Phẫu Thuật Giảm Béo (Bariatric Surgery)

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Nadey S Hakim Franco Favretti Gianni Segato Bruno Dillemans Editors BARIATRIC SURGERY Imperial College Press

Bariatric
Surgery

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Imperial College Press
ICP
Bariatric
Surgery
Editors
Nadey S Hakim
Imperial College Healthcare NHS Trust London, UK
Franco Favretti
Vicenza Regional Hospital, Italy
Gianni Segato
Vicenza Regional Hospital, Italy
Bruno Dillemans
St. Jan Hospital, Bruges, Belgium

British Library Cataloguing-in-Publication Data
A catalogue record for this book is available from the British Library.
Published by
Imperial College Press
57 Shelton Street
Covent Garden
London WC2H 9HE
Distributed by
World Scientific Publishing Co. Pte. Ltd.
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Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, USA. In this case permission to
photocopy is not required from the publisher.
ISBN-13 978-1-84816-588-5
ISBN-10 1-84816-588-9
Typeset by Stallion Press
Email: enquiries@stallionpress.com
All rights reserved. This book, or parts thereof, may not be reproduced in any form or by any means,
electronic or mechanical, including photocopying, recording or any information storage and retrieval
system now known or to be invented, without written permission from the Publisher.
Copyright © 2011 by Imperial College Press
BARIATRIC SURGERY

Contents
Contributors
xi
Foreword
xvii
(by Michael G. Sarr, Mayo Clinic, USA)
Chapter 1
Indications for Bariatric Surgery and Selecting
1
the Appropriate Procedure
John B. Dixon
Indications for Bariatric Surgery
1
References
10
Chapter 2
Anaesthesia in Bariatric Surgery
15
Ernesto Pizzirani and Giuseppe Calcarella
Definitions
15
Epidemiology
16
Pathophysiologic Aspects Connected to Obesity
19
Pharmacologic Considerations
31
Evaluating the Patient Before Anaesthesia
37
General Anaesthesia
47
Loco-Regional Anaesthesia
50
Post-Operative Treatment
51
Conclusions
53
References
53
v

vi
Contents
Chapter 3
Intragastric Balloon (BIB®) in the Management
61
of Morbid Obesity Disease
Alfredo Genco, Roberta Maselli and Nicola Basso
Introduction
61
Results
71
Discussion and Conclusion
84
References
86
Chapter 4
Laparoscopic Adjustable Gastric Banding
91
Gianni Segato, Nadey Hakim, Maurizio De Luca
and Franco Favretti
Introduction
91
Indications and Contraindications
91
Preparation for Surgery
93
Surgical Instruments
93
Patient and Surgical Team Positioning
94
Procedural Steps
94
References
102
Suggested Reading
103
Chapter 5
Long-Term Results in Laparoscopic Adjustable
105
Gastric Banding (LAP-BAND®) for Obese Patients
Maurizio De Luca, Luca Busetto, Gianni Segato,
Nadey S. Hakim and Franco Favretti
Introduction
105
Laparoscopic Technique
106
Role of the Balloon
109
Lap-Band® Series at Vicenza Regional
110
Hospital, Padua
Discussion
118
Life Expectancy Study
120
Conclusion
121
References
122

Chapter 6
Laparoscopic Adjustable Gastric Banding
125
(LAP-BAND®): Diagnosis, Prevention
and Treatment of Complications
Maurizio De Luca, Luca Busetto, Gianni Segato,
Nadey S. Hakim and Franco Favretti
Introduction
125
Lap-Band® Series at Vicenza Regional
126
Hospital, Padua
Complications
127
Conclusions
151
References
152
Chapter 7
Roux-en-Y Gastric Bypass
155
Bruno Dillemans and Sebastiaan Van Cauwenberge
Introduction
155
Physiology of the Roux-en-Y Gastric Bypass
156
Preoperative Evaluation
159
Medical Evaluation
160
Psychological Evaluation
160
Technical Aspects of the Laparoscopic RYGB
161
Procedure
Operative Technique of the Fully Stapled
164
Laparoscopic Roux-en-Y Gastric Bypass
Complications of Roux-en-Y Gastric Bypass
171
Side Effects of Roux-en-Y Gastric Bypass
179
Weight Evolution After RYGB
183
Conclusion
188
Acknowledgements
188
References
188
Chapter 8
New Technologies in Bariatric Surgery
199
Matthias Lannoo and Andre D’Hoore
Introduction
199
Contents
vii

Sleeve Gastrectomy
199
New Minimally Invasive Techniques in Bariatric
214
Surgery
References
217
Chapter 9
Imaging of Complications After Bariatric Surgery 223
Jose C. Varghese and Shuvro H. Roy-Choudhury
Introduction
223
Laparoscopic Adjustable Gastric Banding
224
Roux-en-Y Gastric Bypass (RYGB)
245
Summary
273
References
275
Chapter 10
Sequential Treatment of Obesity
285
Maurizio De Luca, Luca Busetto, Gianni Segato
and Franco Favretti
Introduction
285
Classification of Bariatric Operation
286
Effectiveness/Invasiveness of Various Operations
286
Undertreatment and Overtreatment
287
Surgical Treatment of Obesity
290
Conclusions
291
References
292
Chapter 11
Bariatric Surgery: When the Miracle is Not
293
Enough
Melodie K. Moorehead
Introduction
293
Bariatric Surgery is a Behavioural Surgery Too
296
A Holistic Approach to Bariatric Surgery: Recovery
302
Managed by Healthcare Specialists
Establishing a Three-Stage Psychoeducational
305
Recovery Programme
The Initial Psychoeducational Interview
311
What is the Value of Speaking the Same Language
317
in Outcomes?
viii
Contents

Discussion
320
Acknowledgements
322
References
323
Suggested Reading
324
Chapter 12
Effects of Bariatric Surgery on Co-Morbidities
327
Sebastiaan Van Cauwenberge and Bruno Dillemans
Introduction
327
Hypertension
327
Obstructive Sleep Apnoea
331
Dyslipidemia
334
Type 2 Diabetes
337
Other Co-Morbidities
343
Quality of Life After Bariatric Surgery
346
References
348
Chapter 13
Impact on Life Expectancy After Bariatric
359
Surgery
Luca Busetto, Elisa Calo’, Marco Mazza and
Giuliano Enzi
Introduction
359
Impact of Morbid Obesity on Morbidity and
360
Mortality
Effects of Bariatric Surgery on Metabolic
361
Co-Morbidities
Effects of Bariatric Surgery on Respiratory
371
Disturbances
Impact of Bariatric Surgery on Health Related
377
Quality of Life
Impact of Bariatric Surgery on Life Expectancy
378
Conclusion
383
References
383
Index
389
Contents
ix

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xi
Contributors
Nicola Basso
Department of Surgery
La Sapienza University
Policlinico Umberto I
Viale Regina Elena 324
00185 Rome, Italy
Luca Busetto
Department of Medical and Surgical Sciences
University of Padova
Via Giustiniani, 2
32128 Padova, Italy
E-mail: luca.busetto@unipd.it
Giuseppe Calcarella
Anaesthesiology Department
Camposampiero Hospital
Via P. Cosma, 1
35012 Camposampiero, Padova, Italy
E-mail: gcalcarella@ulss15.pd.it

Elisa Calo’
Department of Medical and Surgical Sciences
University of Pad
Via Giustiniani, 2
32128 Padova, Italy
E-mail: elisa1002@libero.it
Maurizio De Luca
Department of Surgery
Vicenza Hospital
Via F. Rodolfi, 37
36100 Vicenza, Italy
E-mail: nnwdel@tin.it
Andre D’Hoore
Department of Abdominal Surgery
Hospital UZ Leuven
Gasthuisberg Campus
Herestraat 49, Leuven, Belgium
E-mail: andre.dhoore@uzleuven.be
Bruno Dillemans
Department of General Surgery
Hospital AZ St.-Jan AV
Ruddershove, 10
B-8000 Brugge, Belgium
E-mail: bruno.dillemans@azbrugge.be
John B. Dixon
Head of Obesity Research Unit
Department of Surgery
Monash University
Victoria 3800, Australia
E-mail: john.dixon@med.monash.edu.au
xii
Contributors

