motion.
well as hiatus without having to “turn around.” Also, by
12
Laparoscopic Gastric Bypass: Technique and Outcomes
141
Fig. 12.1 Operating room
arrangement and port
placement
keeping the initial entry away from the midline, the
vena cava and aorta are not as vulnerable to injury.
2. Primary optical trocar (12 mm)—placement has been
described above. Optimal placement allows for forward
visualization of the proximal small bowel and the hiatus.
Once this trocar is placed, the camera is moved to this
port for subsequent trocar placement. I have not found the
current 5 mm scopes to provide enough light delivery and
therefore resolution for optimal visualization in most
patients.
3. Right-sided trocar (12 mm)—this trocar must be placed
thoughtfully just as all others. Exterior landmarks are irrelevant. It must come in below the liver edge, just to the right
of the midline so as to be able to triangulate on the hiatus as
well as the ligament of Treitz; therefore, it should be angled
toward the root of the mesocolon, rather than perpendicular
to the abdominal wall. It must be 12 mm to accommodate
the stapler that will define the inferior gastric pouch.
4. Left inferior trocar (12 mm)—this is often at the same
level as the primary optical trocar and in the same line as
the initial trocar. This will be the primary stapler entry site
for the jejunojejunostomy (Fig. 12.2) and along with the
Fig. 12.2 Steps in jejunojejunostomy
142
Fig. 12.3 Steps in gastrojejunostomy
right upper quadrant trocar will triangulate very well for a
comfortable manual gastrojejunostomy (Fig. 12.3).
5. Liver retractor—the most consistent placement appears to
be the subxiphoid. A 5 mm trocar can be used here,
depending on the liver retractor of choice. We have found
that a simple 5 mm instrument or similar device will provide excellent exposure and therefore is often placed
without a trocar, through direct puncture, as it will not be
removed until the end of the case.
The Components
The Pouch
Much emphasis is placed on the formation of the gastric
pouch or modification of the gastric pouch to improve performance. Its contribution to the “gastric bypass” effect is
undeniable, yet poorly understood. Collateral evidence suggests that the actual size and configuration of the pouch are
more important for prevention of complications and
improved alimentation rather than maximal weight loss or
metabolic effect. In other words, one would be hard-pressed
to find literature, anecdotal, or otherwise that describes a linear correlation between pouch size and weight loss. Likewise,
attempts at pouch reduction for weight recidivism or inadequate weight loss have been inconsistent and disappointing.
Early gastric bypass descriptions were of horizontal orientations and often nondivided staple lines. Both have been
retired with the adoption of linear cutting stapling devices
K. D. Higa and P. K. Ma
allowing for orientation and construct based on intent, rather
than necessity. One can now orient the pouch vertically with
complete isolation of the gastric pouch with more precision
and less concern for splenic or other visceral injury. This was
made even easier with the laparoscopic stapling devices;
along with the increased visualization of the proximal stomach and hiatus, the laparoscopic approach has improved the
safety and reproducibility of this procedure.
Isolation of the gastric pouch was important to limit the
potential of gastrogastric fistula—relatively common complication of nondivided staple lines. It also allowed for more
precise dissection—nondivided pouches were often created
by placement of a spherical intragastric balloon for sizing,
rather than a cylindrical bougie. This made the pouch consist
primarily of anterior stomach wall with a greater amount of
fundus that accounted for its eventual dilation and increased
capacity. Vertical, lesser curve-based orientation of the pouch
has been shown by Mason to be ideal for gastroplasty, avoiding the distensible fundus, making the pouch more stable in
size, an observation.
The pouch is formed by sequential firing of a laparoscopic
linear cutter stapler, a stapling device around an intraluminal
bougie. The first firing is usually horizontal beginning no
more than 5 cm distal to the esophagogastric junction; subsequent firings are vertically oriented to the angle of His.
Creating a longer pouch may lead to an increased risk of
developing marginal ulcerations in the future [5]. The staple
height depends upon the thickness of the tissue, often requiring 3.8–4.1 mm cartridges. The size of the bougie does not
appear to be controversial; most surgeons use the same size
to calibrate the gastrojejunal anastomosis—usually 1.2–
1.5 mm diameter.
One of the critical steps in creation of the gastric pouch is
posterior visualization at the level of the hiatus. Many surgeons will “bluntly” dissect behind the stomach, but given
the variable level of adhesions to the pancreas and the splenic
vessels, this is unwise. Optimally, it is better to enter the
lesser sac through the gastrocolic omentum and free the posterior gastric adhesions up to the esophageal hiatus. This protects the pancreas and the occasional tortuous splenic artery
from inadvertent injury. After this, the lesser curve, perigastric dissection can be performed with more confidence and
placement of the stapler more precisely so as not to “twist”
the stomach pouch. This occurs when posterior gastric adhesions prevent the initial horizontal stapler from capturing
equal amounts of anterior and posterior gastric wall. The
resultant twist is not as critical as in the gastric sleeve but
looks less than ideal nonetheless.
More controversial is whether or not to dissect the hiatus
and repair a hiatal hernia when present. Autopsy studies
show that a hiatal hernia is present in up to 70% of individuals, similar to our observations when we routinely dissect out
the hiatus in all patients. However, dissection of the hiatus
12
Laparoscopic Gastric Bypass: Technique and Outcomes
can add additional time and potential complications to an
already complicated procedure. Our studies have not shown
that preoperative endoscopy accurately predicts the absence
of a hiatal hernia; the only way to determine its presence is
circumferential dissection of the esophagus. The absence of
the “anterior” dimple is not reliable as the hernia space is
often taken up by a large paraesophageal lipoma that can be
easily reduced into the abdomen once identified. Once identified, the hiatal hernia is best repaired posteriorly with permanent suture.
The question remains: “Is it important to repair every hiatal hernia at the time of gastric bypass?” The answer is not
clear. If one assumes that precise dissection and formation of
the gastric pouch are important to limit postoperative complications, then it would be appropriate to absolutely identify
the location of the gastroesophageal junction—often hidden
in a “sea of fat”—to better perform more consistent reconstruction. It has been our observation that almost all patients
undergoing revision after gastric bypass have a significant
hiatal hernia at the time of reoperation—something not
appreciated at the time of the first intervention.
Dissection of the hiatus and repair of the hiatal hernia
along with removing the fat pad overlying the angle of His
may allow for more precise and consistent pouch formation
and subsequent better long-term performance and lower
complications. However, this has not been proven. In addition, disruption of the phreno-esophageal ligament may predispose the patient to recurrent paraesophageal herniation,
thus complicating their postoperative course. Postoperative
GERD does occur after gastric bypass, but probably not
attributable to an undiagnosed hiatal hernia as much as it is
because of a poorly formed pouch and redundant fundus.
The Bypass
The vertical banded gastroplasty has not been shown to be as
effective as the gastric bypass in terms of long-term weight
loss and quality of life owing to significant GERD and persistence of appetite and hunger. Clearly, the intestinal bypass
is an integral part of the physiology of the gastric bypass
even though the mechanism of its contribution is still largely
unknown.
Overall intestinal length can vary as much as 100%, and
intraoperative measurements are far from precise given the
dynamism of the small bowel. Still, attempts to accurately
measure and modify gastric bypass limb lengths to correlate
with weight loss and malnutrition have been published. Very
few comparative studies exist; most show no difference
except in the super obese population and then only for a few
years. Our data suggests no difference between a 100 and
150 cm Roux limb when stratified to patients with a BMI
greater or lower than 50 kg/m2. Varying biliopancreatic limb
143
lengths up to 100 cm likewise have failed to show a difference. Therefore, it does not seem critical or necessary to
expose gastric bypass patients to excessive diversion beyond
that which is necessary to prevent bile reflux to the gastric
pouch.
Extreme variants of the proximal gastric bypass that
include radically lengthening the Roux limb, shortening the
common channel to 50–150 cm from the ileocecal valve
(type: 2 distal gastric bypass), or shortening the entire alimentary limb length to 3–4 m (type: 1 distal gastric bypass),
effectively creating a biliopancreatic-type diversion, do not
constitute what is commonly referred to by patients and
insurers as “gastric bypass.”
The length of the biliopancreatic limb is not critical,
usually just long enough to provide mobilization of the
Roux limb to the gastric pouch without tension. This
depends on whether or not the Roux limb is to be routed
antecolic or retrocolic, with antecolic naturally requiring
more length. The length of the Roux limb should be at least
75 cm as we have seen bile reflux in patients with 60 cm
Roux limbs. Variants up to 150 cm give no added benefits.
Beyond 150 cm, insufficient data exists to illuminate any
benefit.
The bowel is transected with a linear cutting stapling
device. Surprisingly, little mesentery division needs to be
performed; one must be careful not to transect the superior
mesenteric artery.
Construction of the jejunojejunostomy is usually performed as a side-to-side anastomosis with linear cutter staplers (Fig. 12.2). Attention must be directed to avoid kinking
or twisting the Roux limb or inadvertently performing the
notorious Roux-en-O by not properly identifying each limb
prior to anastomosis.
The Anastomosis
The least controversial but most often studied component
of the laparoscopic gastric bypass is the gastrojejunal
anastomosis. Three distinct methods exist. The original
method proposed by Wittgrove and Clark involved endoscopic retrieval of a percutaneous guidewire that was then
attached to the anvil of a 21 mm circular stapler. This
allowed the anvil to be passed orally into the gastric pouch;
the stapler was passed through an enlarged port site
through an opening of the Roux limb so as to create the
anastomosis. After retrieval, the afferent limb was then
transected. The anastomosis can then be inspected and
tested with the flexible endoscope. Care must be taken
when the anvil passes the cricopharyngeus—the narrowest
part of the esophagus.
Scott and de la Torre modified placement of the anvil
through a gastrotomy prior to gastric pouch formation, elimi-
144
K. D. Higa and P. K. Ma
nating the need for operative endoscopy or transoral passage
of the anvil [6]. The gastrotomy required closure similar to
the enterotomy made on the Roux limb with the Wittgrove
method.
Other surgeons used the linear cutter stapler to create a
side-to-side anastomosis from the Roux limb to the gastric
pouch [7]. This technique required manual closure or the
residual opening, but minimal suturing was required.
The simplest but overlooked method of creating this anastomosis is a handsewn approach familiar to most open bariatric surgeons. It is unclear why many minimally invasive
surgeons dismiss this technique as being too difficult when
much of the operation still requires manual suturing skill.
The handsewn anastomosis remains the most cost-effective
method of gastrojejunostomy. It remains the surgeon’s
choice as to the absorbable suture material, single or two layers, and interrupted or continuous, as well as the diameter of
the thread and size of the needle. We prefer 3–0 absorbable
sutures for this application.
outing of the Roux Limb and Closure
R
of Mesenteric Defects
The Roux limb can be brought through the mesocolon
(retrocolic) or anterior to the colon (antecolic) as well as
anterior or posterior to the gastric remnant. While all
routes are acceptable, one must be familiar with all methods so as to be able to adapt to any situation. For example,
if one has planned, or the situation requires, a gastrostomy
tube, then a retro-gastric placement of the Roux limb will
allow the gastric remnant to attach, unimpeded, to the
abdominal wall.
The antecolic routing eliminates one potential site of herniation—the mesocolon—but introduces additional tension
on the gastrojejunal anastomosis by the weight of the colon
and undivided omentum, if present. When necessary, the
omentum can be shifted to the right of the patient or divided;
under no circumstance is a trans-omental route acceptable
for the potential for herniation through the omental defect
and possible small bowel obstruction. The large Petersen’s
space should be closed either way.
There is no clear advantage of routing the bowel behind
or in front of the colon. If the mesocolon were excessively
short, it would be prudent to go antecolic. If the omentum
is heavy or difficult to manipulate or a short small bowel
mesentery is found, a retrocolic route would be more efficient. When the omentum is adherent to the pelvis or
lower abdomen, as in the case of previous surgery, a
supra-mesocolic approach to the small bowel can be most
efficient.
The retrocolic route for the Roux limb leaves three
potential sites of internal herniation: the jejunojejunostomy
space, the mesocolon, and the Petersen’s space. With continuous closure with nonabsorbable sutures, the internal
hernia rate should approach 1%. Although there are some
advocates for not closing potential sites of herniation (citing personal experience), given the potential serious and
emergent nature of small bowel obstruction after gastric
bypass from internal herniation and the minimal risk of
complications from mesenteric closure, leaving these
spaces open makes little sense [8].
Outcomes
Long-term data regarding gastric bypass have been lacking
due to the complexity of issues regarding follow-up [9–14].
Himpens [14] reported 9-year data consistent with long-term
open gastric bypass data that was comparable to our 10-year
data [13]. Although we experienced poor follow-up, there
was no difference in outcomes between patients who followed up in our office and those who did not; so it is not
unreasonable to extrapolate our results.
Consistent with most series (Table 12.1; Fig. 12.4), there
was gradual weight gain over time, stratified to the severity
of obesity; individuals with BMI < 50 kg/m2 were more
likely to lose a greater percentage of their excess weight
initially but tended to regain weight similar to the super
obese.
Table 12.1 Long-term postoperative BMI
Investigator
Jones [9]
Pories et al. [10]
Sugerman et al.
[11]
Christou et al.
[12]
Higa et al. [13]
Himpens et al.
[14]
Patients
(n)
352
608
1025
Follow-up
(years)
10
10
10–12
Patients eligible for follow-up Patients at follow-up, n
(n)
(%)
71
36 (51)
NR
158 (NR)
361
135 (37)
%
EWL
62
55
52
Postoperative BMI (kg/
m2)
30
35
36
272
12
272
161 (59)
68
38
242
126
10
9
242
126
65 (27)
77 (61)
57
63
33
30
12
Laparoscopic Gastric Bypass: Technique and Outcomes
Fig. 12.4 % Excess weight
loss for patients who had
preoperative BMI < 50 kg/m2
compared to those with
preoperative BMI ≥ 50 kg/m2
[13]
145
preBMI <50 kg/m2 (143 pts)
preBMI ≥50 kg/m2 (53 pts)
% Excess Weight Loss
70
60
50
0
2
4
6
Postoperative Years
8
10
Table 12.2 Postoperative comorbid conditions for patients in Higa et al.’s study [13]
Outcomes of comorbid conditions for 242 study patients and 51 patients evaluated during postoperative year 10
242 study patients
51 patients with 10-year follow-up
Patients
% of
Comorbid condition
(n)
242
Follow-up (%) Resolved or improved (%) Follow-up (%) Resolved or improved (%)
Osteoarthritis
110
45
35
84
100
78
Diabetes
45
19
27
83
75
67
Dyslipidemia
6
2
100
67
100
80
Hypertension
108
45
36
87
100
86
Infertility
5
2
40
50
100
100
Obstructive sleep apnea
45
19
47
76
95
79
Asthma
23
10
30
100
100
100
Gastroesophageal reflux disease 121
50
36
89
94
90
Urinary stress incontinence
35
14
46
69
92
55
Varicose veins
21
9
29
100
63
100
Resolution of comorbid conditions was significant, but
there is a trend for recurrence of diabetes over time
(Table 12.2) [13]. This is consistent with other reports.
Adams [15] showed a reduction of remission of diabetes
after gastric bypass from 75% to 62% from years 2–6 post­op, while Himpens reported no recidivism of diabetes after
9 years but, ironically, a 27.9% incidence of new-onset
diabetes.
Resolution and/or improvement of dyslipidemia, hypertension, asthma, GERD, and obstructive sleep apnea appears
to be sustainable. Despite some weight regain over time,
reduction in overall mortality has been observed [16–18].
Mortality rates now approach 0.16% [19] primarily due to
pulmonary thromboembolism with anastomotic or stapler
leak rates stabilizing at 1%. Early complications (Tables 12.3
and 12.4) are primarily due to gastrojejunal stenosis, amenable to endoscopic balloon dilation. Late complications
include marginal ulceration, biliary tract disease, internal
hernia, and alcohol dependency [20, 21].
Table 12.3 Complications among postoperative patients in Higa
et al.’s study [13]
Complications of 242 study patients and 65 patients evaluated during
postoperative year 10
65 patients evaluated
242 study
during POY 10, n
patients, n
(%)
(%)
Morbidity
Early
Incomplete division of
4 (1.7)
stomach
Staple line failure
2 (0.8)
Thermal injury with
1 (0.4)
perforation
Marginal ulcer perforation
1 (0.4)
Bleeding, observation
1 (0.4)
1 (1.5)
Deep venous thrombosis
1 (0.4)
Stenosis, gastrojejunostomy
12 (5.0)
4 (6.2)
Stenosis, mesocolon
1 (0.4)
Fever
1 (0.4)
Readmission
5 (2.1)
1 (1.5)
Hypoglycemia
1 (0.4)
1 (1.5)
(continued)
146
Table 12.3 (continued)
Complications of 242 study patients and 65 patients evaluated during
postoperative year 10
65 patients evaluated
242 study
during POY 10, n
patients, n
(%)
(%)
Morbidity
Central pontine myelinolysis
1 (0.4)
Subtotal
31 (12.8)
7 (10.8)
Late
Internal hernia
39 (16.1)
Marginal ulcer
11 (4.5)
5 (7.7)
Gastrogastric fistula
1 (0.4)
1 (1.5)
Biliary requiring
17 (7.0)
12 (18.5)
cholecystectomy
Alcohol dependency
6 (2.5)
5 (7.7)
Other substance abuse
1 (0.4)
Hernia, trocar
3 (1.2)
1 (1.5)
Subtotal
78 (32.2)
24 (36.9)
Total
109 (45.0)
31 (47.7)
Data in parentheses are percentages
POY postoperative year
Table 12.4 Postoperative nutritional deficiencies for 136 patients over
10 years
Cumulative incidence of nutritional deficiencies for 136 study
patients tested between postoperative years 1 and 10
Patients with
Percent of 136
Parameter
deficiency (n)
patients tested
81
60
Vitamin B12
Hemoglobin
71
52
Albumin
46
34
Intact parathyroid hormone
36
26
Vitamin B6
23
17
Calcium
18
13
Folate
2
1
Conclusion
The laparoscopic gastric bypass has proven to be superior to
the traditional open approach with respect to complications,
cost, patients’ acceptance, and possibly weight maintenance.
In addition, the minimally invasive approach and current
instrumentation have allowed for refinement, improved precision, and standardization of the procedure through video
documentation and peer review criticism of operative technique not possible with open surgery. Clearly, the laparoscopic approach can now be considered the standard of care,
similar to cholecystectomy—no one should be offered an
open operation in the elective setting.
However, the learning curve for this operation is long,
even with good laparoscopic skills and intense mentorship as
in the case of most MIS fellowship programs. Given the low
incidence of serious complications with the associated
expectations of superior outcomes and the need for a supportive program, it is not reasonable that surgeons can or
K. D. Higa and P. K. Ma
should perform this operation without fellowship training or
mentorship from senior partners.
Although the pathophysiology of the gastric bypass is still
debated, the outcomes, its effect on metabolic syndrome, and
its underutilization cannot be denied. In the absence of
evidence-­based data, surgeons are forced to rely upon anecdotal and observational data when constructing or modifying
their procedures. Given the seemingly infinite variables that
can contribute to results, including reliance upon the compliance of patients themselves, observational data may be more
applicable in a given practice than the illusion of randomized
trials when comparing nuances in operative technique.
Further modifications such as robotic applications and
single-incision surgery have yet to define superior results;
their true advantages, that of marketing, may have relevance
in certain demographics, but as surgeons we must be cautious when defining our role in health care.
Question Section
1. What was the original anastomotic technique described
by Wittgrove and colleagues for construction of the gastrojejunal anastomosis?
A. Handsewn
B. Linear stapler
C. Circular stapler
2. What is the most common cause of death after gastric
bypass?
A. Obstruction
B. Bleeding
C. Sepsis
D. Pulmonary embolism
3. What step is critical in creating the gastric pouch?
A. Posterior visualization at the level of the hiatus
B. Horizontal-based pouch to include the fundus of
stomach
C. Disruption of the phreno-esophageal ligament
D. Pouch size greater than 7 cm
4. Internal herniation can occur in which potential space(s)
after creation of retrocolic gastric bypass?
A. Petersen’s space
B. Jejunojejunostomy space
C. Transverse mesocolon space
D. All of the above
References
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Laparoscopic Gastric Bypass: Technique and Outcomes
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Laparoscopic Sleeve Gastrectomy:
Technique and Outcomes
13
Natan Zundel, Juan D. Hernandez R., and Michel Gagner
Chapter Objectives
1. Describe the surgical technique of laparoscopic
sleeve gastrectomy with attention to the steps that
prevent complications.
2. Present technical modifications that may represent
improvement to the procedure.
3. Summarize the outcomes of laparoscopic sleeve
gastrectomy and their relation to surgical
technique.
Introduction
About 18 years ago, laparoscopic sleeve gastrectomy (LSG)
was proposed as part of a two-stage procedure in high-risk
patients. Today it is not only an accepted stand-alone procedure to effectively treat morbid obesity, but it has become the
most frequently practiced bariatric procedure in the USA
since 2013 when it overtook gastric bypass with a percentage
of 42 versus 34 of the latter [1] and since 2014 worldwide
according to an IFSO survey [2]. LSG experts and the bariatric surgical community in several meetings have also
endorsed it [3, 4]. These same consensuses have underscored
the importance of those procedures being practiced by expert
bariatric surgeons. That is true even considering that low
morbidity and mortality have been advocated as advantages
N. Zundel
Department of Surgery, Florida International University Herbert
Wertheim College of Medicine, North Miami Beach, FL, USA
J. D. Hernandez R.
Surgery and Anatomy, Hospital Universitario Fundación Santa Fe
de Bogotá, Universidad de los Andes School of Medicine,
Bogotá, Colombia
M. Gagner (*)
Department of Surgery, Herbert Wertheim College of Medicine,
Florida International University, Miami, FL, USA
Department of Surgery, Hôpital du Sacré-Coeur,
Montreal, QC, Canada
over more complex procedures such as laparoscopic Roux-­
en-­Y gastric bypass and biliopancreatic diversion with duodenal switch or other restrictive procedures like the
laparoscopic adjustable gastric banding that can have serious
anatomical complications in the mid- to long-term follow­up. It also avoids intestinal surgery with associated complications such as internal herniation, small bowel obstruction,
micronutrient deficiencies, and malnutrition. Additionally, it
is a good alternative when a patient is a transplant candidate
or has inflammatory bowel disease, multiple adhesions, previous bowel resection and other conditions that preclude the
creation of a Roux-en- Y, or a biliopancreatic diversion. It
has also been argued that the follow-up is less demanding
than for the aforementioned procedures [4]. Since long-term
reports are starting to appear, some of these facts are now
supported in the literature. These are some of the reasons that
have made LSG a technique that is growing in popularity and
is offered by most bariatric centers.
The history related to the LSG starts in 1990 with
Marceau’s modification of the classic Scopinaro’s biliopancreatic diversion (BPD) by making a parietal cell gastrectomy to reduce the acid load on the ileum in an effort to
decrease the incidence of marginal ulcerations [5]. This gastrectomy was vertical and evolved into a loose gastrectomy
over a 60-Fr bougie, which was held against the lesser curvature of the stomach far away from the GE junction without
mobilization of the antrum.
Gagner reproduced this operation laparoscopically in July
1999, hence performing the first laparoscopic sleeve gastrectomy over a 60-Fr bougie with a duodenal switch. Thereafter,
LSG alone was initially conceived as the first of two stages
of the biliopancreatic diversion with duodenal switch. The
rationale was that the procedure would be technically easier
and shorter, therefore reducing morbidity and mortality,
since the more technically demanding part of the operation
would be carried out after a period of weight loss [6, 7]. The
idea came from the observation made by the senior author,
after recording a higher mortality associated with super-­
super obesity (BMI > 60) in patients undergoing BPD-DS. A
two-step surgery approach was used to reduce operating time
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_13
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N. Zundel et al.
and surgery complexity [8]. The first step was the LSG, and
after several months, the BPD-DS was completed, with a significant reduction in mortality and good results in weight
loss [9]. In several patients a steady and surprisingly good
weight reduction with the LSG only was noticed, and it was
hypothesized that it could become a primary bariatric procedure on its own, a procedure that still left open the possibility
of a second intervention in case of unsatisfactory weight loss
or weight regain. This suggestion, supported by the author’s
own data, was made by other researchers [10]. It became a
safe alternative for high-risk patients in need of the
operation.
LSG is technically easier when compared to gastric
bypass or biliopancreatic diversion, a primary reason for its
growing popularity among surgeons and patients. It does,
however, as with any other surgical procedure, have a
potential for long-term complications that range from 0.7%
to 6% in different series [11–15]. Some of these complications can be severe and potentially fatal. Therefore, it is
important to be thorough in the appropriate technique, to
observe the correct steps and safety features, and to follow
patients closely after surgery to avoid long-term complications or failure.
Preparation and Surgical Technique
A multidisciplinary team dedicated to treat obese patients
evaluates all patients to ascertain the indication for a bariatric
procedure and works toward improving patient diet, physical
condition, and habits during the preoperative period.
Identified comorbidities are controlled, and patients are fol-
Fig. 13.1 (a) Five-trocar
setting. (b) Six-trocar setting.
The size of the larger trocars
depends on the type of stapler
to be used
a
lowed all through the perioperative period. This includes
gastroscopy, Helicobacter pylori treatment if present, and
respiratory-related measures.
Patients are placed in supine, either with legs spread
(French position) or closed together (American position).
Either way, they are firmly secured to the operating table, to
allow for a steep Fowler (reverse Trendelenburg) position.
Additionally, the table is slightly tilted right side down for an
adequate visualization of the gastroesophageal (GE) junction. Additionally, anti-embolic stockings and intermittent
compression devices are employed to prevent venous
thromboembolism.
Authors’ current LSG technique uses five or six ports.
Figure 13.1 shows the options of port distribution. The first
trocar, 10–12 mm, is placed at the umbilicus, using an open
technique to reach the peritoneal cavity. Two more 5- or
12-mm ports are placed in the supraumbilical region, one
subxiphoid and another in the right upper quadrant. Two
15-mm trocars, wide enough to allow the insertion of the
largest staplers, are placed in the mid-abdomen just medial to
the midclavicular lines. Finally, a 5-mm trocar used by an
assistant for retraction is placed in the left upper quadrant,
high enough to reach the top of the gastric fundus.
A 10-mm, 30° scope is used. The left lobe of the liver is
retracted to expose the entire GE junction and the lesser
curve. The procedure starts by cutting the small branches of
the gastroepiploic arcade and opening the lesser sac. Then,
dissection is carried out along the greater curve, staying very
close to it, dividing the branches of both gastroepiploic arteries, until short gastric vessels are divided using an advanced
bipolar cutting device or the ultrasonic scalpel. The assistant
retracts the omentum laterally during the maneuver and
b
13
Laparoscopic Sleeve Gastrectomy: Technique and Outcomes
keeps repositioning the instrument superiorly to improve
exposure of the vessels and avoid bleeding. The remainder of
the gastrocolic ligament (without gastroepiploic vessels transection) is severed distally up to 2 cm proximal to the pylorus. The objective of cutting the omentum right by the edge
of the greater curve is to minimize the amount of fat attached
to the stomach, to make its extraction from the abdomen
easier at the end of the operation. The stomach is then lifted
to expose its posterior aspect, and all lesser sac attachments
to the stomach are freed. This will allow the appropriate
positioning of the mechanical suture and avoid bleeding.
When cutting these adhesions, it is necessary to be aware of
the presence of the branches of the left gastric artery, identifying and preserving them. If the left gastric branches were
cut, the blood supply to the sleeve would be compromised.
