Integrated Health in Bariatric Surgery-Blanca Rios-V02

Blanca Ríos, MD
INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Blanca Ríos, MD
Copyright 2015, Blanca Patricia Ríos Martínez
Copyright 2015, Instituto de Investigación y Educación en

Ciencias de la Salud (IIECS)
All rights reserved.
This publication may not be reproduced or transmitted or in

part by any means, electronic or mechanical, photocopying,
recording or other reproduction system information without the
written permission of the copyright holders.
The articles in this book are the sole responsibility of the

author. The publisher declines all responsibility for the
contents thereof
1st Edition ISBN: 978-607-97283-0-4
Legal deposit: 03-2016-070111434000-01
Produced in Mexico by: IIECS
Instituto de Investigación y Educación en Ciencias de la Salud
Design and edition: www.bariatric.today
Continuing Education: www.obesity.academy

Blanca Ríos, MD
Index
Prologue
Dr. Prof. Antonio Torres García
Introduction
Dr. Rafael Álvarez Cordero MD, PhD, FACS
Chapter I. Presurgical psychological evaluation

Blanca P. Ríos M. MD, México
Chapter II. Psychiatry disorders and post-operative follow-up

Dr. Adriano Segal and Dr. Debora Kussunoki, Brazil
Chapter III. Revisional surgery and weight regain: New roles for
psychological intervention
Psych. Isabel C.M Plaegle, Brazil and Blanca P. Ríos M. MD, México
Chapter IV. Preoperative preparation of patients posted for bariatric

surgery
Poonam Shah MD, India
Chapter V. Post-bariatric surgery

Dr. Luca Busetto, Italy
Chapter VI. Management of special conditions: Type 2 Diabetes mellitus

Dr. Luca Busetto, Italy
Chapter VII. Compensatory responses to weight loss that contribute to

weight regain: Effects of surgery and lifestyle/dietary intervention
Dr. Cynthia Buffington and Dr. Keth Kim, USA
Chapter VIII. Alcohol metabolism and potential health consequences with

bariatric surgery
Dr. Cynthia Buffington and Dr. Keth Kim, USA
Chapter IX. Dumping syndrome

Poonam Shah, MD and Dr. Shashank Shah, India
Chapter X. Physical activity in bariatric patient

Klga. MSc Johanna Pino Zúñiga, Klga MSc Mariela Olivares Galvez and Prof.
PhD. Jorge Cancino López, Chile
Chapter XI. Anesthetic considerations for obese surgical patients

undergoing bariatric surgery.
Carron Michele, MD, PhD, Italy

Blanca Ríos, MD
Cap XII. Bariatric Sensivity training

ASMBS Integrated Health Clinical Issues Committee 2013-2014.
Curriculum vitae of authors
This electronic book was elaborate with Integrated Health Committee

Members of International Federation for Surgery of Obesity (IFSO).

Blanca Ríos, MD
Introduction
Rafael Álvarez Cordero MD, PhD, FACS

Past IFSO LAC President
Hospital Ángeles Pedregal
More than a half century ago, three residents tried to find an answer to the
repeated questions and complaints of a lady who suffered severe obesity and
did not find the solution for her physical problems; they decided to try an
unknown technique to diminish the absorption of meals and performed a jejuno-
ileal bypass; it was in 1954, and this operation marked the beginning of a new
era, the era of Bariatric Surgery.
The years and the events that follow may be described as a rush to find the
best technique to make an obese patient lose weight no matter what, more than
43 different methods were published, and every one claimed to be the best; we
have to acknowledge that in several cases the published results did not match
with the reality, but at the same time, the real pioneers of bariatric surgery
worked day and night to find the most effective, reliable and efficient technique
to achieve the main goal: make the obese patient lose weight.
But nothing in life is as simple as it looks, and both surgeons and physicians
soon realize that obesity is much more than accumulation of fat to be shed, and
that the obese patient is a human being, whose body and mind suffer disorders
and diseases, some related, some not related to their obesity, and that those
disorders deserve attention from the bariatric surgeon.
Then, in many bariatric centers of the world, surgeons began to form a
multidisciplinary group in order to face the multiple facets of the obese
individual; almost all specialties were invited to form a wise group to handle the
obese patient in a integral way.
The result along this last 25-30 years have been exciting, experts from
Psychology, Psychiatry, Nutrition, Endocrinology, Cardiology, Gastroenterology,
Anesthesiology, Physical training, etc., working together to offer the best
solution for every patient.
Professor Blanca Rios, MD, began to work at the Clinic of Weight Control and
Surgical Treatment of Obesity in México City, and her work attracted the

Blanca Ríos, MD
attention of many international bariatric experts, her lectures and publications

and her active role in several IFSO Meetings, made her to be Chairman of the
Integrated Health Committee for the 20th. IFSO Congress to be held in Vienna
this fall.
Blanca Rios decided to gather the best bariatric specialists to publish this on
line book in which the concept of Integrated Health and Bariatric Surgery is
presented and clearly discussed.
Congratulations for this new achievement; I am sure this on line book will help
bariatric specialists to offer the best of the best for their obese patients.

Blanca Ríos, MD
Prólogue
Antonio J Torres García

President of IFSO (2011-2012)
IFSO ́s Chairman Board of Trustees
President Capítulo Español del American College of Surgeons (ACS)
Chief General Surgery Service Department of Surgery Complutense
University of Madrid.
Hospital Clínico "San Carlos".
Madrid, Spain
It is with a great pleasure that I am writing this prologue to this e-book, designed
and coordinated by Blanca Rios.
I know the outstanding commitment that Blanca has had and still have with the
crucial role that Integrated Health professionals develop in contributing to get an
important long term success in the management of obese patients submitted to
bariatric surgery.
The main challenge of obesity treatment is not weight loss, but long-term weight
loss maintenance. This weight loss maintenance is hindered by a complex
interaction of environmental, biological, behavioral, and cognitive factors, which
are only partly known.
The most recent developments of comprehensive lifestyle modification
programs combine dietary and physical activity recommendations with specific
cognitive and behavior strategies to improve patients’ adherence to a long- term
weight management are present in this e-book
Even more, the different contributors analyze the multidisciplinary approaches
to deal with this challenging topic. The different chapters give information about
the preoperative psychological and nutritional evaluation; the postoperative
follow-up and the most controversial aspects as well (dumping syndrome,
alcohol metabolism, physical activity, .......).
I would like to finish congratulating Blanca, all the authors, as well as Dr. Luis
Pedraza who is in the shade, pushing up the new ways of teaching, learning
and training.

Blanca Ríos, MD
Chapter I
Presurgical psychological evaluation
Blanca P. Ríos Martínez, MD

Obesity of Institute and metabolic syndrom
Hospital Ángeles del Pedregal
Ciudad de México, México
Obesity is a public health problem of global significance which has increased as

the years go by on account of its effects on life expectancy and quality of life.
Research shows the relation between obesity and medical complications (e.g.,
diabetes, hypertension, heart failure, bone problems, among other conditions);
currently, researchers enquire about the connection between obesity and
psychological issues (e.g., depression, anxiety, self-image, personality,
psychopathology). There are many studies on obesity and depression among
men, women and teenagers; some results show that women with a high body-
mass index (BMI) manifest more signs of depression than men, and it has been
concluded that there is a connection between depression in teenagers and a
high risk of developing obesity as a young adult.
Moreover, extreme obesity is related to significant psychosocial stress.2-4

Between 20 and 60 percent of people who look for weight loss treatments, such
as bariatric surgery, have a related mental disorder, usually mood disorders.5-8
In comparison with normal-weight individuals, morbidly obese people often
experience more symptoms of anxiety and depression, a decline on quality of
life, discontent regarding self-image, as well as marital and sexual issues.9-12
There are also studies on the role of the family, a role that influences the risk of
developing obesity. One research mentions the factors which supposedly have
an impact on depression: race, age, marital status, academic achievements,
chronic physical disorders and family history; among which depression within
family history, the most significant one, represents a risk factor for depression in
obese patients. Other researches support the former data by stating that
maternal inheritance contributes with 50 percent to the development of obesity,
while paternal inheritance contributes with 38 percent; likewise, other factors
are moral values, the surrounding environment and family support.1 While it is

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true that genetics affect the risk of “becoming obese” to a large extent, it is the
environment which defines whether a person becomes obese, as well as the
extent of his or her obesity.
Although it is impossible to control everything children do, it is evident that
parents have an impact on their children’s environment inasmuch as they take
decisions regarding the purchasing and availability of food, as well as the
activities related to food preparation and physical activity.13
Usually both parents work nowadays; this situation has led to the deterioration
of many aspects of family life, such as meal schedules, eating out and having
high-fat and high-sugar food in the house, the school and the workplace.
Therefore, it is a matter of importance to provide support to the family and the
individual who suffers from obesity.13
Having said that, there has not been found any significant results regarding the
presence of mental illness while studying psychological aspects such as self-
esteem and personality among obese patients, in comparison with average-
weight individuals, neither has been found a specific personality profile of the
obese patient.1
For some years now, surgery for obesity in Mexico and Latin America has
offered a great opportunity to obese or morbidly obese patients with a view to
improve their health and quality of life. Nevertheless, even today some obesity
surgeons don’t have the full multidisciplinary team, or even a specialized
psychologist to treat the patients eligible for bariatric surgery and offer them
formal monitoring in the long term with an individual or group protocol for
patients and their families. In accordance with our experience, many patients
relapse in the long term, with or without monitoring; another issue is the lack of
academic training on part of the mental health specialist, and this is why this
chapter is important for mental health specialists who deal with obese
patients.14
First appointment
We must take into account the patient’s history when he or she applies for a
bariatric procedure, whether it be intragastric balloon, sleeve gastrectomy,
gastric bypass surgery or gastric plication surgery. We know that most patients

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have a long history of many diet attempts and weight loss treatments, some of
them good; however, most of them are only “miracle” products that make the
assertion of achieving weight loss in a short period of time, a promise that is
never fulfilled.
Hence, the obese patient gets defensive with regard to the procedure during the
interview, but at the same time he or she expects this one to the best option for
losing weight; consequently, the patient arrives to the appointment with high
expectations and looking forward to the definitive solution to his or her problem.
The patient who requests a weight loss treatment, whether it be a surgical
procedure or otherwise, must be evaluated by specialists from the
multidisciplinary team, in order to rule out any physical, nutritional or emotional
issues that may crucially interfere with the treatment.
The purpose of the psychological evaluation is to establish the psychological
condition of the patient, as well as to determine whether is the right time for a
weight loss treatment or a bariatric surgery or not, in which case the patient
must wait in order to be psychologically prepared. This preparation should not
take long and should be used to enquire about the aspects which, according to
research, have an impact on obesity development.
There is controversy regarding some evaluation aspects during the initial
evaluation, such as the number of sessions, nevertheless many of the aspects
mentioned above are supported by most mental health groups and specialists.
Pre-surgical psychological evaluation

One of the most important aspects when starting an interview is rapport
(empathy) with both patient and family, for this contributes to achieving success
during the first part of the interview by acquiring information and a proper bond
with the treatment and the multidisciplinary team. Patients should tell the story
of their body weight inasmuch as this could help to acknowledge their own
evolution, which leads to a better understanding of their condition. On the other
hand, motivation is another essential aspect to evaluate during the interview,
since most patients consider bariatric surgery as a “magic” solution to their
obesity and, therefore, their expectations tend to be unrealistic and their
commitment to change non-existent. It is very useful to know the person who

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takes or accompanies the patient to the appointment, in order to learn who is

interested in the treatment and the concealed profit.
Additionally, one must consider that most patients are not able to identify how
much food they eat, this is the reason why is necessary to get to know the
behavior and symptomatology of the different kinds of eating disorders (usually
binge eating disorder), in order to rule them out or identify them and help the
patient to be more aware of them. Furthermore, the psychologist must look into
the psychological factors which have an effect on the development and
maintaining of obesity by exploring the psycho-emotional development and the
social and familiar environment of the patient, as well as the conscious and
unconscious mental representation of his or her body, self-esteem and self-
image. It is also important to evaluate the psycho-social complications of weight
loss. Therefore, we must assess in which ways obesity has affected the
patients’ physic, emotional, sexual and social life, since having difficulties in any
of those areas may lead them to resort to surgery as a way to solve their
problems.1
Eating habits should also be taken into consideration: under which
circumstances and how often the patient eats, how impetuous or tolerant he or
she is when frustrated, as well as eating habits within the family and the support
network patients have in order to change their eating behaviors.
We must look into the way patients perceive their food (quantity); this is
important for they see their food portions smaller than they really are and are
prone to ignore or deny eating large quantities of food, as well as how often
they eat. It is essential to have knowledge of psychopathology in order to
identify and get the right diagnosis. We must explore whether patients and their
families have psychiatric history or not, if they have been under psychological or
psychiatric treatment, as well as previous hospitalizations related to mental
health. The psychologist must explain the procedure and the importance of pre-
surgical evaluation to patients, along with the purpose of post-surgical
monitoring or psychotherapy, so they understand the significant life changes
they are going to experience due to weight loss. It has been proved that a short
therapeutic process before surgery gives a better prognosis in the short,
medium and long term.1

Blanca Ríos, MD
The motivation interview is widely used, since it focuses on the patient and
contributes to explore and resolve any ambivalence regarding bad habits and to
promote a healthier lifestyle. The purpose is to provide tools to face unsolved
issues, to promote behavior changes and allow the professional to improve the
patients’ motivation while keeping in mind their basal level and final decisions.
The therapist should not have an authoritarian role,15,16 neither try to convince
or discourage the patient regarding bariatric surgery, but rather provide the
information patients need in order to understand the procedure.1
It is also important, as a therapist, to respect the beliefs, customs and moral
values of patients; we must pay attention to the patients’ point of view and let
them choose freely according to the provided information. It is impossible to
motivate people if they don’t see the benefit; the patient is not going to change if
he or she doesn’t have a clear perspective of the magnitude of the task.16
In summary, the points to take into consideration are:
a) First interviews
1. Identification card (name, age, marital status, occupation, education,
religion, evaluation date, etcetera).
2. Initial history and evolution of obesity, evaluation of weight variation

through life stages, cycles of weight loss and gain, related events, beginning
stage, heaviest and lighter weight, incidents related to weight gain, eating as an
emotional disorder, stress management, etcetera.1
Patients must describe their attempts at weight loss starting from the first weight
loss treatment, for instance: an individual who doesn’t adhere to a strict plan will
have little adherence to post-surgical diet.17
3. Reasons for consultation, the patient’s companion, the reason for making
the decision at that point of his or her life, whether it has to do with health
problems, emotional issues, friends or family.

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4. Expectations, motivation, goals and objectives; we try to make patients

realize that surgery is not a “magical” solution, that they must commit to change;
also, we need to make sure they have a proper understanding of the surgery
and the process of losing weight, as well as to enquire about any possible gain
in relation to obesity and the people that surround them.1 This implies to
examine the patient’s responsibility when facing changes, as well as to evaluate
the patient’s motivation and will for change.16
In addition, it is essential to look into what patients expect from weight loss and
the health benefits after surgery, since we must make sure that they have
realistic expectations about the procedure’s result.16 In this manner, we are able
to discover whether patients see their weight as the cause of all their problems
and weight loss as a great solution since, most surely, it won’t work like that.
After the motivational interview, the therapist will know whether an individual is
motivated if: he or she agrees with the therapist, accepts the diagnosis,
expresses a need for help, appears to be affected by the problem and follows
the therapist’s advice.16
The interview describes different stages of change, which are:
Pre-contemplation
 There is neither true will to change nor awareness of the problem.

 Staying obese due to lack of information or demoralization.
 Opposition to external pressure to change.
 Information.
 Asking for help.
 Positive experiences regarding previous attempts.16
Contemplation
 Serious thinking about change through the next six months.

 An open mind towards information and change.
 Ambivalence between advantages and disadvantages.

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 Showing understanding.
 Analysis of the pros and cons of habits.
 Constant meditation, they replace acting with thinking.16
Preparation
 Preparation for acting within a month.

 Resolution of the individual’s ambivalence in favor of changing.
 Little steps.
 Help with choosing strategies.
 Exploring motivation for change and related behavior with the patient.
 Evaluation of family and social support.
 Assessment of previous attempts of change (analysis of relapses).16
Relapse
 Normal process within every behavior change in which the individual goes back
to previous stages.
 Attitudes concerning relapse:
 Avoid drama.
 Recognize relapse as a possibility from the beginning.
 Use it as learning tool.
 Avoid feeling guilty.16
It is relevant to identify in which stage the patient is, and consequently

determine when the pre-surgical preparation should start.
5. Familiar environment (nuclear family and of origin). We know that family

is an important part of the learning process, by reason of the influence of its
members on the obese individual. Obese people learn their eating habits and
behaviors from this environment during childhood, adolescence and even
adulthood, when family has a strong influence on their food preferences.1

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Therefore, we must look into any history of obesity within the family, the use of
reward and punishment methods of learning using food during childhood, food
symbolism, cultural and religious beliefs, the point of view of family and partner
regarding surgery, emotional and economic support, family dynamics and the
sort of family which incites post-surgery sabotage.
Some types of families are:13
Contributor Saboteur Antagonistic Indifferent Competitive Watchful
Well-informed They appear They They ignore the Some of the They
to collaborate, undermine the problem members are mistake
but send treatment also on diet support for
contradictory and question supervision
messages. the patient’s and
treatment monitoring
of
instructions
Creates a They ruin the They criticize Cold They want to They tell on
comfortable patient’s changes environment impose their the patient
environment plans, own during the
whether experience doctor’s
consciously appointment
or
unconsciously
Encourages They search There’s no Weight loss

communication for magical encouragement competition
treatments to adhere to
the treatment
Favors diet
and exercise
6. Life style and history of eating habits, the sort of food they eat and how
they behave on vacations, whether they eat when facing difficult situations,
engage in stressful activities that lead them to eat at different hours through the
day, or have an irregular eating schedule; how they behave during work trips
and how they manage food and work situations (frequent business
appointments in restaurants, social events, et cetera), stress management, how
many food they take each day, the tendency to eat snacks during the day and

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what kind of snacks they prefer, identify if they are candy-eaters, compulsive
eaters (binge) or tend to night eating; enquire about their awareness on how
much food they eat, how long it take for them to eat, which kind of food and
when they prefer to eat, whether they eat fast or not; when are they not hungry,
differentiate between physical hunger and emotional hunger, whether they drink
large quantities of high calorie liquid (flavored water) or alcohol.1
For instance, if a patient has chicken for dinner it is important to know which
brand it is, the way is prepared, which give us information about his or her bad
habits; we must also know the size of the food portion, since generally the
patient prefers to avoid the subject, denies it,17 doesn’t have a clear idea about
servings or someone else serves the food.
Likewise, we must evaluate the eating behaviors of patients and how often they
fall into them, such as the following ones: a) picking at food and eating in the
kitchen while standing, b) eating while cooking or preparing food, c) eating fast,
d) eating without being hungry, e) eating large quantities of food at night, f)
drinking carbonated drinks, g) drinking large quantities of high calorie liquid, h)
drinking at least eight glasses of water a day, i) taking vitamin and mineral
supplements.15
Therefore, it is important to identify the type of eater we are dealing with, as well
as to asses the physical and emotional hunger. (Table 1 and 2)
Table 1. Types of eaters.

Adapted by Blanca P. Ríos M., MD.
I thank the collaboration of Psychologist Diana Pérez Carbajal (Hospital Ángeles Tijuana, Mexico) for the
creation of this classification.
Types of eaters Description

Emotional Patient that eats carbohydrates when subjected to stress
or situations that involve a positive o negative emotion.
Candy eater Patient that, generally, can’t stop eating sweets of
chocolates between meals.
Nibbler or grazer Patient that eats small portions of every type of food

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during the day or at a special schedule.