Guiliano Enzi
Department of Medical and Surgical Sciences
University of Padova
Via Giustiniani, 2
32128 Padova, Italy
E-mail: giuliano.enzi@unipd.it
Franco Favretti
Director
Department of Surgery
Vicenza Hospital
Via F. Rodolfi, 37
36100 Vicenza, Italy
E-mail: ffavret@tin.it
Michael G. Sarr
Department of Surgery
Mayo Clinically
200 First Street S.W.
US-Rochester, MN 55905, USA
E-mail: sarr.michael@mayo.edu
Alfredo Genco
Department of Surgery
La Sapienza University
Policlinico Umberto I
Viale Regina Elena 324
00185 Rome, Italy
E-mail: alfredo.genco@uniroma1.it
Nadey S. Hakim
Max Thorek Professor of Surgery
Fellow of the American Society of Bariatric and Metabolic Surgery
Lead Bariatric Surgeon Highgate Hospital London
Surgical Director, West London Transplant Unit
Imperial College Healthcare NHS Trust
Du Cane Road
London W12 0HS, UK
E-mail: nadey@globalnet.co.uk
Contributors
xiii

Matthias Lannoo
Department of Abdominal Surgery
Hospital UZ Leuven
Gasthuisberg Campus
Herestraat 49, Leuven, Belgium
E-mail: matthias.lannoo@uzleuven.be
Roberta Maselli
Department of Surgery
La Sapienza University
Policlinico Umberto I
Viale Regina Elena 324
00185 Rome, Italy
Marco Mazza
Department of Medical and Surgical Sciences
University of Padova
Via Giustiniani, 2
32128 Padova, Italy
E-mail: marco_mazza78@yahoo.it
Melodie K. Moorehead, Ph.D., ABPP
Honorary Member Psychologist
Board Certified by the American Board of Professional
Psychology in Clinical Health Psychology
1201 Broward Blvd.
Ft. Lauderdale, FL 33301, USA
E-mail: psydrmm@aol.com
Ernesto Pizzirani
Director of Anaesthesiology
Anaesthesiology Department
Camposampiero Hospital
Via P. Cosma, 1
35012 Camposampiero, Padova, Italy
E-mail: epizzirani@ulss15.pd.it
xiv
Contributors

Shuvro H. Roy-Choudhury
Consultant Radiologist
Heart of England NHS Trust
Department of Radiology
Spire Parkway Hospital
1 Damson Parkway
Solihull B91 2PP, UK
E-mail: shuvro.roy-choudhury@heartofengland.nhs.uk
Gianni Segato
Department of Surgery
Vicenza Hospital
Via F. Rodolfi, 37
36100 Vicenza, Italy
E-mail: gsegat@tin.it
Sebastiaan Van Cauwenberge
Department of General Surgery
Hospital AZ St.-Jan AV
Ruddershove, 10
B-8000 Brugge, Belgium
E-mail: sebastiaan.vancauwenberge@azbrugge.be
Jose C. Varghese
Department of Radiology
Boston University Medical Center
88 East Newton Street, 2nd Floor
Boston, MA 02118, USA
E-mail: jose.varghese@bmc.org
Contributors
xv

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xvii
Foreword
With the worldwide epidemic of obesity seemingly just around the corner,
bariatric surgery has exploded onto the surgery scene, having now become
a truly household word. This book, edited by Professor Nadey S. Hakim
and colleagues, should serve as a very readable, practical text for a wide
range of staff, right from the huge number of medical support staff within
a bariatric centre, to the bariatric surgeon, the anaesthesiologist, the baria-
trician, and, most importantly, for the general surgeon who is NOT a
bariatric surgeon! This latter focus on the non-bariatric general surgeon
is becoming a topic of both extreme interest and deep concern to many
general surgeons, as well as Emergency Room physicians.
Currently, bariatric surgery represents the most common gastric oper-
ation in the Western world, since the operative treatment for Peptic Ulcer
Disease has all but disappeared. And, with our increasingly mobile popu-
lation, the ever-increasing number of a spectrum of operations (which are
so well reviewed in this book!), and the growth of medical tourism due to
first-world costs of bariatric surgery, all physicians, as well as non-
bariatric general surgeons, will be exposed on an increasing basis to
patients who have undergone surgery. Thus, the education of all physi-
cians who do not have a bariatric practice is vital. This book will do just
that — the readability, focus, emphasis, and clinically-oriented approach
have been consciously designed to address this topic in a way appealing
to both the bariatric and non-bariatric healthcare provider.
This book addresses most of the practical issues in bariatric surgery.
Separate chapters address patient selection, different bariatric procedures,

including intragastric balloons (this topic is being revisited currently after
its dismal failure 15–20 years ago), the “lap band” or the laparoscopic
adjustable gastric banding (and its complications/success), Roux-en-Y
gastric bypass, and the forms of biliopancreatic diversion. Each procedure
obligates a different set of medical concerns, leads to different mechanical
and/or functional complications, and requires a unique type of follow-up.
The chapter on anaesthetic issues provides a fabulous focus for the
book. These considerations are important, not only for the surgical staff,
but also for the entire team in the operating theatre — and not just for just
bariatric operations but also for other operations performed on the mor-
bidly obese patient.
Finally, the book finishes with the evidence supporting the efficacy of
bariatric surgery from several different aspects — resolution of direct,
weight-related medical co-morbidities, improvements in quality of life,
and even the concept of impact on life expectancy.
As a general and gastrointestinal surgeon for the last 30 years, I have
witnessed (and participated in) the growth, improvements, and finally
general acceptance of bariatric surgery by both the lay public but, also
importantly, by the medical community. In summary, this book accom-
plishes its goals — readability, clinical relevance, and the important topic
of a global view of bariatric surgery. You will enjoy reading every chapter.
Michael G. Sarr, M.D.
James C. Masson Professor of Surgery
Mayo Clinic, USA
xviii
Foreword

Chapter 1
Indications for Bariatric Surgery
and Selecting the Appropriate Procedure
John B. Dixon
Indications for Bariatric Surgery
When is surgery an option for a patient? When should
it be recommended as best care?
In 1991, the National Institutes of Health (NIH) criteria for patient
selection for gastrointestinal surgery for severe obesity were developed at
a consensus conference involving expert surgeons, gastroenterologists,
endocrinologists, psychiatrists, nutritionists and other health care profes-
sionals as well as the public. After weighing the evidence the panel
recommended that:
1.
patients seeking therapy for severe obesity for the first time should be
considered for treatment in a non-surgical programme with integrated
components of a dietary regimen, appropriate exercise and behav-
ioural modification and support;
2.
gastric restrictive or bypass procedures could be considered for well-
informed and motivated patients with acceptable operative risks;
3.
patients who are candidates for surgical procedures should be selected
carefully after evaluation by a multidisciplinary team with medical,
surgical, psychiatric and nutritional expertise;
4.
the operation should be performed by a surgeon substantially experi-
enced with the appropriate procedures and working in a clinical
1

2
J. B. Dixon
setting with adequate support for all aspects of management and
assessment;
5.
lifelong medical surveillance after surgical therapy is a necessity to
monitor for complications and lifestyle adjustments.1
The patient selection criteria recommendations were that surgery is an
option for well-informed and motivated patients who have ‘clinically
severe obesity’ Body Mass Index (BMI) 40, or a BMI 35 and serious
co-morbid conditions.
There were many weaknesses with the NIH approach at the time.
Recommendations came from an expert panel and were not necessarily
evidence-based at the time. The cut-off values of BMI 35 and 40 were
arbitrarily chosen although ‘patient risk’ is clearly a continuous concept
which is based on much more than weight corrected for height and the
presence of a co-morbid condition. Patient selection involves a clinical
assessment of risk versus benefit for the individual patient and while BMI
is one consideration, others include age, ethnicity, weight distribution, a
wide range of obesity related medical and psychological co-morbidities,
and risk factors for future obesity-related morbidity and mortality
An additional concern is the concept of option. The NIH describes a
group of patient characteristics and conditions that are required before
surgery can be considered. This is a far cry from the description of a rec-
ommendation. A recommendation would imply that a caring physician,
after identifying a patient’s specific conditions, recommends that the
patient seek a surgical opinion regarding surgical treatment as best ther-
apy or standard of care. A male aged 25 with BMI 55, severe obstructive
sleep apnoea, type-2 diabetes and steatohepatitis may provide an example
where recommendation for a surgical opinion is appropriate. To withhold
such a recommendation may now be seen as negligent. While it may have
been inappropriate in 1991, current evidence regarding the outcomes of
surgical versus non-surgical therapy indicates a category of patient where
recommendation is now appropriate.
Since 1991 there have also been major advances in our understanding
of the benefits of substantial sustained weight loss which include resolu-
tion or improvement in obesity related co-morbidity,2 improved quality of
life3 and psychological conditions, reductions in disease risk factors, and