Other anatomic relations the surgeon needs to be aware of
are the splenic artery and vein, running along the superior
edge of the pancreas. Splenic artery in older patients may be
redundant and therefore may be in harm’s way during posterior dissection and stapling.
The gastrophrenic ligament is divided, and the fat pad
usually found anterior to the cardia is removed to improve
exposure of the angle of His, adding the full exposure of the
left crus to complete the dissection and to determine the
presence of a hiatal hernia. In case such a hernia is discovered, a formal closure of the hiatus is mandatory, since gastroesophageal reflux disease (GERD) and other complications
are associated with its presence in the postoperative period.
To achieve that, the stomach involved and distal esophagus
are freed of mediastinal attachments and brought down into
the abdomen, leaving at least 3 cm of intraabdominal esophagus. A posterior crural approximation is conducted to close
the gap, using nonabsorbable sutures and pledgets if needed
(Fig. 13.2). It has been proposed in the literature that GERD
with or without a hiatal hernia can be treated or prevented. To
Fig. 13.2 Laparoscopic posterior closure of a hiatal defect is required
in patients with hiatal hernia or GERD
151
that purpose and as mentioned ahead, a modified Hill repair
has been advocated by some surgeons to keep the sleeve in
the abdominal cavity.
Stomach division starts 4 cm proximal to the pylorus, to
preserve a part of the gastric emptying mechanism of the
antrum. Prior to the creation of the sleeve, the anesthetist
introduces a 34–40-Fr bougie to guide the stapling and maintain an adequate lumen of the gastric sleeve. Continuous
communication between surgeon and anesthetist is paramount to ensure adequate positioning of the bougie in a safe
fashion. The bougie should be placed prior to stapling, guiding it to reach the pylorus, and positioned close to the lesser
curve. Care is taken not to divide the stomach too close to the
incisura angularis to avoid kinking or stenosis at this level.
Green (4.8 mm) or black (5 mm) stapler cartridges are used
with absorbable buttress material (Gagner). Green or black
for the first two firings and blue or gold for the rest if no
absorbable buttressing materials are used (Zundel). In any
case, all of them are 60 mm in length. Stapling is performed
in a way that no kinking or twisting of the sleeve is produced
at any level. To achieve this, the stomach is held by the assistant stretching it to the patient’s left, while the surgeon places
the stapler making sure that anterior and posterior edges are
at the same distance from the lesser curve. In other words,
the distance of the anterior aspect of the remaining stomach
should not be shorter than its posterior counterpart.
Additionally, a stapler should be placed right at the angle of
the previous one, avoiding “dog-ears” created on the edge of
the stomach that may produce ischemia. After each firing,
the anesthetist is asked to wiggle the bougie to ensure the
sleeve is not too tight or that the bougie has not been stapled
or cut.
Although the senior author recommended in the past to
cut the fundus at least 1 cm from the gastroesophageal junction, his current practice is to divide it as close as the GE
junction as possible, without actually compromising the
esophagus.
The other authors still cut the fundus 0.5 cm away from
the GE junction and imbricate the staple line with absorbable
suture in an effort to reduce leak rates. This is done without
the presence of buttressing material.
The senior author’s intention is to create a sleeve that goes
in straight line from the GE junction down into the stomach,
since a funnel-shaped sleeve may be more likely to produce
gastroesophageal reflux by dilatation and stretching of the
lower esophageal sphincter. Additionally, the perigastric fat
is mobilized, permitting better identification of the esophagogastric junction, and this may be used to buttress the staple
line. In this technique, the staple line is reinforced only at the
GE junction, where leaks are more frequent, and at the bottom of the staple line on the antrum, the thickest part of the
stomach. This is done using through-and-through figure-­
eight stitches with 3–0 absorbable monofilament sutures.
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N. Zundel et al.
Fig. 13.3 Reinforcement of the stapler line with running suture. Only if the stapler line does not have buttressing materials
The other authors (Zundel and Hernandez) do not routinely
use absorbable buttressing material; conversely, with the bougie in place, the full length of the staple line is oversewn with
a running suture of 3–0 absorbable suture (Fig. 13.3).
The anesthetist removes the bougie under direct vision to
check the final shape of the sleeve. The stomach is removed
through one of the 12–15 mm ports (Fig. 13.4). The integrity
of the staple line is tested with the instillation of 50–100 ml
of methylene blue in saline solution. No drains are left.
Postoperative Period
Appropriate hydration and pain and nausea control is initiated. During in-hospital stay, patients are observed for signs
of leak or bleeding such as tachycardia, tachypnea, or fever.
Abdominal pain and left shoulder pain are not reliable symptoms at this point, but should not be dismissed as normal.
Anti-embolic stockings and intermittent sequential compression devices can be removed as soon as the patient is ready to
walk. The next day, an upper gastrointestinal contrast X-ray
is done to identify any possible leaks (Fig. 13.5). If the study
is negative for leaks, liquid diet is started, and patients are
encouraged to ambulate. Respiratory therapy is initiated and
previous chronic medication is restarted. If early signs suggesting a leak appear, the patient is taken to surgery for a
diagnostic laparoscopy.
Patients are usually discharged home on the first or second postoperative day with liquid pain medications for a
few days and a proton pump inhibitor for 6–8 weeks. Also,
patients are initiated in a liquid diet for 2 weeks, followed
by a semiliquid diet following the first, until progressively
more solid diet is allowed.
A team of dietitian, surgeon, nurse, and according to need
a psychiatrist, internist, or other specialist follows patients.
Results
Weight Loss and Comorbidities
A number of reports on outcomes of LSG with patients followed for more than 5–10 years are being published more
often, giving the scientific community more data to make
possible to reach conclusions about the safety, efficacy, and
durability of LSG. However, it is important to point out
that the large number of variations that still exist in surgical technique may be cause for confusion and difficulty
in establishing comparable outcomes at the present time
[15]. Most patients with longer follow-up were operated
at a time when surgical technique was even less standardized. The bariatric community has made an effort to come
to an agreement in major technical issues through consensus meetings on LSG. Five of these meetings explored the
opinions of experts and the evidence in the literature, creating concurrence that has reduced technical variations in
topics such as bougie size, starting point of stapling, etc.
[4]. Recommendations have been made, and a more homogeneous technique has been developed. These consensus
meetings started in 2007, so as mentioned before, outcomes
that could be attributable to these agreements are only coming to be available now.
13
Laparoscopic Sleeve Gastrectomy: Technique and Outcomes
153
Fig. 13.4 Shape of the resected stomach with a continuous staple line and an additional resection of the fundus. On the right the stomach is insufflated to see its size and shape. Left: regular stapler line. Right: staple line reinforced with buttressing material
Fig. 13.5 Upper GI contrast study showing uniform shape of the
sleeve with no evidence of leaks and good flow through the sleeve
The LSG summit of 2012 [16] reported on a survey
answered during the meeting by 130 surgeons with experience of more than 1 year doing the operation, with a total of
46,133 LSGs. The survey included surgeons with short
experience and minimum follow-up. A calculation on what
surgeons reported rendered a mean % excess weight loss
(EWL) of 59.3% in year 1, 59.0% in year 2, 54.7% in year
3, 52.3% in years 4 and 5, and 50.6% in year 6 [16]. The
authors recommend caution when analyzing these numbers,
since they determined that surgeons marked 0 change in
EWL% when they should have left a blank for not having
patients that far in time. Since it was not possible to discard
the 0% EWL option, they did not eliminate those numbers,
but adjusting the analysis for this bias, % EWL could be
even higher.
On 2014, the Experts Survey carried out before the fifth
consensus in Montreal reported at 5-year follow-up an EWL
of 60.5%, with an average patient BMI post-surgery of
30.2 kg/m2. The average rate of strictures was 2.1% and the
leak rate reported was 2.4%. In what concerns to conversions, 4.7% were due to weight loss failure and 2.9% due to
GERD [4].
154
Studies with a long-term follow-up support better results
in weight loss than those reported by the survey. Bohdjalian
et al. found a 5-year % EWL of 54.8 ± 6.9, which was comparable to the results at 1 year, commenting that LSG leads
to stable weight loss in the long-term follow-up [17]. In a
study with a large number of super obese patients that
extended follow-up to 3 and 5 years, Saif et al. showed that
the percentage of excess BMI lost was maintained. The mean
percentage of excess BMI lost was statistically significant
for all cohorts, being 58.5% at 1 year, 65.7% at 3 years, and
48% at 5 years [18]. Zachariah et al. report the data collected
from 228 patients treated with LSG and followed for 5 years
since 2007. They showed a mean % EWL of 71.2 ± 21 at
3 years and 63 ± 20 at 5 years, with BMI going down to 26
and 28, respectively. Mortality was reported at 0.43% [19]. It
is worth pointing out as a parenthesis that in high-volume
centers mortality is even lower [13, 14]. At 5 years, resolution of diabetes was 66%, 50% for hypertension, and 100%
for hyperlipidemia. In fact, results for diabetes resolution
have been found to be as good as that of laparoscopic Roux-­
en-­Y gastric bypass [20].
Two recent studies have published more than a thousand
patients, each with more than 5 years follow-up. Alvarenga
et al. [13] reported 1020, some of them operated up to 8 years
before. EWL for this series was 92% after 1 year, 89% after
3 years, 75% after 5 years, and 73% after 8 years. The caveat
was a large desertion of patients as the follow-up period was
longer, up to 92% at 8 years. Authors do not give the actual
number, making difficult to judge these results; however,
they argue that the main power of the paper is in the 3–5 years
follow-up and the large number of patients in their cohort. In
the second paper, van Rutte et al. [14] reported on 1041
patients followed for up to 5 years. Percentage of EWL was
69.3% at 3 years, 70.5 at 4 years, and 58.3 at 5 years. Both
studies consider LSG a safe and effective treatment for morbid obesity. Complications are low and comorbidities control
is very good. They also showed that mean EWL after 5 years
remains over 50%, with the overall percentage in 70%.
Interestingly, van Rutte also found that of the 16.4% of
patients who reported GERD before surgery, complaints disappeared in 84.5%. On the other hand, 11.7% developed de
novo reflux disease.
In relation with the metabolic effects of LSG, there was a
concept that therapeutic results were achieved only by reducing the stomach size approximately to 80% of its original
size. Therefore, the resulting weight loss was a consequence
of a mechanical or volumetric variation. This concept has
been abandoned as a number of studies have shown other possible causes. There are indeed humoral changes that impact
metabolism, therefore affecting weight. Several studies have
shown that after the operation, plasma ghrelin levels were significantly reduced in the early postoperative period [21, 22]
and remain consistently low during 5-year follow-up studies
N. Zundel et al.
[17]. This peptide, produced mainly in the stomach, is
secreted when the stomach is empty, increasing hunger and
producing secretions to digest food. Another molecular effect
that is creating interest among researchers is the interaction
between LSG, bile acid circulation, and FXR signaling [23].
It has been reported that levels of circulating bile acids are
higher after LSG [24]. This has an impact on gut microbiota,
contributing to the changes that have been associated with
weight loss. The Farsenoid X receptor, also known as NR1H4,
is a nuclear receptor and, when it binds to bile acids, creates
signaling molecules that take part in regulating several metabolic processes. It has been suggested that these metabolic
processes have great impact in weight reduction, possibly
more than the stomach volume restriction itself [24].
A general belief of minimal nutritional deficiencies has
accompanied the practice of LSG, which originated in the
fact that nutrients follow the normal path in the gastrointestinal tract, as opposed to gastric bypass and biliopancreatic
diversion, where large segments of the small intestine are
excluded from the passage of nutrients. There is still insufficient documentation available to support or dismiss this
assumption. Gehrer et al. [25] found nutritional deficiencies
both before gastric bypass and after LSG with a mean follow-­up of 24 months. Deficiencies in zinc, vitamin D3, folic
acid, iron, and vitamin B12 were present but not clinically
significant and less important than after gastric bypass, and
all were easily treated and resolved. A 5-year follow-up
study showed a different picture, with values for parathyroid
hormone, hemoglobin, and hematocrit just under the normal
values but with no deficiencies [18]. For the authors, the
results show clear health improvements with nutrient indicator levels reaching up to normal values with no signs of nutritional deficiencies and conclude that long-term follow-up is
fundamental to assist patients in maintaining the good weight
loss results.
Complications
On the large series by Alvarenga [13], 39 patients (3.8%) had
long-term morbidity that included strictures in 5 of them
(0.49%) and GERD in 61 (6%). The overall 30-day mortality
rate was 0%. Conversion rate to LRYGB was 1.25% (n = 12),
five of them (0.49%) due to intractable GERD, four (0.43%)
for weight regain, and three (0.29%) for gastric outlet
obstruction.
In the group of van Rutte et al. [14], complications rates
decreased with improved technique over time. No death was
attributed directly to surgery. Of 724 patients, 11.7% developed GERD de novo, and 8.2% presented over time with
dysphagia leading to vomiting.
One of the most feared complications, fortunately rare, is
leaks. However, fistula, stenosis, GERD, and pouch dilata-
13
Laparoscopic Sleeve Gastrectomy: Technique and Outcomes
tion, among others, also can be present [11]. Leakage usually
appears as an acute complication (within 7 days), causing
tachycardia, tachypnea, and fever very early on, and indicates most often that the patient requires immediate intervention. The most common site for leak is along the staple line
immediately below the gastroesophageal junction. Several
strategies can be used including diagnostic laparoscopy with
drainage, insertion of a T-tube in the opening to control the
fistula, insertion of an esophagogastric stent to occlude the
perforation and to open any associated distal narrowing, or
percutaneous drainage with endoscopic stents. Some
European groups have used endoluminal double pigtail catheters to the same end. The most frequent location of the fistula is near the angle of His (at the top of the stapled line) and
secondly in the antrum at the beginning of the gastric stapled
line. Sometimes fistulae can become chronic and therefore
will need a different and more complex treatment [26]. A
laparoscopic Roux-en-Y fistula-jejunal anastomosis can be
performed as early as several weeks after a leak, with a high
success rate, thus avoiding total gastrectomy, a procedure
with higher morbidity.
Another complication and common cause for leakage is
stricture or stenosis at the level of the gastric incisura [27], a
cause of obstruction. Clinical presentation both for acute and
late LSG obstruction is similar with dysphagia appearing
weeks to months after the LSG operation in the latter, starting with dysphagia to solids followed by symptoms to liquids, salivation, and vomiting. Endoscopy with balloon
dilatation is the preferred method for management of the
stricture. Zundel et al. recommend an achalasia balloon with
higher controlled pressure [26]. Acute obstruction cases may
be due to gastric mucosal edema and external compression
and in some cases due to kinking of the sleeve [9]. Cottam
et al. noted that kinking is independent of bougie size and
more correlated with the oversewing of the suture line rather
than with the diameter of the sleeve [27]. Stricture can be
avoided by keeping a safe distance from the bougie at the
level of the incisura angularis. This also applies when the
staple line is oversewn to reinforce it. All along the staple
line, the bougie will prevent stitching through the stomach’s
lumen or further reducing the size of the sleeve. In all these
cases, kinking may appear. The recommended bougie size is
36 F [28], as nearly 40% of surgeons have used this size [16].
The alteration of the pouch architecture caused by asymmetric stapling of the anterior and posterior walls of the stomach
may lead to twisting of the gastric tube, which may also
cause dysphagia [29]. Also, leaving an excessively large posterior wall may twist the sleeve as the stapler is applied, leaving an uneven line of staples. If a stricture becomes permanent
and does not respond to endoscopic treatment such as dilatation or stent, then a laparoscopic longitudinal lateral gastrotomy with transverse hand-sewn closure (like a Mikulicz
pyloroplasty) can be performed. Alternatively an anterior
155
seromyotomy, rarely performed due to the risk of mucosal
perforation and leak, or conversion to Roux-en-Y gastric
bypass can be performed.
The association between GERD and LSG has been one of
the most controversial issues of the technique. There are
multiple causes for pathological reflux in obese patients,
even before surgery. Increased intraabdominal pressure and a
higher rate of hiatal hernia are two of them [30]. De novo
GERD can appear, arguably more after LSG, but also after
RYGBP, and if a hiatal hernia is left untreated at the time of
the operation, the chances of severe or even intractable reflux
are important. Several studies have shown an incidence
between 6% and 16% [13]. On the other hand, Lyon et al.
showed an improvement of GERD if hiatal hernia was
repaired with anterior and posterior hiatal closure [31] in
patients with history of GERD and hiatal hernia diagnosed
both pre- or intraoperatively. They also reported a slight but
not statistically significant rise in reflux symptoms in patients
previously asymptomatic and without hiatal hernia. These
results must be analyzed with caution since it is a retrospective study and patients were only interviewed by phone.
The discussion started when cases of GERD appeared in
relation to LSG [27], blaming the operation for all of them.
It was then reported up to 79% of heartburn in obese patients
in the preoperative period, with regurgitation in 63%.
Additionally near half of them had objective GERD as demonstrated by esophagitis at endoscopy in almost a fifth of the
total [32]. Although several authors attribute mechanisms
for de novo reflux to the destruction of the phrenoesophageal membrane, the section of the sling fibers at the cardial
region and the disappearance of the angle of His [32], others
consider that it is in the technique of the creation of the gastric tube where causes can be found [33]. A review of the
literature in 2015 showed great variability in results, with
some papers showing high incidence of postoperative reflux
either worsening or appearing de novo, while other talked of
reduction or absence of the GERD symptoms present in the
preoperative period [34]. It was true by the time of that publication as it is now that there are no valid studies that shed
light on this topic. On a review of his own experience on a
period of 18 months, and after 6 years of practicing LSG,
Daes et al. give a different picture [33]. They prospectively
followed 373 of 382 consecutive patients undergoing LSG
for up to 22 months, at least 97% of them more than
6 months. Using endoscopy, they found GERD in 44.5% of
patients and hiatal hernia in 51%. The hernia was confirmed
during surgery in 37.2% of patients. According to them,
with a very well-­standardized technique, plus being aggressive in the search and surgical correction of hiatal hernia,
they achieved a very low incidence of postoperative
GERD. They did not use pH analysis or manometry; however the incidence of GERD on 373 patients was only 2.6%,
of the patients with preoperative GERD symptoms 94%
156
were asymptomatic, and only one patient of the previously
asymptomatic patients reported GERD complaints.
A very recent meta-analysis [35] produced a recidivism
rate between 14% and 37% and a revision rate close to 20%,
mostly due to weight regain, and in a small percentage of
near 3%, to GERD. Authors discussed that findings are from
7 to 11 years ago, and therefore surgeon’s experience, standardized technique, and thorough follow-up were not there
yet, and therefore there is still a lot of variation in results.
That is also true, they say, when revisions are analyzed.
Variations in revision rates and their causes are very high,
suggesting differences in experience and technique.
Most of patients with early postoperative symptoms of
GERD respond to prolonged medical therapy; however,
some patients require surgical reoperation with hiatal hernia
repair, or conversion to Roux-en-Y gastric bypass, which has
been advocated as the best alternative in these cases. Hiatal
hernia repair with the use of nonabsorbable mesh is avoided
due to the risk of erosion into the gastric lumen. Current recommendations are to reduce the hernia with an appropriate
length of intraabdominal esophagus and closure of the hiatus, which most surgeons tailor posteriorly [36]. Recent publications advocate for what some authors have called a
modified Hill technique, in reference to Lucius Hill anterior
fundoplication with a gastropexy to the arcuate ligament
[37]. A French group has used the technique since December
2014 [38]. The first 14 patients they described, all symptomatic, had a mean excess BMI loss of 68%. There were no
major complications. Of three patients complaining of persistent GERD symptoms, only one required daily use of
PPIs. They have called their technique simplified laparoscopic Hill repair. The authors consider posterior gastropexy
a more appropriate name for it, since no fundoplication is
possible. It has been used both at the first operation and as a
procedure to correct GERD and hernia [39].
In spite of all measures possible, there will be failures,
and LSG should in this case be considered as a first step
treatment in obese patients and be converted into a second
procedure [15]. Weight regain, GERD, inadequate weight
loss, or inadequate resolution of comorbidities may require
late reintervention, after proper endoscopic and radiological
evaluation. Choice of operation will be dependent on the initial BMI (super obese will respond better with a duodenal
switch), presence or absence of GERD (Roux-en-Y gastric
bypass is preferred), or re-sleeve gastrectomy for fundus
dilatation.
Sleeve Gastrectomy or Gastric Bypass?
Since it is the gold standard of bariatric surgery, it is inevitable to compare RYGBP with today’s more frequently practiced operation for obesity: sleeve gastrectomy. Gastric
N. Zundel et al.
bypass has been practiced for more than 50 years; although
several modifications have been done along the years and
different groups have introduced variations, the technique
has been fairly standardized for several decades. The first
series of LRYGBP was published in 1994, and since then,
minimally invasive approach became the preferred route. On
the other hand, LSG’s longer meaningful series are reaching
only 8 or 9 years, and therefore comparisons that make justice to both procedures are still scarce.
SM-BOSS [40] is a Swiss multicenter randomized trial
that compares LSG and LRYGBP. Both procedures are standardized in the four hospitals that are collecting data. They
recently published an update with 5-year follow-up that
shows no difference in weight loss between both procedures.
There is a slight increase in excess BMI every year for both
procedures; however, the results remain successful for both:
61.1% excess BMI loss for LSG and 68.3% for LRYGBP,
both good and not significantly different (P = 0.22). On secondary observations, complete remission of diabetes was
seen in 61.5% and 67.9%, respectively (P = 0.99); total
remission of dyslipidemia was significantly higher in
LRYGBP than in LSG (62 vs. 42%, P = 0.09). In reference
to a complication extensively exposed before, they found
remission of preexisting GERD after 5 years in 25% of
patients after LSG and 60% after LRYGBP (P = 0.002).
They also reported higher worsening of symptoms after LSG
(31.8% vs 6.3% P = 0.006); additionally, de novo GERD was
found in 31.6% after LSG and 10.7% after LRYGB
(P = 0.01). However, other complications were significantly
less frequent in LSG. Both techniques are nowadays and in
experienced groups very safe, but there were more reinterventions in the 30-day postoperative period, as there were
late complications like internal hernia and obstruction and
dumping, among others. Additionally, there was one dead on
the LRYGBP group only [40].
SLEEVEPASS [41], also a multicenter randomized clinical trial, this one conducted in Finland, has now 5-year follow-­up results published. It was designed to establish if there
was equivalence between LRYGBP and LSG. Two hundred
forty patients were involved. In it, percentage of EWL at
5 years was higher for LRYGBP, but the difference was not
statistically significant. As authors report, “gastric bypass
resulted in statistically greater weight loss than sleeve gastrectomy at 5 years, but the difference was not clinically significant, as the minimal clinically important difference of 9 is
within the confidence interval” [41].
Diabetes remission rate was lower than in the SM-BOSS
trial, and no difference was found between both procedures. A remarkable finding in complications was that de
novo GERD was only 9.1% after 30 days postoperative of
LSG and only 5.8% at long-term follow-up. In terms of
reintervention, GERD was associated with 7 of 10 surgeries. No mention was made of the relation between GERD
13
Laparoscopic Sleeve Gastrectomy: Technique and Outcomes
157
and RYGBP. Additionally, there was no difference in patients, it is going to be the only intervention they need, as
quality of life between both groups.
long as they have discipline and a good team to support them
The merit of SLEEVEPASS and SM-BOSS is high-­ in the process, among other things.
quality evidence, but other papers have shown comparable
However, it may have come the time to consider obesity
results in Israel, Korea, and the USA [42–44]. In a large as other chronic diseases are approached, like hypertension
population study that included surgical and nonsurgical or diabetes, where treatment has to be planned in stages that
patients, after a mean 4.5 year follow-up, Reges et al. [42] grow in complexity. Consequently, for obesity, surgery and
reported a higher survival rate in surgical as compared to endoscopic interventions will have to be part of those steps,
nonsurgical patients. In the surgical group, comprising 8385 and possibly patients will have to be informed that a second
patients, mortality was significantly lower among LSG operation may be needed in the future. In such scenario, LSG
patients, compared to LRYGBP and adjustable gastric band- is probably the most versatile operation: it will be more than
ing. Revisional surgery was a less frequent in the first two enough for most patients but can also be the best first interprocedures and higher in gastric banding. In a study with vention in a stepped program, since it can be redone or conelderly patients comparing both techniques, Janik et al. [43] verted to RYGBP, BPD-DS, or SADIs.
reviewed the Metabolic and Bariatric Surgery Accreditation
and Quality Improvement Program (MBSAQIP) database of
2015 and selected 6742 patients over 60 years that ­underwent Conclusions
one of the two bariatric procedures and matched them 1 to 1.
Compared to LSG, LRYGB had significantly higher anasto- The advantages of LSG are still being confirmed today, but
motic leakage rate (1.01% vs. 0.47%, P = 0.019), more fre- also placed in perspective in the whole spectrum of obesity
quent 30-day readmission rate (6.08% vs. 3.74%, P < 0.001), surgery. This procedure has earned an important place in barand higher 30-day reoperation rate (6.08% vs. 3.74%, iatric surgeons’ armamentarium and has become the most
P < 0.001). There was no significant difference in bleeding, practiced intervention as a stand-alone operation.
infection, sepsis, and pulmonary embolism, among others.
If one considers that LSG’s surgical technique has only
Kim found no significant difference in the mean percentage been well defined in the last 5 or 7 years, it is possible to
of EWL between LSG (63.5%) and LRYGBP (71.2% hypothesize that outcomes reported in the future may be
P = 0.073), although revision was higher in LSG [44].
even better than those currently found in literature. This, of
course, will require good patient selection, expert multidisciplinary teams, and adequate long-term follow-up.
Discussion
One fundamental consideration that has reached consensus among experts is that GERD and hiatal hernia must be
Severe obesity should be considered a chronic and mostly carefully sought after, both in the preoperative and postopincurable disease influenced by many features and with erative periods, and if found, treated aggressively. There are
many etiological factors. In fact, emotional and psychologi- suggestions that an appropriate surgical technique may
cal components in obesity are paramount, not only as a cause reduce its incidence.
for obesity itself but also as a reason of failure of surgical and
Finally, there is still work to be done in standardizing sevnonsurgical treatments. It is worth considering that a multi- eral important steps in the surgical technique, as there is still
factorial chronic disease, with a considerable behavioral controversy in bougie size, suture reinforcement, and how
component, is not best treated with surgery. However, after much of the antrum is to be resected.
several decades, surgery is still the best method to achieve
such a large rate of success, that is, a significant and durable
weight loss and control of comorbidities. However, an Question Section
important and growing number of patients have some sort of
failure. And that is true for all procedures and surgical 1. What was the origin of the sleeve gastrectomy as such?
A. Doctor Gagner’s first staged duodenal switch starting
techniques.
with a laparoscopic sleeve gastrectomy.
One of the items growing more in bariatric surgery today
B. Doctor Marceau’s modification of Scopinaro’s classic
is reinterventions. A larger number of patients are going for
biliopancreatic diversion creating a vertical
a second operation every year, and this can only be expected
gastrectomy.
to grow, as the rate of operations is higher. LSG has demonC. A consensus of bariatric surgery experts created a verstrated to be a safe, reproducible, and effective operation on
tical gastrectomy by removing fundus and body of the
its own to treat morbid obesity with a rate of success that is,
stomach.
arguably, at least as good as the Roux-en-Y gastric bypass,
D. Mason did the first sleeve gastrectomy.
according to several studies. For a large percentage of
158
2. What are the main measures if a hiatal hernia is found?
A. The hiatus is not explored; only the fundus is freed
and prepared for resection.