Compulsive (Binger eating Patient that eats great amounts of food in a short time,
disorders) without being actually hungry. This form can manifest in
three levels: mild (1-3 binge eatings a week), moderate
(4-7), severe (8-13) or extreme (14 or more times a
week). Observe details in the DSM-V diagnosis
criteria.18
Night eating syndrome Morning anorexia with frequent night ingestions,
compulsory wishes to eat, they eat hours after dinner
time, and night food intake makes the organism
concentrates in the digestion, therefore, provoking
constant insomnia that, at the same time, originates the
impulse to eat again, creating a vicious cycle. One can
be a compulsive eater at noons or at night, for being
anxious at night time or for having cravings.18,19
Messy Patient that, generally, doesn't comply with the establish
eating hours.
Junk Food Eater Patient that, generally, eats junk food with an abundance
of carbohydrates and fat.
Mixed Eater Patient that represents two or more of these types of
eaters.
Table 2. Physical Vs. Emotional Hunger. Adapted by Blanca P. Ríos M., MD. and
Psychologist Denise Arcila Martínez.
Physical hunger Emotional hunger
Develops slowly Develops quickly
It's slower and must be satisfied Satisfaction must come immediately
There is a choice and one is conscious about There's no conscience, he/she doesn't know
the food. how, what and when it's eating.
Realizes the amount of food that's going to Demands more food despite being physically
be consumed, stops when satisfied. full.
It's open to different types of food. Prefers specific types of food, generally junk
food (carbs and fat)
There are no guilty feelings Presents guilty feelings
It's a physiological need Generally, it's the result of a painfull situation
(emotional)

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7. Medical information. It is essential to look into how much information the

patient has regarding surgery. Generally patients get this information from the
multidisciplinary team, hence we must find out how much information of their
medical condition they have, as well as their level of understanding in relation to
their health and medical treatments.17
Patients often get information from the internet, which can be a risky option
since the quality of information may be either good or bad, and our task is to
clarify any doubt. It is essential to evaluate the patient’s understanding of
surgical procedures and identify three points: the patient should know the
procedure and the risks that entails, the recovery process and the post-
operative diet plan.
We should worry when the patient has little understanding of the surgery, since
this may be a consequence of lack of knowledge, low motivation or cognitive
limitations.17
8. Self-image. The way patients perceive themselves, how they think other
people perceive them, the idea of their own body image; how they see
themselves in the mirror, since they may see themselves more or less obese
than they really are; evaluate if they have a clear perception of their weight.
We know it is important to evaluate the patient’s body image by reason of the

changes this aspect is going to undergo after surgery. The patient should be
well-informed about it.
9. Sexuality (gender, role and sexual activity). Evaluate past and current
sex life; the way in which obesity affects the intimate life of the patient, in some
cases as a defense mechanism and in others as rejection towards the partner;
growing apart from the partner, because of shame or infidelity.1

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10. Psychopathology. Generally, obese people are impulsive, sedentary,

depressive, they suffer from anxiety and depend on others, they experience
food dependency and strong guilty feelings.1 Because of this, we must rule out
eating disorders associated to obesity (bulimia, mainly in the past), binge eating
disorder, mood or personality disorders, or anxiety.
There are obese individuals with or without psychopathology, but there is not a
mental disorder typical of this condition, and there is a high percentage of obese
individuals who suffer from psychiatric comorbidity.
The most frequent related psychopathologies are: i) Major depressive episode

(MDE) and persistent depressive disorder (dysthymia). ii) Anxiety disorder:
generalized anxiety disorder (GAD) and social anxiety disorder (social phobia).
iii) Obsessive-compulsive disorders: body dysmorphic disorder. iv) Eating
disorders and compulsive eaters: binge eating disorder.
Mental illness should not be a contraindication for surgery, and this is why in
some cases it is important to give the patient a pre-surgical
psychopharmachologic treatment, considering that the patient’s state of mind
helps to determine his or her possibilities of managing the treatment.18
It is relevant to do a full interview and in some cases a deeper one, which is

why the number of initial interviews is one of the most controversial themes.
The appropriate range of evaluation, to my consideration, is between two and
five interviews depending on several factors, an appointment per week;
however this has to do with the interviewer’s and patient’s schedule, the sort of
institution (public or private), the amount of waiting patients, the agreement with
the multidisciplinary team, the cost of sessions, et cetera. Consequently, when
planning activities in the psychology area it is preferable to determine a definite
number of sessions, proposing extra pre-surgical sessions to the
multidisciplinary team in difficult cases, only if necessary and using brief and
formal psychotherapeutic techniques for previous preparation.

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b) Psychological contraindications
There is a strong controversy about contraindications; nonetheless some of

them have been identified in order to have a guide and achieve a better
prognosis for surgery. Next I will explain some relative and absolute
contraindications, taking into consideration the variation of waiting periods,
unless there is an extreme reason against surgery. If necessary, surgery should
be canceled, in which case the patient will receive a brief and formal
psychotherapeutic treatment.
Ignoring these contraindications may put patients, their families or partners at

great psychological/psychiatric risk.1
Absolute contraindications
 The patient has an ongoing emotional crisis (e.g., emotional breakup, recent
mourning, among other things).
 Untreated psychiatric disorders, such as schizophrenia, mania, bipolar
disorder, severe depression, recent suicide attempt, constant thoughts of death.
 Risk situations: active alcohol consumption and drug use, eating disorders
(untreated or ongoing bulimia), binge eating disorder.
 Body dysmorphic disorder.
In some of the above mentioned cases, the patient must receive a

psychopharmacological or psychotherapeutic treatment before having surgery.
Relative contraindications
 Unfavorable familiar environment (dysfunctional).

 Unresolved mourning, divorce, previous suicide attempts (at childhood or
adolescence).
 Previous history of bulimia (at least a year of remission).
 Previous history of alcohol and drug use or abuse (preferably a year of
remission).

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 Identify the secondary profit around obesity.

 The patients’ perspective about surgery solving the problems related to their
surroundings.
 Moderate to profound mental retardation, evaluation of family support.
 Poor support on part of the family and social environment.
Contraindications should be treated with caution and it is also advisable to

discuss them with the multidisciplinary team.
c) Evaluations tools
In some cases, and in order to achieve a more complete evaluation, it is

necessary to rely on psychological tests and surveys, since we must identify or
rule out some disorders that may be incompatible with surgery in the short,
medium or long term, or even permanently. This is the reason why we are going
to mention some of the most efficient tools for identifying obesity-related issues.
There are many evaluation scales and tools; the problem is that some of them
do not have validation in Latin American and obese population, which indicates
there is still a difficult task to carry out, in addition to the generalized use of the
eating disorder diagnostic scale (EDDS). Because of this, it is important to point
out that according to the American Psychiatric Association (DSM V)18 obesity is
not a psychiatric disorder and, therefore, obesity is not considered an eating
disorder unlike binge eating disorder, which is frequent among obese
individuals.1
The most frequent psychological tests and surveys for evaluating some aspects
of obesity are:
Personality
 Multiphasic personality inventory (MMPI 2)20

 Personality factors 16 PF 21

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Depression and anxiety
 Hospital anxiety and depression scale (HAM)22,24

 Beck depression inventory (BED II)23-26 [Validation in Mexican population]
Quality of life
 Health-related quality of life survey (SF-36)27

 The life quality inventory and health (InCaViSa)28 [Validation in Mexican population]
 Bariatric analysis reporting outcome system (BAROS)29

 Health survey (EQ5D)30
 Impact of weight on quality of life-lite (IWQOL)31
Body image
 Body shape questionnaire (BSQ)32

 Stunkard figure rating scale33
Eating behavior
 Overeating questionnaire (OQ)34 [Validation in Mexican population]
Psychopathology
 Symptom checklist (SCL 90-R)35
We must take into account that the use of the above mentioned tools depends
on the place where the therapist works, since they differ according to whether it
is a private hospital or a public one, on account of costs, time and number of
patients.

Blanca Ríos, MD
d) Pre-surgical preparation
In some cases, after having discussed the case with the multidisciplinary team,
the decision about a possible pre-surgical psychological preparation is made
(not in every case), in which a patient could manifest an absolute
contraindication that has not been treated. In such case, the patient must
receive treatment before surgery, for instance when a patient needs
psychopharmacologic drugs to treat a major depression or a severe personality
disorder. Therefore, we must wait some time for the medicine to work. In other
situations, it is necessary to have limited-time sessions (between eight and
twelve sessions), using brief therapy techniques with a focus on the root of the
problem and with the purpose of solving an ongoing situation which affects the
life of the patient, such as a recent mourning.
Some patients receive the treatment individually, while others, especially in

public institutions, have it in groups.
In addition, before surgery, the patient receives a “class” about the pros and
cons of bariatric procedure at some public and private institutions, in order to be
well-informed about the events he or she is going to experience throughout the
process of weight loss, from pre-surgery to post-surgery. This is why is
necessary for us therapists to be well-informed about bariatric procedures and
their complications, so we are able to refer the patient to the doctor in case the
factor which interferes with the process is not psychological; as well as some
nutritional aspects with a view to learn what kind of food affects the patient,
having frequent interaction with the nutritionist and with each specialist from the
multidisciplinary team; occasionally, this sort of communication extends to other
specialists who are asked for consultation, such as orthopedists,
pneumologists, psychiatrists and cardiologists, among others.
Some of the most important general aspects to be discussed with patients

before bariatric surgery, preferably with the assistance of the nutritionist, are: a
brief and clear explanation of the bariatric procedure, nutritional preparation
before and after the procedure, complications and benefits, the importance of

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support networks, the aspects to evaluate during postsurgical monitoring and

lifestyle changes.
The purpose is that the patient is aware of the bariatric procedure with a view to
avoid fears and subsequent surprises, as well as achieving emotional stability to
endure the social, familiar and psychological changes during the postsurgical
period.
Our role at this point is to clarify the patient’s expectations, goals, and
objectives regarding surgery, along with providing clear and precise information
about the surgery in question.
I consider our task as psychologists to be essential for the treatment of the

obese patient. Fortunately, psychologists participate more in healthcare,
although there is yet a difficult task to fulfill within the area of bariatric
psychology.
Bibliographical references
1. Ríos Martínez BP, Sánchez M, Guerrero M, Pérez D, Gutiérrez S, Rico M et
al. El rol del psicólogo en la cirugía bariátrica. Revista de Cirugía General.
2010;32(2).
2. Sarwer DB, Wadden TA, Fabricatore AN. Psychosocial and Behavioral
Aspects of Bariatric Surgery. Obes Res. 2005;13:639-648.
3. Herpertz S, Kielmann R, Wolf AM, Hebebrand J, Senf W. Do Psychosocial
Variables Predict Weight Loss or Mental Health after Obesity Surgery? A
Systematic Review. Obes Res. 2004;12:1554-1569.
4. Herpertz S, Kielmann R, Wolf AM, Langkafel M, Senf W, Hebebrand J. Does
Obesity Surgery Improve Psychosocial Functioning? A Systematic Review.
Int J Obes Relat Metab Disord. 2003;27:1300-1314.
5. Larsen F. Psychosocial Function Before and after Gastric Banding Surgery
for Morbid Obesity: A Prospective Psychiatric Study. Acta Psychiatr Scand
Suppl. 1990;359:1-57.
6. Black DW, Goldstein RB, Mason EE. Prevalence of Mental Disorder in 88
Morbidly Obese Bariatric Clinic Patients. Am J Psychiatry. 1992;149:227-234.
7. Powers PS, Rosemurgy A, Boyd F, Pérez A. Outcome of Gastric Restriction
Procedures: Weight, Psychiatric Diagnoses, and Satisfaction. Obes Surg.
1997;7:471- 477.
8. Sarwer DB, Cohn NI, Gibbons LM et al. Psychiatric Diagnoses and
Psychiatric Treatment Among Bariatric Surgery Candidates. Obes Surg.
2004;14:1148-1156.
9. Fabricatore AN, Wadden TA, Sarwer DB, Faith MS. Healthrelated Quality of
Life and Symptoms of Depression in Extremely Obese Persons Seeking
Bariatric Surgery. Obes Surg. 2005;15:304-309.

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10. Wadden TA, Sarwer DB, Womble LG, Foster GD, McGuckin BG, Schimmel
A. Psychosocial Aspects of Obesity and Obesity Surgery. Surg Clin North
Am. 2001;81:1001-1024.
11. Fontaine KR, Barofsky I. Obesity and Health-related Quality of Life. Obes
Rev. 2001;2:173-182.
12. Sarwer DB, Thompson JK, Cash TF. Body Image and Obesity in Adulthood.
Psychiatr Clin North Am. 2005;28:69-87,viii.
13. García-García E, Kaufer-Horwitz M, Pardío J, Arroyo P. La obesidad.
Perspectivas para su comprensión y tratamiento. 1ª edición. Editorial Médica
Panamericana. México. 2010.
14. Marcondes Franques AR, Salete Arenales-Loli M. Novos corpos novas
realidades: Reflexões sobre o Pós-operatório da Obesidade. 1ª edición.
Editora Vetor. 2012.
15. Fernández R. Tesis de doctorado sobre el Estudio psicológico del paciente
con obesidad mórbida sometido a intervención quirúrgica: Análisis de las
diversas variables que pueden afectar a la pérdida de peso. Universitat de
Valencia. 2009:54.
16. Miller W, Rollnick S (comps.). La entrevista motivacional. Preparación para el
cambio de conductas adictivas. 2ª edición traducida. Editorial Paidós Ibérica.
Buenos Aires. 1999:20-24.
17. Sogg S, Mori DeAnna L. The Boston Interview for Gastric Bypass:
Determining the Psychological Suitability of Surgical Candidates. Obes Surg.
2004;14:370-380.
18. First M. American Psychiatric Association (APA). Diagnostic and Statistical
Manual of Mental Disorders (DSM V). Editorial Masson. 5ª edición. American
Psychiatric Publishing. Arlington. 2014:155-243.
19. Ellenberg C, Verdi B, Ayala L, Ferri C, Marcano Y, Vivas de Vega J.
Síndrome de comedor nocturno: un nuevo trastorno de la conducta
alimentaria. An. venez. nutr;19(1):32-37, 2006.
20. Butcher J, Grant Dahlstrom W, Graham J, Tellegen A, Kaemmer B. MMPI-2.
Inventario Multifásico de Personalidad de Minnesota-2. 1ª edición. TEA
Ediciones. Minnesota. 1989.
21. Catell R. Cuestionario factorial de personalidad: adolescentes y adultos (16
PF). Manual y cuestionario. 5ª edición. TEA Ediciones. Illinois. 2008.
22. López-Alvarenga J, Vázquez V, Arcila D, Sierra A, González J, Salin R.
Exactitud y utilidad diagnóstica del HAD en una muestra de sujetos obesos
mexicanos. Rev Inv Clin. 2002;54(5):403-409.
23. Ríos M, Rangel G, Álvarez-Cordero R, Castillo A, Ramírez-Wiella G, Pantoja,
J et al. Ansiedad, depresión y calidad de vida en el paciente obeso. Acta
Medica. 2008;6(4):147-153.
24. Hamilton M. Development of a Rating Scale for Primary Depressive Illness.
Br J Soc Clin Psychol. 1967;6:278.
25. Beck AT, Ward CH, Mendelson M et al. An Inventory for Measuring
Depression. Arch Gen Psychiatry. 1961;4:53-63.
26. Jurado S, Villegas M, Méndez L, Rodríguez F, Loperena V, Varela R. La
estandarización del inventario de depresión de Beck para los residentes de la
Ciudad de México. Salud Mental. 1998;21(3):26-31.
27. Zuñiga MA, Carrillo-Jiménez GT, Fos P, Gandek B et al. Evaluación del
estado de salud con la encuesta SF-36: resultados preliminares en México.
Salud Pública de México. 1999;41:110-118.

Blanca Ríos, MD
28. Riveros A, Sánchez-Sosa J, Del Águila M. Inventario de calidad de vida y

salud (InCaViSa). Inventario y Manual. El Manual Moderno. México. 2009.
29. Moorehead M, Ardelt-Gattinger E, Lechner H, Oria H. The Validation of the
Moorehead-Aldelt Quality of Life Questionnaire II. Obes Surg. 2003;13:684-
692.
30. EuroQol. A New Facility for the Measurement of Health-related Quality of Life.
Health Policy. 1990;16:199-208. Texto libre en: http://www.euroqol.org
31. Kolotkin RL, Crosby RD, Kosloski KD, Williams GR. Development of a Brief
Measure to Assess Quality of Life in Obesity. Obes Res. 2001;9:102-111.
Texto libre en: http://www.qualityoflifeconsulting.com
32. Ware J, Sherbourne C. The MOS 36 Items Short-form Health Survey (SF36).
Med Care. 1992;30:473-483.
33. Stunkard A, Sorensen T, Schulsinger F. Use of the Danish Adoption Register
for the Study of Obesity and Thinness. Research Publications – Association
for Research in Nervous & Mental Disease. 1983;60:115-120.
34. O’Donnell W, Warren W. Cuestionario de sobreingesta alimentaria (OQ).
Cuestionario y Manual. 1ª edición. El Manual Moderno. México. 2007.
35. Derogatis L. Cuestionario de 90 síntomas (SCL 90-R). Cuestionario y
Manual. 3ª edición. TEA Ediciones. Madrid. 2002.

Blanca Ríos, MD
Chapter II
Psychiatric disorders and post-operative follow-up
Dr. Adriano Segal

Technical director of the Segal Clinic
São Paulo, Brazil
Dr. Debora Kussunoki

Psychiatrist of the Segal Clinic
São Paulo, Brazil
The surgical approach of severe obesity cases is the conduct of choice not only for its
results in terms of weight loss and maintaining that loss, but also as result of its impact
on quality of life and health markers, including mental markers. This is a very well
known fact, as described and explained throughout this book.
Regardless of these facts, there are many concerns, clinical and psychological,
associated to the follow-up of bariatric surgeries (BS). These concerns are, in great
part, justifiable.
This seems to result from, at least, two reasons:
1. BS are obviously not a panacea for obesity. They are not even "the easiest
way" or "the last chance", as many patients, family members (and, sometimes,
even health professionals) think, fear and/or wish for, sometimes concurringly,
confusingly or counterproductively. Patients and team should be aware that
being submitted to this type of procedure is taking on a lifelong commitment of
collaboration (in the true sense of the word, that is, joint work) with the
multiprofessional team as result of a set of care, specially during post-operative
(PO). This care is essential and, it is not exaggerated to say, is the main
responsible for procedure success in the long run, not only in terms of weight
and comorbidity reduction, but also in terms of preventing adverse events and
complications, which are sometimes irreversible.
2. There is also a generalized fear, although not always declared, that there are
some psychological and/or psychiatric complications resulting from the
procedure, regardless of the care offered. It is our opinion that this fear is much

Blanca Ríos, MD
more a consequence of prejudice against obesity, associated or not to

psychosomatic theories in relation to its ethiology, than just caution based on
scientific evidences. As mentioned in another part in this chapter, the
prevalence of psychiatric disorders (PD) in the patient population candidate for
BS is in fact higher than the overall population, for some specific states.
However, at the same time, psychiatric improvement is expected in a large part
of patients,1 probably a result of the removal of an important stressing factor,
that is, severe obesity. This factor exerts stress not only on the psychological
point-of-view (a lot was already said about the stigma of obesity in modern
society), but also based on the biochemistry and hormonal point-of-view, and in
terms of adverse events associated to obesity drugs or drugs used to treat the
diseases associated with obesity.
In this chapter, we will address part of the second item.
Psychiatric disorders identified in PO
For a great part of patients, PO will represent at least half of their lives, usually even
more.
Therefore, in PO there is a greater chance of PD onset, which was not present during
preoperative evaluations. But not necessarily resulting from a cause/effect relation,
instead because it represents a longer period of time. In fact, most of the time, there is
not cause/effect relation, on the contrary to lay people assumptions.1
These new PD may in fact appear in post-op (the patient never presented PD before
surgery) or simply may be diagnosed in post-op (patient had a PD or history of PD,
which for one reason or another, remained unknown to the team). They may or may
not be related to bariatric surgery or weight loss. We would like to reiterate that the
cause/effect relation, which some attribute to BS or to weight loss is far from
consensual in the scientific community.
First of all, some causes of PD onset, not present in preoperative candidates, are:
 Age group and genders common to both events: age group of great part of BS
candidates is usually close to the age of the first psychiatric state. The same applies to

Blanca Ríos, MD
gender, given that most part of the BS candidates are female and there is a higher
prevalence of PD in females, notably mood, anxiety and eating disorders.2,3
 Eating disorders (not present during preoperative), caused by any of the PO changes.
For instance, in 2004, we described a state in post-op BS patients characterized by
important changes in the relationship with food combined with the intense and irrational
fear of weight gain. On the contrary to anorexia nervosa (AN), high calorie foods, which
are tastier and easier to swallow are often chosen. Additionally, the core criteria for AN
and bulimia nervosa (BN) are absent in the post-surgical eating avoidance disorder
(PSEAD).1
 Behavioral changes resulting from specific nutritional shortage.4
 Pharmacokinetic changes of alcohol in some techniques (specially the ones with the
Roux Y), favoring a more effective and, most likely, faster damage to target organs
(liver, pancreas, heart and brain).5,6
 High levels of association between eating disorders and substance abuse.7
 Reward deficiency syndrome (RDS).8-11
We have chosen not to include the last three items under the tempting, wicked and
devoid of scientific support concept of "compulsion change" since we believe it is just a
simplification, which only helps to perpetuate prejudice in an area where they are
already abundant enough.
Secondly, some causes of identification of PD in post-op that already existed in

preoperative are:
 Anamnesis mistake.
 Mood disorders may be confused with "normal" depressive reactions in the presence of
morbid obesity.
 We would like to stress that the bipolar spectrum states may take years to be
diagnosed as such, thereby they are wrongly classified as unipolar depression. The
mistake described in the first line of this item is more likely in the absence of a
psychiatrist.
 Patient and/or family member express omission of information because of shame or
even with the purpose of not being contraindicated for surgery.12 It is worth noting that
the latter could be an iatrogenic consequence of the health professionals prejudice. In
that case, it is essential to define which would be the most appropriate and productive
stance to be taken by the team in the case of psychiatric/psychological contraindication

Blanca Ríos, MD
of BS. And yet today, some teams still use the expression "postpone surgery" as an
euphemism, since the cases in which this is justified are few and well defined and the
cases in which surgeries are "postponed" are much more abundant.
Interference of psychiatry disorders in the outcome of bariatric surgeries
Regardless if PD is pre-existing or latter to the BS, it can interfere with patient

compliance to clinical and nutritional follow-up and, possibly, interfere in patient
outcome. Therefore, each pathology must be detected and treated early to avoid the
impact on weight loss, on the nutritional state, and on the patient's quality of life.
Nevertheless, there is no need for normalization/complete remission of the psychiatric
state(s) before BS, at least from the evidence-based medicine point-of-view. Exception
of that rationale are the states in which the patient cannot argue logically about the
surgery, its needs, limits and consequences and possibly in the states in which there is
significant alcohol consumption. The first group is comprised of active psychotic states
at the time of preoperative procedures and states with innate or acquired cognitive
impairment, reversible or not. In the case of reversible states, when reverted, they do
not constitute contraindication.1,8,9
For some authors,10 slow preoperative evaluations would be useless and could be a
type of prejudice, in face of the current means of scientific evidences.
In the table below,8 some PD and their relations with BS post-op are shown:
Disorder Related symptoms Others