evidence that therapy is cost effective4 and saves lives.5,6 We now have
considerably more information to use when making a risk–benefit assess-
ment of a patient.
Thus the NIH term ‘clinically severe obesity’ needs to have plasticity
with an ability to mould to a range of important considerations. It also
needs to be graded to indicate subjects where surgery should be consid-
ered an option and those where a surgical referral and assessment is
recommended as best care.
Why have I focused on the NIH criteria? This is simply because they
are the most quoted and used. Many surgical societies, health service
providers and third party payers around the world have adopted very
similar, or at times more restrictive, eligibility criteria for bariatric
surgery.
Let us consider some of the factors associated with a patient that
should be considered when selecting a patient for a surgical option or
consideration.
Age
Age is an important factor in the risk–benefit analysis. Obesity-related
excess mortality declines with age at all levels of obesity.7,8 In a German
cohort, older men and women aged 50–74 with a BMI range of 25 to less
than 32 had no excess mortality.7 A US analysis of life table and large
health surveys also estimated that years of life lost are significantly
greater in younger subjects.8 The Seven Countries Study found a BMI of
up to 30 kg/m2 was not associated with increased mortality when middle
aged men became older.9 The American Cancer Society’s Cancer
Prevention Study I also found that the relative risk associated with greater
body weight is higher among younger subjects.10 However, obesity at the
age of 40 years is a predictor of a significantly shortened life and has an
effect similar to smoking.11 A Finnish study demonstrated that years of
disability and poor health related to obesity were likely to be greater in
younger subjects.12 Elderly patients presenting for bariatric surgery may
therefore have limited benefit in both years of life and in years of healthy
life gained. Improving shorter term quality of life may be the primary ben-
efit in operating on elderly subjects, but on the other hand older patients
Indications for Bariatric Surgery and Selecting the Appropriate Procedure
3

have a higher mortality associated with bariatric surgery.13,14 These find-
ings have important implications when assessing benefit versus risk in
older obese subjects presenting for treatment, and emphasizes the impor-
tance of treating clinically severe obesity in younger adults.
One may use the information concerning age when considering bariatric
surgery for adolescents where arguably we may achieve greatest benefit
from treating the clinically severely obese. It is in this age group that static
BMI cut-off levels have limited value as there is a moving target.
Normally with growth and development, BMI rises throughout adoles-
cence in both boys and girls.15,16 Using age adjusted BMI z-scores and
obesity related co-morbidity we may, with further careful evaluation, be
able to set guidelines for bariatric surgery in adolescents. Several attempts
have been made to define criteria for the use of bariatric surgery in ado-
lescents,17 but these are flawed by the same lack of sufficient evidence that
confronted the NIH in 1991. Fortunately many carefully designed studies
are currently in progress and in the near future we should have a better
understanding of the relative benefits and risks of intervening early in
adolescents. In the meantime adolescent bariatric surgery should only be
performed by experienced multidisciplinary teams with experience in
managing the issues and nuances of severely obese adolescents, with data
collected to evaluate long term clinical outcomes.17
Ethnicity
Body Mass Index is used as a surrogate for adiposity and as a marker for
risk associated with increasing body weight. However there are major eth-
nic differences in both the degree of adiposity and risk of obesity related
diseases at any given body mass index. The World Health Organization
(WHO) consultation has recommended that for those with Asian ethnicity
public health BMI action points may be reduced by 2.0–2.5 kg/m2 to
23.0, 27.5, 32.5 and 37.5 kg/m2. Recognizing the increased adiposity and
co-morbidity risk, the WHO and International Obesity Task Force have
also recognized an increased risk of type-2 diabetes at lower BMI levels
in Asian populations18 and the International Diabetes Federation has used
ethnic specific waist circumferences for men and women when defining
the metabolic syndrome.19,20 Ethnic differences in adiposity and disease
4
J. B. Dixon

risk should be considered in determining indications for bariatric surgery.
It is not acceptable to use cut-off values based on the white population for
those of higher risk ethnicity.
Co-morbidity
As already stated there should be graded levels of indications for bariatric
surgery: a level where a patient is eligible for surgery and another where
it is recommended as best care for the patient’s condition (Fig. 1).
On what basis can we assess co-morbidity as an indication or a rec-
ommendation for surgery? It would seem logical that a number of criteria
could be examined for any particular co-morbidity:
•
What is the strength of the relationship between the co-morbidity and
obesity?
•
How serious is the co-morbidity?
•
What is the effectiveness of weight loss for this co-morbidity?
•
How effective is current therapy for the patient’s condition?
Co-morbidities cluster, and patients often present with a range which all
relate to the inflammatory and metabolic consequences of central obesity
such as type-2 diabetes, hypertension, obstructive sleep apnoea, non-
alcoholic steatohepatitis (NASH) and polycystic ovary syndrome. We
Indications for Bariatric Surgery and Selecting the Appropriate Procedure
5
Figure 1.
Indications for surgery.
Surgery may be indicated —
Eligible for surgery
Surgery is indicated — Should be advised
as best care for a patient’s condition

need to recognize that we have far less knowledge about the importance
and severity of psychological co-morbidities and these are rarely seen as
important and pressing indications for bariatric surgery.
Some of the conditions associated with obesity are demonstrated in
Table 1. Those with a relative risk greater than 5 are all strongly related to
obesity. Of these, type-2 diabetes, obstructive sleep apnoea, obesity
hypoventilation syndrome, idiopathic intracranial hypertension and more
advanced forms of NASH may be seen as serious. In the context of
obesity, these have been shown to respond well to substantial sustained
weight loss, but do not respond as well to other therapy.
Bariatric surgery recommended or indicated as ‘best care’
Using the NIH notion that BMI is an important marker of adiposity we
could argue that those with a BMI > 50 or those with a BMI > 40 with one
or more of the serious but responsive co-morbidities should, as best care,
be referred for a bariatric surgical assessment (Table 2). Currently we have
no indications or guidelines that physicians could use for the obligatory
6
J. B. Dixon
Table 1.
Some conditions associated with obesity.
Relative risk > 5
Relative risk 2–5
Relative risk 1–2
Type-2 diabetes
All-cause mortality
Cancer mortality
Dyslipidemia
Hypertension
Breast cancer
Obstructive sleep
Myocardial infarction
Prostate and colon cancer
apnoea
and stroke
in men
Breathlessness
Endometrial carcinoma in
Impaired fertility
women and hepatoma
in men
Excessive daytime
Gallstones and complications,
Obstetric complications,
sleepiness
including cancer
including fetal
abnormalities
Obesity hypoventilation
Polycystic ovary syndrome
Asthma
syndrome
Idiopathic intracranial
Osteoarthritis (knees)
Gastro-oesophageal reflux
hypertension
Nonalcoholic steatohepatitis
Gout
Anaesthetic risk

referral for bariatric surgical assessment as best practice, and health care
providers can use their discretion in providing bariatric surgical services.
Further carefully conducted longitudinal studies of long term outcomes of
patients in these categories are recommended. There would be ethical
concerns about randomized controlled trials for patients with these condi-
tions because it could be seen as negligent not to provide appropriate or
‘best care’. There must be equipoise, a balance of risk and benefit, when
designing and conducting randomized controlled trials.21
Bariatric surgery as an option for therapy
As knowledge about the safety and efficacy of bariatric surgery increases,
there has been a growing interest in its utilization in those with a BMI < 35.
Our Melbourne group has recently reported two randomized controlled tri-
als including subjects in the BMI 30–35 range.22,23 The first showed better
weight loss, health and quality of life outcomes in participants in the BMI
30–35 range for those randomized to laparoscopic adjustable gastric band-
ing (LAGB) surgery when compared to those randomized to an intensive
medical weight loss programme. The second study included participants
with type-2 diabetes in the BMI range 30–40. Subjects were randomized to
LAGB surgery with conventional diabetes therapy or to a best care lifestyle
programme with conventional diabetes therapy. Those randomized to
surgery achieved 73 per cent remission of type-2 diabetes compared to
Indications for Bariatric Surgery and Selecting the Appropriate Procedure
7
Table 2.
The author’s proposed criteria for the two categories.
Surgery an option for therapy*
Surgery is indicated
BMI > 40
BMI > 50
BMI > 35 with a broad range of problems
BMI > 40 with serious weight
related to obesity
loss — responsive co-morbidity**
BMI > 30 with serious weight
loss — responsive co-morbidity
*For ‘at risk’ ethnicity the criteria should be dropped by a BMI of 2–3.
**Serious weight loss responsive co-morbidity could include: type-2 diabetes, obesity hypoventilation
syndrome, severe obstructive sleep apnoea, obesity related raised intracranial pressure and non-
alcoholic steatohepatitis with substantial fibrosis.