B. The procedure is abandoned and the patient informed
of the options.
C. Reduction of the hernia with 3 cm of intraabdominal
esophagus and crural approximation.
D. Create a formal fundoplication to prevent GERD.
3. Metabolic effects of LSG are mainly related to the reduction of the production of:
A. Insulin
B. GLP-1
C. Ghrelin
D. Glucose
4. Where are leaks after LSG more frequently located?
A. Staple line below gastroesophageal junction
B. Staple line at the start near the pylorus
C. Staple line at the incisura angularis
D. Caused by accidental perforation anywhere in the
stomach
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Biliopancreatic Diversion
with Duodenal Switch: Technique
and Outcomes
14
Ranjan Sudan
Chapter Objectives
1. Understand the history of evolution of the duodenal
switch operation.
2. Become familiar with the principles of performing
the duodenal switch operation.
3. Understand comparative effectiveness of the major
bariatric operations.
4. Understand surgical and nutritional complications
of the duodenal switch operation.
Introduction
Nicola Scopinaro described the original biliopancreatic
diversion (BPD) in 1979 in which a distal gastrectomy was
performed with an alimentary limb of 250 cm and a common
channel of 50 cm [1]. In the original BPD, the blind end of
the jejunoileal bypass (JIB) was eliminated. The blind loop
was thought to be responsible for bacterial overgrowth and
cirrhosis. The BPD created a more substantial stomach
pouch of about 250 mL compared to the Roux-en-Y gastric
bypass (RYGB) allowing the patient to eat more normal
sized meals, and the weight loss was attributed primarily to
fat malabsorption. However, the operation was associated
with post-­gastrectomy syndromes such as dumping, marginal ulceration, and the potential for diarrhea. The concept
of developing the duodenal switch was based on the original
studies of DeMeester in dogs that showed when the pylorus
was preserved, marginal ulceration was reduced. Hess et al.
performed the first BPD/DS in 1988 [2], and Marceau et al.
published their results and technique in 1993 [3] in which
SG and a post pyloric anastomosis is performed. Ren et al.
described the first laparoscopic BPD/DS in 2000 [4], and the
R. Sudan (*)
Department of Surgery, Division of Metabolic and Weight Loss
Surgery, Duke University, Durham, NC, USA
e-mail: ranjan.sudan@duke.edu
same year Sudan et al. performed the first robotic BPD/DS
[5].
The BPD/DS is increasingly being recognized as the most
effective bariatric operation for excess weight loss (EWL)
and is the best operation for resolution of diabetes and hyperlipidemia. In a propensity matched analysis of different bariatric operations, the comparative effectiveness of BPD/DS
showed better odds of resolution of diabetes, hypertension,
and more weight loss compared to either the RYGB or the
sleeve gastrectomy (SG). It was also better than the SG for
resolution of reflux disease but less so than the RYGB [6].
However, BPD/DS annual numbers have lagged behind other
bariatric operations [7]. It takes longer to perform, is more
challenging technically, and has the potential for more technical complications and nutritional deficiencies which may
explain some of the reasons behind its slower adoption.
However, with better description of minimally invasive techniques to perform BPD/DS and increasing need to revise
RYGB and SG for inadequate results, there is growing interest in performing this more aggressive operation.
Preoperative Assessment
The indications for performing a BPD/DS are similar to
other bariatric operations with preference given to those
patients who have a high BMI, more severe diabetes, or
hypercholesterolemia. There is evolving evidence that for
patients with a BMI of less than 50 kg/m2, the rates of malnutrition or excess weight loss are not any different than
those for a BMI greater than 50 kg/m2 [6]. Accordingly,
Centers for Medicare and Medicaid allow BPD/DS for
patients with BMI > 40 kg/m2 or >35 with a significant
comorbidity and sufficient attempt to lose weight through
nonsurgical means. Many other payers use similar criteria.
The contraindications for performing a BPD/DS are the
same as for any bariatric operation such as noncompliance,
unresolved psychiatric conditions including substance abuse,
or overwhelming medical risk. Any patient in whom malab-
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_14
161
162
sorption should be avoided or those who have anatomical
considerations such as dense small bowel adhesions is also
not a good candidate for a BPD/DS. Patients are also advised
about the side effects of the BPD/DS, and these may be
incongruent with their preference or lifestyle.
Patients must undergo multidisciplinary evaluations that
include medical nutritional and psychological evaluations.
The ability to comply with follow-up and with nutritional
supplements is even more important with the BPD/DS. Since
the operation takes longer to perform, the ability of the patient
to tolerate a longer duration of anesthesia is assessed from a
cardiopulmonary standpoint. Vitamin deficiencies must be
assessed preoperatively and corrected prior to ­surgery as it is
often harder to do so after the operation. Patient education
regarding appropriate compliance with postoperative followup and adherence to nutritional guidelines is emphasized. In
the era of enhanced recovery, a liver shrinking diet may be
prescribed, and for the patients who are very heavy, preoperative weight loss may enable completion of the BPD/DS in a
single stage. Bowel prep is avoided to prevent dehydration.
Preoperatively, the patients are assessed for duration of DVT
prophylaxis that is required postoperatively [8]. They are
given a high carbohydrate drink in the morning of the surgery
as well as prescribed gabapentin and intravenous acetaminophen. A transverse abdominis plane (TAP) block using lipoidal bupivacaine may also be used to reduce the need for
postoperative narcotic pain management. Details of the
enhanced recovery protocol are available [9].
Technical Details
A few years ago, the BPD/DS was primarily being performed
by laparotomy on account of its complexity. However, over
the last few years, surgeons have become more facile in their
minimally invasive technique, and several techniques have
been described to perform this operation. The essential details
of each technique include a sleeve gastrectomy in which the
stomach pouch has a larger capacity than that of a stand-alone
primary SG operation and is in the range of 150–250 ml. The
pylorus is preserved, and the duodenum is divided where the
first part of the duodenum becomes adherent to the pancreas.
This often corresponds to the location of the gastroduodenal
artery (GDA). A post pyloric anastomosis is performed to the
alimentary channel. The technique by which this anastomosis
is performed has been described variously using the EEA stapler, linear cutter, handsewn, or robotic. The BPD/DS can be
performed in a standard Roux configuration or as a loop duodenoileostomy. Proponents of the duodenoileostomy propose
a lowered risk of internal hernias and technical complication
due to one less anastomosis between the biliary limb and the
alimentary limb, while proponents of the standard configuration think that a leak may manifest with clinically worse signs
R. Sudan
and symptoms because of the presence of bile. Also, biliary
reflux in the single loop version may cause additional longterm problems that have been previously described with
Billroth-type operations. This debate is beyond the scope of
the present chapter, but it is important to note that there are
some variations in the limb length and types of anastomosis
of the alimentary channel. In the standard BPD/DS, a 250 cm
alimentary limb with 100 cm common channel is commonly
used, while the common channel is somewhat longer in the
loop configuration and is in the range of 300 cm. In contrast
to RYGB, the measurements of the bowel in the BPD/DS are
from the ileocecal valve, and the limb lengths are marked
using either suture or clips to perform the anastomoses at the
appropriate distance and in the correct orientation to prevent
twisting of the bowel.
Since the average duration of the operation is longer,
positioning the patient is important, and they need to be adequately padded and protected to prevent pressure sores.
While some surgeons prefer the split-leg position, many others use a standard supine position. Patient positioning, room
setup, and trocar placement are optimized depending on the
technique for performing the duodenoileostomy. It is important to remember that the operation is performed in three
abdominal zones and the room set up accordingly. Access to
the abdomen is most often obtained using a Veress needle in
the left subcostal area, and an optical trocar is then used to
enter the abdominal cavity. Additional ports are placed under
direct visualization. The port size needs to consider the size
and the brand of the stapler that will be used in the operation.
Therefore a liver retractor is placed. The type of liver tractor
used is up to the surgeon (Fig. 14.1). Additionally, the liver is
often bulky, and occasionally a hiatal hernia repair needs to
be performed concomitantly making the liver retractor quite
important.
Another debatable part of the operation is performing a
simultaneous cholecystectomy. Many surgeons believe that
gallstone formation is higher with a BPD/DS than the RYGB
due to more wasting of bile salts. In the event that a stone
slips into the common bile duct, access may be more challenging after a BPD/DS, as there is no remnant stomach.
Also, if the patient develops acute cholecystitis, it may be
harder to perform a cholecystectomy in the area of the duodenoileostomy due to scarring from the previous operation.
However, other surgeons do not want to spend the additional
time and prefer to address a cholecystectomy or common
bile duct storms postoperatively, as and when they develop.
Depending on whether a cholecystectomy is performed or
not, most surgeons will begin the actual BPD/DS operation
by performing the sleeve gastrectomy. The greater curvature
of stomach is mobilized from the left crus of the diaphragm
to the junction of the first part of the duodenum and the pancreas. As mentioned previously, it is important to make the
stomach pouch larger in the BPD/DS compared to the stand-­
14
Biliopancreatic Diversion with Duodenal Switch: Technique and Outcomes
163
Fig. 14.2 Marking bowel at predetermined distances (100 cm and
250 cm) from the ilececal valve. (From: Sudan and Podolsky [24].
Reprinted with permission from Springer Nature)
Fig. 14.1 Sample port pacement: C camera port, LR liver retractor, 1
and 3 are accessory ports, and usually stapling is performed through
port 2 and assistant port (From: Sudan and Podolsky [24]. Reprinted
with permission from Springer Nature)
alone SG. The mobilization can be performed by any energy
device that seals and divides the vessels of the greater curvature reliably. This is often facilitated by entering the lesser
sac close to the greater curvature and dividing the leaves of
the greater momentum close to the stomach and within the
gastroepiploic arcade. The highest short gastric vessel can
easily be avulsed, and gentle but adequate retraction to visualize this area is important to prevent bleeding. In addition, it
is important to avoid lateral spread of thermal energy to the
gastroesophageal junction to avoid leaks in this location.
Similar care is used when mobilizing the first part of the duodenum so as to not cause either burns or bleeding. Bleeding
obscures visualization and prevents safe transection of the
duodenum. A 50–60 French bougie in the stomach is often
used as a guide, and the stomach transection is started
approximately 5 cm proximal to the pylorus on the antrum.
This part of the stomach is thicker than the more proximal
stomach. Therefore, a longer leg length stapler is used.
Newer staplers are automated and facilitate in selecting the
appropriate staple load. More proximally, the stomach
becomes thinner, and the leg length can be downsized appropriately to decrease bleeding. Most surgeons reinforce the
staple lines on the sleeve to prevent leaks or bleeding. The
choice of reinforcement is up to the surgeon, and considerations include cost of the material and the time involved in
applying reinforcement. The available choices are buttress
material, sutures, or clips. When performing the sleeve gastrectomy, it is important not to narrow the sleeve or spiral the
staple line. Appropriate retraction by the assistant and careful application of the stapler prevent these complications.
Since the duodenum is thinner, a shorter leg length stapler
can be used in this location, and reinforcement is optional.
The division of the duodenum is carried out in the area of the
GDA, and the surgeon must be careful to not damage this
vessel, the portal structures, or the duodenum when performing this maneuver. Familiarity with the anatomy in this area
is crucial for safe dissection but not hard to learn with
experience.
The next part of the operation involves performing the
duodenoileostomy at the premarked bowel lengths (Fig. 14.2).
The small bowel at the premarked site (250 cm) is brought up
for anastomosis to the proximal stapled end of the duodenum
(Fig. 14.3). This is typically performed antecolic although
retrocolic techniques have also been previously described.
The division of the omentum or creation of a transomental or
transmesocolic window is performed depending on surgeon
technique and tension being placed on the anastomosis. The
anastomosis in the standard BPD/DS is performed 250 cm
from the ileocecal valve and is longer in the loop duodenal
switch version. It is important to maintain the appropriate orientation of the small bowel so as to prevent a twist that results
in an internal hernia, or worse, a closed loop obstruction. The
method of performing the duodenoileostomy is variable. In
the EEA approach, the anvil of a size 21 stapler is passed
orally through the pylorus and seated at the stapled line of the
proximal duodenum. The EEA stapler is then passed through
164
Fig. 14.3 The sleeve gastrectomy is performed, the duodenum is
divided, and the bowel at the 250 cm mark is anastomosed to the proximal stapled edge of the duodenum (From: Sudan and Podolsky [24].
Reprinted with permission from Springer Nature)
the small bowel and engaged with the anvil. After the anastomosis has been completed, the enterotomy for the stapler is
closed by suture or stapling. This process is more demanding
technically than when performing a circular anastomosis for
the RYGB because the anvil has to pass through the pylorus
and the distal small bowel is often quite narrow. Therefore,
some surgeons have adapted the linear stapler approach to
perform this anastomosis. They close the enterotomy using
another stapler or hand suturing. This stapling technique is
faster and relies less on the suturing skills of the surgeon but
may not use the full length of the duodenum. A totally handsutured technique can be ­performed either laparoscopically
or robotically. While the laparoscopic technique is faster and
less expensive, it demands higher skill levels and may not be
as comfortable ergonomically as the robotic technique. If the
surgeon is planning a loop duodenal switch, the operation is
completed by performing a leak test using either air or methylene blue. In the standard duodenal switch, the distal anastomosis is performed next by approximating the bowel at the
100 cm mark to the biliary limb. The technique for performing the ileoileostomy is more standard. Most often, a 60 mm
stapler is used, and the enterotomy for the stapler is closed
using suturing or stapling. The surgeon must ensure that the
bowel is not narrowed in this process. Finally, the biliary limb
is divided near the duodenoileostomy to complete the standard Roux configuration of the BPD/DS (Fig. 14.4). In order
to prevent internal hernias, the closure of mesenteric defects
R. Sudan
Fig. 14.4 Completion of standard duodenal switch by performing an
anastomosis between the alimentary limb at the 100 cm mark to the biliary limb just proximal to the duodenoileal anastomosis and then dividing the biliary limb (From: Sudan and Podolsky [24]. Reprinted with
permission from Springer Nature)
between the alimentary limb and the biliary limb using a running nonabsorbable suture has been standard practice. In the
antecolic version, and particularly with the loop duodenal
switch, the closure of Petersen’s defect is debatable.
Proponents of closure argue a reduction in internal hernias
due to one less anastomosis, and those who leave it open feel
that a wide open space is less likely to obstruct. Closure of
this space is more difficult in the BPD/DS. Endoscopy with
air insufflation to check for patency, leaks, and bleeding is
often performed prior to completion of the operation.
Methylene blue can also be passed through an orogastric tube
to check for leaks. Specimens are retrieved at the end of the
case. Larger port sites are closed with a port closure device,
and lipoidal bupivacaine can now be injected for TAP block,
if not done preoperative, to help with pain control.
Postoperative Management
After a complex bariatric operation, patients undergoing the
BPD/DS are monitored in a unit with staff that is adequately
trained and equipment that is suitable for managing such
patients. With greater implementation of enhanced recovery
programs in bariatric surgery, the use of narcotic medication
and routine use of patient-controlled analgesia or epidural
anesthesia have become the exception. However, patients
14
Biliopancreatic Diversion with Duodenal Switch: Technique and Outcomes
should still be monitored closely as many suffer from sleep
apnea. There are some nuances in managing the diet of BPD/
DS patients that are highlighted here. Patients undergoing a
BPD/DS have an intact pylorus and have undergone a sleeve
gastrectomy. As a result, it is not unusual for patients to have
some degree of gastroparesis or pylorospasm similar to that
seen in the stand-alone SG patients. This may predispose
them to nausea, and judicious use of anti-nausea medicine,
including scopolamine patches, has been very helpful in alleviating this problem. In the RYGB, the stomach pouch is
small, and there is no restriction to outflow of fluid from the
pouch. Hence, RYGB patients tolerate oral intake sooner
than the SG or the BPD/DS patients. The BPD/DS patients
also have a larger stomach pouch, and therefore high-volume
emesis with subsequent chances of aspiration, needs to be
kept in mind when initiating oral intake. Once the patients
are nausea-free and are on a normal clinical track, liquids are
initiated in small quantities and advanced to protein shakes.
The duration of the liquid diet varies with bariatric program
but is commonly about 2 weeks, at which time patients are
started on a soft diet and gradually progressed to more normal consistency diet, over the next 3 months. Vitamins are
supplemented as per ASMBS recommendations for malabsorptive operations [10]. If a leak test has been performed
during the operation, routine postoperative upper gastrointestinal series is not performed, unless clinically indicated.
Early ambulation with assistance is encouraged, and routine
use of drains, nasogastric tubes, and Foley catheter is not
usually practiced. For DVT prophylaxis, sequential compression devices are used routinely, and appropriate anticoagulation medication is administered, as assessed by the
patient’s need preoperatively. Patients are ready for discharge
when they are tolerating adequate amount of liquid to prevent dehydration, pain is under good control, and they are
ambulating well. The average length of stay for a BPD/DS
patient is longer than that of stand-alone SG or RYGB. When
patients have return of bowel function, they may experience
urgency and frequency. This normalizes to an average of 2–3
soft bowel movements a day. Patients need to be counseled
regarding this expectation. If bowel movements are excessive and an infectious colitis has been ruled out, antidiarrheal
agents such as loperamide or diphenoxylate-atropine can be
used.
Complications
Surgical
Comparative effectiveness among different bariatric operations shows higher complication profile at 30 days and 1 year
for the BPD/DS and is discussed below in greater detail in
the section on outcomes [6]. Leaks and bleeding are man-
165
aged similar to other bariatric operations, and the need to
manage these complications operatively depends on hemodynamic stability as well as radiographic findings. Evidence
of a free leak necessitates an urgent operation. Stenting a
sleeve leak or a DI anastomosis leak, draining any fluid collections percutaneously, making the patient nil per os, and
feeding them through parenteral access, can avoid an operation in suitable patients. Bleeding can be managed with fluid
and blood replacement or endoscopic management using
epinephrine injections or clips. More aggressive bleeding or
one that cannot be accessed endoscopically needs operative
intervention. The chances of PE are also higher after a longer
operation. Bowel obstructions in BPD/DS can be particularly dangerous because these patients do not have a remnant
stomach. Obstruction in the biliary limb or common channel
may therefore manifest itself with the blowout of the duodenum, if not treated in a timely fashion. Abdominal pain
should be investigated with a CAT scan, and patients with
dilation of the biliary limb should be promptly explored to
prevent this from occurring. Typically, the bowel is traced
back from the ileocecal valve to ensure appropriate orientation. Nausea and vomiting may also be attributable to strictures of the sleeve, and a technique to widen the stricture by
performing a strictureplasty has been described [11]. Another
option is to perform a RYGB proximal to the stricture, but
this operation is more complex in the face of a previous
BPD/DS. Conversion to a RYGB may also be considered if
patients have intolerable reflux. Sometimes in the absence of
any anatomic abnormality, nausea is of a metabolic nature
and improves with time. Resolution of nausea may take
months and requires careful monitoring and supplementation
of nutrition in the meantime. Despite the statistically higher
complication rate, the rate of complications from BPD/DS is
still acceptable from a clinical standpoint.
Nutritional Complications
Duodenal switch patients do not suffer from dumping symptoms, and as a result, they can eat larger portions and tolerate
a wider variety of foods. If they are not careful and consume
sugars and starches, weight loss may be inadequate. Also, as
the bowels are bypassed quite distally, many patients will
become lactose intolerant, and most malabsorb fat including
the fat-soluble vitamins such as A, D, E, and K. If patients
are not mindful of the type of food they eat, they may also
have excessive flatulence and steatorrhea. The fat-soluble
vitamins need to be supplemented in their water-soluble analogue form and often need to be specially ordered and cost
more. Noncompliance with these vitamins may result in deficiency states. Duodenal switch patients are often more predisposed to vitamin D deficiency and a concomitant increase
in parathormone level. Deficiencies related to minerals such
166
as iron, copper, zinc, and magnesium can also be seen. In
order to detect and adequately treat these vitamin deficiencies, serum levels need to be assessed at least annually, and
more frequently if needed. Recommended doses of vitamins
and micronutrients are available through ASMBS guidelines
[10]. As stated previously, it is important to obtain these levels preoperatively and correct them prior to surgery. Patients
who have chronic nausea and vomiting are also predisposed
to vitamin B deficiency [12–19].
Another major concern with the BPD/DS is protein deficiencies. Marceau et al. increased the length of the common
channel from 50 to 100 cm and described a decrease in the
incidence of protein deficiency compared to the Scopinaro
BPD. He also demonstrated reduced bowel movements and
improved levels of fat-soluble vitamins [20]. It is conceivable that increasing the length of the common channel in the
loop version of the duodenal switch may further decrease
nutritional deficiencies. BPD/DS shows remarkable stability
in maintaining weight loss over a long period of time, but a
few patients need to have the operation reversed due to
excessive malnutrition or bowel side effects. In experienced
centers, about 2% of the patients may need a reversal for
these reasons. This can be accomplished by either creating a
more proximal side-to-side anastomosis between the biliary
and the alimentary limb, or the Roux limb can be disconnected at its junction with the common channel and moved
more proximally. Another issue with more distal bypass is
the formation of oxalate kidney stones. Normally the oxalates in the gut bind to calcium and are excreted in stool. In
BPD/DS due to inadequate binding in the gut, oxalates are
absorbed and excreted through the kidneys where stones can
form. This can be avoided by consuming supplemental calcium that binds to oxalates and prevents its absorption.
Adequate hydration and making the urine more acidic help
dissolve oxalate crystals in the urinary tract.
Outcomes
The vast majority of studies in the literature are single-center retrospective studies from investigators who have extensive experience with BPD/DS [2, 3, 21]. There is one
randomized study that compares BPD/DS to RYGB and
patients with a BMI greater than 50 kg/m2 [19]. Sudan et al
conducted a multi-institutional propensity matched analysis
on comparative effectiveness of bariatric operations that
included 130,796 subjects, 1,436 patients underwent BPD/
DS and were compared with 5,942 SG and 66,324 RYGB
patients. The remaining underwent LAGB. This study demonstrated that BPD/DS had the greatest BMI change at
1 year, followed by RYGB, SG, and AGB, respectively.
When using LAGB as a reference, patients undergoing
BPD/DS had a BMI reduction of 10.6 units versus 9.3 for
R. Sudan
RYGB and 5.7 for SG. BPD/DS had the greatest odds for
remission for diabetes type II (OR = 5.62, 95% CI: 4.60–
6.88), RYGB (OR = 3.5, 95% CI: 3.39–3.64), and SG
(OR = 2.11, 95% CI: 1.92–2.31). Remission of hypertension
was also the best after BPD/DS. However, for GERD the
best operation was RYGB followed by BPD/DS, and it is
noteworthy that the BPD/DS was still better at resolving
reflux than SG. In this study, adverse events (AE) and serious adverse events (SAE) at 30 days and 1 year for the
unmatched cohort were higher for the BPD/DS compared to
the other operations. At 30 days, unmatched AEs were
8.04% for SG, 11.77% for RYGB, and 20.26% for BPD/
DS. At 1 year, the AE rates were 6.5% for AGB, 10.03% for
SG, 17.99% for RYGB, and 27.52% for BPD/DS. SAE rates
for AGB at 30 days were 0.23% and increased to 0.81% for
SG, 1.35% for RYGB, and 3.63% for BPD/DS. At 1 year,
SAE rates increased slightly to 0.3% for AGB, 0.93% for
SG, 1.58% for RYGB, and 4.60% for BPD/DS [6].
Rates of bleeding at 30 days were 0.63% for SG, 1.38%
for RYGB, and 0.99% for BPD/DS. Leaks were 0.14% for
SG, 0.36% for RYGB, and 0.89% for BPD/DS. PE was
0.11% for SG, 0.13% for RYGB, and 0.54% for BPD/DS. At
1 year, these rates increased only slightly suggesting that
beyond 30 days operative complications remained relatively
stable. After matching, the odds of adverse events and severe
adverse events remained higher for the BPD/DS at 30 days
and 1 year [6].
Longer-term single-center retrospective studies have similarly demonstrated excellent weight loss and resolution of
comorbidities. A study comparing BPD/DS with RYGB in
patients with a BMI of ≥50 kg/m2 demonstrated faster and
better resolution of comorbidities and higher weight loss for
BPD/DS with no significant increase in morbidity or mortality [21]. In another study, 810 BPD/DS patients with a
BMI < 50 kg/m2 demonstrated excellent weight loss and
resolution of comorbid conditions suggesting its appropriateness for lower BMI patients [22]. Patient satisfaction was
also excellent with acceptable complications rates. Quality
of life studies after BPD/DS are limited with regard to gastrointestinal symptoms. The average BPD/DS patient has
been shown to have an average of 2.7 bowel movements a
day [23].
Conclusion
BPD/DS has better weight loss and resolution of certain
comorbid conditions such as diabetes, hypercholesterolemia,
and hypertension. The operation is now being performed
using a variety of minimally invasive techniques, and although
still not very common, its popularity seems to be increasing.
It is associated with nutritional and higher technical complication rates that can be managed by an experienced team.
14
Biliopancreatic Diversion with Duodenal Switch: Technique and Outcomes
Question Section
1. Regarding the biliopancreatic diversion without the duodenal switch, all of the following are true except:
A. There is no blind end.
B. A distal gastrectomy is performed.
C. The operation has shown excellent weight loss.
D. Rate of marginal ulcerations is low.
2. According to a large database analysis comparing
Duodenal switch to Roux-en-Y gastric bypass and sleeve
gastrectomy operations the following is true:
A. Diabetes resolution is the best with a duodenal switch.
B. GERD resolution is best with a duodenal switch.
C. The operative complications are clinically unacceptably high with a duodenal switch.
D. The operative complications are statistically equivalent between a duodenal switch and a gastric bypass.
3. The following is true regarding the duodenal switch:
A. Dumping is common.
B. Steatorrhea is common.
C. Vomiting is common.
D. Marginal ulcer is common.
4. Regarding vitamin deficiencies following a duodenal
switch, the following is true:
A. Vit D deficiency is uncommon.
B. Use of water-soluble analogues of fat-soluble vitamin
is mandatory.
C. Use of fat-soluble analogues of water-soluble vitamins is mandatory.
D. Patients do not need supplementation of vitamin K.
References
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pancreatic bypass for obesity: 1. An experimental study in dogs. Br
J Surg. 1979;66(9):613–7.
2. Hess DS, Hess DW. Biliopancreatic diversion with a duodenal
switch. Obes Surg. 1998;8(3):267–82.
3. Marceau P, Biron S, Bourque RA, Potvin M, Hould FS, Simard
S. Biliopancreatic diversion with a new type of gastrectomy. Obes
Surg. 1993;3(1):29–35.
4. Ren CJ, Patterson E, Gagner M. Early results of laparoscopic biliopancreatic diversion with duodenal switch: a case series of 40 consecutive patients. Obes Surg. 2000;10(6):514–23; discussion 24.
5. Sudan R, Puri V, Sudan D. Robotically assisted biliary pancreatic
diversion with a duodenal switch: a new technique. Surg Endosc.
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Morton JM. Comparative effectiveness of primary bariatric operations in the United States. Surg Obes Relat Dis. 2017;13(5):
826–34.
7. English WJ, DeMaria EJ, Brethauer SA, Mattar SG, Rosenthal RJ,
Morton JM. American Society for Metabolic and Bariatric Surgery
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estimation of metabolic and bariatric procedures performed in the
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8. Aminian A, Andalib A, Khorgami Z, Cetin D, Burguera B,
Bartholomew J, et al. Who should get extended thromboprophylaxis after bariatric surgery?: a risk assessment tool to guide
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Demartines N, et al. Guidelines for perioperative care in bariatric
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McMahon MM, et al. Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient – 2013 update: cosponsored by American
Association of Clinical Endocrinologists, The Obesity Society,
and American Society for Metabolic & Bariatric Surgery. Obesity
(Silver Spring). 2013;21(Suppl 1):S1–27.