(DSM IV)
Major Changes in mobility and/or autonomy, increase in The depressive episodes with
Depressive appetite, weight gain and sleepiness (depressive atypical characteristics are more
Disorder episodes with atypical characteristics), gloominess frequent in BD 1 and BD 2 and
and pessimistic thoughts. Somatic symptoms bring Major Depressive Disorder
patient back to the office with uncommon BS recurring with a seasonal pattern.
complaints. The Mania episodes that present
Risk and/or suicidal behavior include not following after BS could be preceded by
nutritional scheme directions. atypical post-op depression.
Bipolar In mania: lack of impulse control, including eating in Uncontrolled shopping, excessive
Disorder some cases. Abandonment of clinical treatment. The spending, alcohol abuse, as well
(BD) association of BD with absences, school failure, as other substances, uncommon
divorces, and in some more severe cases child or sexual behavior for the person,
spouse abuse or violent behavior. excessive involvement in
Extreme irritability and mood instability. pleasureful activities with a

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Suicide risk. potential for painful

Hypomania episodes. consequences.
Weight gain with mood stabilizers (exception: Higher rates of diabetes mellitus
topiramate and lamotrigine.) and atypical type 2 even before medicine use.
antipsychotics.
BS may help in compliance to the posology scheme in
specific cases.
Some obesity treatments may induce mania or
hypomania episodes in these patients.
Schizophrenia Patients with negative symptoms present a decrease More visceral obesity and
of activities. metabolic syndrome even before
Positive symptoms hindering a clinical approach and starting treatment with
follow-up during a crisis. antipsychotics.
Change in mobility and/or autonomy.
Variable weight gain with antipsychotics. In some
cases with restricted medicine based on the severity
of the case, BS may help in compliance to the
posology scheme.
Panic with or Choking phobia: patient avoids solid foods or food that Possibly using more delivery
without could get "stuck". services such as: pizza,
agoraphobia, agoraphobia with changes to mobility and/or sandwiches and others.
specific autonomy.
phobias
Obsessive Rituals and compulsions that make compliance to Symmetry rituals leading to
compulsive nutritional schemes or to clinical follow-up more hyperphagia
disorder (OCD) difficult.
Prader-Willi Syndrome: impulsive and compulsive
behaviors, hyperphagia
Addiction to Non-compliance to clinical and nutritional follow-up If there is another associated PD,
alcohol and Risk behavior. treating the underlying PD makes
other Easier to become addicted to alcohol and it easier to treat the addiction.
substances exacerbated consequences as result of changes in
alcohol absorption and metabolism.
Malnutrition (crack/cocaine) or sometimes even
insufficient weight loss (cannabis).
BN Maintaining weight as result of inappropriate The presence of inappropriate
compensation practices and potential consequences compensatory practices must be
of this actions (self-induced vomiting, laxatives, investigated, not only in
diuretics, prolonged fasting, excess exercise). preoperative, but also in post-op.
Involuntary vomiting immediately after post-op which

Blanca Ríos, MD
will later evolve to provoked vomiting, be it to lose

weight or as a response to gastric discomfort.
BED and night Difficulty to keep with the proposed nutritional High comorbidity rate with mood
eating schemes and less weight loss. and anxiety disorders.
syndrome
(NES)
PSEAD Higher weight loss than expected and tests are not Anorexia Nervosa is different from
compatible with technique used. PSEAD.
Resistance to any type of dietary or medical
approach. Intense and irrational fear of going back to
weight before BS.
Interference of bariatric surgeries when a psychiatry disorders is present

1. Psychiatric changes resulting from nutritional deficiencies8
A. Pellagra:
Caused by the deficiency of niacin and/or essential amino acids, such as tryptophan.
Pellagra is usually associated to alcohol abuse, unbalanced vegetarian diets and
extreme malnutrition. It is classically described as the five Ds: dermatitis, diarrhea,
delirium, dementia, and death. Replacement promotes a fast recovery, however if the
deficiency is prolonged it could be slower or could cause permanent damage.
B. Beriberi:
Vitamin B1 (thiamine) deficiency, characterized by cardiovascular and neurological
alterations and associated to Wernicke-Korsakoff Syndrome. Symptoms are apathy,
depression, irritability, nervousness and concentration deficit. Long-lasting cases could
cause severe and irreversible memory loss.
C. Vitamin B12 deficiency:

Vitamin B12-which needs the intrinsic factor produced by the gastric mucosa to be
absorbed-deficiency is characterized by megaloblastic anemia, neurological
manifestations resulting from nervous degenerations and mental alterations.
Apathy, depression, and irritability are common. In some cases delirium, illusions,
hallucinations, and dementia are observed in some cases.
Symptoms reversions are fast after early and continuous administration of vitamin B12.

Blanca Ríos, MD
The other dietary deficiencies and the dietary replacement or dietary supplements
approach are also discussed in another chapter.
2. Psychiatric alterations as result of weight loss 9
The idea that diets cause a negative psychological impact is widely disseminated
among lay people. That is possibly a result of or was reinforced by the first trials
carried out on this topic, from 1950 to 1970. These trials were not controlled and their
results were mainly based on non-standardized clinical evaluations. Controlled trials,
with standardized tools carried out from 1969 have shown opposite results, in the
sense that there are no mood swings or anxiety attacks or even, present an
improvement in these parameters. An additional difference between the two trial
groups is the presence of BED in the second group. There is a consensus about the
psychological improvement and quality of life in obese patients that lose weight,
proportional to the amount of weight loss and regardless of the method.
In relation to the effects of weight loss on body image, data is more scarce, for post-op
patients or patients submitted to very low calorie diets, collected in a short period of
time after weight loss showing disparate results. Apparently, the improvement
observed in some trials may be transient, however the topic requires more trials with
longer term follow-up to reach a consensus.
3. Psychiatric alterations as result of surgery8
Here, we will mention the changes in the many different moments of post-op. It is worth
noting that part of them is common to any type of surgery similar in size to BS and
many are associated to dietary deficiencies.
Immediate post-op (POI, first day)
Delirium (state of acute confusion):
 Post-anesthesia and/or
 anesthetics x prior suspended drug interactions, with a half-life longer than the
suspension period
 others (embolism or strokes in the CNS, unbalanced hydroeletrolitics, other
metabolic disorders)
 use and abstinence of substances (licit or illicit).

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Mediate post-op (POM, first month) and late post-op (POT, as from second
month):
 Abstinence of substances (licit or illicit) first weeks

 Intensification of psychiatric syndromes known in preoperative
 Intensification of psychiatric syndromes unknown during preoperative
 States caused by dietary deficiencies (see above and other chapters of book)
 Use of licit or illicit substances leading to psychiatric states (via intoxication or
triggering)
 Attempted suicide11
At any time, in any surgery.

Some psychiatric conditions may be present in post-op of any type of surgery, not just
bariatric. Such as:
Factitious disorder, Münchausen Syndrome and Simulation. The Factitious

disorders are characterized by intentionally produced or simulated physical or
psychological syndromes with the purpose of playing the role of a sick person in the
absence of external incentives. In general, an individual is not aware of the motivation.
Münchausen syndrome is the most chronic and severe variant of its presentation and
seems to be the most frequent in men.
In simulation there is a clear direct gain such as indemnifications, running from the
police or a place to stay at night.3
Somatization. Polysymptomatic state with onset before 30 years of age, which takes
place for many years and is characterized by a combination of pain, gastrointestinal,
sexual, and neurological symptoms. The symptoms are not intentionally produced.3
Epilepsy with psychic and/or behavioral symptoms. Epileptic attacks present signs
and symptoms that reflect the affected area and could present motor, sensitive,
sensory-perceptive, autonomic and even psychic manifestations.12-13 The epileptic
attacks in the temporal lobe often present automatism, including crying, laughing,
shouting, walking, running, and kissing. The aura may involve feelings of fear or
anxiety, changes in gastric motility or a feeling of smelling strange things. The more
common secondary reactions and feelings or feelings and reactions during the epileptic
attacks of the temporal lobe are fear, anxiety, depression, depersonalization, pleasure,
displeasure.

Blanca Ríos, MD
4. Psychopharmacological treatment in post-op
Obviously there are few differences in treatment of PD in post-op compared to other

situations where they are present. The same psychotherapeutic,
psychopharmacological, and social conduct must be instituted.
However, some items must be observed, and only one is unique to BS:
1. Choosing the drug which is less associated to weight gain/metabolic alterations

whenever possible.
2. Be aware of drug and food interactions of psychoactive drugs.
3. Be aware of pharmacokinetic and pharmacodynamic changes that could
change the serum levels of substance(s) used.12,13
Conclusion
There is a high association of PD and obesity, notably in BS candidates. This fact

requires that the presence of a psychiatrist on the multiprofessional team be
mandatory.
On the other hand, BS seem to have a positive effect on some type of pre-existing PD
and a zero effect on others in the short and medium term. It seems that BS do not have
a positive or a negative effect on pre-existing PD in the long term.
There are no evidences that suggest a worsening of pre-existing states with weight
loss, provided the adequate psychiatric approach is implemented.
Likewise, PD that present post-op could be a result of many factors, where a
meaningful part of them can be addressed through prevention or specific treatment and
the minority is caused by BS.
One point worth being discussed is the high risk of suicide in BS post-op mentioned
above.11 In this study, suicide rates of operated patients were compared to the overall
population, paired according to gender and age, but not for BMI or for the presence of
psychiatric or dietary disorders. Therefore, although it is something to bear in mind, it is
not about proven scientific truth, as the media presented at the time.
Nevertheless, knowledge available is still insufficient, specially when the swashing of

indications for surgery and the so-called metabolic surgeries are considered. Specific,
prospective, adequate and ethically designed trials are necessary.

Blanca Ríos, MD
1. Segal, A.; Kussunoki, D.K.; Larino, M.A. Post-Surgical refusal to Eat: Anorexia
Nervosa, Bulimia Nervosa or a New Eating Disorder? A Case Series (2004):14, 353-
360.
2. American Psychiatric Association. Manual Diagnóstico e Estatístico de Transtornos
Mentais 4a Edição - Texto Revisado (DSM-IV-TR). Porto Alegre, Artmed, 2002.
3. Buchwald H; Avidor Y.; Braunwald E. et al. Bariatric Surgery: A Systematic Review
and Meta-analysis. JAMA, 14:1724-37, 2004
4. Fujioka K. Follow-up of nutritional and metabolic problems issues after bariatric
surgery. Diabetes Care 2005;28:481-4.
5. Hagedorn J.C.; Encarnacion B.; Brat G.A.; et al. Does gastric bypass alter alcohol
metabolism? Surg. Obes. Relat. Dis.; 3(5):543-8; discussion 548, 2007 Sep-Oct.
6. King WC, Chen J-Y, Mitchell JE, et al. Prevalence of Alcohol Use Disorders Before and
After Bariatric Surgery. JAMA, Published online June 18, 2012 Downloaded From:
http://jama.jamanetwork.com/ on 06/19/2012
7. Ross, H.E.; Ivis, F. Binge eating and substance abuse among male and female
adolescents. Int. J. Eat. Disord. 1999; 26: 245-260.
8. Kussunoki DK, Segal A. Transtornos Psiquiátricos no Pós-Operatório Tardio. In press.
9. Segal A. Obesidade e comorbidade psiquiátrica: caracterização e eficácia
terapêutica de atendimento multidisciplinar na evolução de 34 pacientes. São
Paulo, 1999. Thesis (Doutorate) - Faculdade de Medicina da Universidade de
São Paulo.
10. Ashton D, Favretti F, Segato G. Preoperative Psychological Testing—Another
Form of Prejudice. Obes Surg (2008)18-10, 1330-1337.
11. Tindle HA, Omalu B, Courcoulas A et al. Risk of Suicide after Long-term Follow-
up from Bariatric Surgery The American Journal of Medicine Volume 123, Issue
11 , Pages 1036-1042, November 2010
12. Giselle G. Hamad, M.D.; Joseph C. Helsel, B.S.; James M. Perel, Ph.D. et al.
The Effect of Gastric Bypass on the Pharmacokinetics of Serotonin Reuptake
Inhibitors Am J Psychiatry 2012;169:256-263.
13. Katharine Semion, M.D.; John Dorsey, M.D.; James Bourgeois, M.D.
Intravenous Valproate Use in Bipolar II Disorder After Gastric Bypass Surgery.
The Journal of Neuropsychiatry and Clinical Neurosciences 2005;17:427-a-429.

Blanca Ríos, MD
Chapter III
Revisional surgery and weight regain:
New roles for psychological intervention
Isabel C. M. Paegle
Gastro Obeso Center, GOC
Advanced Center for Gastroenterology
and Surgery of Obesity, Sao Paulo, Brasil
Blanca P. Rios Martinez

Hospital Ángeles del Pedregal
Ciudad de México, México.
With increasing weight regain after bariatric surgery, it is necessary to

understand the psychic functioning as well, forms of action and search for
complementary practices in patient care. This set of tools are essential for
practicing psychologist inserted in interdisciplinary teams of bariatric and
metabolic surgery.
The purpose of this chapter is to explain the ways of revisional surgery, its
indications and contraindications, assess the association of psychological
causes of weight regain. We opened a discussion on the role of bariatric
psychologist forward new surgeries.
And what would be the conduct of the clinical psychologist in contemporary
bariatric? The bariatric psychologist and his relationship with the team should
present collaborative attitude, approaching the other interdisciplinary knowledge
in order to better meet and following patients.
Ramos1 presented results on patients to perform the revision surgery focusing
on surgical techniques used in the first treatment. It showed the ineffectiveness
of some techniques, early postoperative complications or even a year after the
procedures. His humanized approach expanded the investigation beyond
technical: weight loss short of 50% of the preoperative BMI, feeding behavior in
unbalance. Difficulties patients face in new forms of eating routine, among
which search for hypercaloric foods, frequent tweaks, consumption of drinks,
alcohol abuse, psychiatric disorders.
According Ramos1 psychological predictors found in the population with weight
regain after bariatric surgery are changes in eating behavior: (hipercaloric food -

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sugar, sweets, fat); (snacks all the time); (soft drinks – gas and sugar); (alcohol)
and (psyquiatric disorders).
The indications to revisional surgery due inadequate / inappropriate weight loss
or weight regain are: Sugar/sweets Gastric bypass; Fat Duodenal Switch and
for alcoholism revisional surgery is contraindicated
In view of this research we present hypotheses for changing the bariatric

psychologist job considering associations between regained weight and
psychological factors.
In the literature there is a shortage of these data in our interest.
So far there is no scientific indication of a personality type or unique psychiatric
disorder morbidly obese but types of psychic functioning which comprise some
common features to this population.2
In Brazil, according to a survey carried out between 27% and 47% of patients
who undergo bariatric surgery exhibit binge eating and have difficulty planning
and organization.2
Therefore it is worth reflecting on reshape the practice of bariatric psychologist
to better serve this population with compulsive eating behavior and the
enigmatic psychological functioning difficulties of dealing with goals, objectives,
planning, organization.
In our clinical practice is common heed patients with complaints of difficulty of
financial organization, food, own the routine day-to-day.
We infer that the psychological profile of these patients are linked to dynamic
mental world ruled by anxiety, impulsivity, lack of time for own disorganization
and manifestation of the voracious phenomenon.
The observed weight regain factors happens between 3 and 6 years of post-
operative; They had less weight loss in the immediate post-surgical, did
multidisciplinary approach. Negative implications for change in lifestyle. 2
The need for inclusion in physical activities, care at the times and prepare
meals, practice of proper chewing, time to program and separate vitamins that
will be taken during the day, time to go the market to buy fruits and vegetables,
time and creativity to plan the menu of the week, and so avoid the fast food,
time for consultation of psychological and nutritional counseling.

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Eating behaviors distorsed to grazing, small quantities of food, however, calorie

(chocolate, "peanuts", wine, beer).
After the weight regained patients present intensification of symptoms of anxiety
and depression. The sense of failure and inability are the triggers for recurrence
of binge eating and obesity.
Preoperative clinical disorders related to anxiety, depression and binge eating
have high incidence among the obese.2
Using the questionnaire in psychology service must be guided by psychological
listening serving to describe the socio-demographic profile candidates for
bariatric surgery, analyze the patients' perception of personality traits
associated with obesity and eating disorders in addition to describing the
psychodynamic contents of the narrative the subject. It provides important
information for planning in the pre and post-surgical care. The results showed
psychological characteristics reported by patients: anxiety in 93.7% of
respondents, followed by impulsivity, depression, frustration tolerance, low self-
esteem, resolver of other problems (over 50%). The family history of obesity is
more than 70% depression and alcohol use for 30%; embodiment of
psychotherapy (30%) and drugs for depression and anxiety (10%).3
Patients with previous psychological disorders have 25 times more possibilities
of weight regain.4
A sense of frustration, fear, failure may trigger binge eating, by increasing the
intake of sugar and carbohydrates.5
The fundamentals of the theories and techniques of psychoanalysis allow us to
investigate the mental processes that bring harm to the life of the individual.
Access to mental processes is what will be the psychoanalytic and
psychotherapeutic work as well as knowledge and proper training and
dedication of professional leads him to adapt the techniques for alleviating the
patient's suffering.6-7
Usually doctors expect psychologists accurate and infallible diagnosis stating
the candidate for bariatric surgery and metabolic is favorable or not for the
procedure. Although this is the psychologist's role, the case study should be
continued because some behaviors can be predicted and others do not: some
complex environmental interactions arise at unexpected times.

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It is important to be aware of the professional psychic functioning from the initial

interview and complement the assessment with the use of unique instruments
for psychologists as projective techniques, which give us evidence of the kind of
personality and structure the patient presents.8
The psychologist also makes use of the interview and psychological listening,
which are different techniques of listening that is not psychological, listen to
what is not being said.8
The anamnesis provides clues about the first feelings on the emotional and
intellectual life of the individual and will resort theory of Melanie Klein's object
relations.
The first rewarding experience that the child gets the external world is
satisfaction to be fed; part of the satisfaction appears as famine relief and the
other party to the pleasure in sucking the breast. The absence of satisfaction
can mean a feeling of good mother's loss. The nascent ego and not prepared to
endure the frustration of "no presence" of the breast and avoids in his mental
world's displeasure, discomfort, anger and aggression. If the baby does not feel
good enough internal and external environment and this even in the absence of
the breast will have difficulties in overcoming equizoparanóide position and
reach the depressive position.9-10
The relationship with food since the beginning of life including the lactation and
weaning can be excessive sources of pleasure and greed and gluttony of the
start of the behavior, then seen in adulthood.
The beginning of the process to tolerate the frustrations renouncing the
immediate pleasure is found in our obese population.
If these excesses are not treated, distorted eating habits are revealed in repeat
way into adulthood with mature or not the ego that is linked to reality.
At this stage of development can happen to installation conditions such as
eating disorders, anorexia nervosa and bulimia and Binge Eating Disorder
(BED).
These disorders suggest a failure in preparing the necessary waiver to all the
pleasures of food, beyond emotion called greed by Melanie Klein (1946)

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associated with the desire to put inward parts of the object that early in life are
felt to be loaded integers all pleasurable goodies.9-10
The baby fancy this object within it the deliver of deprivation, but in reality the
organic responses stimulated by hunger, will rise.9
In adults, these sensations can be stimulated by the same forces and the
voracious cycle begins again.
We infer that there is dissociation between emotion and intellect among obese
even carry the conscious knowledge of the obesity condition of harm harvest
failures in non-invasive treatments.
Both the understanding of the psychological development of the individual, the

learning processes, family, social life are always associated with emotional
memory of food experiences, basic principles experiences of assimilation
determine the integration or unhealthy attachment behaviors.
It is indicated that during consultations both pre and postoperative psychologist

make a script, an activity schedule and present a plan for the patient choosing
the subjects and the ability to effectively manage time, focus and ability to
establish goals for weight loss, identify and implement strategies and actions
necessary to achieve the goal.
The bariatric psychologist must help the patient competence to develop skills of
self-control, especially eating impulses and flexibility to adjust your plan as
needed.
The psychologist, "personal emotion", is the professional that will work more
focused on motivation, organization and self-discipline to follow your plan
applying techniques related to human potential, tacking with the mission, values
and food and social beliefs.
The re-learning becomes a difficult process because a narcissistic organization
that guarantee pleasure and avoiding suffering and frustration deserves a
modification to healthy repetition, so at this moment we have the understanding
of psychoanalysis and techniques of positive psychology.
We can work also with the emotional intelligence that involves the ability to
understand their own emotions focused on self-awareness, manage their
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emotions, which is self-control, self-motivate yourself, or use their own emotions

in the service the proposed objective, recognize the emotions of others, such as
empathy, awareness of others and properly deal with the emotions of others.11
We conclude that patients with psychological disorders tend to regain weight
and eating disorders such as BED are the main causes.
The importance of psychodynamic psychodiagnostic reveals the unconscious
aspects that led the person to develop binge eating and obesity, facilitates the
psychologist's work as a guiding tool, as within large services the time factor is
critical for patient demand.
Faced with the difficulty of symbolization that these patients, direct intervention
in relearning to approach positive psychotherapy opens great possibilities to
plan, program and fulfill their tasks and weight loss.
Undoubtedly, the interaction of understanding of subjectivity and the
implementation of complementary practices enrich the psychologist in groups
returning to the clinic for regained weight.
Bibliographic references
1. Ramos AC. LSG Revision: what options do we have? What are the
expected results?. 3rd Annual Fall Education Event; Las Vegas, NV:
ASMBS - The American Society for Metabolic and Bariatric Surgery;
2012.
2. Venzon CN, Alchieri JC. Indicadores de Compulsão Alimentar Periódica
em Pós-operatório de Cirurgia Bariátrica. Psico – PUCRS 2014;
45(2):239-249.
3. Paegle ICM. Uso do protocolo no serviço de psicologia e avaliação
psicodinâmica em candidatos à cirurgia bariátrica. São Bernardo do
Campo, Brasil. Dissertação (Mestrado em Psicologia da Saúde) -
Faculdade de Psicologia e Fonoaudiologia, Universidade Metodista de
São Paulo; 2008.
4. Papapietro KV. Reganancia de peso después de la cirugía bariátrica.
Rev Chilena de Cirurgia 2012; 64(1):83-87.
5. Pajecki D, Halpern A, Cercato C, Mancini M, Cleva R, anto MA. Short-
term use of liraglutide in the management of patients with weight regain
after bariatric surgery. Rev Col Bras Cir. 2012;40(3):191-195.
6. Freud S. Recordar, Repetir e Elaborar (novas Recomendações sobre a
Técnica da Psicanálise II, 1914). In: Salomão J tradutor. Obras
Psicológicas Completas de Sigmund Freud. Rio de Janeiro: Imago
Editora;1974. XII, p.191-203.