only 13 per cent for those on the conventional lifestyle programme when
using an intention to treat analysis. The likelihood of remission was
directly related to the extent of weight loss. Clearly, evidence such as this
provides strong evidence that bariatric surgery is beneficial and may be
indicated in those with a BMI < 35. Further randomized controlled trials
are needed to strengthen this evidence base. Table 2 shows the hypotheti-
cal two-tiered approach to bariatric surgical indications.
Selection of the procedure
Bariatric surgery has evolved as an inexact science. It has advanced
through many dedicated surgeons communicating with one another to
progress an art, and there have been some wonderful achievements.24
Experimental designs have almost all been small series on human
subjects, with surgeons modifying and changing their procedures to
provide greater efficacy and safety, an approach perhaps not unlike the
development of many other surgical therapies.
This must change! Bariatric surgery is now considered a ‘standard of
care’. There are now good data on the efficacy, safety and durability of
specific surgical procedures. Deviation from standard techniques should
be tested, after appropriate ethical approval, in properly designed clinical
trials. If the proposed surgery or technique is a major departure from a
standard of care, animal models should be used.
The current most commonly used procedures are shown below in
Table 3. The proportion of each procedure used varies enormously from
region to region so I have estimated current use based on the 33 interna-
tional societies and countries surveyed in 2002–3.25 Since that survey
there will have been a marked increase in the number of laparoscopic
procedures, a reduction in the proportion of vertical banded and other gas-
troplasties, and an increase in the proportion of laparoscopic adjustable
gastric banding (LAGB) procedures.
While these figures above are hypothetical estimates there is no doubt
the RYGB (Roux-en-Y gastric banding) and LAGB dominate the current
world scene and there are sufficient data regarding safety, efficacy and
durability to justify this trend.
While there are quality data regarding BPD and BPD-DS, the
weight loss efficacy and durability have not been a concern, but safety
8
J. B. Dixon

is problematic as short and long term nutritional concerns abound.26,27
Few surgeons have followed the path of performing these procedures as
primary bariatric surgical procedures. For sleeve gastrectomy (SG) the
efficacy, safety and durability of weight loss remain untested against the
RYGB and LAGB standards as a primary bariatric procedure. It was ini-
tially utilized as a first stage procedure for those at high risk having
BPB-DS, or more recently RYGB, as the definitive procedure.28,29 This
procedure needs further ethical study of a wide range of outcome meas-
ures. The American Society for Metabolic and Bariatric Surgery issued a
statement of caution regarding the use of SG in 2007. The standard of care
provided by RYGB and LAGB means they are the logical choice for
primary bariatric procedures today. I will not address failed or revisional
surgery. The choice of a primary procedure today is between RYGB and
LAGB. There have been a large number of attempts to match the right
patient to the right procedure to ensure great results, but to date these
attempts have largely failed and lack of hard data means they are not
credible.30 The preoperative unpredictability and variability of weight loss
following surgery is problematic. Preoperative BMI, age, co-morbidity,
food choices, eating behaviours, personality testing, quality of life testing,
motivation and many other variables have been tested, and found to
predict a small proportion of weight loss variance.31–33 These preoperative
variables have largely had a common effect on the two candidate procedures
and have not really separated them. Perhaps more relevant is that postop-
erative follow-up and adopted behaviours following surgery are highly
Indications for Bariatric Surgery and Selecting the Appropriate Procedure
9
Table 3.
Commonly used surgical procedures.
Procedure
Global estimate
Roux-en-Y gastric bypass (RYGB) — laparoscopic
40–55%
and open (including variants of long limb gastric
bypass and banded bypass)
Laparoscopic adjustable gastric banding (LAGB)
30–45%
Vertical banded gastroplasty (VBG)
< 5% and falling
Bilio-pancreatic diversion (BPD). (including the
< 5% and steady
duodenal switch variant (BPD-DS)
Sleeve gastrectomy (SG)
Unknown, but gaining
popularity

predictive of outcome variance.34,35 Our difficulties with preoperative pre-
dictability are perhaps largely driven by our lack of knowledge regarding
the actual mechanism of action of bariatric surgery. Just how does surgery
have such a profound effect on energy balance and why is any other cur-
rent therapy so poor in comparison?
One caveat to the comparison of RYGB and LAGB is the very differ-
ent pattern of weight loss. There is rapid weight loss following RYGB and
usually a much steadier loss following LAGB. The difference in mean
weight loss between the procedures is quite substantial with better weight
loss in those treated with RYGB, but at three years and beyond the
percentage of excess weight loss outcomes are comparable.36 One can
argue that more rapid weight loss increases the risk of cholelithiasis, loss
of lean body mass and nutritional deficiencies.
The decision as to which procedure a patient should have comes down
to a range of issues. Clearly the local experience of the surgeon(s)
and multidisciplinary team and their knowledge of the procedures
involved are crucial. Most critical is the availability of excellent long term
follow-up care.
In addition to this peri-operative mortality, the severity of morbidity
and nutritional risk associated with the procedures are important, and
clearly LAGB carries a significant advantage in all of these categories.37
The LAGB procedure is also adjustable and easily reversible providing a
more logical choice of adolescents and those considering a pregnancy in
the future.38,39 It also provides a logical choice for patients at high risk of
mortality with RYGB.14,40 On the other hand while weight loss achieved
with LAGB surgery has a profound effect on the improvement or resolu-
tion of type-2 diabetes, there is growing evidence that in subjects with
diabetes, the diversionary aspects of RYGB have benefit in addition to
that of weight loss.23,41 It may be that this benefit is important to those with
type-2 diabetes who already have significant beta cell dysfunction.
However, the nature and durability of the beta cell stimulatory effects are
yet to be fully determined.
References
1. Hubbard, V.S., Hall, W.H. (1991). Gastrointestinal surgery for severe obesity.
Obes Surg 1(3): 257–265.
10
J. B. Dixon