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12. Aasheim ET, Bjorkman S, Sovik TT, Engstrom M, Hanvold SE,
Mala T, et al. Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch. Am J Clin Nutr.
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13. Binggeli C, Corti R, Sudano I, Luscher TF, Noll G. Effects of
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Bjorkman S, et al. Randomized clinical trial of laparoscopic gastric
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et al. Duodenal switch improved standard biliopancreatic diversion:
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superior weight loss in the super-obese (BMI > or =50 kg/m2) compared with gastric bypass. Ann Surg. 2006;244(4):611–9.
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diversion with duodenal switch: single dock technique and technical outcomes. Surg Endosc. 2015;29(1):55–60.
Single Anastomosis
Duodeno-ileostomy
15
Amit Surve, Daniel Cottam, Hinali Zaveri,
and Samuel Cottam
Chapter Objectives
1. History of the single anastomosis duodeno-­
ileostomy (SADI) procedure.
2. Describe surgical technique with attention to the
steps to prevent common as well as rare
complications.
3. Summarize the outcomes in terms of weight loss,
complications, nutritional outcomes, and type 2
diabetes mellitus resolution.
4. Describe SADI as a revision procedure following
failed sleeve gastrectomy (SG), Roux-en-Y gastric
bypass (RYGB), and adjustable gastric banding
(AGB).
5. Review of literature.
History
In 1986, Dr. Douglas Hess modified the biliopancreatic
diversion (BPD) in order to retain the pylorus as a functioning part of the digestive system. The new procedure was
called a biliopancreatic diversion with duodenal switch
(BPD-DS) [1]. This procedure includes removing a significant portion of the stomach as well as bypassing a segment
of the small intestine. The new procedure was more effective
for long-term weight maintenance than a Roux-en-Y gastric
bypass (RYGB) or a vertical banded gastroplasty (VBG).
However, it became associated with complications such as
chronic diarrhea, smelly stools, flatulence, vitamin deficiencies, and protein-calorie malnutrition.
Because of the complication profile, the BPD-DS did not
gain widespread adoption. Most surgeons gravitated to the
RYGB as the best balance of weight loss and procedural
A. Surve · D. Cottam (*) · H. Zaveri · S. Cottam
Bariatric Medicine Institute, Salt Lake City, UT, USA
related side effects. The RYGB suffered from ulcers, perforations, anastomotic dilation, vitamin and protein deficiencies, dumping syndrome, anastomotic strictures,
gastro-gastric fistula, and internal hernias [2]. The complications of the RYGB are almost all associated with the formation of the Roux limb.
To eliminate the problems with Roux limb formation,
Drs. Torres and Sanchez-Pernaute from Spain introduced a
variant of BPD-DS that involved one anastomosis instead of
two. They named it “Single anastomosis duodenoileal bypass
with sleeve gastrectomy” (SADI-S) [3]. The SADI-S
involved preservation of pylorus like BPD-DS but eliminated
the Roux limb found in RYGB and BPD-DS. They used a
54-size Fr bougie for sleeve creation with a 200-cm common
channel. However, this length was later enlarged to 250 cm
to reduce the risk of hypoproteinemia [4].
In order to reduce a prohibitive risk of short bowel syndrome and provide a margin if the bowel is inaccurately
measured, Drs. Cottam and Roslin from the United States
further modified the SADI-S procedure. Their variant
included a 40-size Fr bougie (vs. 54-size Fr bougie) for better weight loss along with a common channel of 300 cm (vs.
250 cm). This variant was called “Stomach intestinal pylorus-­
sparing surgery” (SIPS) [5]. However, the basic concept of
preserving the pylorus and having a single anastomosis was
the same.
The SIPS, being a fairly new concept in 2015, was considered experimental in the United States [6]. However, by
2018, based on clinical knowledge, expert opinion, and published peer-reviewed scientific evidence, the International
Federation for the Surgery of Obesity and Metabolic
Disorders (IFSO) considered the SADI-S (and its SIPS variant) an established bariatric procedure [7]. In addition, the
IFSO proposed a nomenclature for surgery that combines a
partial gastrectomy with a single anastomosis between the
small bowel regardless of bougie size or common channel
length as SADI-S or one anastomosis duodenal switch
(OADS).
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_15
169
170
A. Surve et al.
Surgical Technique
Sleeve Creation
Retrograde Tracing and Temporary Tacking
With the creation of the SADI-S, the consensus among surgeons who perform this procedure making the sleeve too
“tight” is a problem. By tradition, surgeons have not made
sleeve’s smaller than 40 F. However, just as there are many
ways to create a sleeve, the same applies to the creation of
the sleeve during SADI-S. This would include oversewing,
The first step of the procedure is to locate the ileocecal valve
(Fig. 15.1). Once this is located, the small bowel is traced
retrograde to the desired common channel length (this varies
greatly between authors and around the world) and tacked up
to the gastrocolic omentum (Fig. 15.2).
Fig. 15.1 Location of the ileocecal valve
Fig. 15.2 Temporary tacking of the ileal loop limb to the gastrocolic omentum of varying lengths
15
Single Anastomosis Duodeno-ileostomy
staple line reinforcement, the distance from the pylorus, and
treatment of the hiatus (Fig. 15.3).
Duodenal Dissection and Transection
There are two equally popular techniques for the dissection
of the proximal duodenum. The more traditional technique
involves starting the dissection 4 cm distal to the pylorus
and gently retracting the duodenum taking down attachment
between the colon, pancreas, and liver before division.
171
The other equally popular technique relies on adequate
blood supply from the right and left gastric vessels on the
lesser curve and was popularized by Cottam and Roslin. Once
the sleeve is created, they continue taking down the gastroepiploic perforators after the formation of the sleeve until the
attachments from the duodenum to the pancreatic head stops
easy progress [8]. This is usually 3 cm beyond the pylorus.
This technique spares vessels from the pancreaticoduodenal
arch from injury but sacrifices the gastroepiploic perforators
to do so (Fig. 15.4). A band passer is passed through the space
created under the duodenal bulb, toward the liver, and through
Fig. 15.3 Sleeve creation
with variable sized bougie
Fig. 15.4 Important blood supply to the duodenum that needs to be preserved during duodenal dissection and transection
172
Fig. 15.5 Creation of space under duodenal bulb through the gastrohepatic ligament
A. Surve et al.
nal stump staple line to relieve tension with a running suture
(Fig. 15.7). Then enterotomies are made as large as possible
and approximately the same size on both the small bowel and
the duodenum (Fig. 15.8). A posterior row and an anterior
row are sewn closed with running suture. Some surgeons
also perform a second anterior row.
Other surgeons have perfected a three-stapler technique
to transect the duodenum, connect the small bowel, and close
the enterotomy. This involves dilating the proximal duodenum using air from the sizing tube. Then enterotomies are
made in both the small bowel and proximal duodenum. The
duodenum enterotomy is made 1 cm from the pylorus. The
stapler is fired on the anterior portion of the duodenum away
from the staple line. Next sutures are placed on the proximal
and distal ends of the enterotomy and elevated to apply the
stapler.
Anti-reflux Stitch
Some patients can experience nausea when food goes primarily down the afferent limb of the loop. To prevent this
rare complication, an anti-reflux stitch is placed (Fig. 15.9).
This involves placing an interrupted suture between the
afferent limb to the antrum of the stomach to prevent retrograde filling of the afferent limb [9]. The entire SADI-S procedure can be seen in Fig. 15.10.
Fig. 15.6 Transection of the duodenum
Postoperative Care
the gastrohepatic ligament, with care taken to preserve the
blood vessels (Fig. 15.5). This technique also results in a linear gastric tube since the gastropancreatic ligaments are
responsible for the curve of the stomach, and when you eliminate them, the antrum assumes a linear shape.
Once the duodenum is dissected free with either technique, a linear stapler is placed across the first part of the
duodenum (Fig. 15.6). Before firing the stapler, always try to
feel the pylorus to make sure the stapler is distal to the pylorus since it is not always easy to visualize the pylorus.
The care of the SADI-S patient does not differ substantially
from the care of the sleeve patient or the gastric bypass
patient. Follow-up is similar as well except greater emphasis
is placed on the patient’s postoperative supplementation.
Current recommendations for postoperative labs are at
6 months, 1 year, and then yearly thereafter. The recommended yearly nutritional evaluation includes folate, ferritin,
parathyroid (PTH), vitamins A, D, E, K, B1, and B12, copper, and zinc. Depending on circumstances, we may also
measure hemoglobin A1C, complete blood count (CBC),
comprehensive metabolic panel (CMP), lipid panel, prealbumin, phosphorus, fasting insulin levels, thyroid-stimulating
hormone (TSH), and free T4.
Duodeno-ileostomy (DI)
Unlike the gastrojejunal anastomosis in the gastric bypass,
practitioners of duodenal switch surgery do not believe the
duodenal small bowel connection plays any role in short- or
long-term weight loss or maintenance. Therefore, the emphasis is not on size but safety.
Currently, the most popular technique worldwide is the
totally hand-sewn technique. For the hand-sewn technique,
the mesenteric border of the loop limb is sewn to the duode-
Weight Loss Outcomes with SADI-S
Following the procedure, the patients can lose 78–95% of the
excess weight at 18 months (weight loss peak) depending on
their starting BMI [4, 10–15]. These results seem to be maintained out 4–6 years from surgery [10, 14].
15
Single Anastomosis Duodeno-ileostomy
173
Fig. 15.7 Approximation of the loop limb to the proximal duodenal stump
Fig. 15.8 Creation of the hand-sewn duodeno-ileostomy
Complications
One of the reasons Drs. Torres, Sanchez-Pernaute, Cottam, and
Roslin introduced the SADI-S procedure and its variant was to
minimize the complications seen with BPD-DS and RYGB. The
primary advantage of SADI over BPD-DS is that there is no
distal anastomosis or Roux limb. They postulated that with one
anastomosis and no Roux limb, the complications related to
174
Fig. 15.9 Creation of the anti-reflux stitch
A. Surve et al.
anastomoses could be lowered. In a recent study, Surve et al.
specifically studied the incidence of complications related to
one anastomosis (loop DI) following 1,328 SADI-S cases as
well as compared the anastomotic complication rates to the
reported rates following BPD-DS and RYGB in the literature
[16]. They found that the anastomotic leak, ulcer, and bile
reflux occurred in 0.6%, 0.1%, and 0.1%, respectively. None of
the patients experienced volvulus at the DI or an internal hernia. The overall incidence of complications associated with
loop DI was far lower than the reported incidence of anastomotic complications following BPD-DS and RYGB. These
numbers from the study included the learning curve of each
practitioner; so long-term results are expected to be even better
than those reported in the study.
The most common short- and long-term complications
one can expect are nausea (2.2%), wound infection (2.2%),
and sleeve stricture (2.9%), respectively [10, 12]. However,
Fig. 15.10 Hand-drawn sketch of a single anastomosis duodeno-ileostomy with sleeve gastrectomy procedure along with an upper gastrointestional series
15
Single Anastomosis Duodeno-ileostomy
these complications are not explicitly related to the SADI-S
procedure.
The most common complication related to the SADI-S
procedure is chronic diarrhea that is seen in approximately
2% patients [10]. Not all the patients that experience chronic
diarrhea require limb lengthening. In some patients, it can be
treated with dietary manipulation, probiotics, and Lomotil as
well. With 300 cm approximately, 1% of the patients will
need limb lengthening over a 5-year period [10].
The overall short- and long-term complication rates
seen following SADI-S were 7.7% and 10.9%, respectively [10].
Rare Complications and Their Management
Retrograde Filling of Afferent Limb
So far there have been only two cases reported in the literature [9]. In both cases, scar tissue was found distal to the DI
that pulled the efferent limb superior to the DI, causing the
flow of food and secretions down the afferent limb. Tacking
the afferent limb to the antrum of the stomach hopefully can
prevent such complication.
Miscounted Bowel
Miscounted common channel could be a part of the learning
curve. Usually, such patients present with chronic diarrhea
and are usually treated by lengthening the common channel.
The length of the additional common channel depends on the
miscounted bowel. The symptoms are usually resolved following this procedure [17].
Reversed Loop
The reversed loop is another rare complication that can occur as
a part of learning curve. The patients usually present with persistent nausea and vomiting. The ideal way to fix this complication is redoing the duodenal small bowel anastomosis [10].
Nutritional Outcomes
Contrary to popular belief, there is minimal nutritional malabsorption seen following the SADI-S procedure, and no
author has presented evidence of primary malnutrition with
250–300 cm of small bowel for absorption [18].
Typically, in a patient with a 300-cm common channel,
65% fat malabsorption can be seen. Even though the percent-
175
age of fat malabsorption with SADI-S is higher when compared to the RYGB procedure [11], with the recommended
postoperative multivitamin regimen, the patients usually do
not experience fat-soluble vitamin deficiency.
Zaveri et al. in the 4-year outcome paper on SADI-S studied the fat-soluble vitamin levels, pre- and postoperatively
[10]. At 4 years, even though 7.5% patients had a vitamin A
deficiency, there was no statistically significant difference
when compared to the preoperative abnormal levels.
Prevalence of vitamin D deficiency is reported to be as high
as 90% in patients with obesity. In their study, 48.2% had
vitamin D deficiency preoperatively. However, at 4 years,
only 23% patients experienced vitamin D deficiency. This
shows that despite the shorter bowel lengths, vitamins can
still be replete.
Vitamins E and K are fat-soluble but are far easier to
absorb with any vitamin regimen. At 1 year in a recent study,
no patients experienced vitamins E and K deficiency [10].
The nutritional deficiencies that are reported in the literature
can be seen in Table 15.1 [4, 11, 13–15, 19–23].
To conclude, the SADI-S procedure is not associated with
apparent nutritional changes; however, postoperative supplementation with iron, multivitamins, calcium, and vitamin D
may be required continuously to prevent nutritional
deficiency.
T2DM Resolution
The SADI-S procedure is a variant of the DS procedure. As
such, it retains the expected long-term diabetes mellitus
(DM) resolution seen in DM. Sanchez-Pernaute et al. studied
the effect of SADI-S on patients with obesity and
DM. Absolute remission for patients with oral therapy was
seen in 92.5% in the 1st year and 75% in the 5th year [14],
while absolute remission for patients under insulin therapy
was seen in 47% in the 1st year and 38.4% in the 5th year.
Overall remission rate (HbA1c <6%) was seen in 71.6%,
77%, 75.8%, 63.3%, and 52% at one-fifth year, respectively.
A short DM history and no requirement for insulin therapy
were related to higher remission rate, while Zaveri et al.
found the complete remission rate (HbA1c < 6% without
antidiabetic medication) of 78.6%, 77.8%, 81.3%, and 81.3%
after one-fourth year, respectively [10]. Similarly, 97.6% of
the patients were able to maintain HbA1c < 6% with or without the medication at 4 years.
Cottam et al. compared the DM resolution rate at differing
levels of HbA1c between RYGB and SADI-S [12]. At each
differing level, SADI-S had a statistically higher amount of
diabetic resolution compared to RYGB. At 1 year, HbA1c < 6%
was controlled in 88% of SADI-S patients versus 58% of
RYGB patients without any antidiabetic medications.
8
16
29
8
10
7.6
13
8
3
1
1
1
1
2
Protein Def
(%)
1
2
Post-op
year
11
8
3.1
12
8
12
13
6
Albumin Def
(%)
–
5
5.1
–
18
6
13
0
Calcium Def
(%)
–
–
–
–
–
54
–
42
PTH Def
(%)
–
–
45
–
–
53
31
40.5
10.8
29
34
23
Vitamin def
(%)
A
D
–
46
–
6
SADI-S single anastomosis duodeno-ileostomy with sleeve gastrectomy, Def deficiency, Zn zinc, Cu copper, Fe iron, Se selenium
Nelson (2016) [21]
Sanchez-Pernaute
(2013) [4]
Sanchez-Pernaute
(2015) [14]
Cottam (2016) [11]
Cottam (2017) [15]
Enochs (2015) [22]
Neichoy (2016) [23]
Surve (2017) [13]
Author
Table 15.1 Published nutritional deficiencies following SADI-S
–
–
–
–
–
7
–
E
–
–
–
–
–
–
–
K
29
38
15.3
10.4
0
8
B12
0
20
16
–
–
–
–
3
Folate
–
10
–
–
–
–
–
33
–
–
–
–
–
11
–
–
–
–
–
–
Mineral def (%)
Zn
Cu
Fe
–
–
–
–
–
4
–
–
–
–
–
28
Se
–
2.5
176
A. Surve et al.
15
Single Anastomosis Duodeno-ileostomy
The overall T2DM remission rates following SADI-S
can be around 81–90% without antidiabetic medication
[10, 14, 23].
SADI as Revision Procedure
SADI Following Failed SG
Weight loss failure and weight recidivism over the long term
have been a common concern following SG. Moreover, SG
has also shown poor results in patients with BMI >50 kg/m2
[24]. This is one of the reasons why revision procedures following failed SG have been increasing in recent years. The
question that remains for the bariatric surgeons is what revision options are now available for patients who fail SG?
The SADI-S procedure is increasingly becoming popular
as a second step revision procedure or as a staged procedure,
primarily for weight loss failure following SG. The mean
EWL at 1 and 2 years following the second step SADI has
been around 69% and 72%, respectively [25]. More importantly, postoperative complications have been minimal with
no reported incidence of small bowel obstruction or internal
hernias, which are commonly seen following RYGB and
BPD-DS. Zaveri et al. showed that if SADI is performed
within the 1st year of performing SG, the patients could lose
a similar amount of weight as a primary SADI-S procedure
[26]. However, this approach will need a longer follow-up to
understand its limitation.
177
Although the data are limited, the initial data have shown to
have favorable outcomes. The EWL following revision
SADI-S for failed RYGB at 1 year has been reported between
53% and 61% and at 2 years has been reported around 55%
[31]. This is similar to patients who have an RYGB to traditional DS [32].
ADI-S Following Failed Adjustable Gastric
S
Band
Multiple studies have demonstrated a high incidence of
weight recidivism and long-term complications with AGB
[33–35]. In addition, multiple reports have been published
on the different approach to revising the failed AGB patients
to SG, RYGB, or BPD-DS. However, EWL has not been that
favorable, and complications have been high [36–38].
Therefore, the controversy exists regarding the choice for
patients with failed LAGB.
The outcomes of SADI-S as a revision option following failed AGB have been only reported by Surve et al. in
the literature [39]. Technically, it is simpler than BPD-DS
and RYGB. Three years report showed 90% EWL following revision of AGB to SADI-S. The weight loss mirrors
the weight loss seen following primary SADI-S procedure. The only caveat with this procedure is careful dissection to avoid leaks and strictures from scar tissue below
the band.
Review of Literature
SADI-S Following Failed RYGB
The RYGB has been associated with long-term good weight
loss outcomes. However, approximately 25% of patients
have weight recidivism [2, 27].
Various techniques such as resizing the pouch or lengthening the Roux limb have been used but with limited or no
success [28, 29]. The SADI-S is an effective option for failed
RYGB patients due to its pyloric preserving capacity. Most
of the patients who fail RYGB usually eat small, frequent,
high-carbohydrate meals. This is a physiologic response to
vacillating blood sugar levels causing hunger [30]. The
SADI-S with its pylorus preserving capacity plays an important role in maintaining blood sugar levels and satiety.
Although technically possible this revision is challenging
and has been shown to have high complication rates [31].
The outcomes with primary and revision SADI/SADI-S that
have been published in the literature are summarized in
Table 15.2. Unique data sets have been included [4, 5, 10, 18,
21, 23, 25, 31, 39–43].
Conclusion
Effective weight loss, high T2DM resolution rates, low
anastomotic complication rates compared to other established procedures, minimal nutritional changes, effective
second stage, or revision option following failed bariatric
procedures make SADI/SADI-S one of the best options
for patients with morbid obesity and coexisting
conditions.
178
A. Surve et al.
Table 15.2 Published outcomes with primary and revision SADI/ SADI-S
Article
Procedure
Primary SADI-S procedure
SIPS
Mitzman
et al. [5]
SADI-S
Zaveri
et al. [10]
SADI-S
Sanchez-­
Pernaute
et al. [4]
Neichoy
et al. [23]
Morales
et al. [40]
Abd-Elatif
et al. [18]
Gebelli
et al. [41]
Nelson l
et al. [21]
SIPS
SESDID
SADI-S
SADI-S
SADI-S
Bougie size and Sample
common channel size
Follow-up
42 F and
300 cm
40 F and
300 cm
54 F and
200 cm
(50 patients)
250 cm
(50 patients)
40 F and
300 cm
34 F and
300 cm
36 F and
250 cm
36 F and
300 cm
34 F and
250 cm
SADI procedure following failed SG
SADI
42–54 F and
Sanchez-­
250 cm
Pernaute
et al. [25]
Vilallonga
et al. [42]
Balibrea
et al. [43]
SADI
SADI
Bougie size is
unk and 300 cm
32 F and
200–300 cm
SADI procedure following failed RYGB
SADS
40 F and
Surve
et al. [31]
300 cm
SADI procedure following failed AGB
SIPS
40 F and
Surve
et al. [39]
300 cm
Weight loss
T2DM
Rem. rate
Complication
Fat-soluble vitamin
deficiency
123
1 year
72.3%EWL
N/A
6.5%
N/A
437
4 years
85.7%EWL
81.3%
100
3 years
>95% EWL
>90%
Early = 7.7%
Late = 10.9%
5–9%
Vit A = 7.5% (4 years)
Vit K = 5.8% (1 year)
Vit D = 6% Def
40% Ins
225
2 years
88.7% EWL
88.8%
N/A
N/A
Early = 4.8%
Late = 8%
12%
100
N/A
N/A
37
1 year
67
1–1.5 years
23 kg/m2 BMI
red
N/A
N/A
2.7%
N/A
N/A
12.8%
N/A
69
1 year
61.6% EWL
50% Rem,
33.3%
Imp
10.1%
Vit D = 45.8%
16
2 years
32.5% EWL
(SADI)
72% EWL
(SADI+ SG)
N/A
88%
6.2%
Vit A = 25%,
Vit D = 6% Def, 50
Ins, Vit E = 0%
3
3–9 months
33.3%
Imp
71.4%
0%
N/A
30
2 years
Early = 13.3%
Vit D = 55.5%
44.2%EWL
(SADI)
78.9% EWL
(SADI+ SG)
N/A
Late = 50%
23
2 years
54.5% EWL
N/A
Early = 17.3%
Late = 13%
Vit D = 9%
27
3 years
90% EWL
75%
Early = 40.7%
Late = 25.9%
Vit A = 0%
Vit D = 41.1%,
Vit E = 5.8%,
Vit K = 0%
SESDID Single end-to-end anastomosis duodenoileal, Def deficiency, Ins insufficiency, mos months, Rem remission, Imp improvement, DIOS
distal loop duodeno-ileostomy, SADS single anastomosis duodenal switch, SIPS stomach intestinal pylorus-sparing surgery, SG sleeve gastrectomy, RYGB Roux-en-Y gastric bypass, AGB adjustable gastric banding
Question Section
1. Which of these is false about SADI surgery?
A. Technically it is more difficult than BPD-DS.
B. There is an alimentary as well as biliopancreatic limb
involved.
C. Conversion of failed RYGB to SADI is a feasible
option.
D. It has fewer ulcers than BPD-DS.
2. One of the main advantages of SADI over RYGB
A. Nutritional deficiencies
B. Weight loss
C. Dumping syndrome
D. Protein-energy malnutrition
3. The weight loss between SADI-S with a 300-cm common
channel and BPD-DS with a 150-cm common channel
and 150 cm Roux limb is
A. The same amount of weight loss between the two
B. Less weight loss with SADI-S
C. Much better weight loss with SADI-S
D. Much worse weight loss with SADI-S
15
Single Anastomosis Duodeno-ileostomy
4. What is the percentage of bile reflux seen following SADI
surgery in the literature?
A. 0.1%
B. 1%
C. 0.8%
D. 2%
179
16. Surve A, Cottam D, Sanchez-Pernaute A, et al. The incidence of
complications associated with loop duodeno-ileostomy after single
anastomosis duodenal switch procedures among 1328 patients: a
multicenter experience. Surg Obes Relat Dis. 2018;14:594–601.
17. Surve A, Zaveri H, Cottam D. A step-by-step surgical technique
video with two reported cases of common channel lengthening in
patients with previous stomach intestinal pylorus sparing surgery
to treat chronic diarrhea. Surg Obes Relat Dis. 2017;13(4):706–9.
18. Abd-Elatif A, Yousser T, Farid M, et al. Nutritional markers after
loop duodenal switch (SADI-S) for morbid obesity: a technique
with favorable nutritional outcome. J Obes Weight Loss Ther.
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responsiveness predictors after two-step single-­
anastomosis
duodeno-ileal bypass with sleeve gastrectomy. Obes Surg.
2017;27(5):1302–8.
Laparoscopic One Anastomosis Gastric
Bypass: History of the Procedure
Surgical Technique and Outcomes
16
Helmuth T. Billy, Moataz M. Bashah, and Ryan Fairley
Chapter Objectives
1. Familiarize the reader with the evolution of one
anastomosis gastric bypass.
2. Present two common techniques described when
performing one anastomosis gastric bypass.
3. The reader will understand the controversial issue
of bile reflux as well as other complications, how to
diagnosis these conditions, and therapeutic options
for treatment.
4. Compare and understand the benefits of one anastomosis procedures versus two anastomosis bypass
with Roux reconstruction.
History
In 2001, an article was published in the journal Obesity
Surgery reporting operative technique and outcomes in a
series of 1274 cases utilizing a single anastomosis version of
a gastric bypass [1]. The procedure described a simplified
version of a traditional Roux-Y gastric bypass, avoided creation of a small gastric pouch or permanent gastric resection,
and eliminated the second distal anastomosis which was
required for the Roux-Y gastric bypass or duodenal switch.
The concept of anastomosing a loop of jejunum to a long,
narrow, gastric pouch created 2–3 cm below the crow’s foot
H. T. Billy (*)
Metabolic and Bariatric Surgery, Community Memorial Hospital,
Ventura, St. John’s Regional Medical Center, Oxnard, CA, USA
M. M. Bashah
Division of Metabolic and Bariatric Surgery, Hamad General
Hospital, Hamad Medical Corporation, Doha, Qatar
R. Fairley
Surgical Education, Community Memorial Hospital,
Ventura, CA, USA
along the lesser curve was first introduced by Rutledge.
Rutledge coined the phrase “mini gastric bypass” (MGB)
and described a less complicated operative strategy that was
easier to perform and eliminated the need for a Roux limb. It
was hypothesized that a one anastomosis approach to gastric
bypass could obtain similar results as the Roux-Y gastric
bypass while also reducing the side effects and complications associated with the creation of the Roux limb necessary
in RYGB and duodenal switch. Attempts at introducing a
loop gastric bypass as a bariatric operation had been introduced by Mason 30 years earlier [2]. The “mini gastric
bypass” operation introduced by Rutledge differed quite significantly from the original loop gastric bypass described by
Mason. Mason’s attempt to create a weight loss operation
utilizing a horizontal gastroplasty and a simple loop jejunostomy was based very closely on the Billroth II gastrojejunostomy. Despite the simplicity of the operation, the initial loop
gastric bypass created by Mason resulted in uncontrolled bile
reflux and exposure of the distal esophagus to the deleterious
effects of bile and acid. The controversy created by the
esophageal complications following the introduction of the
Mason loop gastric bypass has persisted over the two decades
since the introduction of the “mini gastric bypass” by
Rutledge. Mason’s operation and the reflux producing side
effects were quickly abandoned due to the severe and excessive presence of bile reflux on the distal esophagus.