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7. Freud S. Inibições, Sintomas e Ansiedade (1926). In: Salomão J

tradutor. Obras Psicológicas Completas de Sigmund Freud. Rio de
Janeiro: Imago Editora;1974. XX, p.107-108.
8. Paegle ICM, Gatto ME. Teorias psicodinâmicas e avaliação psicológica
em candidatos à cirurgia bariátrica. In: Segal A, Franques ARM,
coordenadores. Atuação Multidisciplinar na cirurgia bariátrica - A visão
da COESAS- SBCBM. São Paulo: Miró Editorial; 2012. p.131-138.
9. Klein M. Notas sobre alguns mecanismos esquizóides. In: Barros EMR,
Chaves LP, coordenadores. Inveja e Gratidão e outros trabalhos (1946-
1963). Rio de Janeiro: Imago, 1991. p.17-43.
10. Klein M. O desmame. In: Barros EMR, Chaves LP, coordenadores.
Amor, Culpa e Reparação e outros trabalhos. Rio de Janeiro: Imago,
1996. p.330-345.
11. Goleman D. Emotional intelligence-why it can matters more than IQ.
Bloomsbury; 1996.

Blanca Ríos, MD
Chapter IV
Pre-operative preparation of patients posted for

bariatric surgery.
Poonam S. Shah, M.D

Laparo-Obeso Centre,
Pune, India.
Role of the dietian in a bariatric program

In many Asian countries where ‘Bariatric surgery’ has recently started, ‘bariatric
nutrition’ is not a part of the Dietitian’s curriculum. Bariatric patients with their
many existing co morbidities and many post-operative nutritional challenges,
require regular dietary advice. These patients need tailor-made dietary tips as
per their procedure, pre-existing nutritional deficiencies, lifestyle and
affordability of nutritional supplements. Any successful bariatric program
therefore requires dedicated dietitians.
The role of the dietitian starts in the pre-operative period. It includes
understanding the lifestyle and eating habits of the patient, supervising a good
dietary preparation before surgery and educating the patient to the
postoperative dietary phases and requirements. It is important to coordinate
with other team members as to identifying the nutritional deficiencies, their
causes, identifying eating disorders etc.
Bariatric procedures bring about various physiological challenges made by the
anatomical changes of the surgical procedure. The dietian’s responsibility is
therefore, to understand the changes in the absorption of nutrients in every
procedure and find out the challenges expected. Understanding this therefore
helps them in educating patients and ensuing adequate nutrition to prevent of
any of the expected deficiencies.
Gaining knowledge of previous weight loss attempts i.e type of program, the
duration, results, reasons for failure or weight gain, helps the dietian to
understand the compliance, motivation level of the patient. The dietitian can
now help the patient to form realistic goals.
To ensure cooperation of the patients the dietian’s need to develop a good
rapport with the patient from the beginning of the preoperative period. It also
helps to identify the caretaker of the patient- a person whether related or

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unrelated to the patient but has a positive attitude towards the patient’s goals.
The caretaker therefore encourages the patient to follow-up regularly and also
attend the Support group meetings to educate themselves, which helps success
of the weight loss procedure.
There are special situations during which the patient needs the dietitian’s
guidance and support.
Patients need the dietitian’s help during weight loss plateau, especially if the
plateau is within the first year of surgery, when target weight not yet reached.
Even later on after target weight loss achieved but weight gain started. Patients
may go through anxiety of gaining back all the lost weight, sometimes guilt of
being responsible for the same. It is important for the dietitian of the unit to
support and guide the patient through such challenging periods. If the patient
happens to get pregnant during the first one and half year when the weight loss
is still going on, she will need supervised dietary advice during the pregnancy
as well as post-partum period.
To help prevent patients from developing any nutritional deficiencies the

dietitian keeps in touch with the patient and the caretaker encouraging the
patient to follow-up regularly and do the required nutritional work-up when
indicated.
The ‘Support group meeting’ is a good platform for the dietitian to educate the
patients and their families- by discussing various aspects of nutrition,
demonstrating receipes, helping make right choices, reading nutrition labels
correctly etc. Various small studies have shown that patients who attend the
Support Group meetings do much better than those who don’t.1-3
Nutritionist need:
1. Identifying nutritional deficiencies and eating disorders preoperatively.

2. Understanding patient’s lifestyle, eating habits, choices and availability of
nutritionally rich food.
3. Supervising pre-operative preparation.

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4. Educating for post-operative nutritional challenges.

5. Identifying patient’s caretaker.
6. Supervising post-operative diet phases, ensuring adequate calorie and liquid
intake.
7. Educating through Support Group meetings- recipe demonstration of nutritional rich
food, reading nutrition labels, etc
8. Ensuring follow-up of long distance patients through phone, emails, chatting
etc.
Pre-operative preparation of patients posted for bariatric surgery.

Why do patients posted for bariatric Surgery need to be evaluated and
prepared before surgery?
Obesity is a multi-organ disease with various co morbidities which pose a risk

for anesthesia and also with a range of existing nutritional deficiencies which
may affect wound healing and post-operative quality of life.
The Pre-operative evaluation helps in identifying peri –operative and post-
operative challenges.
1. Comorbidities like OSA, DM, HT, varicose veins increase the risk to life
during anesthesia and immediate post-operative period, if not controlled before
surgery.
2. Identifying psychological problems and judging the severity of eating
disorders is important before accepting patient for surgery, as they may affect
the long term results of the procedure.
3. Knowing if the patient has a support system at home and identifying the
caretaker of the patient, for educating along with the patient, is again important
to help the patient prepare correctly before surgery and also be able to maintain
the achieved results after the procedure.
4. It is important to make the patient understand and choose realistic targets
before surgery, so as to be prepared to work towards achieving the same during
the posoperative journey.
Preoperative evaluation and supervised preparation is therefore a team work.

Proper selection and training of all team members is important.

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Preoperative Evaluation by the bariatric team
*Detail history of patient, including past and existing Medical Problems,

medications past and present.
*Details of past Surgical procedures especially abdominal surgeries, open/lap,
healing period.
*Details of any previous weight loss procedure- type, open/lap, peri-operative
period, diet plan followed post-surgery, complications, weight loss pattern,
weight gain.
*Details of Weight gain pattern, Attempts at weight loss and their duration,
results, causes of failure.
* Life style of the patient- working hours, daily physical activity, diet pattern and food
choices.
* Family history-of Obesity, DM, Hyperlipidemia, Cancers etc
* Physical Examination- including Anthropometry.
* Evaluation by Team Dietitian
*Evaluation by Team Psychologist
* Laboratory Evaluation – Co-morbidities evaluation, Fitness for Anesthesia, nutritional
assesment tests.
* Evaluation by Specialists as indicated after above preliminary testing:
Cardiologist/pulmonologist/gynecologist/endocrinologist/paediatrian /
orthopedic /ophthalmologist/neurologist, etc
Importance of Nutritional assessment

Obesity is a assumed to be a state of ‘Over Nutrition’ but in fact it is a state of
‘Malnutrition’ -as it is seen to be associated with multiple nutritional deficiencies.
The following deficiencies are commonly seen in Obese patients before
surgery.4-9,
-Vitamin D, Calcium –(Secondary Hyperparathyroidism)
-Viamin B-Complex – B12, Folic Acid, B1, B6. (Diabetics, Vegetarians)
-S. Fe, Ferritin, TIBC
-Vitamin A, E, K

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-Zinc, Copper, Selenium

-Protein (vegetarians)
The deficiencies would worsen post-surgery, more so, if the patient undergoes
malabsorptive procedures. Therefore diagnosing and correcting these
deficiencies before surgery will help wound healing and prevents post-operative
deficiencies.
Pre-operative evaluation by a dietitian
1. Daily Routine- including amount of Physical Activity

2. Daily Diet:
- Eating habits- when, what, where?
- Eating choices-Vegetarian, Non-vegetarian, sweet? Fluid intake – water,
aerated drinks, fruit juices, alcohol?
- Affordability, access to nutritional food, use of supplements
- Commitment to following instructions?
past weight loss attempts – results…
3. Coordinate with Physician and Psychologist- to

* Identify pre-existing deficiencies,
* Identify eating disorders
Psychological Assessment Pre-Surgery

- Life style,
- Identifying eating disorders,
- Identifying addictions- Past, Present.
- Identifying psychiatric illnesses and medications being used
- Evaluating commitment of patient and family.
Physical Evaluation Pre-Surgery

1. Anthropometry to judge severity of Obesity- height (HT)*, weight (WT), body
mass index (BMI),diabetes Mellitus, Waist: Hip ratio.
*Waist, Neck, Arms, Chest, Abdomen, Thighs, Calf circumference.

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2. General Examination including for signs of internal diseases like Pre- DM,
Hypothyroidism, Cushings, Alcoholism, Hyperlipedimia etc – e.g
acanthosis, warts; neck fullness, moon facies, xanthomas, buffalo hump,
strai, parotid swelling, pedal edema, varicose veins, pallor, skin dryness,
discolouration,
3. Systemic examination.
Laboratory Tests:
Co-morbidities Evaluation And Fitness for Anesthesia
- Haemogram, Hematocrit, PBS,
- GTT with S. Insulin levels (non-diabetics/ prediabetics)
- BSL F & PP, HbA1c, S. Insulin and C. Peptide F &PP (Diabetics)
- Anti-Insulin antibodies, Anti –Gad etc* (Type I DM?)
- Liver function Tests
- Coagulogram:
- S.Iron Studies- Ferritin, TIBC etc
- Renal Function: BUL, S. Creatinine, Urine protein loss over 24 hrs.
- Urine microscopic examination
- S. Uric acid
- S. B12, Folic Acid, S.B1.
- S. Calcium, Vitamin D, PTH.
- S. Proteins, Prealbumin.
- Lipid Profile,
- HIV / AuAg
Hormonal
- S. FSH / LH / Prolactin* (PCOD)
- Thyroid function tests,
- S.Cortisol*
Radiological
-Chest x-ray, X-rays of affected joints*,
-UltraSonography of Abdomen & Pelvis,

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-CT SCAN for Liver volumetry*,

-DEXA scan*.
-Venous Doppler studies of lower limbs
Cardiac
ECG, 2-D ECHO.
Stress test / Stress Thallium/ Thallium Scan*.
Pulmonary Function
PFTs*-Baseline ABG,
Sleep studies*, Baseline ABG.

Upper GI Endoscopy & Manometry*
Preparation for Surgery by bariatric team
(*In Selected cases only)
- Comorbidities- review of severity and medications, control.

- Dietary Preparation-
 Very Low Calorie Diet (VLCD) for decreasing Liver size & Friability
 Optimization for Anasthesia.
 Weight record- judge commitment
- Lung preparation-
 Breathing exercises, Spirometry, Steam Inhalation,

 BiPAP or CPAP for Obstructive Sleep Apnea (OSA)
- Physical activity -
1. Walks
2. Limb exercises, Physiotherapy
3. Deep Vein Thrombosis (DVT) prevention
4. Stockings,

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5. DVT Prophylaxis-
*Education of patient and family- regarding procedure, post-operative diet plans.
Pre-operative dietary preparation: Does it help?

This is a topic of controversy. So each Bariatric program has its own protocol.
Few small studies have found favorable short term results of dietary preparation
like:-
• Decreases liver size/volume and intra-abdominal fat.
• Improves visual field for the surgeon.
• Shortens operating time.
• Decreases post-operative risks/complications.
• Decreases Hospital Stay.
• Controls co-morbidities.
• Increases patient’s understanding of post-op dietary requirements.
• Opportunity to correct pre-operative nutritional deficiencies
*Improves post-op healing
*Prevents exacerbation of existing preoperative nutritional deficiencies.
In fact pre-operative dietary preparation prepares the patient physically and
mentally for the surgery and post-surgery life long journey.
Pre-operative Diets and Duration

In many of the Asian countries bariatric surgeries are not supported by
insurance, but in those countries where some procedures are covered by
insurance, the Insurance company may make it mandatory for the patient to
show 10% weight loss before surgery. However this maybe mainly for judging
the patient compliance, than attempting to improving any specific medical
condition. Therefore the pre-operative diet preparation for such cases is
because it is made mandatory by the insurance company.
However in majority of bariatric centers worldwide the pre-operative dietary

preparation is made mandatory by the team physicians to improve the existing
co morbidities of the patient to make the operative (under anesthesia) and
immediate post-operative period safer and comfortable for the patient. The time

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period for preparation is anytime from 48 hours to 6 months depending on the

team’s decision for that particular patient. Most centers make it mandatory for 2
weeks i.e 15 days at least.
Depending on the duration of diet the consistency could be liquid or soft/solid i.e
when the preparation is for smaller periods like 2 to 3 weeks the diet advised is
‘high protein, low carb, no fat liquid diet.
When the diet period is longer a ‘high protein, low-carb, low fat non-liquid diet’
works better to maintain the patient hunger control and hence the compliance.
Therefore the diet should decide by patient and the bariatric team depending
upon the ‘waiting time’ period for surgery.
The waiting time could be decided by various factors from the patient’s side
(making financial arrangements, getting mentally prepared etc) or it could be the
team’s opinion. The medical indications for longer waiting time could be many
e.g Uncontrolled co morbidities like.
Uncontrolled hypertension, uncontrolled diabetes especially with a chronic
infection of urinary or respiratory system; recently detected severe
hypothyroidism; uncontrolled irritable bowel, any stage of renal insufficiency
with high S. creatinine and S. potassium; recent episode of ischemic heart
disease on anti-coagulants; recent major surgery especially bone surgery
requiring patient to be bed-ridden; uncontrolled Bronchial asthma etc.
**Supervised preparation-
In our centre super-obese patients with respiratory insufficiency, sleep apnea,
uncontrolled diabetes with an infection, varicose veins with limb swelling or
chronic non-healing ulcer, renal insufficiency, anasarca, patient unable to follow
diet as alone or out-station-- an in-hospital preparation is made mandatory.
This helps the team to medically supervise the patient well and maintain his/her
motivation.
How does pre-operative dietary preparation help the Surgeon and the
Patient?
The intraabdominal organs like the liver, pancreas, omentum are laden with fat in the
obese. The fat laden liver is big, heavy and brittle – It therefore obstructs the visual field

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of the surgeon, who is operating on the stomach just below the liver. Manipulating the
liver to clear the operating field may injure the liver.
The body normally converts carbohydrates to glucose to be used as a main

source of energy. So if there is a shortage of carbohydrates going inside the
body, the body has to shift to fat, to be broken down and use for energy. Once
the liver has used all of its stored glucose, it therefore begins to metabolize fatty
acids. This helps in mobilizing the fat from the storage sites, which when done
for longer time decreases the fat from the liver. This decreases liver volume and
makes it softer.
The glucose is stored in the liver and muscles as glycogen which is stored with
water-So when the glycogen stores deplete water loss from liver also occurs,
probably causing a decrease the volume of the liver too. These changes
probably improve the ‘visual field’ for the surgeon.
A low carbohydrate diet for a long time decreases brings about a generalized
‘weight loss’ also. The decrease in liver volume and generalized weight loss
probably decreases the pressure of the abdomen on the lungs, improving lung
expansion. Doing breathing exercises, blowing balloons or frequent spirometry
also helps to improve the lung function also.
Use of Meal Replacements for dietary preparation
Meal replacements powders, which contain High Protein, Low Carbohydrate, no

Fat with vitamins and trace elements, can be included in the long time non-
liquid diet and are an important part of the short-time liquid diet too. They are
lower in carbohydrates, so body has to breakdown and use the stored fat for
energy. The protein which is high quality and easily digestible gives satiety and
also prevents muscle loss, hair loss etc. The added vitamins trace elements,
minerals correct/prevent deficiencies. Therefore the weight loss is without a
feeling of weakness or hunger.

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Side-Effects of Low Carbohydrate /High protein Diet
 Hypoglycemia –Lowering of the blood glucose to below normal can occur in

diabetic patient on anti-diabetic drugs. So the blood sugar levels need to be
frequently monitored to adjust drug doses to prevent hypoglycaemia. e.g the
OHA may be required to be decreased to half and ideally patient shifted to short
acting Insulin especially for last 48 hrs, as the insulin doses are easy to titrate.
 Starvation Ketosis: If the patient is on a severely calorie-restricted diet that is

extreme or is unmonitored, there is depletion of stored glucose and
subsequently can lead to a state of ketosis. If this remains undetected, the
starvation ketosis can result in ketoacidosis, a condition in which ketones can
reach abnormally high levels that can be dangerous or life threatening. So all
patients on dietary preparation have to be well supervised by the team. Those
patients who do the dieting at home a relative/caretaker should also be involved
and educated to supervise.
 Renal Function to be monitored in those with nephropathies, or on diuretics.
Patient can end up with a renal colic or even acute renal failure. Those with mild
renal insufficiency can deteriorate.
 Constant hunger especially if diet options not correct or timings not followed or
liquid intake inadequate, the patient may become irritable. It may discourage the
patient from following the instructions and may give up the preparation.
 Loose motions, frequency of urination may give rise to dehydration.
Some Clinical Studies on ‘Effect of pre-operative weight loss’
Cassie et al,1 did a systematic review of 27 studies in which they found only two
randomized control trials (RCT), which were from same patient population. They
concluded that little evidence is available in their review to support or refute the
routine use of preoperative weight reduction in bariatric surgery. They suggest a
large-scale, multicenter, randomized, controlled trial with sufficient power is
necessary to clarify this significant aspect of preoperative care.

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Another systematic review was done by Ochner CN et al,2 ‘Pre-bariatric surgery

weight loss requirements and the effect of preoperative weight loss on
postoperative outcome’ they even looked at the insurance mandated
preoperative requirements. They concluded that ‘preoperative weight loss may
lead to improvements in at least some relevant postoperative outcomes’. They
also comment that ‘a preoperative weight loss mandate may lead to the denial
of surgery and subsequent health benefits to individuals who are unable to
achieve a pre-specified amount of weight.
A prospective randomized trial was done by Alami et al,3 to study the benefit of
preoperative 10% weight loss in gastric bypass patients, whether preoperative
weight loss results in better outcomes after laparoscopic gastric bypass as
compared to the pre-operative non-weight loss group. They studied the peri-
operative complications, operative time, postoperative weight loss, and
resolution of co-morbidities. They concluded that the weight loss was
associated with a decrease in the operating room time and an improved
percentage of excess weight loss in the short term. However it had no effect on
co morbidity resolution or did not affect any major complication or conversion
rates.
In 2011, American Society for Metabolic and Bariatric Surgery (ASMBS),4
published a Position Statement on ‘Preoperative Supervised Weight Loss
Requirements’ which provides an evidence-based review of the medical
literature regarding the common healthcare insurance requirement for patients
to provide documentation of supervised diet attempts for various periods of time
before authorization to pay for bariatric surgery services. They conclude that
there are no Class I studies or evidence-based reports that document the
benefits of, or the need for, a 6 to 12 month pre-operative dietary weight loss
program before bariatric surgery. The current evidence supporting preoperative
weight loss involves physician-mandated weight loss to improve surgical risk or
to evaluate patient adherence. Studies 5 to 23 are reviewed during making of
this position statement.
The ASMBS with the AACE and the TOS have published guidelines for the pre-
operative preparation of the obese patients.9

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Biblioghapical references
1. Livhits M, Mercado C, Yermilov I, Parikh JA, Dutson E, Mehran A, Ko

CY, Shekelle PG, Gibbons MM.: Is social support associated with greater
weight loss after bariatric surgery?: a systematic review:Obes Rev. 2011
Feb;12(2):142-8. doi: 10.1111/j.1467-789X.2010.00720.
2. Kaiser KA, Franks SF, Smith AB: Positive relationship between support
group attendance and one-year postoperative weight loss in gastric
banding patients. 2.2011 Jan-Feb;7(1):89-93. doi:
10.1016/j.soard.2010.07.013. Epub 2010 Aug 11.
3. Song Z, Reinhardt K, Buzdon M, Liao P: Association between support
group attendance and weight loss after Roux-en-Y gastric bypass. Surg
Obes Relat Dis. 2008 Mar-Apr;4(2):100-3. Epub 2007 Apr 2.
4. Flancbaum L, et al. Preoperative nutritional status of patients undergoing
Roux-en-Y gastric bypass for morbid obesity. J Gastrointestinal Surg
2006;10:1033-7.
5. Buffington CK, et al. Vitamin D deficiency in the morbidly obese. Obes
Surg 1993;3:421-4.
6. Carlin AM, Rao DS, Meslemani AM, et al. Prevalence of vitaminosis D
depletion among morbidly obese patients seeking bypass surgery. Surg
Obes Related Dis 2006;2:98 –103.
7. Madan AK, et al. Vitamin and trace mineral levels after laparoscopic
gastric bypass. Obes Surg 2006;16:603-6.
8. El-Kadre LJ, Roca PR, de Almeida Tinoco AC, et al. Calcium metabolism
in pre and postmenopausal morbidly obese women at baseline and after
laparoscopic Roux-en-Y gastric bypass. Obes Surg 2004;14:1062– 6.
9. ASMBS Allied Health Nutritional Guidelines for the Surgical Weight Loss
Patient:Linda Aills, R.D. (Chair)a, Jeanne Blankenship, M.S., R.D.b,
Cynthia Buffington, Ph.D.c, Margaret Furtado, M.S., R.D.d, Julie Parrott,
M.S., R.D. Surgery for Obesity and Related Diseases 4 (2008) S73-S108