2. Buchwald, H., Avidor, Y., Braunwald, E. et al. (2004). Bariatric surgery: a
systematic review and meta-analysis. JAMA 292(14): 1724–1737.
3. Dixon, J.B., Dixon, M.E., O’Brien, P.E. (2001). Quality of life after Lap-
Band placement: influence of time, weight loss, and comorbidities. Obes Res
9(11): 713–721.
4. Clegg, A., Colquitt, J., Sidhu, M. et al. (2003). Clinical and cost effectiveness
of surgery for morbid obesity: a systematic review and economic evaluation.
Int J Obes Relat Metab Disord 27(10): 1167–1177.
5. Adams, T.D., Gress, R.E., Smith, S.C. et al. (2007). Long-term mortality
after gastric bypass surgery. N Engl J Med 357(8): 753–761.
6. Sjostrom, L., Narbro, K., Sjostrom, C.D. et al. (2007). Effects of bariatric
surgery on mortality in Swedish obese subjects. N Engl J Med 357(8): 741–752.
7. Bender, R., Jockel, K.H., Trautner, C. et al. (1999). Effect of age on excess
mortality in obesity. JAMA 281(16): 1498–1504.
8. Fontaine, K.R., Redden, D.T., Wang, C. et al. (2003). Years of life lost due
to obesity. JAMA 289(2): 187–193.
9. Visscher, T.L., Seidell, J.C., Menotti, A. et al. (2000). Underweight and over-
weight in relation to mortality among men aged 40–59 and 50–69 years: the
Seven Countries Study. Am J Epidemiol 151(7): 660–666.
10. Stevens, J., Cai, J., Pamuk, E.R. et al. (1998). The effect of age on the asso-
ciation between body-mass index and mortality. N Engl J Med 338(1): 1–7.
11. Peeters, A., Barendregt, J.J., Willekens, F. et al. (2003). Obesity in adulthood
and its consequences for life expectancy: a life-table analysis. Ann Intern
Med 138(1): 24–32.
12. Visscher, T.L., Rissanen, A., Seidell, J.C. et al. (2004). Obesity and unhealthy
life-years in adult Finns: an empirical approach. Arch Intern Med 164(13):
1413–1420.
13. Murr, M.M., Martin, T., Haines, K. et al. (2007). A state-wide review of con-
temporary outcomes of gastric bypass in Florida: does provider volume
impact outcomes? Ann Surg 245(5): 699–706.
14. DeMaria, E.J., Murr, M., Byrne, T.K. et al. (2007). Validation of the obesity
surgery mortality risk score in a multicenter study proves it stratifies mortal-
ity risk in patients undergoing gastric bypass for morbid obesity. Ann Surg
246(4): 578–582; discussion 583–574.
15. Cole, T.J., Bellizzi, M.C., Flegal, K.M. et al. (2000). Establishing a standard
definition for child overweight and obesity worldwide: international survey.
BMJ 20(7244): 1240–1243.
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16. Flegal, K.M., Ogden, C.L., Wei, R. et al. (2001). Prevalence of overweight in
US children: comparison of US growth charts from the Centers for Disease
Control and Prevention with other reference values for body mass index. Am
J Clin Nutr 73(6): 1086–1093.
17. Inge, T.H., Krebs, N.F., Garcia, V.F. et al. (2004). Bariatric surgery for
severely overweight adolescents: concerns and recommendations. Pediatrics
114(1): 217–223.
18. Misra, A., Wasir, J.S., Vikram, N.K. (2005). Waist circumference criteria for
the diagnosis of abdominal obesity are not applicable uniformly to all popu-
lations and ethnic groups. Nutrition 21(9): 969–976.
19. Ford, E.S. (2005). Prevalence of the metabolic syndrome defined by the
International Diabetes Federation among adults in the U.S. Diabetes Care
28(11): 2745–2749.
20. WHO Expert Consultation (2004). Appropriate body-mass index for Asian
populations and its implications for policy and intervention strategies.
Lancet 363(9403): 157–163.
21. Lilford, R.J. (2003). Ethics of clinical trials from a bayesian and decision
analytic perspective: whose equipoise is it anyway? BMJ 326(7396): 980–981.
22. O’Brien, P.E., Dixon, J.B., Laurie, C. et al. (2006). Treatment of mild to mod-
erate obesity with laparoscopic adjustable gastric banding or an intensive
medical program: a randomized trial. Ann Intern Med 144(9): 625–633.
23. Dixon, J.B., O’Brien, P.E., Playfair, J. et al. (2008). Adjustable gastric banding
and conventional therapy for type 2 diabetes: a randomized controlled trial.
JAMA 299(3): 316–323.
24. Buchwald, H., Buchwald, J.N. (2002). Evolution of operative procedures for
the management of morbid obesity 1950–2000. Obes Surg 12(5): 705–717.
25. Buchwald, H., Williams, S.E. (2004). Bariatric surgery worldwide 2003.
Obes Surg 14(9): 1157–1164.
26. Newbury, L., Dolan, K., Hatzifotis, M. et al. (2003). Calcium and vitamin D
depletion and elevated parathyroid hormone following biliopancreatic diver-
sion. Obes Surg 13(6): 893–895.
27. Papadia, F.S., Adami, G.F., Marinari, G.M. et al. (2007). Bariatric surgery in
adolescents: a long-term follow-up study. Surg Obes Relat Dis 3(4): 465–468.
28. Ren, C.J., Patterson, E., Gagner, M. (2000). Early results of laparoscopic
biliopancreatic diversion with duodenal switch: a case series of 40 consecu-
tive patients. Obes Surg 10(6): 514–523.
12
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29. Regan, J.P., Inabnet, W.B., Gagner, M. et al. (2003). Early experience with
two-stage laparoscopic Roux-en-Y gastric bypass as an alternative in the
super-super obese patient. Obes Surg 13(6): 861–864.
30. Buchwald, H. (2002) A bariatric surgery algorithm. Obes Surg 12(6):
733–746; discussion 747–750.
31. Dixon, J.B., Dixon, M.E., O’Brien, P.E. (2001). Pre-operative predictors of
weight loss at 1-year after Lap-Band surgery. Obes Surg 11(2): 200–207.
32. Lanyon, R.I., Maxwell, B.M. (2007). Predictors of outcome after gastric
bypass surgery. Obes Surg 17(3): 321–328.
33. van Hout, G.C., Verschure, S.K., van Heck, G.L. (2005). Psychosocial pre-
dictors of success following bariatric surgery. Obes Surg 15(4): 552–560.
34. Colles, S.L., Dixon, J.B., O’Brien, P.E. (2008). Grazing and loss of control
related to eating: two high-risk factors following bariatric surgery. Obesity
(Silver Spring) 16(3): 615–622.
35. Colles, S.L., Dixon, J.B., O’Brien, P.E. (2008). Hunger control and regular
physical activity facilitate weight loss after laparoscopic adjustable gastric
banding. Obes Surg 18(7): 833–840.
36. O’Brien, P.E., McPhail, T., Chaston, T.B. et al. (2006). Systematic review
of medium-term weight loss after bariatric operations. Obes Surg 16(8):
1032–1040.
37. Chapman, A., Kiroff, G., Game, P. et al. (2004). Laparoscopic adjustable
gastric banding in the treatment of obesity: a systematic review. Surgery
135: 326–351.
38. Dixon, J.B., Dixon, M.E., O’Brien, PE. (2005). Birth outcomes in obese
women after laparoscopic adjustable gastric banding. Obstet Gynecol
106(5): 965–972.
39. Fielding, G.A., Duncombe, J.E. (2005). Laparoscopic adjustable gastric
banding in severely obese adolescents. Surg Obes Relat Dis 1(4): 399–405;
discussion 405–397.
40. DeMaria, E.J., Portenier, D., Wolfe, L. (2007). Obesity surgery mortality risk
score: proposal for a clinically useful score to predict mortality risk in
patients undergoing gastric bypass. Surg Obes Relat Dis 3(2): 134–140.
41. Rubino, F., Gagner, M. Gentileschi, P. et al. (2004). The early effect of the
Roux-en-Y gastric bypass on hormones involved in body weight regulation
and glucose metabolism. Ann Surg 240(2): 236–242.
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Chapter 2
Anaesthesia in Bariatric Surgery
Ernesto Pizzirani and Giuseppe Calcarella
Definitions
On accessing the Medline data-bank, you find the following definition for
‘morbid obesity’: ‘the condition of weighing two, three, or more times the
ideal weight, so called because it is associated with many serious and life-
threatening disorders’.
This very concise sentence emphasises some aspects which concern
the anaesthetist:
•
the enormous (pathological) increase in the body mass, to which we
attribute the difficulty in performing manoeuvres which are generally
simple if related to patients whose weight is close to the ideal;
•
the danger due to serious pathophysiologic alterations associated with
obesity, that affect the anaesthesiological and intensive care treatment
of the obese person; and
•
the reference to the ideal weight that compels us to pay attention to
the use of drugs in anaesthesia.
Obesity concerns a state of diversity referred to individuals in which, the
accumulation of adipose tissue has so increased that both mental and
physical health are compromised. The subject’s life expectancy is
reduced, and it is convenient to divide these individuals into grades or
classes according to the severity of the state.
15

16
E. Pizzirani and G. Calcarella
It is useful to underline that in the literature we constantly quote the
ideal weight, known by the acronym IBW (Ideal Body Weight), a term
coined in 1835 by the Belgian statistician Quetelet. Its value is calculated
on the basis of tables worded by insurance companies (for instance the
Metropolitan Life Insurance Company) that consider parameters such as
height, physical constitution, sex and age. They specify the ideal weight
in connection with an estimate of the lower mortality risk relative to the
above mentioned parameters.
Others, more simply, are referred to the so-called Broca Index, which
allows us to calculate the ideal weight (kg) by subtracting from height (in
cm) an x value equal to 100 for adult males and 105 for adult females.
On the other hand, should we calculate the excess of weight, we could
refer to the relative weight, which is the connection between real weight
and actual weight, or to the most common and widespread system, Body
Mass Index (BMI), which represents the numerical ratio between the
weight (expressed in kg) and the height squared (expressed in metres).
The BMI is surely the most used measuring parameter for clinical and
epidemiologic studies and it has been validated by the World Health
Organization and by other acknowledged international institutes. On the
basis of its estimate, we can define an individual as underweight if they
have a BMI < 18.5 and normal if their BMI is between 18.5 and 25.
Overweight is between 25 and 29.9 and covers three obesity classes:
Class I: BMI 30−34.9
Class II: BMI = 35–39.9
Class III: BMI > 40
Subsequently, some specialists in bariatric surgery coined the term ‘super
obese’ for patients whose BMI exceeded 50 and to these patients, accord-
ing to some specialists, we should reserve the so-called Class IV.1
Epidemiology
Once the classification of obesity has been agreed upon, it is easier to
study the relative risks of co-morbidity within a specific population. As a
matter of fact, the risk is estimated as low, moderate, high and very high
according to the passage from the simple overweight to the three obesity