Subsequently, the potentially harmful effects of combining
bile with acid and exposing the distal esophagus to this combination were well described by DeMeester [3, 4]. Fifty
years after Mason first described his looped gastric bypass,
the concerns that biliopancreatic reflux reaching the distal
esophagus from the afferent limb of a loop gastrojejunostomy persist. Fear that bile induced esophageal inflammation, Barrett’s changes, and esophageal cancer has limited
adoption of one anastomosis gastric bypass (OAGB) in the
United States. In the 20 years since the mini gastric bypass
and OAGB procedures were described, there have been no
publications definitively linking these single anastomosis
procedures with the development of any cases of esophageal
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_16
181
182
or gastric cancer. On the other hand, reflux secondary to
sleeve gastrectomy may contribute to development of
Barrett’s esophagus in as much as 17% of patients undergoing vertical sleeve gastrectomy [5]. It has been hypothesized
that the low-pressure environment of gastric bypass procedures and the longer length of the gastric pouch in OAGB
operations may play a protective role in limiting reflux episodes from reaching the distal esophagus in patients undergoing OAGB.
While single anastomosis gastric bypass has been slow to
gain traction in the United States, the opposite has been true
in Europe, Asia, and the Middle East. Since 2001, over
16,000 patients have been reported in publications reporting
OAGB outcomes [6]. The most comprehensive literature
review identifying studies reporting outcomes following
­single anastomosis gastric bypass procedures was recently
published as an IFSO position statement on March 29, 2018
[7, 8]. Included in the IFSO position statement was the recommendation that the “One Anastomosis Gastric Bypass is a
recognized bariatric/metabolic procedure and should not be
considered investigational.” The IFSO Task force contributing to the review was composed of a multinational group of
22 recognized and accomplished bariatric surgeons. The
United States was represented by two former ASMBS presidents. The task force reviewed, summarized, and correlated
the findings of 52 studies reporting outcomes of 16,546
patients to report on the safety and efficacy of one anastomosis gastric bypass procedures.
H. T. Billy et al.
staged approach [9, 10]. Reversal of a single anastomosis
gastric bypass is also relatively and technically easy should it
be necessary in the future.
OAGB is a simpler, less costly operation to perform.
Shorter operative times, less postoperative pain, decreased
nausea and vomiting, early ambulation, and little more than
an overnight hospitalization have been reported in comparative studies evaluating OAGB to RYGB [11]. The simplification in operative technique allows an inpatient hospitalization
for RYGB to become an outpatient procedure for OAGB. The
enteroenterostomy in RYGB can require up to four additional staple cartridges and closure of three mesenteric
defects. OAGB is a procedure that can be offered by facilities
at a significantly reduced overhead cost than that associated
with gastric bypass. The improved economics associated
with OAGB can significantly increase access to care for
those patients who do not have the insurance coverage or
economic means to afford more expensive procedures. The
widespread adoption of this less expensive, less complex,
and possibly safer alternative than RYGB has allowed bariatric surgery to be offered in large numbers to patients who
might otherwise not have access to bariatric procedures
across Asia, the Middle East, and Europe.
There is neither data nor established consensus as to an
ideal or recommended operative technique. The initial operation described by Rutledge (MGB) and used in his 2001
series describes a gastric pouch based on the lesser curve of
the stomach [12]. The initial staple line is created 1–2 cm
below the crow’s foot followed by a vertical extension along
the body of the stomach and completing the pouch by stayIntroduction
ing just lateral to the angle of His as the stomach is transected. The anastomosis between the pouch and the jejunum
One anastomosis gastric bypass (OAGB) is a technically is a wide, end to side anastomosis utilizing the entire length
easier operation than Roux-Y gastric bypass or biliopancre- of a 45 mm stapler and is created between 180 and 220 cm
atic diversion with duodenal switch. The hallmark of the distal to the ligament of Treitz. There is also no consensus on
OAGB is the elimination of the Roux Limb. The well-­ the optimal length of the afferent loop. Variations in the
recognized complications associated with the creation of the length of the afferent limb have been described for the
RYGB enteroenterostomy are eliminated. Morbidity and elderly, vegetarian patients, and diabetics [13]. Fluctuations
mortality rates are lower due to simplified operative dissec- in the distance from the gastrojejunostomy to the ligament of
tion. Both the duodenal switch and the Roux-Y gastric Treitz have been reported from 180 to about 250 cm to
bypass require the creation of a second enteroenterostomy. greater than 300 cm depending on the age, eating habits, and
Well-known complications following RYGB can occur at the comorbid conditions of the patient (Fig. 16.1).
enteroenterostomy and include internal anastomotic staple
An alteration to the original procedure described by
line bleeding, intussusception, internal hernia, and leakage Rutledge using a side-to-side (lateral to lateral) anastomosis
from a second anastomosis. These complications are avoided between the jejunal loop and the gastric pouch was described
completely with the OAGB. OAGB offers reductions in by Carbajo in 2001 [14]. The modification was designed speoperative time and less aggressive liver retraction. Division cifically to allow the afferent limb to experience less bile
of small bowel mesentery is unnecessary in OAGB. The reflux into the gastric pouch. Carbajo and Caballero described
preservation of small bowel mesenteric blood flow may the operation as a “one anastomosis gastric bypass” (OAGB).
result in a decrease in the incidence of DVT, portal vein Their technique utilized this variation of the anastomosis
thrombosis, and bleeding. Large, super-morbidly obese described by Rutledge and lengthened the distance between
patients whose BMIs exceed 50 can undergo OAGB without ligament of Treitz and the gastrojejunostomy to between 250
the need for a longer operation or one that would require a and 350 cm (Fig. 16.2).
16 Laparoscopic One Anastomosis Gastric Bypass: History of the Procedure Surgical Technique and Outcomes
Fig. 16.1 Technique of the “mini gastric bypass” as described by
Rutledge consists of a long conduit from below the crow’s foot extending up to the left of the angle of His. The operation has a wide gastrojejunal anastomosis to an anti-colic loop of jejunum 150–200 cm distal to
the ligament of Treitz. The gastrojejunostomy between the posterior
wall of the gastric pouch and the antimesenteric border of the jejunum
is typically stapled using a 45 mm stapler in an end-to-side-type
configuration
Since 2001, the variations in technique have resulted in
multiple different versions of essentially the same operation
[15]. These operations can be found in the medical literature
described as:
1. Mini gastric bypass (MGB)
2. One anastomosis gastric bypass (OAGB)
3. Omega loop gastric bypass (OLGB)
4. Single anastomosis gastric bypass (SAGB)
This chapter will present the basic construction, operative
technique complications, and outcomes we have employed
and experienced with the introduction of OAGB into our
practice. There is as yet no “gold standard” method with
which to perform this procedure. Much of the operative
­techniques preferred by individual surgeons are based on
opinions and personal experience. Anastomotic techniques
vary between practices, and there are no comparative studies
evaluating these differences in operative technique. Variations
in technique regarding pouch size, bougie size, gastrojejunostomy technique, or afferent limb length among surgeons
183
Fig. 16.2 “One anastomosis gastric bypass” procedure as described by
Carbajo [14] utilizes a side-to-side configuration and a 5–6-cm-long
“anti-reflux” suture to approximate the mesenteric border of the jejunal
loop to the lateral wall of the gastric pouch. Following this configuration, an enterotomy is made in the distal gastric pouch and the antimesenteric border of the jejunal loop. A stapled gastrojejunostomy in a
side-to-side configuration completes the anastomosis
performing OAGB are common. The most common consensus agreement between various authors appears to be a long
narrow gastric tube which extends to at or below the crow’s
foot of the lesser curve [16].
As surgical innovation continues, new operations that are
cheaper, safe, and effective are the drivers that will improve
access to bariatric surgery. Participation in national and
international registries will allow for the collection of long-­
term data, outcome, and complication analysis. Analysis of
the outcomes data is essential to the further advancement in
the understanding of new and innovative metabolic and bariatric procedures. As we come to develop a consensus on
procedures such as the OAGB, we can expect that future
improvement in insurance coverage may ultimately benefit
access to care nationally.
Patient Selection and Preparation
The 1991 National Institutes of Health Consensus
Development Conference Statement on Gastrointestinal
Surgery for Severe Obesity established guidelines for identifying appropriate candidates for metabolic and bariatric sur-
184
gery operations [17]. Although these guidelines are more
than 20 years old, they remain a foundation of bariatric surgery patient selection despite their likely outdated and historical significance. Evaluations of patients for possible
MGB-OAGB, in our opinion, require utilization of a multidisciplinary team providing medical, surgical, psychiatric,
and nutritional expertise. Evaluation of potential surgical
candidates as per NIH guidelines is recommended and allows
for appropriate discussions of both surgical and nonsurgical
approaches to weight loss operations. In 2004, the American
Society for Metabolic and Bariatric Surgery published a
Consensus Conference statement on Bariatric Surgery for
Morbid Obesity which discussed the expansion of available
operative procedures, the growth in laparoscopic techniques,
and the significant reductions in perioperative morbidity and
mortality that have occurred since the 1991 NIH statement.
In the years following the 2004 ASBS statement, societies
including the American Society for Metabolic and Bariatric
Surgery (ASMBS), the Obesity Society, the American
Association of Clinical Endocrinologists (AACE), and the
International Diabetes Federation (IDF) have endorsed consideration of lower BMI patients (30–34.9) for metabolic
and bariatric operations [18].
Surgical Technique
The introduction of one anastomosis gastric bypass into our
practice evolved from our extensive experience with Roux-Y
gastric bypass, handsewn and stapled anastomosis, and revisional procedures. Experience with laparoscopic anastomosis is essential when performing OAGB. Complications that
can develop from a poorly done anastomosis can result in
intractable reflux, outlet obstruction, afferent loop syndrome,
and bile leakage. Surgeons whose experience is limited with
respect to laparoscopic suturing of gastrojejunal anastomosis
are encouraged to spend time improving their skills with
respect to anastomotic technique. Advanced laparoscopic
suturing skills are required to manage complications of these
procedures. Surgeons with limited experience in performing
laparoscopic suturing will find themselves at a disadvantage
when performing the OAGB procedure or managing complications that may occur at the gastrojejunostomy. Educational
courses featuring experts and faculty with extensive experience performing OAGB are becoming more widely
available.
All patients receive a form of subcutaneous heparin and
pneumatic compression devices to prevent DVT formation
during the surgery. Patient positioning can either be via the
French or split-leg positioning or standard supine position.
We have performed our procedures using both techniques
and find that either positioning is adequate, and there is relatively no advantage offered by one positioning technique
H. T. Billy et al.
over the other. Arm positioning is at 90° to the operating
table, and padded straps to secure the lower extremities are
used in all procedures as well as a foot rest to prevent patient
movement and sliding during the procedure.
Access to the peritoneum is performed using an optical
12 mm trocar technique at the umbilicus utilizing a paraumbilical crease for the access incision. Establishment of pneumoperitoneum is followed by placement of a right upper quadrant,
subcostal 12 mm trocar. Two additional trocars are positioned
slightly higher than utilized in traditional RYGB operations
and include a 5 mm port in the left upper lateral abdomen and
a 12 mm port in the left mid-abdomen lateral to the umbilicus.
We prefer a 10 mm 30° operating laparoscope although surgeons preferring a 5 mm scope could utilize that and downsize
the umbilical port to a 5 mm as per their preference.
If the patient is positioned supine, the surgeon is standing
on the patient’s right side. The majority of our patients have
been placed on a 2-week liquid diet to facilitate reduction in
the size of the liver. In most cases, the decrease in liver size
will be sufficient so as to allow the use of internal liver retraction devices which typically suspend the liver using three
hooks attached to suture technique. A deceased liver size
avoids the deployment of external retraction devices such as
the Nathanson hook which requires an additional incision
and significant torque on the liver in order to provide exposure. We have also subjectively observed less congestion of
the liver and less aggressive retraction using internal liver
retraction.
Creating the Gastric Pouch
Creation of the gastric pouch begins with a lesser curve dissection and identification of the crow’s foot as the critical
landmark to insure optimal pouch length in order to minimize any likelihood that refluxed biliopancreatic secretions
could reach the esophagus (Fig. 16.3). The limitations of the
Mason loop gastric bypass were largely due to the combination of a short pouch which was horizontal in nature with a
loop reconstruction [19]. In order to perform a successful
OAGB, and minimize any biliopancreatic reflux, the identification of the crow’s foot of the lesser curve is the key to a
successful operation. The majority of surgeons begin their
perigastric dissection at the crow’s foot although we prefer
beginning our dissection 1–2 cm or so below the crow’s foot
(Fig. 16.4). Our preferred bougie is a 34 French oral gastric
tube, but we have used 36 and even 40 French bougies when
necessary. Unlike a sleeve gastrectomy, the goal when creating the gastric pouch is to avoid hugging the bougie and to
create a pouch in which the stapler is positioned a bit wider
and lateral to the bougie.
Once the perigastric dissection has been completed and
the lesser sack has been entered, we position a 45 mm linear
16 Laparoscopic One Anastomosis Gastric Bypass: History of the Procedure Surgical Technique and Outcomes
Fig. 16.3 Operative inspection of the stomach. Key landmarks include
the crow’s foot and the planned path for stapling to create the gastric
pouch as well as the pylorus
Fig. 16.4 Dissection for the initial path of the stapler occurs 1–2 cm
below the crow’s foot along the lesser curve
stapler via the left upper quadrant 12 mm port just below the
crow’s foot (1–2 cm) and perpendicular to the antrum
(Fig. 16.5). The initial firing is with a cartridge used for the
thickest tissue. Caution is taken so as to not transect the
antrum or narrow the outflow of what will be the retained
body and fundus of the bypassed portion of the stomach. A
60 cm linear stapler is then introduced through the left upper
quadrant 12 mm port and positioned so as to create a staple
line curving toward the angle of His while staying a bit lateral to the 34 French bougie and not hugging the bougie as is
typically done with sleeve gastrectomy (Fig. 16.6). The initial firing is again with a cartridge used for the thickest tissue, and then adjustments in cartridge selection can occur
based on the thickness of the tissue encountered. We consider bioabsorbable buttressing to limit staple line bleeding
185
Fig. 16.5 Initial positioning of the first staple cartridge 1–2 cm below
the crow’s foot for one anastomosis gastric bypass
Fig. 16.6 Positioning of the second staple firing for creation of the
gastric pouch for one anastomosis gastric bypass
on all firings after the first 60 mm firing. Multiple 60 mm
cartridges are deployed until the stomach is transected just
lateral to the angle of His separating the long gastric pouch
from the gastric remnant. It is essential to stay a bit wide of
the bougie in order to insure that staple cartridges are positioned in the same horizontal plane and at the apex of each
staple firing. This careful attention to detail is to prevent a
spiral of the staple line which can result in a functional
obstruction and severe reflux. We do not routinely oversew
our staple lines and address any persistent bleeding with
additional sutures or surgical clips.
Creation of the loop begins by revealing and exposing the
ligament of Treitz. We use a 200 cm afferent limb for patients
with a BMI under 50 and consider 250 cm afferent limb for
patients with a BMI over 50. We utilize bowel graspers with
186
Fig. 16.7 Completion of the initial suture line in preparation of a side-­
to-­side linear stapled anastomosis for one anastomosis gastric bypass
marks signifying 5 cm and 10 cm lengths to measure as precisely as possible, and we do not estimate the measurements
via visual estimations. Once a 200 cm afferent limb has been
measured, we favor the anti-reflux technique described by
Cabajo and Caballero utilizing a side-to-side anastomosis of
the afferent limb to the distal pouch. The gastric pouch which
is typically 15–18 cm in length is positioned adjacent to the
afferent limb to create a 200 cm biliopancreatic limb length.
The site of the 200 cm measurement is marked with a stay
suture, and measurements are continued distally to insure
that there is at least 250–300 cm of small bowel distal to the
proposed site of the gastrojejunostomy.
Once the site of the 200 cm afferent loop is confirmed, a
posterior row of suture using 3–0 absorbable suture is placed
to approximate the mesenteric serosa of the afferent limb to
the lateral suture line of the distal pouch (Fig. 16.7). This
suture line not only protects from leaks but also is essential in
taking any unnecessary tension off the staple line. Once complete, an opening is made in the distal gastric pouch and the
antimesenteric portion of the afferent limb so as to allow positioning of a 45 mm stapler to create a 3–4 cm gastrojejunal
anastomosis. The stapler is positioned intraluminally in the
gastric pouch and the afferent loop and then fired (Fig. 16.8).
The 34 French bougie is advanced across the anastomosis and
the remaining gastrojejunal defect is closed anteriorly with
3–0 absorbable suture followed by a second layer of 3–0
absorbable suture to oversew the anastomosis and approximate the serosa of the afferent limb to the serosa of the gastric
pouch (Fig. 16.9). By utilizing this technique, the initial running suture line suspends the afferent limb above the anastomosis and secures the loop to the gastric pouch. We believe
this technique not only will decrease the incidence of symptomatic bile reflux but will also decrease the possibility of
developing an afferent loop syndrome postoperatively.
H. T. Billy et al.
Fig. 16.8 Intraluminal positioning of linear stapler for a side-to-side
2.5–4 cm stapled anastomosis one anastomosis gastric bypass
Fig. 16.9 Handsewn closure of stapled side-to-side anastomosis, one
anastomosis gastric bypass
The anastomosis and vertical staple line are tested for
leaks by occluding both afferent and efferent limb and insufflating with oxygen or air under saline submergence. Any
evidence of leak or visible air bubbles are addressed using
intracorporeal suturing until there is no evidence of any air
leak. Caution must be taken not to over-distend the pouch
and afferent limb, and rarely do we need to insufflate with a
pressure greater than 2 L per minute inflow. There must be
excellent communication between the surgeon and the anesthesiologist during the leak test to avoid any rupture of the
bowel or anastomosis due to over-distension. Alternatively,
we have utilized the injection of methylene blue diluted into
1 L of saline as an alternative. Injection of 100–150 cc of
diluted methylene blue is done by our anesthesiologist to
accomplish distension of the gastric pouch as well as a short
segment of the afferent and efferent limbs. Both limbs are
16 Laparoscopic One Anastomosis Gastric Bypass: History of the Procedure Surgical Technique and Outcomes
187
5. Measure 200 cm distal to the ligament of Treitz, and anastomose the loop to the gastric pouch in a side-to-side
fashion with the afferent limb superior and the efferent
limb inferior.
6. Close the mesenteric defect.
Postoperative management is similar to traditional gastric
bypass. We keep our patients overnight and start them immediately on a clear liquid diet. Almost all patients can be discharged postoperative day 1. We do not use routine upper GI
swallows immediately post-op.
Reversal of One Anastomosis Gastric Bypass
Fig. 16.10 Same patient 1 year after one anastomosis gastric bypass.
Visualized during laparoscopic cholecystectomy. The gastrojejunostomy is easily visualized below the liver and sits close to the transverse
colon. The antrum and previous staple line are also visualized. EGD
revealed no evidence of bile reflux, ulcer, or stricture. One year post-op,
this patient has achieved a BMI of 25 and has no complaints
occluded by laparoscopic bowel clamps during the air insufflation or methylene blue tests.
Finally, we choose to close the mesenteric defect created
by the afferent limb between the root of the mesentery of the
afferent limb and the transverse mesocolon. Because the
loop is an antecolic path the creation of a mesenteric defect
between the mesentery of the loop and the transverse mesocolon is a recognized site of potential internal hernia. The
defect is addressed using 3–0 nonabsorbable suture. The root
of the mesentery of the loop is identified and sutured to the
mesentery of the transverse colon until the mesenteric defect
is closed. After completing a final secondary look for bleeding or leaks, the retractors are removed, and the 12 mm
­fascial defects are closed, and the procedure is completed
(Fig. 16.10).
Our technique can be summarized by identifying several
steps as all our OAGB procedures are done in the same
manner:
1. Begin a perigastric dissection 1–2 cm distal to the crow’s
foot along the lesser curve.
2. Position a 45 mm stapler using a staple cartridge for thick
tissue at the point of the perigastric dissection staying
perpendicular to the lesser curve of the stomach.
3. Position a 34 French bougie intragastric followed by a
60 cm stapler just lateral to the bougie.
4. Transect just lateral to the angle of His to create a somewhat generous and straight gastric pouch.
Postoperative complications following one anastomosis gastric
bypass procedures are a rare but recognized reason for considering reversal of the procedure. Malnutrition, excessive weight
loss, severe lower extremity edema, and motor deficits can
present as a refractory malnutrition syndrome after any malabsorptive procedure. Genser et al. reported on a series of 2934
patients who had undergone mini gastric bypass over a 10-year
period [20]. Of the 2934 patients, 26 were identified as having
developed severe and refractory malnutrition syndrome which
responded to reversal of MGB to normal anatomy.
Even with variations in surgical technique, reversal of a
one anastomosis gastric bypass is straightforward allowing
for complete restoration of normal anatomy. There are essentially three steps involved in reversing an OAGB operation:
1. Identification of the gastrojejunostomy
2. Resection of the gastrojejunostomy
3. Anastomosis of the gastric pouch to the body of the gastric remnant
Identification and dissection of the gastrojejunostomy
away from adjacent structures allow for a straightforward
transection of the distal gastric pouch disconnecting the
stomach from the afferent limb. Following this, the gastrojejunostomy can be similarly removed from the afferent limb
by careful placement of a 60 cm stapler along the antimesenteric border of the jejunum and then resecting the anastomosis off of the jejunum. Once the gastrojejunal anastomosis
has been resected, all that remains is to reestablish continuity
between the gastric pouch and the gastric remnant. We
accomplish this by approximating the two stomachs using an
absorbable 3–0 suture and then completing the anastomosis
with a linear stapler followed by closure of the new anastomosis over a bougie using 3–0 absorbable suture in two layers. The anastomosis is tested for leaks using methylene blue
or air insufflation and the reversal is completed. Patients are
started on clear liquids postoperatively and are discharged
after an overnight stay.
188
H. T. Billy et al.
Benefits of a Single Anastomosis Procedure
Mesenteric Defects
Mesenteric defects created by RYGB are a potential source of
internal hernia, bleeding, and bowel obstruction. Obstruction
from internal hernia following Roux-Y gastric bypass is relatively common. Internal hernia as the primary cause of obstruction following gastric bypass represents up to 41% of cases
presenting with intestinal obstruction [21]. Roux-Y gastric
bypass requires the creation of a gastrojejunostomy and a second enteroenterostomy. Depending on whether an antecolic
approach or a retrocolic approach is undertaken, there can be up
to 3 potential spaces where internal herniation can occur. OAGB
eliminates the need for the enteroenterostomy created when a
RYGB is performed. The second anastomosis which is created
between the biliopancreatic limb and the alimentary limb is
unique to RYGB and creates a potential site for internal hernia
that does not exist in an OAGB operation. The herniation of
bowel through this kind of defect creates a surgical emergency
that must be evaluated quickly to avoid bowel ischemia and
infarction. Closure of mesenteric defects can reduce the risk of
internal hernia from 3.3% to 1.2% but cannot eliminate the risk
[22]. If a retrocolic passage of the Roux limb to gain access to
the gastric pouch is used, a third potential site of herniation
through the mesenteric defect is created which also must be
closed. The simplicity of the OAGB eliminated two of these
three potential sites of internal herniation. As a result, the potential for internal hernia is lower in OAGB than in RYGB. Internal
hernia following OAGB is a rare complication [23, 24].
The benefit of decreasing the potential defects associated
with internal hernia following gastric bypass is not new. The
modification of the retrocolic gastric bypass to the antecolic
technique of passage of the Roux limb from the midgut to the
foregut eliminated one of the three potential sites of internal
hernia [25, 26]. As a result, the risk of internal hernia through
the mesentery of the transverse colon was eliminated, reducing morbidity and mortality from internal herniation [27,
28]. OAGB has the benefit of decreasing morbidity and mortality further by eliminating one of the two remaining sites of
potential internal herniation that exist in RYGB.
Internal hernia rates following RYGB have been reported.
Iannelli et al. reported findings of 11,918 patients following
RYGB. Internal herniation was discovered in 300 patients
for an internal hernia rate of 2.51% [29]. Internal herniation
occurred at the level of the transverse colon in 69% of cases,
at the level of the Peterson’s defect in 18% of cases, and at
the level of enteroenterostomy in 13% of cases. OAGB creates no defect at the level of the transverse colon or at the
enteroenterostomy. Eighty-two percent of the cases of internal hernias reported in RYGB are associated with these two
defects. Internal hernia reported with OAGB are relatively
rare compared to the incidence reported with RYGB [30].
Fig. 16.11 Closure of the only mesenteric defect in one anastomosis
gastric bypass is accomplished by closing the defect between the efferent limb and the mesentery to the transverse colon. Nonabsorbable
suture is used to close the defect beginning at the root of the mesentery
and approximating it to the transverse mesocolon until the lower border
of the colon is reached
The OAGB utilizes a single gastrojejunal anastomosis
with a single mesenteric Peterson hernia defect created by
the loop anastomosis of jejunum to gastric pouch. Closure of
this mesenteric defect is relatively easy and is associated
with significant decrease in the rate of internal hernia from
this single remaining site (Fig. 16.11).
Intussusception
Jejuno-jejunal intussusception is a known complication following RYGB. Obstruction, bowel ischemia, and bowel
necrosis are potential sequela following development of
intussusception. The rate of intussusception following
RYGB at the level of the enteroenterostomy occurs at less
than 1% (0.4%) [31]. Diagnosis can be difficult as symptoms
are generally nonspecific. Both operative and nonoperative
approaches to the treatment of intussusception do not reliably prevent recurrence of the problem. The single anastomosis OAGB eliminates the potential of intussusception of
the enteroenterostomy further decreasing postoperative morbidity and mortality from RYGB-related complications.
Simplified Reversal/Revision
Reversal of OAGB can be accomplished via two approaches.
Complete anatomic reversal requires simple transection of
the gastrojejunostomy on the jejunal side of the anastomosis
followed by creation of a gastro-gastrostomy between the
gastric pouch and the gastric remnant. Alternatively, func-
16 Laparoscopic One Anastomosis Gastric Bypass: History of the Procedure Surgical Technique and Outcomes
tional reversal of the OAGB can be accomplished by simply
reconnecting the stomach to the gastric remnant.
Conversion to Roux-Y Configuration
In the rare event that bile reflux is suspected, diversion of the
bile away from the gastrojejunostomy can be accomplished by
simply transecting the afferent limb at the level of the gastrojejunostomy and diverting the flow at least 50–70 cm below
the gastrojejunostomy utilizing a new enteroenterostomy.