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Chapter V
Post-bariatric surgery nutrition
Luca Busetto, MD
Department of Medicine
University of Padua – Italy
Any bariatric procedure induces significant changes in morbid obese patients

nutritional status and habits. Gastric restriction is a part of any traditional
bariatric procedures and requires the adaptation of patients eating behavior to
the reduced stomach size. Furthermore, other nutritional problems and
symptoms may be caused by procedure-specific characteristics. The absorption
of macro- and micro-nutrients may be affected in different ways according to the
anatomical clues of the procedure and differential schemes of vitamins and
minerals supplementation should be advised. The nutritional management of
the post-bariatric patients requires therefore specific nutritional skills and should
be followed by experienced nutritionists and dieticians. Detailed guidelines for
post-operative bariatric nutritional management has been published1,2 and
recently updated.3 In this chapter, we will perform a brief overview of the most
relevant aspects of post-bariatric surgery nutrition and we refer to more detailed
guidelines and position statements for further information.
General aspects in post-surgical nutritional management

Post-op diet
Any traditional bariatric procedure (adjustable gastric banding, sleeve
gastrectomy, Roux-en-Y gastric bypass, bilio-pancreatic diversion or bilio-
pancreatic diversion with duodenal switch) includes the reduction of the volume
of the stomach and the creation of a small gastric pouch. Post-op gastric edema
and inflammation usually precludes the ingestion of solid foods in the first days
after surgery and a very gradual progression of food consistencies in the first
post-op weeks may help the patients to minimizes vomiting, which can threaten
the integrity and safety of the recent surgical procedure. A low-sugar clear liquid
meal program can usually be initiated within 24 hours after any of the bariatric
procedures.1-3 Thereafter, patients should be instructed to gradually and
progressively increase foods consistency, moving from clear liquids to soft or

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creamy foods and then to solid chewable items over first 2-4 weeks. Before
discharge patients should receive a consultation for postoperative meal initiation
and progression with an experienced bariatric dietician and education in a
protocol-derived staged meal progression based on their surgical procedure.3
Specific protocols for meal progression have been suggested for most of the
bariatric procedures,1 but individual protocols may be designed by single
bariatric centers, taking into account personal and regional variations in food
preferences.
Long-term dietary advice

After the end of the post-op diet, patients should be regularly counseled by an
experienced dietician about long-term dietary modifications, in order to
maximize the results of the bariatric procedure and reduce the risk of late
weight regain. Dietary counseling is particularly important after pure restrictive
procedures, but its role should not be neglected even after mixed or
malabsorptive procedures. Sarwer et al. randomized 84 bariatric patients to
receive either regular dietary counseling or standard postoperative care for the
first 4 months after surgery and observed that patients who received dietary
counseling achieved greater weight loss than those who received standard
postoperative care that did not involve this counseling, although this difference
did not reach statistical significance.4 Patients in the dietary counseling arm did
report significant changes in several eating behaviors believed to be important
to successful long-term weight maintenance.4 Dietary counseling should be
centered on the adaptation of patients eating behavior to the surgical procedure
and on the general qualitative aspects of a healthy diet. Patients with gastric
restriction should be counseled to eat three small meals during the day and
chew small bites of food thoroughly before swallowing, without drinking
beverages at the same time (at least 30 minutes apart).1-3
Physical activity
The role of regular physical activity after bariatric surgery has been recently
reviewed by Jacobi et al.5 This literature search identified 19 observational
studies analyzing self-reported physical activity data in relation to bariatric

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surgery. The time frame for physical activity assessment varied: before surgery
in two publications, after surgery in nine, and longitudinal pre- to post-operative
evolution in nine. The latter nine publications found an increase in physical
activity after bariatric surgery. In 10/13 studies where it was described, there
was a positive relationship between physical activity level and amount of weight
loss.5 In conclusion, on the basis the available observational evidence, regular
physical activity should be encouraged after bariatric surgery. Patients should
be advised to incorporate moderate aerobic physical activity to include a
minimum of 150 minutes per week and goal of 300 minutes per week, including
strength training 2 to 3 times per week.3 More detailed guidelines for prescribing
exercise may be derived from specific position statements of the American
College of Sport Medicine (ACSM).6,7
Protein intake
Protein intake is generally reduced following bariatric surgery.8 Protein-deficient
meals are common after all the procedures having a restrictive component, they
are generally more frequent in the first months after surgery and may be
attributed to the development of gastric intolerance to protein-rich foods.1
Usually, most food intolerances tend to diminish over time and protein intake
may resume, but protein intake may be lower than recommended in the first
year after surgery, when most part of weight loss is achieved. A higher protein
intake (80-90 g/day) may be protective against the loss of lean body mass in the
phase of rapid weight loss after surgery.9 Therefore, dietary counseling should
address the problem of protein intake, particularly in the first months after
surgery, guiding the patients to assume a minimal protein intake of 60 g/day
and up to 1.5 g/kg ideal body weight per day.3 Adequate protein intake can be
facilitated through the use of protein supplements, though a causal effect of
protein supplement use and favorable body composition change has not been
demonstrated.10
Protein malnutrition
Protein malnutrition remains the most severe macronutrient complication
associated with malabsorptive bariatric procedures and its frequency strictly

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depends from the degree of the malabsorption, as well as from patients dietary
habits and protein requirements. A frequency of 13% has been reported 2 years
after a distal RYGB with a Roux limb ≥150 cm in super-obese patients,11
whereas a much lower rate (<5%) has been reported after RYGB with a Roux
limb <150 cm.12 The frequency of protein malnutrition after bilio-pancreatic
diversion or duodenal switch have been reported to vary between 3 and 18% of
patients.1 Protein malnutrition may be precipitated in individual patients by the
occurrence of any pathologic (infections) or physiologic (pregnancy) state
characterized by an increase of protein requirements. Prevention of protein
malnutrition involves regular assessment of protein intake and encouraging the
ingestion of protein rich foods (>60 g/d) and use of modular protein
supplements.1 Nutritional support with parenteral nutrition is warranted in case
of severe protein malnutrition and surgical revision and lengthening of the
common channel to decrease malabsorption should be considered if a patient
remains dependent on parenteral nutrition or has recurrent episodes of protein
depletion.13,14
Nutritional support
Nutritional support with enteral or parenteral nutrition should be considered in
bariatric surgery patients at high nutritional risk.3 Specific guidelines for the use
of enteral or parenteral nutrition in bariatric patients have not been developed,
but advanced clinical practice general guidelines for nutritional support in
critically ill patients are disposable15,16 and they may be adapted to the field of
bariatric nutrition. Parenteral nutrition should be considered in those patients
who are unable to meet their nutritional needs using their gastrointestinal tract
for at least 5-7 days in the presence of a noncritical illness or for 3-7 days in the
presence of a critical illness.3 Parenteral nutrition should also be considered in
patients with severe protein malnutrition not responsive to oral or enteral protein
supplementation.3 The opportunity to start nutritional support in an individual
patient should be guided by overall clinical status and it may be facilitated by
the calculation of the Nutrition Risk Score 2002 (NSR 2002), a validated
instrument to identify patients who would benefit from nutrition support.17 The
NSR 2002 is reported in table 1.

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Table 1. Nutrition Risk Score (NSR 2002): a validated instrument to identify

patients who would benefit from nutrition support [modified from Ref # 17].
Impaired nutritional status Severity of disease (≈ stress

metabolism)
Absent Normal nutritional status Absent Normal nutritional
Score 0 Score 0 requirements
Hip fracture
Mild Wt loss >5% in 3 months Mild Chronic patients with acute
Score 1 Or Score 1 complications: cirrhosis
Food intake 50-75% of COPD
normal requirement in Chronic hemodialysis
preceding week Diabetes
Oncology
Wt loss >5% in 2 months
Moderate Or Moderate Major abdominal surgery
Score 2 BMI 18.5-2035 + impaired Score 2 Stroke
general condition Severe pneumonia
Or Hematologic malignancy
Food intake 25-50% of
normal requirement in
preceding week
Wt loss >5% in 1 month
Severe Or Severe Head injury
Score 3 BMI <18.5 + impaired Score 3 Bone marrow
general condition transplantation
Or Intensive care patients
Food intake 0-25% of
normal requirement in
preceding week
Score +
Total score:
Calculate the total score:
1. Find score (0-3) for Impaired Nutritional Status and Severity of Disease.
2. Add the two scores (→total score).
3. If age ≥70 years: add 1 to the total score to correct for frailty of elderly.
4. If age-corrected total score ≥3: start nutritional support.
Management of specific nutritional problems and symptoms

Food intolerance, vomiting and regurgitation
Food intolerances are common after any bariatric procedure having a restrictive

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component. The foods most frequently involved are meat products. Intolerance
to bread, rice and pasta may also occur. Food intolerances tend to diminish
over time, but patients may remain intolerant to particular foods even in the long
term. Food intolerances are frequently related to patients inability to comply with
the changes in eating behavior requested by gastric restriction and may be
facilitated by rapid eating, insufficient chewing or drinking during meals.
Continuous educational support and reinforcement by experienced dieticians
and nutritionists has been proved to be important in facilitating patients
behavioral adaptation.4 The use of alternative foods may be suggested. Food
intolerances and behavioral errors may cause episodes of vomiting or food
regurgitation during meals. Occasional episodes of vomiting occur frequently in
the first months after surgery, when the patients are still adapting to a small
gastric pouch,1 and they should be viewed as a minor side effects of surgery.
Episodes are frequently described by the patients as “spitting up” or “food
getting stuck”1 and they are usually self-limiting. However, in case of persistent
(>6 months) and/or frequent vomiting, an organic cause (obstruction, stomal
erosion, stomae stenosis) should be suspected and a radiologic/endoscopic
evaluation should be considered.1 In case of persistent vomiting heavily
disturbing normal eating and greatly reducing energy intake, the possibility of
the onset of an acute state of thiamine deficiency should be considered (see
below).
Banding adjustments
In adjustable gastric banding, the size of the band and by a consequence the
diameter of the proximal gastric pouch outlet may be modified after surgery,
thus regulating the degree of gastric restriction. Banding adjustments may be
performed on an outpatient basis, through a percutaneous injection of some of
sterile saline solution in to the sub-cutaneous port placed at the abdominal
level, with or without radiologic checking.18 Adjustments of the banding volume
are a major feature of the procedure and should be considered integral to the
follow-up process.19 In case of large or underinflated band, the patients may
experience a very low sense of satiety during meals, thus having difficulties in
following an appropriate hypo-caloric diet. On the other hand, if the band is too

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tight or overinflated, the patient may have difficulty with solid foods and may be
forced to consume mainly liquids or very soft foods, frequently having a high
caloric content. This type of maladaptive eating behavior has been indicated as
“soft calories syndrome” and it is associated to poor weight loss or weight
regain.20 An excessively tight gastric banding, in combination with poor eating
behavior, including frequent regurgitation, is believed to be a significant factor in
the development of gastric pouch dilatation.21 Appropriate banding adjustment
is considered therefore critical in determining the success of gastric banding in
the long term. The maximum band filling volume and the volume of saline
solution that should be added or removed during each adjustment procedure
depend on the type and size of the banding. In general, prudent and more
frequent step-by-step adjustments at regular follow-up visits should be preferred
to uncontrolled large variations of banding volume. Some simple symptoms-
driven suggestions for guiding band adjustments are proposed in Table 2.
Table 2. Indicators for symptoms-driven adjustable gastric banding post-

operative regulation [modified from Ref # 18].
Consider adding Adjustment not Consider removing fluid
fluid required
Inadequate weight Adequate rate of weight Vomiting, heartburn, reflux
loss loss
Rapid loss of satiety Eating most types of Coughing, wheezing and
food choking, especially at night
Increased meals No negative symptoms Difficulty coping with broad
volume range of foods
Hunger between Maladaptive eating
meals behavior*
* Usually characterized by the consumption of high-calorie liquid or very soft foods.
Dumping syndrome
Dumping syndrome refers to symptoms and signs that are elicited by the rapid
transit of calorie-dense food to the small bowel and it is a frequent side effect
after bariatric surgery, typically gastric bypass. Some dumping symptoms occur
initially in a high proportion (70-75%) of patients who have had a gastric

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bypass,1 but the frequency of clinically troublesome episodes is much lower and
tends to diminish after the first post-operative year.1 Dumping has been
suggested as a possible mechanism contributing to weight loss after gastric
bypass, through the negative conditioning of consuming high energy-dense
foods.22 However, there is no convincing evidence proving an association
between the amount of weight loss following gastric bypass and the severity of
dumping syndrome.23 Dumping was classically attributed to a rapid increase in
osmolarity of the intestinal content which led to an influx of fluid into the
intestinal lumen with subsequent intestinal distention, fluid sequestration,
decreased intravascular volume and hypotension.24,25 More recent data
suggests that dumping may be at least in part caused by the abrupt changes in
the secretion of gut peptides (GLP-1) induced by gastric bypass and involved
also in the regulation of glucose metabolism and weight loss.26 In clinical
practice, symptoms of dumping syndrome can be classified as early or late,
depending on how soon after ingestion they occur.24,25 Early symptoms occur
about 10–30 minutes after meal and comprise both gastro-intestinal and
vasomotor symptoms. Gastro-intestinal symptoms include abdominal pain,
diarrhea, nausea and bloating. Vasomotor symptoms include fatigue, a desire to
lie down after meals, facial flushing, palpitations, perspirational tachycardia,
hypotension and syncope.22 Early symptoms can usually be controlled with
certain nutritional manipulation, such as eating small frequent meals, avoiding
ingestion of liquids within 30 minutes of a solid-food meal, avoiding simple
sugars and increasing intake of fiber and complex carbohydrates, and
increasing protein intake.1 If these nutritional measures are unsuccessful,
octreotide, 50 μg subcutaneously 30 minutes before meals, may be helpful
symptoms in some patients.1
Late symptoms occur 1–3 hour after ingestion of a meal and include symptoms
like perspiration, palpitations, hunger, fatigue, confusion, aggression, tremor,
and syncope.22 Late dumping is more strictly related to “reactive hypoglycemia”
and can often be managed with nutritional manipulation or be treated
prophylactically by having the patient drink half a glass of orange juice (or taking
the equivalent small sugar supplement) about 1 hour after eating.1 However, in
case of severe hypoglycemic events with neuroglycopenic symptoms,

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alternative causes of hyperinsulinemic hypoglycemia (pancreatic beta-cells

hyperplasia, insulinoma) should be considered and actively searched.27,28
Diarrhea – steatorrhea
Disordered bowel habits are frequent after malabsorptive bariatric surgery, as a
consequence of fat and carbohydrate malabsorption and the changes in the
equilibrium of intestinal flora with bacterial overgrowth syndrome. Patients
undergoing classic bilio-pancreatic diversion or duodenal switch frequently
reported an increased number of bowel movements with loose stools or
diarrhea, fecal urgency, abdominal bloating and smelling flatulence.29 Bowel
symptoms after malabsorptive bariatric procedures may impair quality of life and
may be controlled by dietary manipulation, with the avoidance of fatty or
carbohydrate-rich foods, and by regular or intermittent use of intestinal anti-
bacterials.
Vitamins and minerals deficiencies and supplementation

General concepts
The frequency and severity of vitamins and minerals deficiencies after bariatric
surgery depends primarily on the type of the surgical procedure. Purely gastric
restrictive procedures are not associated with alterations in intestinal continuity
and do not alter normal digestive physiologic processes. As a result, selective
nutritional deficiencies are uncommon. On the other hand, the anatomic
changes imposed by malabsorptive surgical procedures increase the risk for
various nutrient deficiencies.1 However, other factors besides surgical technique
may be relevant to the occurrence of nutritional deficits after bariatric surgery,
such as regular food intake and vitamin supplementation. Reduction in the
quantity and quality of food intake and irregular use of vitamin supplementation
may be caused by clinical, socio-economic and psychological factors. Intestinal
adaptation, a compensatory phenomenon occurring in short bowel patients in
which anatomic and functional changes progressively increase the gut’s
digestive and absorptive capacity, may occur also after bariatric procedures.
Intestinal adaptation begins in the early postoperative

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period, but may take up to three years to complete. It is unclear if and how
intestinal adaptation processes may affect long term weight maintenance and
nutritional status.2
Detailed descriptions of vitamins and minerals deficiencies that may be
encountered after bariatric surgery, their symptoms and consequences, and the
rationale for vitamin supplementation have been published.1-2
Iron
Iron deficiency and iron deficiency anemia are common after Roux-en-Y gastric
bypass, biliopancreatic diversion and biliopancreatic diversion with duodenal
switch, especially in women with menorrhagia.1 Iron deficiency has been
reported also after sleeve gastrectomy30 and more rarely after adjustable gastric
banding.2 Etiology of iron deficiency after bariatric procedures is multi-factorial.
Although the absorption of iron can occur throughout the small intestine, it is
most efficient in the duodenum and proximal jejunum, which is bypassed after
mixed or malabsorptive procedures.2 Decreased hydrochloric acid production in
the stomach and accelerated gastric emptying may also affect the reduction of
iron from the ferric (Fe3+) to the absorbable ferrous state (Fe2+). Reduced
dietary intake of iron-rich foods, such as meat, enriched grains, and vegetables
may also participate.2 Finally, iron deficiency may also beexacerbated in
bariatric patients as a result of a nutrient-nutrient inhibitory absorptive
interaction between iron and calcium, another mineral that is routinely
supplemented during the postoperative period.1 Most studies show that iron
absorption is inhibited up to 50-60% when consumed in the presence of calcium
supplements (calcium carbonate, calcium citrate, and calcium phosphate) or
with dairy products.1 On the basis of these considerations, routine periodic
surveillance of iron status (serum iron, total iron binding capacity and ferritin
levels 6 months after surgery and then annually) and hemoglobin/hematocrit
levels is recommended.2 Prophylactic empiric iron supplementation is
recommended after Roux-en-Y gastric bypass, biliopancreatic diversion,
biliopancreatic diversion with duodenal switch1 and sleeve gastrectomy.30 Iron
supplementation (65 mg of elemental iron orally twice a day) prevented the
development of iron deficiency after gastric bypass in a randomized controlled

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trial.31 Iron supplementation may be given in a multivitamin and mineral oral

preparation with the inclusion of vitamin C, that is able to increase iron
absorption,1 and without taking iron and calcium supplements in the same
moment of the day. Additional iron supplementation should be considered in
adolescents and menstruating women.1,2 Because the poor absorption and
adverse gastrointestinal effects of oral iron supplementation, parenteral
administration should be considered in case of established iron deficiency
anemia.
Vitamin B12 and Folate

Vitamin B12 deficiency can occur after bariatric surgical procedures that bypass
the lower part of the stomach, typically the gastric bypass,1 and it has been also
observed after sleeve gastrectomy.30 Gastric bypass patients have both a
decreased production of stomach acid and a decreased availability of intrinsic
factor, which both decrease the digestion and the absorption of vitamin B 12.1 In
normal subjects, cobalamin stores are usually fair higher than daily vitamin B12
requirements. Therefore, vitamin B12 deficiency is rare in the first year after
surgery and its prevalence tend to increase over years in the absence of
adequate supplementation. Anemia as a result of vitamin B12 deficiency has
been reported to occur in more than 30% of patients 1 to 9 years after Roux-en-
Y gastric bypass.32 Despite the absence of evidenced-based recommendations,
vitamin B12 regular checking and supplementation should be considered after
most of the bariatric procedures (Roux-en-Y gastric bypass, sleeve
gastrectomy, biliopancreatic diversion or biliopancreatic diversion with duodenal
switch).1 Some controversies also exist about the preferred route of
administration. Most of vitamin B12 is absorbed in the ileum only in the presence
of the Intrinsic Factor, but approximately 1% of supplemented B12 may be
absorbed by passive diffusion even in the absence of the factor.2 Therefore, an
oral dose of 350-500 μg / day is considered sufficient to guarantee the
absorption of 3.5–5.0 μg of vitamin, which is greater than the daily
requirements.2 Alternative suggested regimens of administration are 1000
μg/month intramuscularly, 3000 μg every 6 months intramuscularly or 500 μg
every week intranasally.1 In comparison with vitamin B12, folate deficiency is far

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less common after bariatric surgery because folate absorption occurs

throughout the entire small bowel.1 Folic acid is usually contained in the
multivitamin and mineral supplements routinely used in bariatric patients. The
pregnant bariatric patients should have routine folic acid supplementation for
the prevention of fetal neural tube defects.1
Calcium, vitamin D and bone metabolism

Calcium is absorbed preferentially in the duodenum and proximal jejunum, and
its absorption is facilitated by vitamin D in an acid environment. Calcium
absorption would therefore decrease after any bariatric procedure involving the
bypass of the first intestinal loops and a reduction in gastric acid production.
Vitamin D levels are frequently low in morbid obese patients even before
surgery, particularly in women.33 Low vitamin D levels in obesity have been
attributed to low intake of foods rich in vitamin D (vegetables), to reduced sun
exposure, to hydroxilation reduced to 25(OH)D3 in the fatty liver, and to
sequestration of the fat-soluble 25(OH)D3 in the adipose tissue.33 Increasing
evidence sugges a link between low vitamin D levels and the risk ok type 2
diabetes in obese patients.34 Vitamin D is a fat-soluble vitamin absorbed
preferentially in the jejunum and ileum and a further reduction of vitamin D
levels after surgery may be expected after Roux-en-Y gastric bypass,
biliopancreatic diversion and biliopancreatic diversion with duodenal switch.2
Indeed, a 50-60% incidence of vitamin D deficiencies has been reported after
biliopancreatic diversion35,36 and after gastric bypass37 despite routine
supplementation. No significant decrease in vitamin D levels has been observed
after adjustable gastric banding38 or sleeve gastrectomy.30 Coupled calcium and
vitamin D deficiencies lead to metabolic bone disease and bone
demineralization bolstered by a state of secondary hyperparathyroidism.35-37
Despite no having yet any conclusive evidence for a long term increase in
fracture risk after bariatric/surgery, a recent review of bone density studies
confirmed a sizable reduction (8-10%) of bone mineral density both at the
femoral neck and at the lumbar spine after malabsortive procedures.39
Increased awareness regarding the prevalence of metabolic bone disease after
malabsorptive procedures has led to recommendation of calcium and vitamin D

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routine supplementation.1-3 Pre-operative vitamin D deficiencies should be

corrected with an oral vitamin D load.2 After surgery, current guidelines
recommend the regular assumption of 1.200–2.000 mg / day of elemental
calcium along with 400-800 U of vitamin D.1 Calcium citrate should be preferred
to calcium carbonate because of it better absorbability in the absence of gastric
acid2 and vitamin D is usually included in standard multivitamin preparations.
However, these standard relatively low doses of vitamin D may result largely
insufficient to protect bone density in patients with severe vitamin D
malabsorption and much higher oral doses may be required. In case of very
poor results with oral formulation, parenteral vitamin D administration may be
considered. The consistency and adequacy of calcium and vitamin D
supplementation should be checked in any patients with regular controls of
bone mineral metabolism markers. Supplementation may be considered
adequate when levels of serum calcium, bone-specific alkaline phosphatase or
osteocalcin, vitamin D, PTH and 24-hour urinary calcium excretion rates are
normal.1,2 Persistently elevated Serum PTH levels in the presence of normal
vitamin D and inappropriately high serum calcium levels should raise the
suspecious a primary hyperparathyroidism. In bariatric surgery patients with
established osteoporosis pharmacologic treatment with bisphosphonates may
be considered. Care must be exercised before starting bisphosphonates use
after surgery to ensure that vitamin D deficiency is fully corrected, in order to
avoid severe hypocalcemia, hypophosphatemia, and osteomalacia.1 If therapy
is indicated, then intravenously administered bisphosphonates should be used,
as concerns exist about adequate oral absorption and potential anastomotic
ulceration with orally administered bisphosphonates.3 Recommended
intravenous dosages of bisphosphonates include zoledronate (5 mg once a
year) or ibandronate (3 mg every 3 months).3 If concerns about absorption or
potential anastomotic ulceration are obviated, oral bisphosphonate
administration can be provided: alendronate (70 mg/week), risedronate (35
mg/week or 150 mg/month), ibandronate (150 mg/month).3 However, the
effectiveness of both intravenous and oral bisphosphonates in bariatric surgery
patients has never been proved by specific randomized trials.