Anaesthesia in Bariatric Surgery
17
Table 2.
Obesity classes and treatment.
Physical
Drug
Class
BMI
activity
treatment
Surgery
I
30–35
1st choice
3rd choice
Not applicable
II
35–40
2nd choice
3rd choice
Not applicable
III
> 40
3rd choice
2nd choice
3rd choice
IV
> 50
3rd choice
1st choice
1st choice
classes, reserving the highest class of risk (IV) for the small sub-
population of the so-called super obese (Table 1).2
The proposed classification is considered more efficacious than other
general indexes. It allows us to avoid approximate terms such as ‘severe’,
‘morbid’ and ‘extreme’ obesity, and it can be used as a rational approach
to the choice of the most appropriate treatment (Table 2).
From the epidemiologic point of view, it is recognized that there is a
rising rate of obesity in the world, and in particular in Europe, with an
increase of 10–20 per cent, and higher peaks in some regions, resulting in
economic fallout. It has been estimated, for example, that in the
Netherlands in 1994 the direct and indirect annual sanitary costs associ-
ated with overweight and obesity corresponded to 4 per cent of the total
sanitary costs.3 The situation is even worse in the United States. In the first
half of the 1990s obesity reached 15 per cent and, according to a later sur-
vey, the figure reached 26 per cent (BMI > 30 kg/m2).4 Together with these
studies highlighting a worrying increase of obesity, a series of other
researches came out confirming that subpopulations with very high BMIs
Table 1.
Relationship between obesity classes and risks of co-morbidity.
Risks of
Number of
Class
BMI (kg/m2)
co-morbidity
fat cells
I
30–35
Low
Normal
II
35–40
Moderate
Normal
III
> 40
High
Normal or increased
IV
> 50
Very high
Increased

were more susceptible to health risks, with high rates of work absenteeism
and higher social costs.5
Obesity in general, and high class obesity in particular, are associated
with a certain number of alterations in organs and systems, reflecting
considerable increases in the mortality rate (Tables 3 and 4).
18
E. Pizzirani and G. Calcarella
Table 3.
Incidence of co-morbidity in obese patients.
Co-morbidity
Incidence (%)
Osteoarthritis
50–65
Hypertension
25–60
Gastro-oesophageal reflux
30–50
Urinary stress incontinence
30–40
Gall-bladder disease
25–45
Depression
20–40
Alteration of lipid metabolism
20–35
↓HDL-cholesterol
20
↑blood cholesterol
35
Diabetes
10–20
Hyperisulinemia/increased insulin resistance
10–20
Asthma
10–20
OSA/OSH
5–40
Heart failure
7–12
Table 4. Relative risk of co-morbidity in the obese.
Co-morbidity
Female (%)
Male (%)
Vascular Disease
Claudicatio
25–100
5
Coronary disease
7–35
15
Myocardial infarction
0.7
5
Stroke
0.7
—
Hypertension
≥155/ 95 mmHg
1.5–5.3
1.8
≥175/ 105 mmHg
1.2–4.2
2.3
Diabetes (glycaemia > 7.1 mmol/L)
8–20
5
Dyspnoea
5.5
4
Low back pain
1.5–2
2
Biliary calculosis
2.5
1

As underlined by Adams and Murphy,6 the contemporaneous
involvement of cardiovascular, respiratory, endocrine and gastroenteric
systems has a substantial impact on mortality and morbidity rates, and in
particular is much more likely to expose obese patients to the possibility
of a sudden death compared with normal subjects. It is also useful to
underline the point that risks are proportional to the duration of obesity,
to the level of obesity, and that they are higher for males than for
females.7
A study published in JAMA in 1999 estimates a figure of about
280,000 adult deaths per year due to obesity in the United States, whereas
in 2002 the European figure was 279,000 (equal to 7.7 per cent of
all deaths), with regional variations ranging from 5.8 per cent (France) to
8.7 per cent (United Kingdom). Of these European deaths, 175,000
occurred in obese subjects and 104,000 in overweight ones. Broken down
it was shown that about 70 per cent of the deaths (195,000) were due to dis-
eases in the cardiovascular group and 20 per cent (53,000) due to cancer.
In conclusion, at least one death in 13 in the EU is attributed to being over-
weight.8
Today we believe that both the distribution and quantity of fat signifi-
cantly contribute to the classification of the obese into two groups
characterized by specific factors of co-morbidity: those mainly associated
with weight (mass), and those associated with an altered metabolism
(Tables 5 and 6).9
Pathophysiologic Aspects Connected to Obesity
Overweight due to a positive caloric balance in consequence of excessive
intake and/or reduced physical activity involves a series of both metabolic
and functional alterations at the level of different systems (respiratory,
cardiovascular, gastroenteric and endocrine).10
Metabolic alterations
The obese patient presents alterations with respect to the metabolism of
carbohydrates, proteins and amino acids and other metabolic alterations
caused by the thyroid and the sympathetic nervous system.
Anaesthesia in Bariatric Surgery
19

The increase in fat within the portal system causes the activation
of hepatic gluconeogenesis and the secretion of lipoproteins at very
low density (VLDL) as well as the reduced clearance of the hepatic
insulin.
The hyperinsulinaemia and increased resistance to insulin, increased
gluconeogenesis and the reduction in the peripheral uptake of glucose are the
cause of the reduced tolerance to glucose and therefore of the development
of non insulin dependent diabetes. Furthermore, the hyperinsulinaemia
20
E. Pizzirani and G. Calcarella
Table 5.
Co-morbidity of the obese associated with weight.
1. Arthropathies
2. Hyperdynamic state with increased intravascular blood volume
Heart failure
Fluid imbalance (oedema)
Prolonged QT tract
Sudden death
3. Increase of renal blood flow (RBF)
4. Respiratory disease
Increase of intrathoracic pressure
Increase of O2 consumption
Hypoventilation
OSA
Sudden death
5. Skin lesions
Intertrigo
Ulceration
6. Increase of intra-abdominal pressure
Pseudotumor cerebri
Hernias
Oesophageal reflux
Eclampsia
Urinary incontinence
Venous stasis
7. Obstetric diseases
Poor fertility or infertility
Increased incidence of Caesarian section
Pre-eclampsia

Anaesthesia in Bariatric Surgery
21
Table 6.
Co-morbidity of the obese associated with an alteration of metabolism.
Sistemic Co-morbidity
1. Neurormonal/behaviour alterations
Dysfunction of hypothalamo-pituitary axis
Stress intolerance
Hypercortisolism
Gonadic trouble
Bulimic behaviour, smoke, alcohol, no physical activity, drugs
2. Due to a positive caloric balance
Glucose intolerance, hyperinsulism, insulin resistance
Diabetes type II
Alterations of lipidis metabolism, ↓HDL-cholesterol, ↑blood cholesterol
Inflammatory markers: free radical, oxidative radical, protein C reactive
3. Atherogenic
Stroke
Myocardial infarction
4. Carcinogenic
Breast, endometrial, prostate
Oesophagus, colon
Bladder, kidney
5. Trombogenic
Increase of viscosity
Increase of fibrinogen
Decrease of ATIII
Increase of plasminogen activator inhibitor (PAI-1)
6. Immunologic
Hypercortisolism
Disfunction of leucocytes
Alterations of cytokine
Organ Correlate Co-morbidity
1. Adipose tissue
Hypertension
Alteration of gonadic steroids
2. Liver
Post-hepatic increase of blood glucose
Steatosis, fibrosis
3. Kidney
Increase of glomerular filtration volume
Microalbuminuria
Sodium reabsorption
4. Pancreas
Beta-cells hypertrophy

which helps the reabsorption of sodium and stimulates the sympathetic tone,
favours the appearance of arterial hypertension.11
The factor inhibiting the activation of the plasminogen, which is lib-
erated by the adipose tissue in large quantities, associated with the
increase in the concentration of the fibrinogen, would explain the ten-
dency to hypercoagulate that is present in the severely obese patient
(Fig. 1).12
Respiratory disorders
The most common dysventilatory syndrome associated with obesity is
Obstructive Sleep Apnoea (OSA) which includes Obstructive Sleep
Hypopnoea (OSH) (Table 7).
22
E. Pizzirani and G. Calcarella
↑ Body Fat Mass
↑ Abdominal
Pressure
Ipercoagulability
↑ FFA
↑ Fibronectin
Venous Stasis
Diabetes/ ↑ Blood Glucose
↑ Viscosity
↑ Fibrinogen
↓ ATIII
↓Physical
Activity
↑ Lipids
↑ PAI-1*
↓ Plasminogen
* PAI-1 = Plasminogen Activator Inhibitor
Figure 1.
Contribution of increased body fat mass to thrombogenesis.