Complications
Bile Reflux
Perhaps the most contentious, widely discussed topic surrounding one anastomosis gastric bypass has been the issue
of potential bile reflux (Figs. 16.12 and 16.13). The topic
remains controversial with potential concerns regarding
Barrett’s esophagus and possible esophageal cancer persisting although no reported cases of esophageal cancer appear
in peer reviewed publications. Despite the large number of
publications and low incidence of reflux-related revisions,
this controversy continues to persist and has resulted in a
189
delay of acceptance of the procedure particularly in the
United States. Most authors report an improvement in GERD
symptoms following OAGB [32]; however, some authors
report reflux symptoms that have required revision to either
RYGB or implementation of Braun’s anastomosis distal to
the gastrojejunostomy of the single anastomosis of the gastrojejunostomy [33]. The incidence of symptomatic acid
reflux in our patients that have undergone OAGB procedures
is higher than what we have experienced in our RYGB
patients. The majority of these patients are easily treated
with once-a-day PPI therapy, and many reflux symptoms dissipate over time. The few patients that have had significant
reflux symptoms following OAGB have been successfully
revised to a Roux-Y gastric bypass with complete resolution
of their symptoms. Many surgeons have reported an incidence of symptomatic reflux following one anastomosis gastric bypass at less than 0.5%.
Despite positive effect in terms of weight loss and
improvement of obesity-related comorbidities, there still
exist concerns about symptomatic biliary reflux gastritis and
esophagitis requiring revision surgery following OAGB procedures [34]. Concerns regarding the risk of esophageal cancer with this procedure because of chronic biliary reflux
persist [35]. There is no prospective data to suggest there is a
legitimate concern for gastroesophageal reflux following
OAGB to progress to Barrett’s esophagus or cancer.
Fig. 16.12 Classic bile reflux following mini gastric bypass performed as described by Rutledge in a patient with previous repair of a large para
esophageal hiatal hernia and poorly functioning lower esophageal sphincter
190
H. T. Billy et al.
complaints of reflux occurring in patients having had no history of hiatal hernia or reflux symptoms prior to surgery. Our
only two findings of significant reflux have occurred in two
patients both of whom had significant abnormalities of the
distal esophagus and esophagogastric junction prior to their
OAGB. It has been our experience that patients with symptomatic bile reflux can be confirmed on endoscopic examination and can be successfully treated with revision to a
Roux-Y configuration if necessary with complete resolution
of symptoms [37].
Bile Scintigraphy
Fig. 16.13 Esophageal view, bile reflux following mini gastric bypass.
Same patient as Fig. 16.12
Tolone et al. evaluated 15 patients (5 males/10 females),
with a mean age of 38 years, a median preoperative weight of
141.1 kg (121–174), and a mean BMI of 46.4 (38–60) kg/m2,
who had undergone OAGB [36]. At the 1-year postoperative
follow-up, the median weight was 81.2 kg (72–111), the
median BMI was 31 kg/m2 (28–42), and the excess weight
loss (EWL, %) was 63 (56–69). The OAGB was compared to
a control group consisting of 25 adult patients who underwent sleeve gastrectomy. The sleeve gastrectomy group was
age- and sex-matched with patients who underwent
OAGB. Their median preoperative weight was 130.8 kg
(119–156), and median BMI was 46.1 (38–58); 1-year postoperative median weight was 98 kg (72–110), and median
BMI was 34.7 (28–46), with 56% excess weight loss. In this
study, the OAGB group (15 patients) reported no symptoms
of reflux prior to surgery. Following OAGB, none of the 15
patients reported reflux/GERD symptoms, and there was no
esophagitis on endoscopic examination.
Using high-resolution impedance manometry and 24-h pHimpedance monitoring, Tolone discovered a significant reduction in esophageal acid exposure as well as reflux episodes in
all patients undergoing OAGB. The control group of patients
undergoing sleeve gastrectomy developed an increase in both
esophageal acid exposure and reflux episodes.
They concluded that patients undergoing OAGB developed
no changes in esophageal gastric junction function or motility
patterns in obese patients without preoperative GERD or large
hiatal hernia 12 months after surgery. In contrast to patients
having undergone sleeve gastrectomy, those who had undergone OAGB demonstrated diminished esophageal acid exposure and total number of reflux. Although this study reports a
rather small patient population, it remains perhaps the most
elegant and complete study exploring the function of the
esophageal gastric junction following OAGB operations.
Our experience with bile reflux following OAGB has
been similar to many published studies with virtually no
Bile scintigraphy has been published and is a possible modality to assess the presence of bile reflux in patients following
mini gastric bypass [38] (Fig. 16.14). In this study, nine consecutive patients who underwent OAGB underwent hepatobiliary scintigraphy and a reflux questionnaire 8–13 months
after their operations. In addition, every patient with a positive bile scintigraphy scan underwent gastroscopy with biopsies. Five of the nine patients demonstrated positive reflux
into the gastric tube; however, bile reflux was not present in
the esophagus of any of the nine patients. The findings demonstrated that transient bile reflux was common after MGB
but only in the gastric tube and not in the esophagus. The
clinical relevance of bile reflux and loop bariatric procedures
has not been adequately studied. The debate regarding
OABG procedures and the clinical significance of reflux following these procedures will continue, and further prospective studies both short-term and long-term are necessary to
further define the clinical relevance of bile reflux.
Malabsorption
Multiple studies have confirmed that malabsorption can
occur following OAGB, and careful postoperative monitoring of nutritional status is recommended following this procedure [39]. Unlike Roux-Y gastric bypass where no
standardization of the alimentary, biliopancreatic, and common limb lengths has been defined, OAGB procedures typically describe a biliopancreatic alimentary limb length of
between 150 and 200 cm. Nutritional outcomes utilizing
these limb lengths have been extensively reported [40, 41].
One hundred fifty centimeters of limb length has been proven
to be effective in patients with class II obesity. Regardless of
the method used to determine if the limb length should be
150 cm or 200 cm, a risk of revisional surgery for excess
weight loss was reported by Noun to be 0.4% [42]. Lee
reported a 1.0% and Musella et al. [43] reported an incidence
of excess weight loss at 0.2%. Authors who have used a fixed
200 cm biliopancreatic loop in the creation of a one anasto-
16 Laparoscopic One Anastomosis Gastric Bypass: History of the Procedure Surgical Technique and Outcomes
191
Fig. 16.14 Nuclear medicine bile scintigraphy following one anastomosis
gastric bypass demonstrates no significant bile reflux. The scan correlates
with the endoscopic findings which were devoid of any bile reflux in the
gastric pouch or esophagus. Arrow depicts very small uptake in the gastric
pouch but below the diaphragm which may represent trace amounts of bile
reflux but no significant reflux entering the distal esophagus
mosis gastric bypass report a much lower rate of malnutrition of 0.05% and 0.1% by Chevallier and Kular [44].
ditions following OAGB/MGB was published in 2019. In
it, type 2 diabetes mellitus remission rate was 83% and
70% at 1 and 3 years, respectively. Hypertension resolution
was 61%, 58%, and 58% at 1, 2, and 3 years post-op.
Ninety-nine percent of sleep apnea patients improved
symptomatically and went off their CPAP machines. The
study reported on outcomes of 527 OAGB patients. Mean
follow-up was 2.5 years and the mortality was zero.
Multiple additional authors report similar results with
comorbidity resolution following laparoscopic OAGB and
similar procedures [42, 45–50].
esolution of Comorbidities and Nutritional
R
Complications
The major comorbid conditions commonly associated with
one anastomosis gastric bypass which include diabetes,
hypertension, obstructive sleep apnea, hyperlipidemia, and
joint pain all show significant improvement after 5 years of
follow-up. Bruzzi et al. published a series of 126 patients
with 72% follow-up at 5 years [46]. No mortalities were
reported, and percent excess body mass index lost was an
impressive 71%. Complete remission of type 2 diabetes
occurred in 82% of patients. Fifty-two percent of patients
with hypertension and 81% of patients with hyperlipidemia
were able to stop medications at 5 years follow-up. Sleep
apnea resolved in 50% of patients.
The largest UK study showing safety and acceptable
results for metabolic syndrome and obesity comorbid con-
utcome Comparison Roux-Y Gastric Bypass
O
vs Sleeve Gastrectomy vs One Anastomosis
Gastric Bypass
The most recent prospective randomized series comparing
long-term results between Roux-Y gastric bypass versus
sleeve gastrectomy versus one anastomosis gastric bypass
was recently published by Ruiz-Tovar et al. [51]. In this
192
study, 600 patients undergoing primary bariatric surgery
were prospectively randomized into a clinical trial consisting
of three groups. Patients were randomized into those undergoing sleeve gastrectomy (SG), Roux-Y gastric bypass
(RYGB), and one anastomosis gastric bypass (OAGB). The
study reports on the long-term findings with respect to BMI,
excess BMI loss, remission of type 2 diabetes, hypertension,
and dyslipidemia.
Six hundred patients were randomized into three groups,
200 patients in each group. The authors achieved 91% follow-­up at 5 years in the SG group, 90% follow-up in the
OAGB group, and 92% follow-up in the RYGB group. The
study reports significantly greater excess BMI loss in the
OAGB group versus that achieved in the SG and RYGB
group at 5 years follow-up. Similarly the OAGB group
achieved greater remission of type 2 diabetes, hypertension,
and dyslipidemia than RYGB or SG. The results build upon
findings observed with previous studies and continue to confirm the findings that OAGB is a safe and efficacious operation. Prospective randomized studies continue to confirm
short-term and long-term outcomes that meet or exceed
those of SG and RYGB. The importance of these studies in
contributing to the worldwide adoption of the OAGB as an
acceptable, safe, and effective primary bariatric operation
cannot be underestimated.
Insurance Coverage USA
Insurance coverage for one anastomosis gastric bypass procedures has been slow to obtain adoption by commercial
insurance companies in the United States. At the current
time, there are no know commercial payers in the United
States who have included MGB, OAGB, or single anastomosis gastric bypass as a covered benefit for bariatric surgery. In
our review of over 20 different benefits of coverage policies
for virtually every major insurance company in the United
States, we were unable to find a single policy which did not
specifically exclude these procedures, and in every instance
they were identified as being investigational. In every policy
reviewed, the OAGB procedures, procedures using a loop
gastrojejunostomy or Billroth II-type anastomosis, or procedures described as mini gastric bypass, for the purpose of
weight loss, were specifically identified as procedures which
were not a covered benefit of the insurance plan with respect
to the surgical treatment of morbid obesity.
Summary
One anastomosis gastric bypass/mini gastric bypass is
clearly a promising bariatric operation, one that still continues to polarize bariatric surgeons. Despite the many thou-
H. T. Billy et al.
sands of procedures published in the world literature, there
remain objections to the one anastomosis procedures.
These objections have led to a slow, almost insignificant
adoption of the procedure in the United States as the concern regarding symptomatic bile reflux, malnutrition, and
risk of esophageal cancer remains the most common objections voiced by those surgeons reluctant to perform this
operation. Those surgeons having demonstrated significant
expertise with the one anastomosis approach to gastric
bypass report favorable outcomes with excellent resolution
of comorbid conditions and low complication rates. In
addition, the technical simplicity of the operation and short
learning curve, standardized approach, and relative ease
with which the operation can be reversed or revised lead
many surgeons to advocate for a more widespread proliferation of this operation as a preferred operation for the
treatment of obesity.
Multiple publications including prospective and randomized trials have demonstrated that OAGB/mini gastric bypass
is at least comparable to Roux-Y gastric bypass in the treatment of obesity. Our personal experience with OAGB
exceeds 5 years, and thus far we have experienced results
similar to that described in the world’s body of published
literature. The single anastomosis approach to gastric bypass
can be performed in less time than a Roux-Y gastric bypass,
utilizes less resources, and has a very low complication rate.
Time will tell over the next few years if this procedure develops more widespread adoption among American surgeons
and if the major insurance plans in the United States will
begin to recognize this approach as an effective alternative.
Question Section
1. One anastomosis gastric bypass
A. Consists of a short gastric tube similar to a RYGB.
B. Consists of a long gastric tube created below the
crow’s foot of the lesser curve.
C. Must consist of a tight narrow gastric tube to avoid
weight regain.
D. A 40 French Bougie is to be avoided.
2. Malnutrition associated with one anastomosis gastric
bypass
A. Increases as the afferent biliopancreatic limb exceeds
250–300 cm
B. Can be avoided by insuring that there are at least 250–
300 cm of bowel distal to the loop gastrojejunostomy
C. Can be improved by revision of the biliopancreatic
loop to a 150–200 cm length
D. All of the above
3. Reversal of one anastomosis gastric bypass
A. Requires small bowel resection and reconstruction
into a Roux-Y configuration
16 Laparoscopic One Anastomosis Gastric Bypass: History of the Procedure Surgical Technique and Outcomes
193
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16. Lee WJ, Lin YH. Single-anastomosis gastric bypass (SAGB):
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17. Gastrointestinal Surgery for Severe Obesity. Consens Statement.
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19. Mason E, Printen K, Lewis J, et al. Gastric bypass criteria for effectiveness. Int J Obes. 1981;5(4):405–11.
20. Genser L, Soprani A, Tabbara M, et al. Laparoscopic reversal of
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23. Kermansaravi M, Kazazi M, Pazouki A. Petersen’s space internal
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Part III
Management of Bariatric Complications
Management of Gastrointestinal Leaks
and Fistula
17
Ninh T. Nguyen and Shaun C. Daly
Chapter Objectives
1. Recognize signs and symptoms of gastrointestinal
leaks after bariatric surgery.
2. Understand the management of acute gastrointestinal leaks after bariatric surgery.
3. Understand the management of chronic gastrointestinal fistula after bariatric surgery.
Introduction
Bariatric operations involving gastrointestinal resection and/
or reconstruction can be associated with gastrointestinal
leaks and fistula. Common bariatric operations that can lead
to development of gastrointestinal leaks include Roux-en-Y
gastric bypass, sleeve gastrectomy, and the duodenal switch
operation. Of these procedures, sleeve gastrectomy is the
most commonly performed operation in the USA. Sleeve
gastrectomy as a primary bariatric operation has surpassed
Roux-en-Y gastric bypass for the most commonly performed
bariatric operation, accounting for 58.2% of cases [1]. The
duodenal switch is only being performed at specialized centers and consists of less than 1% of all bariatric procedures
performed in the USA.
Gastrointestinal leak is one of the most dreaded complications following bariatric surgery as it can lead to significant
morbidity and mortality. The incidence of leaks after bariatric surgery varies widely. In a review of the published literature, the mean incidence of leaks after Roux-en-Y gastric
bypass was reported to be 0.8%, and the incidence of leaks
after sleeve gastrectomy has been reported at 0.7% [2].
N. T. Nguyen · S. C. Daly (*)
Department of Surgery, Division of Gastrointestinal Surgery,
University of California, Irvine Medical Center, Orange, CA, USA
e-mail: shaund@uci.edu
Expeditious recognition and early institution of management
for gastrointestinal leaks are keys to minimize the progression from systemic inflammatory response to sepsis and septic shock. Recognition of leaks can be particularly difficult in
the morbidly obese. A high index of suspicion is crucial in
order to recognize these leaks early on. Prompt management
of gastrointestinal leak can also minimize the risk for development of a chronic fistula, which is often difficult to treat.
This chapter reviews the etiologies of gastrointestinal leaks,
common presenting signs and symptoms, diagnostic evaluation, and management of acute gastrointestinal leaks and
chronic fistula.
Etiologies
The causes for leaks are multifactorial and can be divided
into technique-related and patient-related factors. Technical
factors that can lead to development of leaks include issues
such as poor technique in construction of the anastomosis,
the presence of excessive tension on the anastomosis, the
presence of staple line bleeding, and the presence of tissue
ischemia. In most instances, all of the aforementioned factors may play a role in the development of leaks. Patient-­
related factors contributing to the development of leaks
include the presence of poor nutrition, current or recent
smoking history, liver cirrhosis, and renal failure. Sites for
leaks after gastric bypass include the gastrojejunostomy, the
gastric remnant, and the jejunojejunostomy with the gastrojejunal anastomosis being the most common site for leaks.
The primary reason for the higher leak rate observed at the
gastrojejunal anastomosis is the presence of tension at this
anastomosis. Additionally, tissue ischemia plays a role both
due to the division of the jejunal mesentery, which can compromise tissue perfusion to the antimesenteric jejunum, and
the creation of an anastomosis adjacent to a staple line. The
site of leak after sleeve gastrectomy can be anywhere along
the long gastric staple line, but the most common site of leak,
75–85% of cases, is along the proximal staple line near the
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_17
197
198
N. T. Nguyen and S. C. Daly
gastric angle of His. The main reason for leaks in this region
is the high intraluminal pressure associated with construction of the sleeve gastrectomy [3]. This phenomenon can be
explained by Bernoulli’s principle of fluid dynamics, which
states that as fluid moves within a column from an area of
higher to lower surface area, the pressure within that column
increases. The increased intraluminal pressure can lead to
increase in luminal radial force, which can potentially lead to
disruption of the staple line. Additionally, the presence of a
partial obstruction at the level of the incisura angularis can
also lead to additional proximal pressure and can be a contributing factor in the development of leaks after sleeve
­gastrectomy. Other factors that contribute to proximal leaks
are the relative tissue ischemia due to ligation of the short
gastric vessels and the relative thin tissue of the gastric cardia compared to antral thickness.
cumstances. With regard to the vital signs, tachycardia is
often the first vital sign to be abnormal [4]. Tachycardia in
the early postoperative period should raise suspicion for possible gastrointestinal leaks. Other clinical symptoms include
epigastric abdominal pain and fever. Laboratory examination
suggestive of a leak includes leukocytosis and an elevated
C-reactive protein level. In a study of 17 patients with leaks
after gastric bypass, C-reactive protein level of greater than
229 mg/l was able to reliably indicate a leak [5]. CT scan is
the radiographic modality of choice for detection of leaks as
it can delineate the site of leak and the presence of local or
distant fluid/abscess collections (Fig. 17.1). An upper GI
study can also be performed for detection of leaks, but unlike
CT scan, it will not be able to identify the presence of
abdominal fluid collections. CT scan should be performed
with PO and IV contrast, as leaks from the gastrojejunal
anastomosis or from the sleeve gastrectomy staple line can
often be identified by the presence of contrast extravasation.
In 2015, the American Society for Metabolic and Bariatric
Surgery (ASMBS) published a position statement on prevention and detection of gastrointestinal leak after gastric bypass
including the role of imaging and surgical exploration [2].
The sensitivity of upper GI contrast study varies among
reports between 22% and 75%. When upper GI and CT are
combined, up to one-third of patients with leaks will have
both studies interpreted as normal. Therefore, the position
statement suggested that laparoscopic or open reexploration
should be an appropriate diagnostic option when gastrointes-
Presentation and Diagnostic Evaluation
Evaluation for gastrointestinal leaks in the postoperative
period includes analyses of the vital signs, thorough physical
examination with emphasis on the abdominal exam, laboratories including white blood cell count, radiologic studies
such as upper GI study, and computed tomography (CT) scan
of the abdomen and pelvis with PO and IV contrast. Upper
endoscopy can play a role in defining the characteristics of a
leak and may provide a therapeutic option in appropriate cir-
a
Fig. 17.1 (a) Upper GI contrast study demonstrating a leak from the
proximal staple line following sleeve gastrectomy. (b) Computed
tomography (CT) scan of the abdomen showing the staple line of the
b
sleeve gastrectomy with contrast extravasation proximally into an
extraluminal collection (arrow) immediately adjacent to the gastric
sleeve staple line
17 Management of Gastrointestinal Leaks and Fistula
tinal leak is suspected, as reliance on false-negative imaging
studies may delay operative intervention.
Management
Management of leaks after bariatric surgery varies and
depends on the extent of the disruption, the abdominal
contamination, the site of the leak, and timing of presentation. The initial treatments should include NPO (nothing per oral), early initiation of broad-spectrum
antibiotics, and fluid resuscitation. Leaks can be classified as acute (within 7 days), early (1–6 weeks), late
(6–12 weeks), and chronic (>12 weeks) [2]. The treatment options for postoperative leaks after bariatric surgery depend on the timing of presentation. Management
of early and acute leaks can include nonoperative management, reoperation with abdominal washout with or
without closure of the defect or placement of a T-tube in
the defect, and wide peritoneal drainage. Alternatively,
there have been few reports on the use of intraluminal
stenting for gastric leaks after Roux-en-Y gastric bypass
and sleeve gastrectomy [6–11]. For late and chronic
leaks, management may require performing a proximal
gastrectomy with esophagojejunostomy [12].
Nonoperative Treatment
Nonoperative treatment can be considered for small, contained leaks, particularly in hemodynamically stable
patients without peritoneal signs on abdominal exam. The
patient should be kept NPO (nothing per oral) with total
Fig. 17.2 Management
strategies for staple line leak.
Acute presentations can often
be managed successfully with
(a) insertion of intraluminal
stent to cover the staple line
defect or (b) drainage and
T-tube insertion. (c) Chronic
leaks from the staple line
occasionally warrant resection
of the involved area with
Roux-en-Y reconstruction
a
199
parenteral nutrition, and broad-spectrum intravenous antibiotic should be administered. The course for nonoperative treatment should be followed with measurement of
serial white blood cell (WBC) count, vitals, and physical
exam. Patients with increasing WBC, persistent tachycardia, or worsening of abdominal pain should proceed to
endoscopic or operative management. In a relatively large
study of leaks after gastric bypass, Gonzalez and colleagues reported successful nonoperative treatment in 23
of 26 patients, with an overall morbidity of 62% and no
mortality [13].
Reoperation and Drainage
The mainstay of surgical treatment includes drainage of all
fluid collections and placement of abdominal drains with
exclusion of the leak by endoluminal stent placement.
Additionally, some surgeons make an attempt at closure of
the defect; however, these closures tend to break down due to
poor tissue integrity at the leak site. Leaks at the jejunojejunostomy or the gastric remnant may be more amenable for
primary closure, and revision of the anastomosis is rarely
needed [14]. An alternative approach to control the leak site
is placement of a T-tube directly into the defect [10]. This
technique consists of obtaining a conventional T-tube drain
and placing directly into the defect (Fig. 17.2). The drain is
then exteriorized and placed to bag drainage. The T-tube is
left in place for 4–6 weeks and is slowly withdrawn over
time (1–2 in. per week). The idea here is to create a track
along the drain, thus creating a controlled fistula. Upon
­withdrawal of the tube, the well-formed fistulous track will
collapse and eventually close.
b
200
Fig. 17.2 (continued)
N. T. Nguyen and S. C. Daly
c
Endoscopic Stent
Endoscopic stenting for management of bariatric leaks was
developed from the experience of using endoscopic stenting
in management of esophageal anastomotic leaks after esophagectomy [15]. It is important to note that the use of endoscopic esophageal stent for management of leaks is an
off-label use of a US Food and Drug Administration (FDA)approved device for malignant esophageal strictures or fistulas. Table 17.1 demonstrates selected series describing the
use of endoscopic stent for treatment of gastric bypass or
gastric sleeve leaks (Fig. 17.3) [6–11, 16]. To summarize the
case studies, the use of endoluminal stents for the management of sleeve gastrectomy leaks has demonstrated a success
rate of 55–100%. While stenting allows for early oral feeding during the healing process, stent migration, erosion, and
intolerance remain risks of their use. Often, multiple interventions and stent exchanges are needed before complete
healing is achieved [2].
Several principles should be followed when an esophageal stent is considered for management of a gastric leak
after sleeve gastrectomy or gastric bypass. First, an endoscopy must be performed to evaluate the site of the leak, the
size of the leak, and viability of the conduit. Second, appropriate drainage of abdominal collection is of utmost importance using either laparoscopic or percutaneous technique in
combination with nothing per oral and nutritional support
using either total parenteral nutrition or jejunostomy feeding.
Third, the size of the endoscopic stent should be selected erring on the larger size in an effort to prevent migration.
Endoscopic Stent Technique
The procedure starts with an endoscopy to determine the site
and extent of the leak. Upon confirmation of the site of leak,
it is important to make sure that there is an adequate landing
zone above the leak site. Additionally, it is important to estimate the luminal diameter of the esophagus in selection of
the size and length of the stent. It is also important to use
only fully covered stents rather than partially covered stents,
which can lead to tissue ingrowth and possibly compromise
its removal at a later date. There are two techniques for
deployment of the esophageal stent, fluoroscopic guidance
and endoscopic guidance. In the fluoroscopic guidance technique, the site of the leak is confirmed on fluoroscopy, and
radiopaque markers (paper clips) are placed to outline the
proximal and distal extent of the esophageal stent. An ultra-­
stiff guidewire is placed into the gastric antrum for sleeve
gastrectomy patients or passed into the jejunal Roux limb for
Roux-en-Y gastric bypass patients and confirmed under fluoroscopy. The endoscope is then removed, leaving the remaining guidewire in place. The selected esophageal stent is
inserted transorally over the guidewire down the esophagus
and positioned between the two radiopaque markers. The
17 Management of Gastrointestinal Leaks and Fistula
201
Table 17.1 Outcomes in management of leaks after selected series of gastric bypass and sleeve gastrectomy
Authors/year/(reference)
Sakran (2013) [12]
Procedure (# patients Incidence of
with leaks)
leaks (%)
Sleeve
44
De Aretxabala (2011) [18]
Sleeve (n = 9)
–
Csendes (2010) [19]
Sleeve (n = 16)
4.7%
Tan (2010) [10]
Sleeve (n = 14)
–
Casella (2009) [16]
Sleeve (n = 6)
3.0%
Freedman (2013) [20]
Bypass
(n = 69/2214)
3.1%
Thodiyil (2008) [21]
Bypass (n = 46)
1.7%
Ballesta (2008) [22]
Bypass (n = 59)
4.9%
El Mourad (2013) [17]
Sleeve (n = 26)
Bypass (n = 18)
–
Spyropoulos (2012) [23]
Sleeve (n = 12)
Bypass (n = 5)
BPD (n = 13)
2.0%
Serra (2007) [7]
Eisendrath (2007) [24]
Sleeve or DS (n = 6)
Bypass (n = 8)
Sleeve gastrectomy
(n = 4)
DS (n = 8)
BPD (n = 1)
–
–
Eubanks (2008) [25]
–
Treatments
Reop (n = 27)
Perc drain (n = 28)
Stent (n = 11)
Lap reop (n = 5)
Perc drain (n = 1)
Open reop (n = 3)
Stent (n = 4)
Nonoperative
(n = 8)
Reop (n = 8)
Nonoperative
(n = 4)
Reop (n = 7)
Stent (n = 8)
Perc drain (n = 5)
Stent (n = 3)
Nonoperative
(n = 6)
Stent (n = 35)
Reoperation
(n = 28)
Reop (n = 27)
Conservative
(n = 33)
Reop (n = 23)
Conservative
(n = 36)
Stent (n = 41)
Laparoscopy
(n = 5)
Endoscopic fibrin
(n = 1)
Stent (n = 9)
Reop (n = 3)
Nonoperative
(n = 27)
Stent (n = 6)
Stent (n = 21)
Reoperation (n = 3)
Stent (n = 19)
Resolution of leaks following stent
insertion (%)
Endoscopic stent with
laparoscopic drainage
Overall
mortality
9.1%
75%
0%
–
0%
50%
0%
100%
0%
100%
0%
–
0%
–
8.5%
96
0%
100%
3.3%
83%
81%
0%
19%
84%
0%
Reop reoperation, Perc drain percutaneous drainage, BPD biliopancreatic diversion, DS duodenal switch
stent is then deployed under fluoroscopic guidance. In the
endoscopic guidance technique, the ultra-stiff guidewire is
placed as above, and the endoscope is removed and then
reinserted and positioned next to the guidewire at the level of
the proximal aspect of stent deployment. The selected esophageal stent is inserted transorally over the guidewire under
endoscopic guidance, and the stent is deployed. The endo-
scope is used to ensure that the proximal aspect of the stent
is positioned at the optimal position. Upon deployment of
the stent, the guidewire is removed. A completion endoscopy
is then performed with care to avoid dislodgement of the
stent. In cases where migration is a high risk, the endoluminal stent may be either clipped or sutured into place at the
proximal edge of the stent.