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Fat-soluble vitamins
Apart from vitamin D, the absorption of any other fat-soluble vitamin (A,E,K)
may be reduced after bariatric malabsorptive procedure with steatorrhea.
Vitamin A deficiency, with its related ocular xerosis and night blindness
symptoms, occurs in 5-60% of patients 2-4 years after biliopancreatic diversion
with or without duodenal switch.1 Vitamin E deficiency can lead to anemia,
ophthalmoplegia and peripheral neuropathy and has been reported in less than
5% of patients having undergone biliopancreatic diversion with or without
duodenal switch.1 Finally, in patients who have had a biliopancreatic diversion
with or without duodenal switch, vitamin K deficiency and easy bleeding occurs
in approximately 50-70% within 2 to 4 years postoperatively.1 Giving these high
prevalence figures, fat-soluble vitamins supplementation should be
recommended to all patients having undergoing biliopancreatic derivation or
biliopancreatic derivation with duodenal switch procedures.1 Routine
supplementation does not preclude completely the occurrence of a deficiency
and therefore laboratory monitoring should be regularly performed (every year)
and low levels and/or deficiencies symptoms should be treated with additional
specific supplements.
Thiamine
The water-soluble vitamin thiamine (vitamin B1) is stored in high concentrations
in the brain, heart, muscle, liver and kidneys. However, without regular and
sufficient intake, these tissues become rapidly devoid of vitamin.2 Thiamine
deficiency may be caused by bypass of the jejunum, the major intestinal site for
its absorption, but it is more frequently caused by impaired nutritional intake
from severe and continuous emesis. Giving the relatively low level of body
storage capacity, thiamine deficiency may arise only after a short period (a few
weeks) of persistent vomiting.2 Severe thiamine deficiency has been described
after a few weeks of intractable vomiting after bariatric surgery, even shortly
after the procedure, and usually as a consequence of mechanical problems,
such as stomal stenosis after Roux-en-Y gastric bypass,40,41 excessive band
tightness or band slippage after adjustable gastric banding 42 or stomach edema
with impaired nutrition after sleeve gastrectomy.43 Several cases of thiamine

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deficiencies have been reported also after biliopancreatic derivation.44 The

rapidity of the onset of thiamine deficiency clearly differentiates this specific
nutritional problem from the other post-bariatric nutritional deficiencies, usually
arising in a more long term timing. Thiamine deficiency in bariatric patients often
presents symptoms of peripheral neuropathy or Wernicke’s encephalopathy and
Korsakoff’s psychoses.2 These neurologic symptoms are rapidly aggravating
and may cause permanent neurologic deficits and even death. Therefore, it is
important to remember that any case of persistent vomiting after bariatric
surgery should be aggressively treated to prevent this devastating complication
and that aggressive measure to prevent and treat thiamine deficiency should be
promptly considered in every bariatric patient having their nutritional intakes
persistently and importantly disturbed by vomiting. Thiamine status may be
checked by determining erythrocyte transketolase activity.1 However this
dosage is not frequently routinely performed in all hospitals and any deferral of
the appropriate treatment should not be justified by the absence of a laboratory
data. Even in the absence of laboratory measurement, oral or parenteral
supplementation of thiamine should be initiated in any patient with persistent
vomiting (50-100 mg/d) and in case of active neurologic symptoms (100 mg/d
parenteral).1,2 In symptomatic patients, oral supplementation may be used only
after a 7-14 days course of parenteral administration and until neurologic
symptoms resolve.1
Other micronutrients
Other minerals (zinc, copper, selenium, magnesium, potassium) and vitamin
(B6) deficiencies have been described after bariatric surgeries.1,2 The clinical
relevance of these minor nutritional deficiencies remains unclear and routine
supplementation with multivitamins and minerals should be sufficient to prevent
major clinical problems.
General recommendations for vitamin and mineral supplementation

Routine multi-vitamin and mineral supplementation is recommended in all
patients after a bariatric procedure. However, routine supplementation cannot
ensure an absolute prevention of the occurrence of deficiencies over time,

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mainly because of individual variations in micro-nutrients absorption, nutritional

requirements and compliance. Therefore, periodic laboratory routine
surveillance for nutritional deficiencies is recommended and supplementation
should be individualized accordingly, with patients who demostrate
micronutrient insufficiencies or deficiencies treated with the respective
micronutrient.3 A reasonable scheme for minimal periodic nutritional surveillance
after bariatric procedures is proposed in Table 3.
Table 3. Minimal routine periodic laboratory surveillance for nutritional

deficiencies after bariatric surgery.
AGB SG RYGB BPD –

BPD/DS
Timing Every 6 mo. Every 3-6 mo. Every 3-6 mo. Every 3 mo.
in the first in the first in the first in the first
year. Every year. year. year.
12 mo. there Every 12 mo. Every 12 mo. Every 6-12
after. there after. there after. mo. there
after.
Assessment CBC, CBC, CBC, CBC,
platelets platelets platelets platelets
Electrolytes Electrolytes Electrolytes Electrolytes
Iron, ferritine Iron, ferritine Iron, ferritine Iron, ferritine
Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12
Folate Folate Folate Folate
Vitamin D Vitamin D Vitamin D Vitamin D
PTH PTH PTH PTH
24-H U- 24-H U-
calcium calcium
Osteocalcin Osteocalcin
Vitamin A
Vitamin E
INR
Albumin
Prealbumin
AGB: adjustable gastric banding; SG: sleeve gastrectomy; RYGB: gastric bypass; BPD: biliopancreatic diversion;
BPD/DS: biliopancreatic diversion with duodenal switch; CBC: complete blood count; PTH: intact parathyroid hormone;
24-H U-calcium: 24-hour urinary calcium. In RYGB, BPD and BPD/DS, Dual-energy x-ray absorptiometry (DEXA)
should be performed annually to monitor bone mineral density.

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Dual-energy X-ray absorptiometry (DEXA) should be performed annually to

monitor bone mineral density in patients undergoing gastric bypass or
biliopancreatic diversion with or without duodenal switch. Minimal daily
nutritional supplementation for patients with gastric bypass and sleeve
gastrectomy should include 2 adult multivitamin plus mineral supplements (each
containing iron, folic acid, and thiamine), 1200 to 1500 mg of elemental calcium
(in diet and as citrated supplement in divided doses), at least 3000 international
units of vitamin D (titrated to therapeutic 25-OH vitamin D levels >30 ng/ml), and
vitamin B12 (parenterally or orally) as needed to maintain B12 levels at the
normal range.3 After biliopancreatic diversion with or without duodenal switch, a
routine supplementation with adequate amounts of fat-soluble vitamins should
be added to this regimen.1 Minimal daily nutritional supplementation for patients
with adjustable gastric banding should include 1 adult multivitamin plus mineral
supplement (including iron, folic acid, and thiamine) and at least 3000
international units of vitamin D (titrated to therapeutic 25-OK vitamin D levels)
with or without 1200 to 1500 mg of elemental calcium (in diet and as citrated
supplement in divided doses).3
Biblioghafical references
1. Mechanick JI, Kushner RF, Sugerman HJ, et al. American Association of

Clinical Endocrinologists, The Obesity Society, and American Society for
Metabolic & Bariatric Surgery Medical: Guidelines for clinical practice for
the perioperative nutritional, metabolic, and nonsurgical support of the
bariatric surgery patient. Endocr Pract. 2008;14 Suppl1:1-83.
2. Aills L, Blankenship J, Buffington C, Furtado M, et al. Allied Health
Sciences Section Ad Hoc Nutrition Committee. ASMBS Guidelines.
ASMBS Allied Health Nutritional: Guidelines for the surgical weight loss
patient. Surg Obes Related Dis. 2008;4:S73-S108.
3. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for
bariatric surgery patient-2013 update: cosponsored by American
Association of Clinical Endocrinologists, The Obesity Society, and
American Society for Metabolic & Bariatric Surgery. Endocr Pract.
2013;19:337-72.
4. Sarwer DB, Moore RH, Spitzer JC, et al. A pilot study investigating the
efficacy of postoperative dietary counseling to improve outcomes after
bariatric surgery. Surg Obes Relat Dis. 2012;8:561-8.

Blanca Ríos, MD
5. Jacobi D, Ciangura C, Couet C, et al. Physical activity and weight loss

following bariatric surgery. Obes Rev. 2011;12:366-77.
6. Donnelly JE, Blair SN, Jakicic JM,et al. Appropriate physical activity
intervention strategies for weight loss and prevention of weight regain for
adults. Med Sci Sports Exerc. 2009;41:459-71.
7. Garber CE, Blissmer B, Deschenes MR, et al. Quantity and quality of
exercise for developing and maintaining cardiorespiratory,
musculoskeletal, and neuromotorfitness in apparently healthy adults:
Guidance for prescribing exercise. Med Sci Sports Exerc. 2011;43:1334-
59.
8. Bavaresco M, Paganini S, Pereira Lima T, et al. Nutritional course of
patients submitted to bariatric surgery. Obes Surg. 2010;20:716-21.
9. Faria SL. Dietary protein intake and bariatric surgery. Obes Surg.
2011;21:1798-805.
10. Andreu A, Moize V, Rodriguez L, et al. Protein intake, body composition,
and protein status following bariatric surgery. Obes Surg. 2010;20:1509-
15.
11. Brolin RE, LaMarca LB, Kenler HA, et al. Malabsorptive gastric bypass in
patients with superobesity. J Gastrointest Surg. 2002;6:195-203.
12. Faintuch J, Matsuda M, Cruz ME, et al. Severe protein calorie
malnutrition after bariatric procedures. Obes Surg. 2004;14:175-81.
13. Scopinaro N, Adami GF, Marinari GM, et al. Biliopancreatic diversion.
World J Surg .1998;22:936-46.
14. Byrne TK. Complications of surgery for obesity. Surg Clin North Am.
2001;81:1181-93.
15. Martindale RG, McClave SA, Vanek VW, et al. and American College of
Critical Care Medicine, ASPEN Board of Directors. Guidelines for the
provision andassessment of nutrition support therapy in the adult
critically ill patient: Society of Critical Care Medicine and American
Society for Parenteral and Enteral Nutrition: Executive Summary. Crit
Care Med. 2009;37:277-316.
16. Singer P, Berger MM, Van den Berghe G, et al. ESPEN Guidelines on
parenteral nutrition: Intensive care. Clin Nutr. 2009;28:387-400.
17. Kondrup J, Rasmussen HH, Hamberg O, et al. and an ad-hoc ESPEN
Working Group. Nutritional risk screening (NSR 2002): A new method
based on analysi of controlled clinical trials. Clin Nutr. 2003;22:321-36.
18. Favretti F, O’Brien PE, Dixon JB. Patient management after lap-band
placement. Am J Surg. 2002;184:38S-41S.
19. Burton PR, Brown WA, Laurie C, et al. Effects of gastric band
adjustments on intraluminal pressure. Obes Surg. 2009;19:1508-14.
20. Busetto L, Segato G, De Marchi F, et al. Post-operative management of
laparoscopic banding. Obes Surg. 2003;13:121-7.

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21. Brown W, Burton P, Anderson M, et al. Symmetrical pouch dilatation

after laparoscopic adjustable gastric banding: incidence and
management. Obes Surg. 2008;18:1104-8.
22. LaureniusA, OlbersT, Näslund I, et al. Dumping syndrome following
gastric bypass: Validation of the Dumping Symptom Rating Scale. Obes
Surg. 2013;23:740-55.
23. Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypassfor
obesity: Mechanisms of weight loss and diabetes resolution. J Clin
Endocrinol Metab. 2004;89:2608-15.
24. Deitel M. The change in the dumping syndrome concept. Obes Surg.
2008;18:1622-4.
25. Tack J, Arts J, Caenepeel P, et al. Pathophysiology, diagnosis and
management of postoperative dumping syndrome. Nat Rev
Gastroenterol Hepatol. 2009;6:583-90.
26. Yamamoto H, Mori T, Tsuchihashi H, et al. A possible role of GLP-1 in
the pathophysiology of early dumping syndrome. Dig Dis Sci.
2005;50:2263-7.
27. Cui Y, Elahi D, Andersen DK. Advances in the etiology and management
of hyperinsuline michypoglycemia after Roux-en-Y gastric bypass. J
Gastrointest Surg. 2011;15:1879-88.
28. Ceppa EP, Ceppa DP, Omotosho PA, et al. Algorithm to diagnose
etiology of hypoglycemia after Roux-en-Y gastric bypass for morbid
obesity: case series and review of the literature. Surg Obes Relat Dis.
2012;8:641-7.
29. Potoczna N, Harfmann S, Steffen R, et al. Bowel habits after bariatric
surgery. Obes Surg. 2008;18:1287-96.
30. Damms-Machado A, Friedrich A, Kramer KM, et al. Pre- and
postoperative nutritional deficiencies in obese patients undergoing
laparoscopic sleeve gastrectomy. Obes Surg. 2012;22:881-9.
31. Brolin RE, Gorman JH, Gorman RC, et al. Prophylactic iron
supplementation after Roux-en-Y gastric bypass: a prospective, double
blind, randomized study. Arch Surg. 1998;133:740-4.
32. Stocker DJ. Management of the bariatric surgery patient. Endocrinol
Metab Clin North Am. 2003;32:437-57.
33. Earthman CP, Beckman LM, Masodkar K, et al. The link between obesity
and low circulating 25-hydroxyvitamin D concentrations: Considerations
and implications. Int J Obes. 2012;36:387-96.
34. Mezza T, Muscogiuri G, Sorice GP, et al. Vitamin D deficiency: A new
risk factor for type 2 diabetes? Ann Nutr Metab. 2012;61:337-48.
35. Slater GH, Ren CJ, Seigel N, et al. Serum fat-soluble vitamin deficiency
and abnormal calcium metabolism after malabsorptive bariatric surgery.
J Gastrointest Surg. 2004;8:48-55.

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36. Newbury L, Dolan K, Hatzifotis M, et al. Calcium and vitamin D depletion

and elevated parathyroid hormone following biliopancreatic diversion.
Obes Surg. 2003;13:893-5.
37. Johnson JM, Maher JW, De Maria EJ, et al. The long term effects of
gastric bypass on vitamin Dmetabolism. Ann Surg. 2006;243:701-4.
38. Giusti V, Gasteyger C, Suter M, et al. Gastric banding induces negative
bone remodeling in the absence of secondary hyperparathyroidism:
Potential of serum telopeptides for follow-up. Int J Obes. 2005;29:1429-
35.
39. Scibora LM, Ikramuddin S, Buchwald H, et al. Examining the link
between bariatric surgery, bone loss, and osteoporosis: A review of bone
density studies. Obes Surg. 2012;22:654-67.
40. Salas-Salvado J, Garcia-Lourda P, Cuatrecasas G, et al. Wernicke’s
syndrome after bariatric surgery. Clin Nutr. 2000;12:371-3.
41. Loh Y, Watson WD, Verma A, et al. Acute Wernicke’s encephalopathy
following bariatric surgery: clinical course and MRI correlation. Obes
Surg. 2004;14:129-32.
42. Bozboa A, Coskun H, Ozarmagan S, et al. A rare complication of
adjustable gastric banding: Wernicke’s encephalopathy. Obes Surg.
2000;19:274-5.
43. Makarewicz W, Kaska L, Kobiela J, et al. Wernicke's syndrome after
sleeve gastrectomy. Obes Surg. 2007;17:704-6.
44. Primavera A, Brusa G, Novello P, et al. Wernicke-Korsakoff
encephalopathy following biliopancreatic diversion. Obes Surg.
1998;3:175-77.