This syndrome is characterized by:
•
frequent episodes of apnoea during sleep with the total interruption of
flux into the airways for more than ten seconds due to an interrupted
inspiratory effort;
•
snoring due to the loss of tone in the three pharyngeal segments (veil-
or naso-pharynx, oropharynx, laryngo- or hypo-pharynx) during the
diaphragmatic contraction in inspiration;
•
alteration of the sleep/wake rhythm, fragmentation of nocturnal sleep
and day-time somnolence that causes disorders of both concentration
and memory;
•
pathophysiological alterations resulting from prolonged periods of
apnoea involving hypoxia, hypercapnea and systemic pulmonary
vasoconstriction.
Description of the obesity is complicated by OSA and OSH which are
characterized by an abnormal accumulation of the adipose tissue in the
pharyngeal tissues and involve the uvula, tonsils, palatine arches,
aryepiglottic plicae and the pharynx side walls.
The increase of fat causes a reduction in the patency of the pharyngeal
cavity, which increases the possibility for collapse of the oropharynx due to
the muscular relaxation of the upper airways that could occur during sleep.
Also, in the obese patient suffering from OSA, the pharyngeal extraluminal
pressure (external to airways) is raised due to the deposit of the adipose
mass in the neck compressing the upper airways from the outside.13
During apnoea, there is a decrease in PaO2, an increase in PaCO2 and
a progressive increase in ventilatory effort which corresponds to the dura-
tion of the apnoea; finally the pressure in the airways becomes negative.
All these phenomena stimulate the ascending reticular system and this
causes the subject to regain consciousness. Regained consciousness
Anaesthesia in Bariatric Surgery
23
Table 7.
Definitions of obstructive sleep apnoea and obstructive sleep hypopnoea.
↓Airway flow
Frequency of
↓SaO2
Fragmentation
Day-time
>10 sec
apnoea (n°/h)
of sleep
somnolence
OSA
100 per cent
> 5
≥4
Yes
Yes
OSH
> 50 per cent
> 15
≥4
Yes
Yes

results in the reinstatement of the muscular tone of the upper airways and
reopening of the same. Everything comes together as ventilation restarts,
hypoxia is corrected and hypercapnea, which was caused by apnoea,
occurs. This sequence of events can occur repeatedly and, if it happens
many times, can cause serious pathophysiologic sequences: hypoxia,
hypercapnea and systemic vasoconstriction. The first, in particular, can
cause secondary polycythaemia involving an increasing risk of ischaemic
cardiopathy and cerebrovascular accidents.
It is very important for the anaesthetist to know the impact of both the
anaesthetic drugs and sedatives on the patency of airways of the obese
suffering from OSA. It is essential to highlight the effect of these drugs on
the tone of the pharyngeal muscles that lead to a pharyngeal collapse in a
situation already altered by the adipose pharyngeal deposits. Among the
most common drugs causing these deleterious effects are thiopental, ben-
zodiazepine, propofol and nitrous oxide. Drugs containing opium, in
particular, are characterized by the fact that they lead to a decreased ven-
tilatory response which in turn leads to the occurrence of hypoxia and
hypercapnea.
It is useful to complete the general picture of the effects of obesity on
the ventilatory parameters. They particularly occur when this kind of patient
is under anaesthesia, aside from the presence of OSA. The most important
datum, observed in studying the functionality respiratory tests, is the con-
stant reduction in the functional residual capacity (FRC) of the expiratory
volume reserve (EVR) and of the total pulmonary capacity (TPC).14
The reduction in FRC in the obese patient is explained by the con-
temporaneous EVR reduction with the conservation of the residual
volume (RV) within normal limits, whereas the forced expiratory volume
in one second (FEV1) and the forced vital capacity (FVC) can both be
kept within normal limits.15
All of the changes to both dynamic and static volumes are attributa-
ble to the charge effect of the adipose mass on the thorax and abdomen,
together with the increased abdominal pressure and the dislocation of the
diaphragm in a higher position. These alterations can contribute to reduce
FRC over the limit of the alveolar closing capacity (CC), affecting the
closure of the small airways, alteration of ventilation/perfusion ratio
(V/Q), shunt right–left (up to 20–25 per cent) and arterial hypoxia.16
24
E. Pizzirani and G. Calcarella

Furthermore, a reduced pulmonary (< 50 per cent) and thoracic
(< 30 per cent) compliance and an increase in the elastic pulmonary resist-
ance (>15 per cent) have been observed. The reduced thoracic compliance is
the consequence of increased intercostal, peri-diaphragmatic and abdominal
adipose tissue. These factors are also associated with both a dorsal kyphosis
and a lumbar hyperlordosis (due to the accumulation of abdominal fat).17
More recent studies have suggested that the reduction in the total
compliance is above all due to the pulmonary compliance reduction due
to the increased haematic pulmonary volume.18
The combined action of these elements is responsible for the increase
in the work of breathing (WOB) and in the reduced efficiency of the res-
piratory function. In normocapnic obese patients about 30 per cent of
WOB is often due to the pulmonary inflation. In hypercapnic obese
patients this increases some 100 per cent owing to pulmonary inflation
and some 200 per cent owing to the mobilization of the thoracic wall. The
explanation for this is that accelerated ventilation, increasing the energetic
expenditure and O2 consumption, might cause alveolar hypoventilation.
Association with the increased mechanic pressure (intra- and extra-
abdominal), reduction in the pulmonary compliance and increase in metabolic
demands of the respiratory muscles all determine a certain degree of respira-
tory muscular inefficiency and finally an increase in the WOB. Clinically, all
this is characterized by rapid and superficial breathing, together with a limi-
tation of the maximum ventilatory capacity and a very high energetic cost. All
this is accentuated when the patient is in a supine position.
The alterations in the ventilatory mechanics in the obese patient bring
about important consequences during anaesthesia. The supine position,
anaesthetic induction and the use of relaxant drugs causes a reduction in
FRC in the healthy patient of normal weight that, in the dependent areas
of the lungs, can exceed the closing capacity (CC) of the small airways
without any cartilaginous support. This leads to the formation of atelecta-
sis, V/Q mismatch and shunt right–left, with the possibility of reduction
in the arterial oxygenation (PaO2).19 This mechanism of formation of
atelectasic areas is far more accentuated in the obese patient due to the
above mentioned alterations of the ventilatory mechanics, so that
the occurrence of intra-operative arterial hypoxias is frequent, above all
during videolaparoscopic surgeries.
Anaesthesia in Bariatric Surgery
25

This has led to a study of the ventilation strategies available to allevi-
ate the occurrence of these phenomena. The first measure was to use
particularly high current volumes (up to 10–15 ml/kg) and this determined
only modest increases in PaO2.
20 Later, positive end-expiratory pressure
(PEEP) was used in anaesthaetized and paralyzed obese patients and a sig-
nificant increase in O2 was found in the partial arterial pressure in the
group treated with 10 cm H2O of PEEP.18
In 1999 Pelosi et al. measured pulmonary volumes by using the
helium technique and recorded the elastance of the respiratory system,
lungs and thoracic wall, pressure-volume curves and the endo-
abdominal pressure at PEEP 0 and 10 cm H2O. They reached the fol-
lowing conclusions: during anaesthesia and paralysis, PEEP
ameliorates the respiratory function in obese patients, but not in normal
subjects.21 It is important to notice that application of PEEP has
unpleasant side-effects, in particular on the cardiac output (CO), as
underlined by Santesson in 1976.22
More recently it has been suggested that one should carry out the
recruitment manoeuvres followed by the high level PEEP in order to open
the atelectasic pulmonary areas and keep them open.23 In particular,
Whalen et al.24 proposed high level PEEP for at least three respiratory acts
from 4–20 cm H2O as a recruitment manoeuvre, making sure the peak
pressures of 50 cm H2O, followed by a 12 cm H2O PEEP, are not
exceeded. This ventilatory strategy has been applied to two groups of
obese patients subject to laparoscopic surgeries. The results in terms of an
increase in PaO2 have been significant, as have those concerning the
improvement in dynamic compliance, and no substantial difference has
been registered in the occurrence of post-operative respiratory complica-
tions. Therefore, these manoeuvres are effective in the prevention of
intra-operative atelectasis but their effect is to be considered as transitory.
Further and wider studies are necessary so that the utility of these strate-
gies in the prevention of post-operative complications can be assessed;
however we should not exclude the possibility that post-operative, non
invasive ventilatory techniques of positive pressure such as continuous
positive airway pressure (CPAP) with helmet or facial-nasal mask could
also be used.
26
E. Pizzirani and G. Calcarella