N. T. Nguyen and S. C. Daly
202
present with a localized leak and without signs of systemic
toxicity can include nonoperative management by rendering
the patient NPO, providing parenteral nutrition and broad-­
spectrum antibiotic therapy, as well as percutaneously draining any intra-abdominal fluid collections. Endoscopic
stenting has become an appropriate adjunct to this strategy
and can obviate the need for reoperation for some patients.
Surgical treatment including reoperation with drainage
remains the mainstay of therapy for patients presenting with
obvious signs of sepsis. In addition, chronic leaks and fistulae often require surgical reexploration with proximal gastrectomy and esophagojejunostomy.
Question Section
Fig. 17.3 Upper gastrointestinal contrast study showing a stent
deployed for treatment of a proximal staple line leak after sleeve gastrectomy. Oral contrast passed entirely through the stent without evidence of contrast extravasation
Chronic Fistula
1. Appropriate management for acute postoperative leaks
includes all except:
A. Endoluminal stent
B. Laparoscopy with drainage
C. Resection of the leak site and reconstruction
D. IR drainage and IV antibiotic
2. In patients with suspected postoperative leaks, what is the
first vital sign to be abnormal?
A. Elevate systolic blood pressure
B. Temperature greater than 101°
C. Increase respiratory rate
D. Tachycardia >100
Management of chronic fistula is often difficult due to the
persistent leak into a well-contained cavity and often a well-­
defined epithelialized fistula tract. Initial management can References
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ing, endoscopic clipping, and/or injection of endoscopic
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surgical intervention such as surgical takedown of the fistula
2. Clinical Issues Committee of the American Society for Metabolic
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[12]. Other authors have advocated using a Roux limb at the
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DB, Provost DA. Clinical predictors of leak after laparoscopic
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Conclusion
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surgery and is associated with significant morbidity and mortality. Early identification and management are very important in an effort to minimize the morbidity associated with
the systemic inflammatory response and sepsis. A high index
of suspicion is vital to facilitate expedient diagnosis and
treatment of a staple line leak. Treatment of patients who
5. Warschkow R, Tarantino I, Folie P, Beutner U, Schmied BM, Bisang
P, et al. C-reactive protein 2 days after laparoscopic gastric bypass
surgery reliably indicates leaks and moderately predicts morbidity.
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leak after laparoscopic sleeve gastrectomy: early covered self-­
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17 Management of Gastrointestinal Leaks and Fistula
9. Oshiro T, Kasama K, Umezawa A, Kanehira E, Kurokawa
Y. Successful management of refractory staple line leakage at
the esophagogastric junction after a sleeve gastrectomy using the
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Szomstein S, et al. Diagnosis and contemporary management of
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Stamos MJ. Management of gastrointestinal leaks after minimally
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et al. Nonsurgical treatment of staple line leaks after laparoscopic
sleeve gastrectomy. Obes Surg. 2009;19(7):821–6.
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Endosc. 2013;27:808–16.
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19. Csendes A, Braghetto I, León P, Burgos AM. Management of leaks
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D. Treatment of leaking gastrojejunostomy after gastric bypass
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M. Management of anastomotic leaks after laparoscopic Roux-­
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Gastrointestinal Obstruction After
Bariatric Surgery
18
Neil A. King and Daniel M. Herron
Chapter Objectives
1. Address the evaluation of the most common presentations of partial and complete obstruction that
occur after Roux-en-Y gastric bypass (RYGB),
sleeve gastrectomy (SG), adjustable gastric band
(AGB), and biliopancreatic diversion with duodenal switch (BPD-DS).
2. Explore management options for treating partial
and complete obstructions following bariatric
surgery.
Introduction
Obstruction After Roux-En-Y Gastric Bypass
An understanding of the anatomy of RYGB is critical when
diagnosing the bypass patient with obstruction, since the
clinical presentation is determined by the location of the
obstruction (Fig. 18.1). In RYGB, the gastric pouch is very
small, 30 ml or less in volume and 5 cm or less in length.
When the patient eats, food passes first through the pouch
and then enters the Roux limb, a segment of jejunum typically 75–150 cm in length leading to the distal anastomosis.
Food then passes through the “common channel”—the
length of jejunum and ileum between the distal anastomosis
and the ileocecal valve. The bypassed segment of the stomach, referred to as the “gastric remnant,” is no longer part of
Obstruction of the gastrointestinal tract is one of the most
common complications occurring after bariatric surgery. It
may occur after any type of bariatric procedure and may
range in severity from a minimal, spontaneously resolving
problem to a life-threatening emergency. It is important to be
familiar with the different types of strictures, partial obstructions, and complete obstructions that can occur postoperatively so that the patient can be expeditiously evaluated and
appropriately treated. This chapter will address the evaluation and management of the most common presentations of
partial and complete obstruction that occur after Roux-en-Y
gastric bypass (RYGB), sleeve gastrectomy (SG), adjustable
gastric band (AGB), and biliopancreatic diversion with duodenal switch (BPD-DS).
N. A. King · D. M. Herron (*)
Garlock Division of Surgery, Mount Sinai Hospital, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
e-mail: daniel.herron@mountsinai.org
Fig. 18.1 Roux-en-Y gastric bypass
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_18
205
206
a
N. A. King and D. M. Herron
b
Fig. 18.2 (a) This plain film of a gastric bypass patient with obstruction of the biliopancreatic limb is not particularly revealing. (b) CT
imaging of the same patient reveals a tremendously enlarged gastric
remnant filled with fluid. The antegastric Roux limb containing a small
amount of contrast can be appreciated anteriorly
the alimentary path but continues to secrete mucus and gastric acid. These gastric secretions join with bile and pancreatic fluid in the duodenum before passing though the ligament
of Treitz into the biliopancreatic limb. The biliopancreatic
limb is the bypassed segment of the intestine extending to the
distal anastomosis.
In general, obstruction of the Roux limb or common
channel will result in obstructive symptoms familiar to the
general surgeon, including nausea, vomiting, food intolerance, abdominal pain, and distention. Obstruction of the biliopancreatic limb is more challenging to diagnose, since the
alimentary path may remain unblocked. In biliopancreatic
limb obstruction, the gastric remnant may become severely
distended with fluid yet remain invisible on plain film
(Fig. 18.2a). This may result in abdominal fullness, bloating,
hiccups, and pain but no nausea or vomiting. For this reason,
computed tomography (CT) scan of the abdomen and pelvis
is a critically important component of the evaluation of the
patient with possible bowel obstruction, as it will reveal
obstruction of both the bypassed and non-bypassed bowel
(Fig. 18.2b). Obstruction of the biliopancreatic limb will
result in severe distension of the gastric remnant and generally requires emergent decompression, either surgically or
percutaneously.
lowing gastric bypass varies from 0.9% to 34% [1–3]. A
2015 study including 1500 patients reported a gastrojejunal
stricture rate requiring endoscopic intervention of 3.4% [4].
While a significant majority of gastrojejunal strictures present within the first 90 days after surgery, some patients may
present much later, even a year or more postoperatively [5].
The typical stricture patient presents 4–6 weeks after surgery
with solid food intolerance progressing to liquid intolerance
as the stricture narrows. In severe cases, patients may be
unable to swallow their own oral secretions.
The diagnosis of stricture can usually be made based on
history alone and confirmed with upper endoscopy.
Radiographic contrast studies may or may not be helpful;
they are not very sensitive in detecting strictures and pose the
risk of contrast aspiration. Upper endoscopy is the primary
diagnostic modality of choice, as it allows both rapid diagnosis and therapeutic intervention via balloon dilatation [6]. It
is difficult to precisely measure a stricture, as no widely
accepted definition of stricture exists, but most endoscopists
consider an anastomosis that is too narrow to permit passage
of a standard upper endoscope (approximately 9.5 mm in
diameter) to represent a stricture. After being diagnosed
endoscopically, the stricture can be immediately dilated
using a through-the-scope dilating balloon up to a diameter
of 12–15 mm. While most patients respond to a single dilatation, some will require a second or third; up to 13% may
require four to five treatments [7].
Prior to the widespread use of dilating balloons, treatment
of anastomotic stricture was achieved using bougie dilators
like the Savary-Gilliard dilator (Wilson-Cook Medical Inc.,
Winston-Salem, NC). Some studies have demonstrated
Gastrojejunal Stricture
Stricture of the proximal anastomosis, or gastrojejunostomy,
is one of the more common complications after gastric
bypass. The reported incidence of gastrojejunal stricture fol-
18 Gastrointestinal Obstruction After Bariatric Surgery
excellent results with this technique, with no serious complications and most patients requiring only one to two dilations
[8, 9].
While balloon dilation is a safe and effective procedure,
perforation may rarely occur. A 2012 review of 760 patients
undergoing endoscopic dilation found perforation to be the
most common complication occurring in 14 patients (1.8%).
Of note, only two of these patients required operative intervention. The authors reported that only 15 patients (2%)
required surgical revision for recurrent stenosis [10].
The etiology of gastrojejunal stricture formation is not
well understood. Some believe it is related to ischemia, while
others feel that suture material or staples may be causative.
Stricture formation appears to be related to the initial size of
the anastomosis; a 2012 study demonstrated a nearly fourfold incidence of intraluminal stenosis associated with the
21-mm circular stapler compared to the 25-mm circular stapler [11]. For stapled anastomoses, firm apposition or compression of the tissue edges may be helpful in reducing
stricture rate. A recent study found that a circular stapler with
a 3.5-mm height resulted in lower stricture rate than one with
a 4.8-mm height (3.5 v 13.9%) [12]. The use of staple line
reinforcement materials has also been shown to reduce stricture rate [13]. Some surgeons feel that handsewn anastomoses are less likely to stricture, while others prefer linear
stapled or circular anastomosis. A meta-analysis of over
13,000 patients found no difference in stricture rates between
handsewn and stapled anastomoses [14].
Although obstruction at the distal anastomosis is sometimes described as a “distal stricture,” these obstructions are
most likely due to kinking of the anastomosis or excessive
narrowing of the common enterotomy closure due to technical error. True stricture formation along a 60-mm stapled
jejunojejunostomy anastomosis is exceedingly rare.
Obstruction from Internal Hernia
Internal hernias are relatively common after gastric bypass
and may result in bowel obstruction, intestinal ischemia, or
both. A recent study of 594 patients found internal hernia
rates as high as 6.2% following Roux-en-Y gastric bypass
[15]. A 2007 series from the Cleveland Clinic reported that
internal hernia was the single most common cause of bowel
obstruction in their gastric bypass patients, representing 41%
of all obstructions [16]. In a gastric bypass patient with an
antecolic Roux limb, two different types of internal hernias
may potentially occur:
• Distal anastomosis mesenteric hernia—this space is bordered by the divided mesentery of the biliopancreatic
limb and the mesentery of the Roux limb at the distal
anastomosis (Fig. 18.3).
207
Fig. 18.3 Internal hernia potential space at the mesenteric defect of the
distal anastomosis
• Petersen hernia—the space between the mesentery of the
Roux limb and the mesocolon/colon (Fig. 18.4).
Some bariatric surgeons perform a retrocolic gastric
bypass in which the Roux limb is brought up behind the transverse colon through an opening in the mesocolon. These
patients have the potential to suffer from a “mesocolic hernia”
in which the Roux limb herniates up through the defect in the
mesocolon through which the Roux limb passes. If the Roux
limb is placed in an antecolic position, no such opening is
created, and there is no potential for mesocolic herniation.
Retrocolic gastric bypass is associated with a higher rate of
internal hernias. A Mount Sinai study from 2003 found
patients with retrocolic anastomoses to have nearly double
the risk of developing an internal hernia (3.3% v 6.0%) [17].
While the majority of bariatric surgeons close these internal hernia spaces with permanent suture, some do not. A
2017 study found that closure of mesenteric defects resulted
in a 2.5% internal hernia rate compared to nearly 12% in
patients without mesenteric closure [18]. It is important to
remember that even if hernia spaces have been sutured
closed, hernia defects may still form at these sites.
208
N. A. King and D. M. Herron
If the small bowel becomes entrapped within an internal
hernia, its venous outflow may become partially or completely occluded, ultimately resulting in bowel ischemia and
severe abdominal pain far out of proportion to the physical
exam findings (Fig. 18.5). Typically, patients complain of
intense pain in the midepigastrum, often radiating to the
back. The pain may occasionally be relieved by leaning forward or getting “down on all fours,” maneuvers that serve to
reduce the compression on the entrapped bowel. Entrapped
bowel may reduce itself from the hernia spontaneously,
bringing with it rapid resolution of symptoms, or it may persist until surgical intervention. Obstruction of the bowel
lumen may or may not occur at the same time (Fig. 18.6).
Physical exam is generally unrevealing in the patient with
an internal hernia. Laboratory studies are similarly unhelpful. Computed tomography (CT) scan may demonstrate findings such as the “swirl sign,” a spiraling of the mesentery,
mesenteric fat haziness, or intestinal distention in the upper
abdomen [19]. However, these findings are neither sensitive
nor specific, and it is essential to understand that a negative
CT scan of the abdomen in no way rules out an internal hernia. Bowel obstruction may be absent even with a severe
internal hernia causing intestinal ischemia. Thus, the gastric
bypass patient with severe unrelenting abdominal pain but a
normal CT scan still represents a surgical emergency.
Fig. 18.4 Internal hernia potential space at between the Roux limb
mesentery and the mesocolon, frequently referred to as a Petersen
hernia
Fig. 18.5 Petersen-type internal hernia after biliopancreatic diversion
with duodenal switch, resulting in irreversible small bowel ischemia
Fig. 18.6 Plain film of a patient with an incarcerated internal hernia,
showing dilated small bowel loops. Bowel obstruction may or may not
be present with internal hernia
18 Gastrointestinal Obstruction After Bariatric Surgery
Definitive diagnosis of internal hernia can only be
achieved through surgical exploration, either laparoscopic or
open. If a significant length of bowel is entrapped within an
internal hernia, intestinal anatomy may become so distorted
that it becomes difficult to reduce the herniated bowel. In this
situation, it is helpful to start by locating the ileocecal junction and then running the bowel in a retrograde fashion until
the distal anastomosis is identified and the anatomy clarified.
Once the herniated bowel is reduced, the hernia defect should
be securely closed with a nonabsorbable running continuous
suture. Some surgeons advocate the addition of a second
layer of suture material or fibrin sealant to reinforce the hernia closure. If irreversibly ischemic bowel is identified, it
will need to be resected; questionably viable bowel may warrant a “second-look” procedure within 24–48 h.
mall Bowel Obstruction from Scars
S
and Adhesive Bands
The surgeon should always remember that bariatric surgery
patients are also general surgery patients and may suffer
from intestinal obstruction due to intra-abdominal adhesions. In a review of bowel obstruction after gastric bypass,
Elms et al. found that adhesions were the most common
cause of bowel obstruction, accounting for 48% of the 93
patients that occurred in their series of 2395 patients [20].
Adhesions may form anywhere within the abdomen and
can potentially obstruct the Roux limb, biliopancreatic limb,
or common channel. Thus, plain films and even upper GI
series may miss adhesive bowel obstructions that occur outside the alimentary path. CT scan with oral contrast is preferred since it will image the entire intra-abdominal
gastrointestinal tract and may reveal the location of a transition zone where the obstruction is located. In the Cleveland
Clinic series, plain films identified 35% of obstructions,
while CT had a sensitivity of 51% [16].
If the Roux limb is placed in a retrocolic position at the time
of surgery, it must necessarily pass through a surgically created
defect in the mesocolon. This opening may potentially scar to
the point of stricture formation. In the Cleveland Clinic series,
this was the second most common cause of bowel obstruction
in bypass patients, comprising 20% of all obstructions [16].
The risk of mesocolic stricture formation or mesocolic hernia
can be completely eliminated at the time of initial surgery, if
the surgeon places the Roux limb in an antecolic position.
209
hernia following laparoscopic Roux-en-Y gastric bypass
[21]. The vast majority of these patients were asymptomatic,
and only 2 of the 59 patients with ultrasound evidence of
hernia required surgical repair during the study period. Elm’s
review of 2395 laparoscopic bypass patients found just 1
case of incisional hernia requiring surgical repair [20]. To
minimize the risk of incisional hernia, it is often recommended that surgeons close trocar sites 10 mm or larger.
While this will not eliminate the risk of trocar site herniation
entirely, it may significantly decrease the incidence [22].
The treatment of preexisting ventral hernias at the time of
laparoscopic Roux-en-Y gastric bypass is more controversial.
Most surgeons are reluctant to implant prosthetic mesh to
repair large hernias during a clean-contaminated operation.
Others feel that it is most prudent to wait until after the patient
has achieved significant weight loss before performing the
repair. Khorgami et al. reported a higher incidence of return to
the operating room, readmission, discharge to rehabilitation
facility, and a longer hospital length of stay among patients
having concomitant ventral hernia repair and bariatric surgery
when compared to patients having bariatric surgery alone [23].
Bariatric surgery with simultaneous mesh repair of ventral
hernia does not yet constitute the standard of care.
Intussusception
Small bowel intussusception is a far less common cause of
bowel obstruction after gastric bypass, with scattered case
reports in the literature. The distal anastomosis can serve as a
lead point for intussusception. If CT imaging can be obtained
during the obstruction episode, the classic finding of the “target
sign” will be pathognomonic for the condition (Fig. 18.7).
Intussusception may or may not resolve spontaneously. If surgery is required, the intussusception should be reduced, with
resection or revision of the presumed lead point if identifiable.
Incisional Hernia
Incisional hernias may form at open incisions or laparoscopic trocar sites or may exist as sequelae of earlier surgery.
The true incidence of trocar site hernias may be underappreciated; a 2014 study using ultrasound to assess the abdominal wall found that 39% of patients developed a trocar site
Fig. 18.7 CT imaging showing the classic finding of the “target sign”
consistent with intussusception
210
bstruction from Intraluminal Blood Clot or
O
Bezoar
Intraluminal causes of obstruction are exceedingly rare after
gastric bypass. Koopman’s review in 2008 identified only ten
reported cases [24]. Intraluminal blood clots, or hemobezoars,
may form in the immediate postoperative period and can cause
occlusion at the distal anastomosis. If the location of the bezoar
is accessible endoscopically, the obstruction can be relieved
nonsurgically. Otherwise, surgical exploration may be required
with evacuation of the bezoar and confirmation of hemostasis.
eneral Approach to the Bypass Patient
G
with Obstruction
When approaching the gastric bypass patient with intestinal
obstruction, it is important to remember that the clinical presentation is dependent upon the segment of bowel that is
obstructed; an obstruction of the Roux limb will present far
differently from an obstruction of the biliopancreatic limb.
CT imaging with oral and IV contrast should be considered
early in the diagnostic process as it will reveal obstruction in
the Roux limb, biliopancreatic limb, and common channel.
In contrast, plain films and upper gastrointestinal (UGI)
series will generally be unhelpful in diagnosing obstruction
of the bypassed bowel.
Nasogastric tube decompression is frequently employed
in management of the general surgical patient with bowel
obstruction but is often unhelpful in the obstructed gastric
bypass patient unless the blockage is extremely proximal and
the patient is actively vomiting. Placement of a nasogastric
tube may be harmful, as the tube can potentially disrupt a
fresh gastrojejunal anastomosis or penetrate through the
blind end of the Roux limb (“candy-cane end”) if forced.
Finally, it should be repeated and emphasized that the
patient with abdominal pain but no distended bowel on CT
imaging may be suffering from an internal hernia. Internal
hernias cause pain due to compression and ultimately
obstruction of the intestinal vasculature and thus present
with symptoms more suggestive of intermittent bowel ischemia than obstruction.
N. A. King and D. M. Herron
tive complications. Adjustable gastric bands are generally
placed very high on the stomach, just beneath the gastroesophageal junction (Fig. 18.8). The band is designed to be appropriately sized for this location only and may cause excessive
restriction or obstruction if it slips down to a wider area of the
stomach or if the stomach prolapses up through the band.
Bands are generally secured in place through a combination of natural anatomic factors and sutures placed specifically for this purpose. Most bands are placed using the “pars
flaccida” technique, in which the posterior portion of the
band is placed through the soft tissue of the retroperitoneum
above the lesser sac. Because this portion of the band is not
free in the intraperitoneal space, it is held in position by surrounding retroperitoneal soft tissue and surgical scar. In contradistinction, the anterior portion of the band is
intraperitoneal and rests against the serosal surface of the
anterior stomach. To secure this portion of the band, most
surgeons imbricate the stomach over the band using simple
interrupted or running sutures.
Because gastric bands are located in the very proximal
portion of the gastrointestinal tract, obstructions caused by
them result in dramatic and easily recognizable symptoms.
Patients present with nausea, vomiting, and the inability to
tolerate solids or even liquids. In complete obstruction, the
patient may even be unable to manage oral secretions. If the
patient complains of epigastric pain, or is found to be tachycardic or febrile, the possibility of gastric ischemia should be
considered and should prompt expeditious evaluation and
bstruction in the Laparoscopic Adjustable
O
Gastric Band Patient
The laparoscopic adjustable gastric band (LAGB) has significantly declined in popularity due to the emergence of data suggesting poor long-term outcomes and the availability of
alternative operations such as sleeve gastrectomy [25, 26].
Nonetheless, hundreds of thousands of patients worldwide
have bands in place, and it behooves both the general and bariatric surgeon to understand the band’s potential for obstruc-
Fig. 18.8 Laparoscopic adjustable gastric band
18 Gastrointestinal Obstruction After Bariatric Surgery
211
management. Generally, the most appropriate first interven- anterior projection), a band will generally be viewed side-on.
tion is to remove all fluid from the band. While this will not The left side of the band is normally somewhat higher than
change the position of a slipped or prolapsed band, it may the right side; a line drawn through the body of the band is
reduce the gastric obstruction enough to relieve symptoms, generally sloping upward to the left at 30–45° from the horiand its effect is immediate.
zontal (Fig. 18.9). A plain film showing a completely flat
If there is any question about the diagnosis, imaging of band suggests the possibility of anterior gastric slippage,
the abdomen can be very useful to determine whether a band while a film showing a vertical band suggests posterior slipis in normal position. If a plain film is obtained (poster-­ page (Fig. 18.10). In the presence of gastric obstruction, an
Fig. 18.9 (a) Plain film of
the abdomen showing normal
positioning of a gastric band.
An upward angulation of the
left side of the band of 30–45°
is normal. (b) Esophagram
showing normal positioning
of a gastric band. This band is
not yet filled and causes
minimal holdup of contrast
through the band. The band is
angulated with the left side up
about 30°, which is normal
a
b
Fig. 18.10 Esophagram showing a slipped band with posterior gastric prolapse. Note the near-vertical orientation of the band and the excessively
large stomach pouch
212
upper gastrointestinal series will quickly demonstrate lack of
passage of contrast beyond the band. Care needs to be taken
to avoid aspiration of contrast material in this setting, as this
may result in severe aspiration pneumonitis.
bstruction After Laparoscopic Adjustable
O
Gastric Band Placement
The adjustable gastric band is designed to intentionally cause
partial obstruction of the upper stomach. As a result, many
gastric band patients report intermittent vomiting or regurgitation of food even when the band is appropriately positioned
and adjusted. This “restrictive” effect can rapidly progress to
complete obstruction if the band is aggressively overtightened or if it shifts out of position. Rapid recognition and
intervention is essential to avoid gastric ischemia, necrosis,
or perforation from an overly occlusive band.
Early Postoperative Band Obstruction
Gastric obstruction in the immediate postoperative period
was not uncommon in the early days of the adjustable gastric
band. A 2003 series of 56 patients described an 11% incidence of gastric obstruction within 24 h of band placement
[27]. While three of the six obstructed patients in this series
required immediate band removal, two others improved with
conservative management, and one required surgery to reposition the band. The authors felt that the perigastric surgical
technique they were using at the time resulted in a too low
position on the stomach and reported a reduction in this complication after switching to the now-ubiquitous pars flaccida
technique, which places the band just beneath the gastroesophageal junction.
Newer bands are larger in diameter than earlier bands and
allow a greater range of adjustment. The larger size, in conjunction with the use of the pars flaccida surgical technique for
placement, has reduced the incidence of early obstruction [28].
Late Postoperative Band Obstruction
Late obstruction may be caused by overly aggressive tightening of the band or by slippage of the band out of its original
position. A review by Tice et al. found the incidence of band
slippage to range from 1% to 20% [29]. The risk of band
slippage persists during the patient’s lifetime, and the incidence will likely continue to increase as follow-up extends
over longer periods.
The band patient presenting with new obstructive symptoms should be queried regarding any recent adjustments.
Regardless of the presumed cause of band obstruction,
N. A. King and D. M. Herron
removal of some or all of the fluid from the band is a prudent
first step that may result in full resolution of symptoms. The
band port should be accessed with a non-coring Huber-type
needle if at all possible. However, if such a needle is not
available, a narrow-gauge standard hypodermic needle can
be used instead. If the access port cannot be localized by
palpation alone, visualization of the port with fluoroscopy
may be helpful. The patient should also be queried about the
ingestion of food immediately prior to the obstructive symptoms; impacted food material may be easily removed with
endoscopic intervention. The presence of epigastric or chest
pain in addition to nausea or vomiting should raise the possibility of gastric ischemia; expedited workup and intervention is mandatory in this setting. If pain resolves immediately
after deflation of the band, it may be safe to defer definitive
therapy to a more elective setting. Persistent pain after band
deflation warrants emergency reoperation. Similarly, the
presence of fever or elevated white blood cell count suggests
the possibility of gastric ischemia.
In a 2006 report of 1275 banding patients, Ponce et al.
described six different forms of band slippage [30]. Type I
slippage involves prolapse of the posterior stomach through
the band and is thought to be associated with the now-­
abandoned perigastric (intraperitoneal) band placement
technique. Imaging will reveal a vertically positioned band
(Fig. 18.10). Type II slippage describes anterior gastric prolapsed and may be associated with inadequate suture fixation
of the band or excessive vomiting resulting in downward
pressure on the device. Plain films may show a horizontally
oriented band or one angulated downward to the left. Finally,
type III slippage describes concentric pouch dilatation
caused by excessive eating or an overly tight band and may
be associated with a hiatal hernia or dilated esophagus [30].
Unusual Types of Band Obstruction
Gastric bands may very occasionally cause obstruction by
eroding into the lumen of the stomach or esophagus.
Ruutiainen et al. described a patient whose band eroded
completely into the stomach and migrated upward, causing
obstruction at the gastroesophageal junction [31].
Alternatively, a fully eroded band may travel distally and
occlude the small intestine. Operative intervention is required
in these circumstances to remove the band and relieve the
obstruction. It should be noted that erosion of the band
through the gastric wall may occur without the emergence of
sepsis or peritonitis. Additionally, it should be appreciated
that this type of presentation is quite rare; erosion more
­commonly presents with sudden loss of restriction than with
obstruction.
Although uncommon, the tubing that connects the adjustable band to the subcutaneous port may cause bowel obstruc-
18 Gastrointestinal Obstruction After Bariatric Surgery
tion. Several case reports have described this rare
complication and its management [32, 33]. Surgical reduction of the bowel is required in this situation. Removal of the
band, tubing, and port will eliminate the possibility of
recurrence.