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Chapter VI
Management of special conditions:
Type 2 Diabetes Mellitus
Luca Busetto, MD
Department of Medicine
University of Padua – Italy
Patients with type 2 diabetes represent a sizable proportion of patient

candidates for bariatric surgery. Type 2 diabetes represents a classic indication
for bariatric surgery and is included in the number of comorbidities that allowed
the reduction of the Body Mass Index (BMI) threshold for surgery from 40 to 35
kg/m2.1-4 In a large systematic review and meta-analysis on the effects of
bariatric surgery on type 2 diabetes, Buchwald et al. reported a total prevalence
of 22.3% for type 2 diabetes in morbid obese patients treated with several
bariatric procedures.5 The growing interest in the metabolic effects of bariatric
procedures would probably increase these figures in the future, with the
prioritization of more morbid obese diabetic patients for surgery and the
increasing eligibility of patients with type 2 diabetes and lower BMI levels.6
The efficacy of bariatric and metabolic procedures in improving and even

normalizing the metabolic profile of type 2 diabetic patients has been proved by
a large body of uncontrolled clinical observations5 and by a small but significant
number of randomized controlled trials.7-9 On the other hands, sub-optimal
management of type 2 diabetes in the peri-operative phase and thereafter may
have an important negative role in determining safety, outcomes, and cost of
the same bariatric procedures frequently used to treat or to improve type 2
diabetes itself. The issue of type 2 diabetes management in bariatric patients
has been specifically addressed in the medical guidelines for clinical practice for
the peri-operative nutritional, metabolic, and non-surgical support of the bariatric
surgery patients jointly endorsed by the American Association of Clinical
Endocrinologists (AACE), the Obesity Society (TOS) and the American Society
for Metabolic and Bariatric Surgery (ASMBS).10 The section on type 2 diabetes
of these guidelines has been recently updated.11 Moreover, the more general
problem of recognition and management of hyperglycemia in the hospital was

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addressed in great details by the American Diabetes Association (ADA)

standards of medical care12 and in a recent updated consensus statement by
AACE and ADA.12 In this chapter, clinical recommendations for the
management of type 2 diabetes in the bariatric patients will be briefly reviewed,
moving through the pre-operative, peri-operative and post-operative phases.
Medical clearance before surgery: Type 2 diabetes

Current guidelines for the medical clearance before bariatric surgery
recommend that all patient candidates for surgery should undergo evaluation for
causes and complications of obesity, with special attention directed to those
factors that could affect a recommendation for bariatric surgery, including type 2
diabetes.10 Therefore, a laboratory screening for the presence of type 2
diabetes is usually included in the pre-operative diagnostic work-up for all the
candidates for surgery.10 In all patients with a positive diabetes history, and in
the new cases of type 2 diabetes identified during pre-operative screening, a
complete assessment of major cardio-vascular risk factors (lipids, blood
pressure, microalbuminuria) should be carried out and, giving the strong
association between diabetes mellitus and cardio-vascular diseases, a more
detailed diagnostic work up for the detection of ischemic heart disease or
carotid artery atherosclerotic lesions may be recommended. Ideally, not a single
patient with type 2 diabetes should arrive at surgery unrecognized.
Good preoperative glucose control has been associated with decreased peri-
operative infectious complications after general surgery. Dronge et al. analysed
post-operative infections (pneumonia, wound infection, urinary tract infection or
sepsis) according to pre-operative glycatedhemoglobin (HbA1c) value in 490
diabetic patients undergoing several types of surgical procedures at the Veteran
Affairs Connecticut Healthcare System, a tertiary referral centre and major
university teaching site. Both before and after adjustment for several possible
confounding variables (age, race, diabetic treatment, ASA classification,
Activities of Daily Living assessment, elective vs emergent procedure, wound
classification and operation length), a HbA1c level of more than 7% was found
to be associated with a two-fold increased rate of infectious complications, with

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an adjusted odds ratio of 2.13 (95% confidence interval: 1.23-3.70).13-14

Therefore, optimisation of the metabolic control should be targeted before
surgery in all patients known or found to have type 2 diabetes, in order to
reduce the rate of serious surgical complications.
Preoperative glycemic control should be optimized using a diabetes

comprehensive care plan, including healthy dietary patterns, medical nutrition
therapy, physical activity, and as needed, pharmacotherapy.11 Orally
administered agents and insulin should be introduced according to standard
diabetes medical care guidelines.12 Reasonable targets for preoperative
glycemic control, which may be associated with improved bariatric surgery
outcomes, include a HbA1cvalue of 6.5%-7.0% or less, a fasting blood glucose
level ≤110 mg/dL, and a 2-hour postprandial blood glucose concentration ≤140
mg/dL.11 More liberal preoperative targets, such as anHbA1c of 7-8%, should be
considered in patients with advanced micro-vasculaor macro-vascular
complications, extensive co-morbidconditions, or long-standing diabetes in
which the general goal has been difficult to attain despite intensive efforts.11 It
should be noted, however, that the use of these targets is translated from
evidence related to long-term type 2 diabetes outcomes and their application to
this surgical setting is not supported by strong evidence-based data. In patients
with HbA1c>8% or otherwise uncontrolled diabetes, clinical judgment should
determine the need for and the risk of bariatric surgery.11
Glucose control in the hospital

Surgical stress can be associated with exacerbation of hyperglycemia in
patients with type 2 diabetes and “stress hyperglycemia” in non-diabetic
patients. Among hospitalised patients, adverse outcomes (hospital mortality,
infection, heart failure, need for admission to intensive care unit and increased
length of hospital stay) are more frequent in patients with hyperglycemia
compared to those with normal glucose levels.15 In particular, the presence of
hyperglycemia has been associated with poorer outcomes in critically ill
patients,16 in patients undergoing coronary arteries by-pass,17 and in patients
with myocardial infarction18 and acute ischemic stroke.19 On the other hand,

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severe hypoglycaemia may provoke strong neurological insult with stroke or

coma, can impair cognition, and may have extended long-term adverse
consequences.15 Therefore, clinical goals for bariatric specialists during hospital
stay and early post-operative recovery should be the implementation of
therapeutic algorithms aimed to obtain an acceptable metabolic control, but
avoiding an excessive risk of severe hypoglycemic events. Cornerstones of
these algorithms should be frequent glucose levels monitoring, intravenous
insulin therapy with predefined target glucose levels during surgery and in the
intensive care unit, basal-bolus subcutaneous insulin therapy in non-critically ill
patients after surgery (table 1).
At admission, all patients with diabetes should have an order for blood glucose
monitoring, with results available to all members of the bariatric team.10
Because of the high risks of stress hyperglycemia, patients recognised in the
pre-operative phase to have impaired fating glucose or impaired glucose
tolerance, and even patients without any evidence of impaired glucose
regulation, should have their glucose values regularly checked in the peri-
operative period.10 Point-of-care finger stick blood glucose monitoring should
occur before meals and at bedtime (or every 4-6 hours in patients receiving
nothing by mouth). Glucose levels and insulin requirements should be
reassessed even more frequently (every 30 minute or 2 hours) in patients
receiving continuous insulin infusion, immediately after any change in nutrition
status, in patients receiving large amounts of dextrose solutions or drugs known
to affect insulin sensitivity or secretion, and in case of symptoms of
hypoglycaemia.
The safety and efficacy data on the use of oral agents and injectable noninsulin
therapies for metabolic control in the hospital are very limited.12 Oral agents and
injectable noninsulin therapies may be generally discontinued in the morning of
surgery.10,11 A particular caution is required with metformin, due to the
possibility that a contraindication may develop during the hospitalization, such
as renal insufficiency, unstable hemodynamic status, or need for an imaging
study that requires a radio-contrast dye.12 It is advisable to suspend metformin
therapy at least 48 hours before surgery.

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During surgery, in the intensive care unit and in critically ill patients, the most
appropriate regimen for obtaining optimal and safe metabolic control is a
continuous intravenous insulin infusion with predefined targets for glucose
levels. The definition of what glucose levels should be targeted in these clinical
settings has been in the last years the subject of a few randomized controlled
trials which produced some conflicting results. Glucose targets in critically ill
patients have been therefore recently modified as soon as new clinical evidence
was made available. The story started in 2001, when Van den Berghe et al.
randomised patients admitted to a single surgical intensive care unit to an
intensive treatment arm, with fasting plasma glucose targets of 80-110 mg/dl,
and to a conventional treatment arm, with fasting plasma glucose targets of
180-200 mg/dl. In this trial, a 34% decrease in mortality was observed in the
intensively treated group.20 Five years later, the same research group replicated
the original protocol in 1200 patients admitted to a medical intensive care unit.21
In the medical setting, intensive insulin therapy reduced blood glucose levels
but did not significantly reduce in-hospital mortality (40.0% in the conventional-
treatment group vs 37.3% in the intensive-treatment group). However, in a post-
hoc analysis based on the length of stay, mortality was greater among those
receiving intensive therapy in patients staying in the intensive care unit for less
than three days, whereas mortality was reduced from 52.5 to 43.0 % in the arm
receiving intensive therapy in patients staying in the intensive care unit three or
more days.21 The largest study to date, nice-sugar, a multicenter, multinational
randomised controlled trial, compared in 2009 the effect of intensive glycemic
control (target 81–108 mg/dl) to standard glycemic control (target 144–180
mg/dl) on outcomes among 6.104 critically ill participants.22 Ninety-day
mortality was significantly higher in the intensive versus the conventional group
(27.5% vs. 24.9%) in both surgical and medical patients. The precise reason for
the increased mortality in the tightly controlled group is unknown, but severe
hypoglycemia was largely more common in the intensively treated group (6.8%
vs. 0.5%). It is important to note that, in difference to previous trials, the control
group in nice-sugar had a more reasonably good blood glucose management.
Finally, in a recent meta-analysis of 26 trials, including the NICE-SUGAR data,
the pooled relative risk of death with intensive insulin therapy was 0.93 (95% CI

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0.83–1.04) as compared to conventional therapy.23 Approximately half of these

trials reported hypoglycemia, with a pooled relative risk for intensive therapy of
6.0 (95% CI 4.5–8.0). The clinical setting influenced the findings, with patients in
surgical intensive care units appearing to benefit from intensive insulin therapy,
while patients in medical intensive care units did not. It was concluded that,
overall, intensive insulin therapy increased the risk of hypoglycemia but
provided no overall benefit on mortality in the critically ill, although a possible
mortality benefit to patients admitted to the surgical intensive care unit may be
suggested.23
On the basis of these poled results, ADA standards of medical care suggest
that in critically ill patients insulin therapy should be initiated for treatment of
persistent hyperglycemia starting at a threshold of no greater than 180 mg/dl
and that once insulin infusion is started, a glucose range of 140–180 mg/dl is
recommended for the majority of critically ill patients.12 More stringent goals,
such as 110 –140 mg/dl may be appropriate for selected patients, possibly the
surgical ones, as long as this can be achieved without significant
hypoglycaemia.12 More specifically referring to the bariatric patient, the first
AACE/TOS/ASMBS medical guidelines, released in 2008 and largely influenced
by the very optimistic results coming from the first study by Van den Berghe et
al.,20 suggested that blood glucose levels in the intensive care unit should be
maintained ideally within the range of 80-110 mg/dL by using an intravenous
insulin infusion.10 This recommendation has been however tempered in the
updated version of the guidelines edited in 2013.11 New AACE/TOS/ASMBS
medical guidelines now suggest that, in the intensive care unit, intravenous
regular should be used to control hyperglycemia to a 140-180 mg/dL blood
glucose target.11 Anyway, continuous insulin infusion should be delivered with
frequent glucose monitoring in place and with strict protocols for the prevention
and avoidance of hypoglycaemia (table 1).
To date, we have no prospective randomised control trials to inform specific

glycemic targets for non-critically ill patients with type 2 diabetes or “stress
hyperglycemia” and outside the intensive care unit. Therefore,

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recommendations are based on clinical experience and judgment.12 ADA

standards of medical care suggest that for the majority of non-critically ill
patients treated with insulin, pre-meal glucose targets should generally be <140
mg/dl with random blood glucose levels <180 mg/dl, as long as these targets
can be safely achieved.12 In order to avoid hypoglycaemia, insulin regimen
should be reassessed in case of glucose levels <100 mg/dl and modified in
case of glucose levels <70 mg/dl, unless the hypoglycemic event may be easily
explained (i.e missed meals).12 Day-to-day decision regarding insulin dosing
should be guided by clinical judgment, taking into account prior history of
successful tight glycemic control in the outpatient setting, present clinical and
nutritional status and concurrent use of medications that might affect glucose
levels.12 The updated version of the specific AACE/TOS/ASMBS bariatric
guidelines also suggests that insulin therapy should be used to attain glycemic
targets of 140-180mg/dL in non-intensive care unit hospitalized patients11 (table
1).
The preferred method for achieving and maintaining glucose control in non-
critically ill patients and outside intensive care unit should be scheduled
subcutaneous insulin with basal, nutritional, and correction components (“basal-
bolus”)12 (table 1).
“Basal” insulinization should be provided with a long-acting insulin analogue
(glargine or insulin detemir) given once daily at bedtime. Long-acting insulin
analogues, and not traditional insulins, should be used, because they have no
or little peak effect, provide more consistent glycemic control, reduce the risk of
nocturnal hypoglycaemia, and confer a lower overall blood glucose variability.15
“Bolus” preprandial insulinization and “correction” doses should be provided
with a rapid-acting insulin analogue (insulin aspart, insulin glulisine, or insulin
lispro). As compared to traditional regular human insulin, rapid-acting insulin
analogues may be administered closer to or even at the beginning of meals,
providing advantage in the post-operative bariatric setting where amount of
dietary intake may be difficult to predict.15 Moreover, the short duration of action
of rapid-acting insulin analogues may reduce the risk of between-meal
hypoglycaemia.15 In patients shifting from continuous insulin infusion to basal-

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bolus subcutaneous insulin regimen, proper overlap may be ensured by

administering the first dose of a long-acting insulin analogue 2-3 hours before
discontinuation of the intravenous infusion.15
Type 2 diabetes management after surgery

In the few days and weeks after bariatric surgery, patients with type 2 diabetes
may experience profound changes in their metabolic profile and anti-diabetic
therapy requirements. The combination of the very low post-operative caloric
intake and the direct metabolic effects of some of the bariatric procedures, may
induce rapid (within days) normalization of glycemic control and can consent the
complete withdrawal of anti-diabetic therapy.24,25 This phase of rapid metabolic
modifications should be carefully managed in order to avoid the risk of
iatrogenic hypoglycaemia caused by excessive anti-diabetic treatment. Before
discharge, a reasonable approach would be to instruct the patients about
regular and frequent monitoring of glucose concentrations at home to guide
adjustments in glucose-lowering therapy.10,11 Medication prescription at
discharge should take into account the metabolic control and insulin
requirements during the last days of hospital stay and the nutritional status. The
use of all insulin secretagogues (sulfonylureas and meglitinides) should be
avoided and insulin doses should be adjusted postoperatively (due to low
calorie intake) to minimize the risk for hypoglycemia.11 Metformin may be
continued postoperatively until prolonged clinical resolution of diabetes is
demonstrated by normalized glycemic targets.11 An outpatients follow-up visit
should be scheduled within one month from discharge in order to promptly
revaluate metabolic control and glucose-lowering therapy. Scheduled or
emergency phone contacts may be useful for the at home management of
difficult situations.
In patients with type 2 diabetes not having diabetes remission after surgery,
continued surveillance and preventive care according to the currents standards
of diabetic care should be continued as before the procedure.10 The case of
what levels of preventive care should be applied to diabetic patients with
diabetes remission after surgery remains however less clear. The question has

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been addressed by a consensus group comprising experts in endocrinology,

diabetes education, transplantation, metabolism, and bariatric/metabolic
surgery.26 According to the consensus group, complete type 2 diabetes
remission should be defined as normal glycemic levels for at least one year
without active pharmacologic therapy and prolonged remission as a complete
remission of at least 5 year duration.26 Partial remission should be defined as
sub-diabetic hyperglycemia (HbA1c not diagnostic of diabetes and fasting
glucose 100–125 mg/dl) of at least one year duration in the absence of active
pharmacologic therapy. In case of partial or complete remission of less than 5
years duration, experts recommended that treatment goals for comorbid
conditions (hypertension, dyslipidemia) and screening programme for micro-
vascular complications should be the same as those for patients with type 2
diabetes.26 Only in case of prolonged 5 years remission, treating physicians
could consider adopting treatment goals for comorbid conditions appropriate for
patients without diabetes, as long as there is no recurrence of diabetes and no
cardiovascular disease, screening at a reduced frequency depending on the
status of each complication and stopping screening for a particular complication
only if there is no history of that complication.26 It should be noted however, that
these recommendations have been endorsed purely on the basis of expert
opinions and were not supported by firm clinical evidence. The benefits of a
multifactorial therapy targeted at the control of multiple risk factors in terms of
mortality, macro-vascular and micro-vascular complications are so important in
patients with type 2 diabetes that discontinuation of pharmacologic treatments
and deviations from strict preventive targets should be adopted very cautiously
in the absence of clear evidence.
Table 1. Main steps for hyperglycemia management during hospital staying.

Regular blood glucose monitoring since admission
Suspend oral anti-diabetic and injectable noninsulin therapies
Continuous intravenous insulin infusion during surgery and in the ICU
 Intravenous insulin infusion started at glucose levels >180 mg/dl
 Insulin infusion regulated with a target glucose range of 140 –180
mg/dl

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 Insulin infusion protocol designed in order to avoid severe

hypoglycaemic events
“Basal-bolus” subcutaneous insulin regimen after surgery and non in the
ICU
 Shift form intravenous insulin infusion to basal-bolus
subcutaneous insulin
 “Basal” insulinization with a long-acting insulin analogue
 “Bolus” preprandialinsulinization with a rapid-acting insulin
analogue
 Target: premeal glucose <140 mg/dl with random blood glucose
levels <180 mg/dl
In conclusion, attention and special care should be dedicated to the optimal

management of type 2 diabetes in the peri-operative phase of bariatric surgery,
in order to minimize risk of complications, reduce the length of stay, and
improve outcomes. Management of type 2 diabetes during different clinical
phases (screening and medical clearance, surgery, intensive care unit stay,
hospital stay, discharge and follow-up) involves different health care
professionals (endocrinologists, surgeons, anesthesiologists, intensionists,
nurses, dieticians) treating the same patients at different moments and in
different settings and locations. A team approach with clear case-management
protocols and a functional system for the sharing of clinical information should
be considered of paramount importance in the delivery of a correct
multidisciplinary high-quality care.
1. Gastrointestinal surgery for severe obesity. National Institutes of Health

Consensus Development Conference draft Statement. Obes Surg.
1991;1:257-66.
2. National Institutes of Health. National Heart, Lung and Blood Institute:
Clinical guidelines on the identification, evaluation and treatment of
overweight and obesity in adults. The Evidence Report. 1998 June.
3. National Institute for Health and Clinical Excellence. Obesity: Guidance
on the prevention, identification, assessment and management of

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overweight and obesity in adults and children. Nice Clinical Guidelines.

2006;43:1-84.
4. Fried M, Hainer V, Basdevant A, et al. Inter-disciplinary European
guidelines on surgery of severe obesity. Int J Obes. 2007;31:569-77.
5. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes
after bariatric surgery: systematic review and meta-analysis. Am J Med.
2009;122:248-56.
6. Dixon JB, Zimmet P, Alberti KG, et al. Bariatric surgery: an IDF
statement for obese type 2 diabetes. Diabet Med. 2011;28:628-42.
7. Dixon JB, O’Brien PE, Playfair J, et al. Adjustable gastric banding and
conventional therapy for type 2 diabetes. A randomized controlled trial.
JAMA. 2008;299:316-23.
8. Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus
intensive medical therapyin obese patients with diabetes. N Engl J Med.
2012;366:1567-76.
9. Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus
conventional medical therapy for type 2 diabetes. N Engl J Med.
2012;366:1577-85.
10. Mechanick JI, Kushner RF, Sugerman HJ, et al. American Association of
Clinical Endocrinologists, The Obesity Society, and American Society for
Metabolic & Bariatric Surgery Medical: Guidelines for clinical practice for
bariatric surgery patient. Endocr Pract. 2008;14:1-83.
11. Mechanick JI, Youdim A, Jones DB, et al. Clinical practice guidelines for
bariatric surgery patient-2013 update: Cosponsored by American
Association of Clinical Endocrinologists, The Obesity Society, and
American Society for Metabolic & Bariatric Surgery. Endocr Pract.
2013;19:337-72.
12. American Diabetes Association. Standards of medical care in diabetes –
2011. Diabetes Care. 2011;34:S11-61.
13. Moghissi ES, Korytkowski MT, Di Nardo, et al. American Association of
Clinical Endocrinologists and American Diabetes Association:
Consensus statement on inpatient glycemic control. Diabetes Care.
2009;32:1119-31.
14. Dronge AS, Perkal MF, Kancir S, et al. Long-term glycemic control and
postoperative infectious complications. Arch Surg. 2006;141:375-80.
15. Moghissi ES. Addressing hyperglycemia from hospital admission to
discharge. Curr Med Res Opin. 2010;26:589-98.
16. Krinsley JS. Association between hyperglycemia and increased hospital
mortality in a heterogeneous population of critically ill patients. Mayo Clin
Proc. 2003;78:1471-8.

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17. Estrada CA, Young JA, Nifong LW, et al. Outcomes and perioperative
hyperglycemia in patients with or without diabetes mellitus undergoing
coronary artery bypass grafting. Ann Thorac Surg. 2003;75:1392-9.
18. Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycaemia and
increased risk of death after myocardial infarction in patients with and
without
1. diabetes: A systematic overview. Lancet. 2000;355:773-8.
19. Williams LS, Rotich J, Qi R, et al. Effects of admission hyperglycemia on
mortality and costs in acute ischemic stroke. Neurology. 2002;59:67-71.
20. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin
therapy in critically ill patients. N Engl J Med. 2001;345:1359-67.
21. Van den Berghe G, Wilmer A, Hermans G, et al. Intensive insulin therapy
in the medical ICU. N Engl J Med. 2006;354:449-61.
22. Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional
glucose control in critically ill patients. N Engl J Med. 2009;360:1283-97.
23. Griesdale DE, De Souza RJ, Van Dam RM, et al. Intensive insulin
therapy and mortality among critically ill patients: A meta-analysis
including NICE-SUGAR study data. CMAJ. 2009;180:821-7.
24. Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought
it? An operation proves to be the most effective therapy for adult onset
diabetes mellitus. Ann Surg. 1995;222:339-50.
25. Shauer PR, Burguera B, Ikramuddin S, et al. Effect of laparoscopic
Roux-en Y gastric bypass on type 2 diabetes mellitus. Ann Surg.
2003;238:467-84.
26. Buse JB, Caprio S, Cefalu WT, et al. How do we define cure of diabetes?
Diabetes Care. 2009;32:2133-5.

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Chapter VII
Compensatory responses to weight loss that contribute to weight regain:
Effects of surgery and lifestyle/dietary intervention
Cynthia K. Buffington, Ph.D.*

Keith Kim, M.D.*
*Metabolic Medicine and Surgery Institute
Florida Hospital Celebration Health
The majority of bariatric patients, prior to their surgery, have been on numerous
diets. With each weight loss cycle and while eating fewer and fewer calories,
the patient has regained all of their weight and, often, even more. Weight
regain following a diet occurs, at least, in part, from physiological compensatory
responses to weight loss that work in concert to promote rapid and efficient
weight regain.1 These compensatory responses (figure 1A) include: 1) a
persistent and increasing gap between energy intake and energy expenditure
and 2) defects in fat handling and metabolism.
In this chapter, two questions pertaining to these physiological contributors to
weight regain are addressed. First, does bariatric surgery, in comparison to diet,
generate similar biological weight-promoting responses to weight loss?
Secondly, are there lifestyle and nutritional interventions that can favorably
modulate these physiological responses to improve weight loss success?
Question 1. Does bariatric surgery, in comparison to diet, generate similar
biological weight-promoting responses to weight loss?
Compensatory responses to weight loss with diet and surgery
1. Energy gap
With dietary weight loss, energy expenditure (EE) is reduced to levels below
those predicted by reduction in body size or composition, i.e. fat and,
particularly, fat free mass.2-4 This means that two people may weigh the same,
have the same body composition, may be consuming the same number of
calories and engaging in identical physical activities. However, the EE of the
individual who has previously lost weight through dieting will be lower than the
person who has never been on a diet. Furthermore, diet-induced reduction of
EE is not an acute response to dietary weight loss but persists long-term.3
Studies4 find with weight loss an increase in muscle efficiency during low-grade

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physical activity. This means for the reduced-weight individual that fewer
calories would be expended for a given amount of exercise than before weight
loss, resulting in a decrease in overall non-exercise energy expenditure
(NREE). In addition to a decrease in NREE following weight loss, the thermal
effect of food (TEF), i.e. postprandial energy expenditure, and, to a lesser
extent, resting energy expenditure (REE) are reduced.2-4 Because of these
reductions in EE, the person who has been on a weight-loss diet must eat fewer
calories than someone of comparable body weight in order to maintain weight
loss.
With surgery, 24-hour REE also significantly declines and, depending upon the
type of surgical procedure, by as much as 20 to 25%. Nonetheless, most
studies find that, unlike dietary weight loss, the fall in energy expenditure that
occurs with bariatric surgery is not greater than predicted by changes in body
size or composition.5-8 In fact, there are several studies,9-16 both animal and
human, that have reported an increase in EE with surgery.
Stylopoulos et al.9 found in diet-induced obese rats that Roux-en-y gastric
bypass (RYGB) increases total EE and REE relative to body size (VO2/kg/h).
Bueter and associates,10 likewise, found in rodents that RYGB not only
increases weight-adjusted total EE but also the TEF (postprandial energy
expenditure). These same investigators more recently11 reported significantly
higher diet-induced thermogenesis or TEF and weight-adjusted (cal/min/kg)
postprandial and total 24-hour EE for RYGB as compared to vertical banded
gastroplasty patients and proposed that the higher postprandial EE may play a
significant role in the weight loss success of the RYGB procedure. Faria and
associates12,13 also found that RYGB significantly increases weight-adjusted
REE for patients > 6 months postoperative and that the TEF of RYGB patients
is more than 200% higher than that of non-surgical severely obese controls.
Other studies have, likewise, reported increases in EE with RYGB14,15 and the
biliopancreatic diversion (BPD).16 Therefore, with surgery, unlike diet, EE
relative to body size is not reduced with weight loss and, with RYGB and BPD,
EE may even be increased. Differences between surgery- and diet-induced
changes in EE may explain, at least, in part, the significantly lower risk for
weight regain with surgery.