Cardiovascular disorders
Cardiovascular disorders are a consequence not only of the adaptation of
the cardiovascular system to obesity and to increased metabolic request but
also to the anatomic changes to the cardiac structure caused by obesity.
They are also a consequence of the accumulation of adipose tissue in the
myocardium which provokes severe consequences on mechanic and elec-
tric performance. It has been observed that cardiovascular diseases play a
major role in the clinical situation of the obese. Cardiovascular disease
affects both morbidity and mortality and all the studies underline that an
increase in BMI corresponds to an increase in cardiovascular diseases.25
It is however useful to note that the highly reduced mobility of obese
patients is able to utterly conceal the presence of cardiovascular diseases,
even serious ones. Consequently the clinical occurrence of the disease
appears only when the subject makes a physical effort, even if moderate,
or if he is under stress, such as undergoing surgery. In these cases the onset
of certain symptoms such as polypnoea, dyspnoea, and anginous crises are
very common. This compels the anaesthesiologist to request very detailed
cardiovascular tests in order to look for the symptoms of possible car-
diorespiratory deficiency (increase of venous pressures, symptoms of
pulmonary stasis, hepatomegaly, etc.). The clinical examination must be
completed with a series of instrumental tests in order to quantify the severity
of the dysfunction. An ECG, echocardiography and a chest X-ray can give
us all the information necessary in drawing up a therapeutic pre-operative
plan and to quantify the risk associated with planned surgery (Fig. 2).
The genesis of obese myocardiopathy is due to the strict relationship
between hypertension, ischemic cardiopathy and pneumopathy. The latter,
affected by ventricular dilatation and increase in stroke volume, stresses
the wall of the left ventricle leading to hypertrophy.26 This left eccentric
ventricular hypertrophy, accompanied by a reduction in the efficiency of
the left ventricle, compromises the ventricular filling up and results in
increasing left ventricular tele-diastolic pressure (LVEDP) and also of
pulmonary oedema.27 It is clear that the possibility of a dilated ventricle
being hypertrophized is rather unlikely, so that when the parietal thickness
cannot increase due to the excessive dilatation, one immediately observes
the occurrence of a systolic dysfunction.28
Anaesthesia in Bariatric Surgery
27

28
E. Pizzirani and G. Calcarella
↑ Body Mass
↑ Intrathoracic pressure /↑ Chest load
↓ Lung volume / ↓ FRC
↓ Inspiratory strength
↓ Brain stem CO2 response
↓ Oxygenation / ↑ O2 consumption
↑ CO2 Retention
↑ Respiratory rate
↑ Small airway closure// ↑ Shunts / ↑ Pulmonary vasoconstriction
↑ Pulmonary artery pressure
Hypertension
CHF
Figure 2.
The role of increased body mass in the pathophisiology of hypertension and
cardiac heart failure (CHF).

A review of the factors involved in cardiovascular disorders of the
obese includes:
•
An increase in both the circulating blood volume and the cardiac
output necessary to satisfy the needs of an abnormal body mass. The
increase in volume is not proportional to the increase in body mass
(haematic volume/body weight ratio of the obese patient = 45 ml/kg
instead of the corresponding value 75 ml/kg in the non obese
patient) and the majority of the haematic volume is distributed in the
adipose tissue.29 In the meantime, we observe a splanchnic haematic
flux increased by 20 per cent whereas the cerebral and renal fluxes
are normal.
•
Reduced vascular systemic resistance due to the increase in the
cardiac output together with a constant arterial pressure. It is not clear
whether this situation is caused by alterations of the sympathetic tone
since there have been cases of some patients with increased, normal
or reduced sympathetic activity.
•
Cardiac frequency is generally normal, although some studies estab-
lish a positive relation between obesity and increased cardiac output.30
•
Increase in cardiac output, essentially due to the increase in the sys-
tolic volume and/or the cardiac work (increases up to 40 per cent)
even if the indexed parameters are normal, which indicates that the
increase is proportional to obesity. As a result of dilatation and eccen-
tric hypertrophy of the left ventricle, the reduction in compliance and
the increase in the filling up pressures, there is a predisposition to the
occurrence of cardiac insufficiency. Studies have also described
reductions in the left ventricular function,31 which exceed 50 per cent
in the obese patients (without symptoms), whereas the hypertrophic
dilatative pathology of the left ventricle is more often observed in
patients suffering from Pickwickian syndrome.
•
Systemic arterial hypertension (IPT) due to different factors including
the increased activity of the renin–angiotensin–aldosterone system,
the increase in the haematic volume, sympathetic tone and hyperin-
sulinism. It has also been observed that 50–60 per cent of obese
patients suffer from light or moderate IPT, whereas only 5–10 per cent
have the severe form,32 but the exact mechanism causing IPT in the
Anaesthesia in Bariatric Surgery
29

obese patient is not perfectly known even if many researchers
attribute it to a mix of haemodynamic, genetic and hormonal factors.
It is important to stress that weight loss reduces hypertension.33
•
Arterial pulmonary hypertension due to the increase in the cardiac
output, hypoxic pulmonary vasoconstriction and increase in left ven-
tricle diastolic and pulmonary pressure (Fig. 2).
•
Cardiac arrhythmias due to the combined action of different factors:
myocardial hypertrophia, hypoxia, hypokalaemia due to diuretic ther-
apy, coronary disease, increase in circulating catecolamine and
infiltration of the adipose tissue into the conductive tissue of the
myocardium. We should notice that in serious obesity associated with
OSA, episodes of sinusal bradycardia occur during apnoea and
sinusal tachycardia when the patient starts to breathe again.
•
The coronary pathology present in a high percentage of the obese34
results in an increase in myocardial infarction, coronary insufficiency
and sudden death. Most of the epidemiologic studies have shown a
strong connection between the amount of adipose tissue with a central
distribution and ischemic cardiac disease, so that nowadays it is
accepted that obesity represents an independent risk factor for
ischemic cardiopathy (Fig. 2).35
Gastroenteric disorders
These consist of an increased prevalence of gastro-oesophageal reflux and
hiatal hernia, and are strictly correlated with an increase in intra-abdomi-
nal pressure. According to certain studies, 75 per cent of obese patients
had a gastric stagnation greater than 25 ml with pH < 2.5. This condition
is associated with increased abdominal pressure and was correlated to the
risk of inhalation of the gastric content and the development of pneumo-
nia ab ingestis. Later studies attributed these possible complications more
to the pathology of the gastro-oesophageal junction than to the increase in
the gastric stagnation, which in the obese has not been observed as
increased if compared to the normal subject.36
At the hepatic level, we find processes of steatosis, fibrosis, cirrhosis
and biliary calculosis more frequently than in normal patients. Tests of
hepatic functionality often do not indicate the real gravity of the pathology
even if the determination of a decrease in blood albumin concentration, an
30
E. Pizzirani and G. Calcarella

increase in the duration of prothrombin time and an increase in serum
transaminases, indicate a serious hepatopathy.
Endocrine disorders
Obese patients show an increased production of triiodothyronine (T3)
and also a consequential increase in metabolism with which an increased
sympathetic tone is associated.
In females a state of hyper-androgenesis has been observed and
in males the opposite condition3 and this could explain the different dis-
tribution of the adipose tissue in both males and females.
Pharmacologic Considerations
In the obese patient the distribution of drugs is altered. This is due to
various factors:
•
lower corporal water content;
•
increased content of adipose tissue;
•
reduced lean mass;
•
changes in the linking capacity of the tissue proteins;
•
increased haematic volume and cardiac output;
•
increased haematic concentration of free fatty acids, cholesterol and
alpha-glycoproteins.
Liposoluble drugs
Liposoluble drugs such as thiopental, xilocaine and most benzodiazepines
have an increased distribution volume, a more selective accumulation in
the adipose tissue and a longer elimination half life, even though clear-
ance values are normal or increased.37
Hydrosoluble drugs
Drugs in this category react in the same way both in the obese patient and
in those of normal weight. The increased haematic concentration of alpha
1 glycoproteins and hyperlipidemia modify the proteic bond of drugs,
reducing the quantity of free drugs in circulation.
Anaesthesia in Bariatric Surgery
31

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