Obstruction After Sleeve Gastrectomy
Sleeve gastrectomy is now the most common bariatric operation in the United States. Generally, the operation involves
resection of the greater curvature of the stomach with preservation of a banana-shaped stomach based on the lesser curvature (Fig. 18.11). Calibration of the stomach is
accomplished by placing a bougie—typically 12–14 mm in
diameter—along the lesser curvature during stapling. While
the most feared and difficult-to-manage complication of the
operation is gastric leakage, obstruction of the sleeve due to
stenosis, twisting, or kinking can also present clinical
challenges.
It should be noted that many sleeve patients present with
nausea and vomiting in the immediate postoperative period
within 1–3 days after surgery. Upper GI series can be helpful
to determine whether true mechanical obstruction is present.
Patients with nausea and vomiting but without frank obstruction should be treated medically. Ondansetron and other antiemetic medications may be very helpful in relieving nausea,
while some patients respond favorably to hyoscyamine, an
anticholinergic. In our experience, some sleeve patients with
Fig. 18.11 Laparoscopic sleeve gastrectomy
213
continued food intolerance without obstruction have
responded favorably to the administration of mirtazapine, an
antidepressant with beneficial gastrointestinal side effects.
If upper GI series demonstrates true obstruction, endoscopic or surgical intervention is required. A 2013 review of
717 patients found symptomatic gastric stenosis in 5 patients
(0.69%). Four of the five patients were successfully managed
with endoscopic dilation, while one patient failed endoscopic
treatment and underwent conversion to a Roux-en-Y gastric
bypass [34].
bstruction After Biliopancreatic Diversion
O
with Duodenal Switch
Biliopancreatic diversion with duodenal switch (BPD-DS) is a
relatively uncommon bariatric/metabolic operation, less frequently performed than RYGB due to its greater technical complexity and short- and long-term morbidity. However, it has
received some recent attention due to its extraordinary effectiveness with regard to both weight loss and metabolic improvement. A sleeve gastrectomy provides the restrictive component
of BPD-DS. The duodenum is then divided just distal to the
pylorus and anastomosed to the distal 250 cm of small intestine
(Fig. 18.12). The remainder of the small bowel forms the biliopancreatic limb and is diverted from the alimentary tract. The
biliopancreatic limb and the alimentary channel are anasto-
Fig. 18.12 Biliopancreatic diversion with duodenal switch (BPD-DS)
214
mosed 50–100 cm from the ileocecal junction to form the common channel, where food and digestive juices intermix.
Obstructive complication after BPD-DS are similar to
those in gastric bypass, except that there is no gastric remnant present. Additionally, for reasons that are not clear, the
risk of stenosis at the proximal anastomosis is much lower
than that seen for gastric bypass. BPD-DS patients suffer
from the same types of internal hernias as gastric bypass
patients. The evaluation and management of a BPD-DS
patient with abdominal pain or symptoms of obstruction are
essentially identical to that of the bypass patient.
N. A. King and D. M. Herron
adhesions, incarcerated ventral hernias, inguinal hernias, etc.
Thus, while we need to consider the many causes of bowel
obstruction unique to bariatric operations, we should never
forget that more conventional causes of obstruction may be
present as well.
As with general surgical patients, bariatric patients suffer
significant morbidity and even mortality as a result of postoperative gastrointestinal obstruction. Hopefully, as knowledge regarding the evaluation and management of these
obstructions is more widely disseminated, negative outcomes
as a result of gastrointestinal obstruction will become
increasingly rare.
Obstruction from Implanted Medical Devices
Many bariatric surgery patients suffer from gastroesophageal
reflux disease (GERD) [35]. Magnetic sphincter augmentation was approved by the FDA in 2012 for use in treating
GERD [36]. The LINX® Reflux Management System (Torax
Medical, Shoreview, MN) is a magnetized beaded titanium
band, which is placed laparoscopically around the
­gastroesophageal junction to control symptoms of reflux.
Reports of treating GERD with the LINX® device in patients
following bariatric surgery have been reported, with good
outcomes [37, 38]. The LINX® device has been shown to
have low complication or reoperation rates [39]. The most
common reason for removal of these devices is severe dysphagia [39]; additionally isolated cases of the magnetic
beads eroding into the esophagus have been reported in the
literature [40, 41]. The LINX® device may play a larger role
in treating bariatric patients with GERD in the future. The
general surgeon should be aware of this novel technology
and its potential risks and benefits.
Intragastric balloons (IGB) are inflatable medical devices
that are temporarily placed into the stomach to reduce weight.
There are currently three devices that are approved by the
FDA, the Orbera® (Apollo Endosurgery, Austin, TX), the
ReShape Duo® (ReShape Medical, San Clemenete, CA), and
the Obalon® (Obalon Therapeutics, Carlsbad, CA) [42].
Although uncommon, intragastric balloons can cause gastric
outlet obstruction or can deflate and migrate causing distal
small bowel obstruction. Gastric outlet obstructions can be
treated with gastric decompression and endoscopic removal.
Less than 1% of deflated balloons require surgical removal as
most balloons will pass spontaneously from the rectum [43].
Conclusion
Patients who have undergone bariatric surgery clearly present special concerns with regard to postoperative bowel
obstruction. However, it is important to remember that bariatric patients are also general surgical patients and can suffer bowel obstruction from traditional sources such as
Question Section
1. A patient presents to the emergency room 6 weeks after
gastric bypass surgery. Although she was initially eating
soft solid food without difficulty, she recently developed
food intolerance that progressed to liquid intolerance as
well. The most likely cause is:
A. Obstruction from adhesions
B. Internal hernia
C. Intussusception
D. Gastrojejunal stricture
2. A patient presents to the emergency room 2 years after
Roux-en-Y gastric bypass complaining of severe unrelenting epigastric pain radiating to the back. The abdomen is only mildly tender on examination. Ultrasound
and CT of the abdomen are unrevealing. The pain does
not abate. The most appropriate next step is:
E. Upper gastrointestinal series with small bowel
follow-through
F. HIDA scan
G. Pain service consultation
H. Surgical exploration
3. A patient with a history of adjustable gastric band placement 4 years ago presents with new-onset severe vomiting. A plain film shows the band to be vertically oriented.
The best first step in managing this patient is:
A. Withdraw all saline from the band
B. Place a nasogastric tube
C. Upper endoscopy
D. Immediate surgical exploration
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19
Postoperative Bleeding in the Bariatric
Surgery Patient
Federico J. Serrot, Samuel Szomstein,
and Raul J. Rosenthal
Chapter Objectives
1. Classification of bleeding, etiologies, diagnosis,
and management of bleeding in bariatric surgery
patients.
Introduction
Bleeding is an uncommon complication in bariatric surgery.
The reported incidence ranges between 0% and 4.4% and
varies according to the different procedures performed [1–4]
(gastric bypass (GBP), gastric banding, sleeve gastrectomy,
and biliopancreatic diversion with duodenal switch).
Bleeding after bariatric surgery can be classified based on
time of onset (acute, early, late, and chronic) and based on
bleeding site (intra-abdominal [IA] and intraluminal [IL]).
The incidence of bleeding has decreased steadily due to
the development of hemostatic agents (i.e., fibrin glue) and
the use of staple-line reinforcement products, sophisticated
stapling devices and energy sources, and the overall improvement of laparoscopic techniques. However, despite these
advancements, bleeding remains a known complication that
can be difficult to diagnose and manage in the bariatric surgery population. Failure to diagnose and manage bleeding in
a timely manner can result in a significantly prolonged hospital stay and increased morbidity and mortality.
F. J. Serrot
Section of Minimally Invasive Surgery,
Department of General Surgery, The Bariatric and Metabolic
Institute Cleveland Clinic Florida, Weston, FL, USA
S. Szomstein (*) · R. J. Rosenthal
Department of General Surgery, The Bariatric and Metabolic
Institute Cleveland Clinic Florida, Weston, FL, USA
e-mail: szomsts@ccf.org
Definition/Causes
Bleeding, or hemorrhage, can be defined as the presence of
hematemesis or melena and persistent large bloody output
from a surgical drain, with or without the presence of tachycardia, hypotension, oliguria, and a decreasing hemoglobin
and hematocrit [1]. Postoperative bleeding can be classified
based on bleeding site into intraluminal bleeding (ILB, or
into the gastrointestinal tract) or intra-abdominal bleeding
(IAB, or into the abdominal cavity). ILB can occur anywhere
in the gastrointestinal tract and can be classified based on
time of onset into acute (1–7 days), early (1–6 weeks), late
(6–12 weeks), and chronic (more than 12 weeks) (Table 19.1).
Whereas IAB occurs mainly in the acute postoperative
period and is near trocar sites, vascular pedicles, and/or staple lines, ILB can occur at any time and varies in etiologies
from surgical reasons to medical reasons (peptic ulcer disease) or neoplastic (tumors) [5–7].
Acute or early postoperative bleeding usually occurs
within the first 12–48 h after a surgical procedure but can
still manifest as late as 42 days [5, 6]. In gastric sleeve
patients, bleeding is mainly related to the long staple line,
short gastric vessel pedicles, or trocar sites. In gastric bypass
(GBP) patients, bleeding is usually related to an anastomotic
or staple-line bleed as well as a stress ulcer or gastritis. The
bleeding can be either IL or IA. Other potential causes of
IAB in the acute phase can be related as mentioned to trocar
sites, surgical dissection sites, or incomplete hemostasis of
surgical sites prior to disinflation of the abdominal cavity.
Late and chronic bleeding will usually present more than
42 days after the procedure, and it is mostly related to marginal ulceration, gastritis, or neoplasm. It can occur after any
bariatric procedure but is most commonly seen with GBP
Table 19.1 Postoperative bleeding classification based on time of
onset
Acute
1–7 days
Early
1–6 weeks
Late
6–12 weeks
© Springer Nature Switzerland AG 2020
N. T. Nguyen et al. (eds.), The ASMBS Textbook of Bariatric Surgery, https://doi.org/10.1007/978-3-030-27021-6_19
Chronic
>12 weeks
217
218
F. J. Serrot et al.
patients due to the ulcerogenic nature of the gastrojejunal
anastomosis. These ulcers can be seen anywhere at the gastrojejunostomy, in the excluded gastric remnant and duodenum.
The etiologies of these ulcers are multifactorial, including
local ischemia due to poor blood supply, anastomotic tension,
the use of nonabsorbable sutures, increased gastric acidity,
Helicobacter pylori infection, tobacco use, and nonsteroidal
anti-inflammatory drug (NSAID) therapy [6, 7].
Chronic bleeding in the sleeve gastrectomy (SG) patient is
uncommon but can be related to ulcers that can develop but
are not as prevalent as in the GBP patient. Cases of chronic
bleeding in gastric band (GB) patients have been reported in
cases of band erosion, where patients can present with melena
or hematemesis. Neoplasms that were not detected preoperatively or arise de novo after the bariatric procedure should be
also kept in mind when a patient p­ resents with new onset of
signs or symptoms of bleeding [8–11].
plications and tends to increase gradually and be cyclical in
bariatric surgery patients with postoperative hemorrhage.
This cyclical behavior of tachycardia in bleeding episodes
differentiates from the septic pattern that ensues in patients
with anastomotic leaks where tachycardia stays up and above
120 beats per minute without a cyclical pattern [7] (Fig. 19.1).
In the acute setting, one of the biggest challenges is differentiating between IL and IA bleeding, as this will guide
further decision-making. Clinical presentation can be helpful
when symptoms are typical of IL bleeding like melena and
hematemesis. When the symptoms are not present, the use of
surgical drains in the immediate postoperative period can
guide the surgeon to the appropriate diagnosis as mentioned
by Chousleb et al. [2]. If the drains are filling up with bright
red blood, it is safe to assume the bleeding is IA.
IL bleeding is more commonly seen after laparoscopic
Roux-en-Y gastric bypass (LRYGB) due to the many staple
lines that are present (gastrojejunostomy, jejunojejunostomy,
and gastric remnant) (Fig. 19.2). Heneghan et al. described
that 40% of staple-line bleeds are from the gastric remnant,
30% from the gastrojejunostomy, and 30% from the jejunojejunostomy [12]. Nguyen et al. demonstrated that the most
common site of bleeding is at the gastrojejunostomy [6].
Aside from clinical signs, important diagnostic modalities
are upper endoscopy and computed tomography (CT). The
latter is only an option when patients are clinically and
hemodynamically stable. A CT scan can demonstrate collections/hematomas if bleeding is IA and sometimes show fluid
in the gastric remnant, which is a sign of IL bleeding. CT
scan with intravenous contrast can also potentially show,
though rare, if there is active bleeding with the presence of a
Diagnostic Algorithm
Acute and Early Bleeding
Diagnosis of hemorrhage in the acute postoperative period,
the first 48 h, is a challenging task. The bariatric population’s
body habitus and the new anatomy result in difficult clinical
decision-making. Some of the common signs of acute bleeding are increased bloody output if drains are left behind at the
time of the primary procedure, abdominal distension, and/or
tachycardia, hypotension, and oliguria. Tachycardia has been
shown to be a very important indicator of postoperative com-
Heart Rate (bpm)
a
Tachycardia Pattern in Leak after LRYGB
140
120
100
80
60
40
20
0
0
20
40
60
80
100
120
140
160
140
160
Time elapsed after surgery (h)
b
Heart Rate (bpm)
Fig. 19.1 Patterns of
tachycardia after (a) leak is
sustained >120 bpm, (b)
bleeding is cyclical LRYGB
laparoscopic Roux-en-Y
gastric bypass
Tachycardia Pattern in Bleeding after LRYGB
140
120
100
80
60
40
20
0
0
20
40
60
80
100
Time elapsed after surgery (h)
120
19
Postoperative Bleeding in the Bariatric Surgery Patient
219
biliopancreatic limb. A laparoscopic utility gastrotomy can
also be performed to gain access to and evaluate the gastric
remnant with an endoscope when a double-balloon endoscopy is not possible. If all of the above are negative, new
modalities such as capsule endoscopy to identify unusual
small bowel pathology can be helpful [20–22].
Treatment Strategies
Acute and Early
Fig. 19.2 Potential sites for bleeding after gastric bypass and sleeve
gastrectomy
blush/active extravasation. Upper endoscopy is a very useful
diagnostic modality since an intervention can be done without delay at the bedside with the patient in the intensive care
unit (ICU) to stop the bleeding. Endoscopy should be performed with caution in the immediate postoperative period
to avoid disruption of the anastomosis [13–16].
A negative esophagogastroduodenoscopy (EGD) should
prompt the surgeon about a possible bleeding site from the
jejunojejunostomy or gastric remnant.
Late and Chronic Bleeding
Chronic postoperative bleeding (>30 days) is mostly IL and
often presents with clinical signs of upper gastrointestinal
bleeding. Upper endoscopy tends to be the diagnostic method
of choice [17–19]. Double-balloon enteroscopy can be performed to assess the excluded stomach and duodenum that
can be the site of an ulcer or neoplasm. This tends to be a
tedious procedure for gastroenterologists because it is easy
to get lost in the anatomy and difficult to access the excluded
Treatment of acute postoperative hemorrhage begins with the
clinical assessment. It is important to make sure that the patient
is hemodynamically stable. When bleeding is suspected, the
patient should be placed in a monitored unit. A Foley catheter
should be in place to assure adequate fluid resuscitation, and
type and screen and serial blood hemoglobin/hematocrit
should be obtained to determine the trend of blood loss and the
need for possible blood transfusion. If the patient is clinically
stable, further tests such as EGD can be performed, but if there
is hemodynamic instability that is not responding to resuscitation, immediate surgical intervention might be required. The
majority (>80%) of acute postoperative bleeding will resolve
with conservative management, without the need for another
procedure or reoperation [6, 13, 14].
It is very important to differentiate IL bleeding from IA
bleeding in the immediate postoperative period. IA bleeding
rarely requires a reoperation; the incidence of bleeding has
dramatically decreased recently with wide use of staple-line
reinforcement during bariatric procedures and with the
advancement of hemostatic dissection devices (ultrasonic
scalpel/bipolar vessel sealant). In the event that the bleeding
does not stop and reoperation is warranted, diagnostic laparoscopy is an excellent option. If during the exploration no
obvious source of bleeding is identified, all staple lines
should be carefully examined and oversewn if considered
appropriate [1].
If IL bleeding is diagnosed, conservative management
remains an acceptable option; however, if the patient fails
conservative management or is unstable, an invasive
approach is the next step. Upper endoscopy is not only an
excellent diagnostic modality but also a good treatment
option in patients with acute IL postoperative bleeding. An
endoscope can be used to treat bleeding in the gastric pouch
of GBP patients and, with the aid of a laparoscopic gastrotomy, has access to the excluded small bowel/stomach.
Endoscopic treatment options range from heat to injections
to hemostatic clips. In the acute setting, the use of a heat
source to stop bleeding is not recommended due to potential
disruption of a fresh anastomosis; if possible, clips should be
used. Many experts recommend that all endoscopic interventions should be done under laparoscopic observation to mon-
220
F. J. Serrot et al.
Fig. 19.3 Algorithm for
diagnosis/treatment of acute/
early bleeding. EGD
esophagogastroduodenoscopy,
Dx and Tx diagnosis and
treatment
ACUTE/EARLY
BLEEDING
Intra-abdominal
Intraluminal
Stable
EGD (Dx and Tx)
Drain Output
Clinical
Judgement
Unstable
Laparoscopy/
Laparotomy w/wo
Intraoperative
EGD
NEGATIVE
Stable
Observation
Unstable
Laparoscopy/
Laparotomy
Gastrotomy and
Endoscopy
itor for perforation [15]. If bleeding persists despite
endoscopic management, oversewing of the affected area
will be the definitive option (Fig. 19.3).
Late and Chronic Bleeding
When bleeding occurs 42 days or more after the procedure,
it is most likely IL and presents with signs and symptoms of
an upper or lower gastrointestinal bleed. This bleeding is
more likely seen with GBP than other bariatric procedures.
Since the most likely cause is ulcer disease, medical treatment with proton-pump inhibitors is an acceptable initial
treatment method. If bleeding persists despite medical treatment or if there is hemodynamic instability, endoscopy is the
best treatment option [19].
Upper endoscopy is the treatment method of choice for
bleeding ulcers in the gastric pouch. Rabl et al. reported an
80% success rate at controlling bleeding in the gastric
pouch or the gastrojejunostomy [15]. However, other
reports show a success rate of <70% [16, 17]. Gastric and
duodenal ulceration from the bypassed segment is most
commonly due to marginal ulcer and reported to have a 7%
incidence rate, but other sources of bleed include bile gastritis, helical pylori infection, and gastric cancer [23]. When
the ulcers are present in the gastric remnant or the excluded
duodenum, more advanced endoscopic procedures are
required. Double-­balloon enteroscopy is a good option;
however, the ability to access the biliopancreatic limb and
to treat the bleeding is very operator dependent and does
not have a high success rate. A variability of limb length
among surgeons and adhesions from prior surgeries are
some of the potential reasons for an unsuccessful doubleballoon enteroscopy. Following this, tagged red blood cell
scan should be considered if the diagnosis is still lacking
[24, 25]. A technically easier but more invasive procedure
is a laparoscopic-assisted transgastric endoscopy. Using
this method, the endoscopist is directed directly into the
gastric remnant and has full access to the rest of the
excluded duodenum and small intestine [21, 22, 26].
In patients with uncontrolled bleeding or recurrent ulcer
disease, a surgical intervention is required. The aim of surgery is to treat the problem and to prevent a recurrence. For
this reason, the surgical option of choice for patients with
GBP with recurrent ulcers, uncontrolled ulcer bleeding, or
multiple ulcer locations is an excision of the gastrojejunal
anastomosis with reconstruction of a new gastrojejunal anastomosis or remnant gastrectomy, depending on the site of
bleeding. Angiography and embolization have been described
for upper gastrointestinal bleeding; however, in GBP
patients, if the left gastric artery is embolized, ischemia of
the gastric pouch is likely. For this reason, angiography
should be reserved for only select patients who are not good
surgical candidates [19] (Fig. 19.4).
19
Postoperative Bleeding in the Bariatric Surgery Patient
LATE/CHRONIC
BLEEDING
Intraluminal
POSITIVE
(Marginal ulcer)
Endoscopic Tx
PPIs
EGD
NEGATIVE
(Gastric
remanent/duodenal
ulcer)
Bleeding scan
Angiography
Gastrotomy/EGD
Double balloon
endoscopy
(?Tx at same time)
STABLE
Medical
Treatment
IV PPIs
UNSTABLE
Laparoscopy/
Laparotomy
Embolization
Fig. 19.4 Algorithm for treatment/management of late/chronic bleeding. EGD Endoscopic esophagogastroduodenoscopy; Tx and PPIS
treatment and proton-pump inhibitors
Special Considerations
Staple-Line Reinforcement
221
cantly longer [25]. Another randomized trial from Dapri
et al. concluded that buttressing reduces hemorrhage; however, there was no difference in the incidence of a leak or
other postoperative complications [3].
Albanopoulos and colleagues, however, did not observe a
significant difference in their rate of postoperative bleeding
between patients with staple-line suturing or reinforcing buttressing material after LSG. These investigators had a 6%
and 0% complication rate (bleeding and leak) in their suturing and buttressing material arms, respectively, but this did
not reach significance [29].
Recently, Mohamed et al. compared the use of unidirectional barbed suture material (group A) and no reinforcement
(group B). As shown before operative time was significantly
higher in the suture group. Leak occurred in eight cases
(1.7%) in the no reinforcement group and none (0%) in the
barbed suture; leak was significantly lower in group A
(p = 0.008). Bleeding occurred in two patients (0.4%) in
group A and in seven (1.5%) in group B (p = 0.178), with no
statistically significant difference between both groups [30].
Thromboprophylaxis
Obesity is an important risk factor for the development of
venous thromboembolism (VTE), as well as being an indeStaple-line reinforcement (SLR) has been a popular topic of pendent predictor for recurrent thromboembolic disease.
discussion among experts in bariatric surgery. SLR includes VTE remains a leading cause of mortality after bariatric surbuttressing with absorbable materials such as glycolide and gery. Laparoscopic surgery does induce a postoperative
trimethylene carbonate copolymer, porcine small intestine hypercoagulable state, as does open GBP, but it does so to a
submucosa, or bovine pericardium strips. Recently, reports lesser degree. Incidence of VTE ranges between 0.8% and
have described the use of hemostatic agents like Floseal 3.4%, and super obesity (BMI >60) appears to have a close
(bovine-derived gelatin matrix of human-derived thrombin relationship with incidence of VTE and pulmonary embomixed with other components) with excellent results in lism. Low molecular weight heparin (LMWH) use for
decreasing postoperative bleeding and rates of leaks [25, 26]. thromboprophylaxis in bariatric surgery patients has been
SLR in bariatric surgery was initially described by widely accepted in the USA and worldwide. Severe bleedShikora et al. in 2004, when they reviewed buttressing mate- ing complications are infrequent with LMWH prophylaxis
rial to reduce hemorrhage and leakage following GBP. They and lower than using weight-adjusted heparin doses.
concluded that SLR with bovine pericardial strips may Thromboprophylaxis is safe and advised in bariatric surgery
decrease the risk of acute staple-line failures [27]. The use of patients, and LMWH is favored over the unfractionated hephemostatic agents in GBP patients has also been described arin [31, 32].
by Silecchia et al. to prevent leaks, bleeding, and internal
Recent data compared the use of different VTE prophyherniation [26]. A meta-analysis by Sajid et al. showed that laxis protocols and the effects on bleeding and thrombotic
SLR reduces operative time in GBP patients, anastomotic complications following bariatric surgery. As expected, those
leak, and number of clips needed to control hemorrhage at patients not receiving any VTE prophylaxis had the highest
the staple line. However, SLR did not show superiority in rate of thrombotic complications. Following multivariable
terms of controlling staple-line bleeding [28].
logistic regression, after adjusting for other factors, the risk
Buttressing has gained attention with the increased popu- difference in having transfusion among different regimen
larity of LSG. Gantileschi et al. randomized patients to three groups was significant (p value = 0.02), with patients in the
groups with different SLR: oversewing, buttressing with a post-op prophylaxis and pre-post groups being significantly
polyglycolide acid and trimethylene carbonate, and staple-­ less likely to have transfusion than patients with only preop
line roofing with a gelatin-fibrin matrix. They observed no prophylaxis. When comparing results among patients receivdifferences in complications, but oversewing took signifi- ing heparin vs enoxaparin vs mixed, they noticed that those
222
receiving mixed protocols were more likely to have transfusion than patients having only heparin or enoxaparin (4.07 vs
2.50 vs 0.94%, p value <0.0001) [33].
Patients on Long-Term Oral Anticoagulation
There are more than one million patients in North America
requiring long-term oral anticoagulation due to various medical conditions. Perioperative management of the chronically
anticoagulated patient is challenging in the general
­population. Morbidly obese population poses even a greater
challenge due to multiple associated comorbidities and an
increased risk for a thromboembolic event. Special perioperative considerations for patients receiving chronic anticoagulation therapy should include the original indication for
the treatment, the time period from the last thromboembolic
event, urgency of the surgery, risk of thromboembolism and
hemorrhage, consequences associated with bleeding, and the
duration of postoperative bleeding. Mourelo et al. examined
1700 patients undergoing bariatric surgery with 25 of those
on chronic anticoagulation. Twenty-one patients underwent
LRYGB, with three of those having bleeding complications
but only one requiring a reoperation. They concluded that
bariatric surgery can be safely performed in patients on
chronic anticoagulation therapy [34].
ariatric Surgery in Patients Who Refuse Blood
B
Transfusion
Most bleeding after surgery occurs within the first 24 h after
surgery, and more than half of patients with bleeding required
blood transfusion. This poses a problem in patients who
refuse blood transfusions, with the best-known group being
Jehovah’s Witness patients. Refusal of blood transfusion by
Jehovah’s Witnesses has been associated with increased perioperative mortality after cardiac surgery but has not been
demonstrated after other elective surgeries. Kitahama et al.
found a low-average estimated blood loss and acceptable
perioperative morbidity rates in the bloodless surgery
patients who underwent bariatric surgery within the setting
of a multidisciplinary program. Some techniques to minimize blood loss are laparoscopic surgery, meticulous intraoperative hemostasis, SLR, topical hemostatic agents,
hypotensive anesthesia, and additionally using pediatric
blood collection tubes in the postoperative period. A multidisciplinary approach is very important with investigation
and treatment of preoperative anemia and perioperative
advice regarding blood conservation and the use of blood
substitutes [35].
F. J. Serrot et al.
Conclusion
Postoperative bleeding in the bariatric population is becoming rare with advancements in surgical tools. If bleeding
does occur, expedient diagnosis and management is vital.
Bariatric patients are best treated by bariatric surgeons who
are familiar with the operation and anatomy.
Question Section
1. What is the initial diagnostic modality of choice in a
patient 6 months status post-gastric bypass who presents
with melena and weakness?
A. CT scan
B. MRI with IV contrast
C. Diagnostic laparoscopy
D. Upper endoscopy
2. What is/are the therapeutic options for patient who presents with a bleeding ulcer in the gastric remnant?
A. Observation
B. Double-balloon enteroscopy
C. Laparoscopic-assisted transgastric endoscopy
D. Exploratory laparotomy
E. B and C
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Management of Marginal Ulcers
20
Richard M. Peterson and Jason W. Kempenich
Chapter Objectives
1. To understand the pathophysiology and development of marginal ulcer formation in the setting of
Roux-en-Y (RNY) gastric bypass
2. To understand the implications of marginal ulcer
disease and the prevention and treatment strategies
for this disease
Introduction
The increasing incidence of obesity across the globe has led
to a significant rise in the number of bariatric procedures performed for weight loss [1]. Lapar