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Following dietary weight loss, weight regain not only occurs secondary to a
decrease in EE but also from changes in gut-brain interactions that may
increase energy intake (table 1). Weight loss modifies the production of
peripheral hormone regulators of the homeostatic (appetite) and hedonic
(reward) centers of the brain in a manner that leads to an increase in hunger
and the drive to eat,17-20 These modifications include a fall in leptin and an
increase in the hunger hormone, ghrelin. Leptin acts on the homeostatic and
hedonic centers of the brain to enhance satiety and to reduce appetite and the
desire for food; whereas, ghrelin does the opposite. Weight loss also reduces
meal-stimulated production of gut hormones that, under normal conditions,
interact with the appetite centers of the brain to enhance satiety and reduce
appetite. These gut hormones include: glucagon like peptide-1 (GLP-1), peptide
YY (PYY), oxyntomodulin (OXM), cholecytokinin (CCK), and the pancreatic
hormones, amylin and pancreatic peptide. Prospective investigations 17 find that
the adverse changes in gut hormone production with diet, i.e. increased ghrelin
and suppressed meal-stimulated hormone responses, persist long-term and are
associated with perceived hunger and an increased desire to eat. Diet-induced
long-term modification in the production of peripheral regulators of appetite and
reward generate a strong physiological drive to eat, making the post-weight loss
individual more vulnerable to weight regain.
Bariatric surgeries reduce energy intake by anatomically and/or mechanically
inducing food restriction, malabsorption, or both. Many bariatric surgical
procedures, in addition, cause favorable changes in the production of gut
hormone regulators of appetite and satiety (for review see 20-21, table 1). The
sleeve gastrectomy (SG), for instance, not only reduces energy intake via
gastric restriction but also by the effects the surgery has on regulators of
appetite including a persistent long-term decrease in the production of the
hunger hormone, ghrelin, and exaggerated increases in meal-stimulated
production of the appetite suppressing hormones, GLP-1 and PYY. Although
there are conflicting reports with regard to changes in ghrelin following RYGB
and the BPD, these surgeries result in highly exaggerated increases in meal-
stimulated production of GLP-1, PYY and OXM. Furthermore, the increased
GLP-1, PYY responses following surgery persist for years,22 along with a

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decrease in food intake and improved weight loss success.23 Bariatric surgery,
in addition to its anatomical control over food intake, helps to maintain energy
balance via gut-brain interactions that enhance satiety and reduce hunger and
the desire for food.
2. Defects in fat handling

Obesity per se is associated with a reduction in whole body and skeletal muscle
fat oxidation at rest and during aerobic activity, and neither dietary nor surgical
weight loss alone improve fat oxidation.24-28 Moreover, postprandial fatty acid
oxidation is also significantly reduced with weight loss,13,29 and studies that
have examined the fate of radiolabeled fat following its consumption find an
increase in trafficking of dietary fat to adipose tissue for storage.30,31 In addition
to an increase in fat trafficking to adipose depots, weight loss is also associated
with a greater capacity for adipose tissue expansion. Animal studies31 find that
weight regain following a diet is associated with hyperplasia of adipose tissue.
Baptista and associates32 also reported an increased adipogenic potential in
parechymal stem cells of adipose tissue biopsies in postoperative bariatric
patients when compared to that of weight-matched controls. Lofgren et al.33
found that the adipose tissue of bariatric patients three years out from surgery
are characterized by an increased number of small diameter adipocytes,
indicative of adipose tissue hyperplasia. These investigators 34 and others35-37
also found with weight loss (surgical or dietary) an increased potential for
adipocyte hypertrophy via changes in expression and activities of cellular
regulators of fat uptake, synthesis, breakdown, and thermogenesis.
Therefore, both dietary and surgical weight loss are associated with defects in
fat handling that cause a suppression of fat utilization and an increase in its
storage. Under these conditions, a greater proportion of calories consumed
would be stored as fat, contributing to a slow but progressive increase of fat
mass and weight gain with time.
In summary, weight regain following a diet occurs, in part, from compensatory
responses to weight loss. These include: 1) an increasing energy gap caused
by long-term physiological modifications that increase energy intake and reduce
energy expenditure and 2) defects in fat handling that reduce fat oxidation and

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increase the potential for adipose tissue expansion. Does surgery, in

comparison to diet, generate similar compensatory responses? Surgery, unlike
diet, reduces the decline in energy expenditure relative to changes in body size
and composition and, via anatomical and neurohumoral actions, reduces
energy intake and, consequently, the risk for weight regain via energy
imbalance (figure 1B). However, surgical weight loss, similar to diet, is
associated with adverse changes in fat handling that increase the risk for fat
accumulation and weight gain.
Question 2: Are there lifestyle and nutritional interventions that can favorably
modulate the physiological responses to weight loss to improve weight loss
maintenance?
Postoperative lifestyle and dietary interventions

Randomized trials have found that lifestyle interventions postoperatively are
effective in improving the weight loss success, behavior and health of bariatric
patients.38,39 Listed below and illustrated in figure 2 are suggested lifestyle and
dietary interventions that may be helpful in maximizing surgical weight loss
success through their beneficiary effects on fat handling and energy balance.
Intervention 1. Regular physical activity

Regular physical activity produces physiological responses that oppose those
contributing to weight regain and, in doing so, is highly effective in the
maintenance of weight loss. Aerobic activities improve defects in fat handling
by mobilizing fat from adipose tissue and by and stimulating skeletal muscle
mitogenesis, aerobic capacity and the expression of genes regulating fatty acid
oxidation.25,40-43 Studies find that regular bouts of aerobic activity substantially
increase the whole body and skeletal muscle rates of fatty acid oxidation that
are suppressed by dietary and surgical weight loss.25,40-41 Physical activity also
has a salutary effect on energy balance, increasing energy expenditure (total
and resting) and reducing appetite and energy intake.43 Finally, regular
physical activity, particularly when combined with resistance training, helps to
preserve muscle during weight loss and, in this way, improves energy
expenditure and fat oxidation. For weight loss maintenance, current

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recommendations include an exercise regimen consisting of daily performance

of 30 minutes or more aerobic activity (walking, cycling, swimming, etc.) and
two to three sessions per week of resistance training.44
Intervention 2. Reduced sitting time and frequent interruptions

Prolonged sitting contributes to obesity and may offset the benefits of exercise.
Studies find a positive association between time spent sitting and obesity.45
Sitting for prolonged periods not only lowers daily energy expenditure but also
produces physiological changes that favor fat accumulation and weight gain,
including insulin resistance, elevated insulin and triglyceride, inflammation, and
a reduced capacity for muscle to take up, and therefore, to oxidize fat.46-48 A
recent study46 found that one hour per day of vigorous exercise is insufficient to
reverse the metabolic aberrations caused by sitting. However, frequent
interruptions (every 20 to 30 minutes) to time spent sitting by standing, moving
around, taking a short walk, and other such activities, not only increase energy
expenditure but also prevent the metabolic aberrations caused by prolonged
sitting.46,49,50 A reduction in time spent sitting and frequent interruptions to sitting
may be as important as scheduled physical activity for weight loss maintenance.
Intervention 3. Consume foods with anti-obesity actions

Dietary fiber
Foods high in dietary fiber include pulses (legumes), whole grains, nuts, seeds,
fruits and vegetables. Epidemiological studies find an inverse relationship
between the dietary fiber and obesity and weight gain, and clinical studies find a
direct association between dietary intake and weight loss.51 The anti-obesity
actions of fiber are multiple.51-54 Fiber enhances satiety, in part, through gastric
distension and production of the satiety-promoting gut hormone, CCK. In
addition, fiber reduces the absorption of dietary fat and glucose, along with a
decrease in circulating levels of insulin. Furthermore, foods high in fiber are also
high in vitamins, minerals and phytonutrients that have salutary effects on
satiety, fat oxidation and energy expenditure.
Fermentable fiber (soluble fiber and resistant starches) or ‘prebiotics’ have anti-
obesity actions through their interaction with the gut microbiome.52-54 Prebiotics

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promote the growth of beneficial gut bacteria, and studies find that prebiotics
alter the microbiota of obese animals to that of a leaner phenotypes.53 The anti-
obesity actions52-54 of prebiotics involve, in part, the production by the microbiota
of short chain fatty acids and other metabolites that: 1) reduce hepatic fat
production and accumulation, 2) reduce adipose tissue mass, 3) increase
muscle fat oxidation and mitochondrial capacity, 4) and improve gut barrier
integrity to reduce the uptake of endotoxins and associated inflammation. In
addition, prebiotics, though their interaction with the microbiota, increase the
appetite suppressing gut hormones, GLP-1 and PYY, and reduce ghrelin,
contributing to reduced energy intake and significant weight reduction in
animals and humans.53-54 Currently, numerous investigations are in progress to
better understand the interrelationships between diet, the microbiota and
obesity, including studies of change in the profile of gut microbiota with surgery
and concomitant effects on weight and adiposity.55
The recommended intake of dietary fiber51 is between 25 and 30 g per day. As

much as 20 to 25% of the recommended intake should be fermentable fiber or
prebiotics, i.e. barley, pulses, garlic, fruit, onions, soybeans, whole grains,
leeks, fortified foods and drinks. For the bariatric patient, fiber supplements,
particularly those containing prebiotics (such as inulins, oligofructans), will likely
be necessary to maintain adequate fiber intake during the early postoperative
weight loss period. Pulses with their soft texture and high fiber content may
also be helpful in provision of adequate fiber following bariatric surgery.
Furthermore, pulses are not only an excellent source of dietary fiber but are
also high in protein.
Protein
Proteins are an important dietary component of weight loss and maintenance
and have a significant impact on energy balance and fat handling (for
comprehensive review see Faria et al.56 Protein leads to a heightened sense of
satiety and may do so via several potential mechanisms, including the provision
of amino acids as biosynthetic precursors to neuroregulators of appetite, such
as histamine or serotonin, and stimulation of appetite suppressing gut

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hormones, i.e. notably PYY. Protein increases energy expenditure, in

comparison to other macronutrients, and, with weight loss, protein helps to
reduce the associated decline in energy expenditure through the preservation of
muscle. Studies find with weight loss that a protein-rich diet helps to preserve
lean tissue while accelerating the loss of body fat.56,57 The salutary effects of
dietary protein on body composition with weight loss are believed to result, in
part, from branched chain amino acids, particularly leucine. During catabolic
states, leucine stimulates muscle protein synthesis and maintenance of muscle
mass.57 In addition to its role in muscle preservation, leucine has additional anti-
obesity actions including an increase in fat oxidation (whole body, muscle and
adipose tissue), a reduction in adipose tissue fat synthesis, improved insulin
sensitivity, and a reduction in oxidative stress and inflammation.58,59 Dietary
protein, therefore, via suppression of energy intake, stimulation of protein
synthesis and fat breakdown, contributes significantly to weight loss and weight
loss maintenance.
For the bariatric patient, a protein-rich diet is important not only in helping to
prevent loss of muscle with calorie restriction but also to reduce the risk for
protein deficiencies that may occur with the more malabsorptive procedures. As
reviewed by Faria et al.,56 the recommended daily intake for protein with
bariatric surgery varies from 60 to 120 g per day, with preferential intake of
quality protein and, in particular, quality protein high in leucine. Quality proteins,
i.e. those containing all of the indispensable aminoacids, include eggs, dairy,
fish, chicken, turkey, beef, pork and more. The optimal source of leucine is
whey protein, followed by casein, egg, isolated soy, and wheat protein. 56,57
Dairy and dietary calcium

A high content of leucine in dairy is believed to explain, in part, dairy’s anti-
obesity actions.58 Meta-analyses and literature reviews of studies of dairy’s anti-
obesity actions58,60,61 mostly agree that with calorie restriction an increase in low
fat dairy consumption enhances weight and fat mass loss, increases lean tissue
mass and reduces waist circumference. Approximately 50% of the anti-obesity
actions of dairy is believed to be attributable to its high content of dietary
calcium.58,61 As has been reviewed58,61 studies find that an increase in dairy

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calcium stimulates rates of whole body fat oxidation (postprandial and 24-hour).
In addition, high (1,500 mg) dairy calcium versus low (500 mg) substantially
increases fecal fat and reduces fat absorption. Furthermore, an increase in
dietary calcium helps to prevent the fat-promoting effects that elevated systemic
calcitriol, associated with low dietary calcium, have on adipose tissue, i.e.
reduced fat oxidation and lipolysis, increased de novo fat synthesis. In all of
these ways, an increased intake of calcium, particularly dairy calcium, may
benefit weight loss success.
Bariatric patients are likely to have inadequate intake of dietary calcium
postoperatively for several reasons: 1) low nutrient intake, 2) low vitamin D and
3) reduced absorption of calcium and vitamin D, as may occur with the RYGB,
BPD, and BPD/DS. For these reasons, the ASMBS Nutritional Guidelines
Committee62 suggests the following daily intakes of dietary calcium for bariatric
patients: 1,500 mg for the adjustable gastric band (AGB), 2,000 mg for the
RYGB and > 2000 mg for the BPD or BPD/DS, to be obtained through calcium
supplements and calcium-rich foods, including low fat dairy. Other foods or
beverages high in calcium are dairy alternatives and orange juice enriched with
calcium, sardines, shrimp, oysters, cooked broccoli, collard greens, turnip
greens, and rhubarb.
Omega 3 essential fatty acids

Agriculture practices such as grain feeding animals, fish and foul and genetic
engineering of plant foods have produced deficiencies in long-chain omega 3
(n-3) polyunsaturated essential fatty acids (EFA). Furthermore, most cooking
oils and processed foods sold at the grocery contain high amounts of omega 6
(n-6) EFA that oppose the actions of n-3. For these reasons, it is believed a
large portion of the population has measureable or functional n-3 deficiencies
and that such deficiencies are exacerbated by obesity. Significant inverse
relationships between BMI, waist and hip circumference have been found for
obese adults.63 Studies64-65 in obese children also find low plasma n-3 levels in
comparison to lean youth and a significant inverse association between n-3 and
BMI.
Animal and human studies have reported benefits of fish oil (n-3) supplements

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in the prevention of weight gain as well as in reduction of weight and fat mass in
the presence or absence of calorie restriction (for review see 66-67). The anti-
obesity actions of n-3 remain unclear. In humans, fish oil supplements of n-3
stimulate whole body fat oxidation, reduce inflammation, lower circulating levels
of insulin and triglyceride, and reduce stress-induced production of cortisol.68-71
In animals, the protective and weight-loss promoting effects of n-3 EFA involve
salutary effects on central regulation of appetite and changes in gene
expression that shift metabolism toward an increased accretion of lean tissue, a
reduction in fat deposition and adipose tissue numbers, and an increase in fat
oxidation and energy expenditure.66,67
To our knowledge, there are currently no studies of the effects of bariatric

surgery on levels of n-3 EFA. The risk for n-3 deficiencies with surgery,
however, is likely to be high considering the reduced nutrient intake, the low fat
dietary recommendations of some bariatric programs, and the reduced fat
absorption of malabsorptive procedures. An increase in dietary n-3 EFA intake
or supplementation may, therefore, be warranted. Foods high in n-3 EFA
include fatty fish (salmon, sardines, herring, mackerel, black cod, etc.), grass-
fed animals, flax, mustard, and pumpkins seeds, cloves, oregano, walnuts,
chia, rapeseed oil, and more. Supplements high n-3 include fish oil, Krill, and
certain forms of algae. The WHO recommends 0.3-0.5 g per day of the n-3 EFA
docosahexaenoic (DHA) plus eicosapentaenoic acid (EPA), with higher
amounts needed for deficiency or disease, i.e. heart disease, hypertension,
hyperlipidemia, depression, diabetes. Amounts higher than 3 g/d DHA + EPA
should be taken under the supervision of a physician.
Intervention 4. Reduce significantly the intake of obesity-promoting foods

Just as there are foods with anti-obesity qualities there are also those that are
obesigenic (for review see 72-74). Processed grains, sugar, and high fructose
corn syrup cause a rapid rise in blood glucose, along with surges in insulin with
its anti-lipolytic actions. In addition, the fructose in high fructose corn syrup
stimulates hepatic lipogenesis and fat production. Excessive intake of saturated
fat not only increases calories but may also may cause inflammation and, alter

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the gut microbiome in a manner that favors obesigenesis.74,53,54 Trans fats, i.e.
partially hydrogenated vegetables oils, are also fat-promoting and longitudinal
studies find that trans fats cause weight gain even in the absence of an energy
imbalance.74-76 Processed meats are not only associated with an increased
risk for cancer, heart disease and diabetes but are believed to be fat promoting,
as well. Processed meat is generally high in monosodium glutamate (MSG).
Population studies find a direct correction between the amount of MSG in the
diet and increasing body size,77 and animal studies find MSG to be toxic to
homeostatic regulation of appetite.78 Therefore, in an effort to prevent weight
gain, bariatric patients should attempt to reduce their intake of foods with
obesigenic actions, including saturated and trans fats, processed meat,
processed grains, sugar, and high fructose corn syrup.
Intervention 5. Take vitamin/mineral supplements

Bariatric patients are at risk for vitamin and mineral deficiencies and such
deficiencies not only increase the risk for bone loss, anemia, neurological
defects and other adverse health conditions but also may affect weight loss
success and maintenance. Micronutrients are needed for appropriate
absorption and metabolism of foods, and deficiencies increase the risk for fat
accumulation and obesity. Eating a wholesome diet and taking additional
micronutrient supplements may help to assure adequate intake of vitamins and
minerals. Epidemiological studies79 find that individuals who take
vitamin/mineral supplements have more favorable body compositions and are
less likely to gain weight over time than individuals who do not take
multivitamins. Prospective studies have also found that vitamin/mineral
supplements reduce hunger and disinhibition,80 cause loss of weight and body
fat,80-82 and significantly increase energy expenditure and fat oxidation.82 These
findings suggest that vitamin/mineral repletion may help to assure greater
weight loss success.
Intervention 6. Obtain adequate amounts of sleep

Adults require 7 to 8 hours of sleep per night and epidemiological studies, both
cross-sectional and longitudinal, have found an inverse association between

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sleep durations that are less than 7 hours and obesity or weight gain.83-84
Studies also find with dietary restriction that partial sleep loss causes
unfavorable changes in body composition, i.e. increased loss of lean tissue,
reduced loss of fat.85 The obesigenic actions of sleep loss are believed to
involve, in part, effects on appetitive hormone regulation that increase ghrelin
and reduce leptin. Studies86 find, after only two days of partial sleep loss, a
significant increase in the ratio of ghrelin to leptin, along with greater energy
intake and desire for calorie-dense foods, such as cookies, cakes, candy, and
chips. Sleep loss also has adverse effects on energy expenditure, fat oxidation,
glucose regulation and the production of hormones that may contribute to
weight gain, including a significant increase in evening levels of cortisol.84,85
Hence, adequate sleep (7 to 8 hours) for the bariatric patient is relevant to
weight loss promotion and weight gain prevention.
Intervention 7. Find ways to reduce stress

Chronic psychological stress and distress increase the risk for weight gain and
may interfere with successful long-term weight reduction.87 Psychological
distress stimulates the hypothalamic pituitary axis resulting in increased
production of cortisol which, in turn, stimulates fat uptake into adipose tissue,
increases hepatic production and release of glucose, promotes insulin
resistance and increased circulating levels of insulin, and reduces muscle
aerobic capacity; all potential contributors to weight gain and obesity. In
addition, stress-induced increases in cortisol as well as other central responses
to stress stimulate appetite and the potential for energy imbalance through an
increased physiological drive to eat. Patients should be assisted in findings
ways to release stress or be provided referrals to healthcare professionals
specialized in the identification and appropriate management of stress.
In conclusion, the human body resists changes in weight through powerful

compensatory mechanisms that include a reduction in energy expenditure
relative to changes in body size, a physiological increase in hunger and the
drive to eat, and defects in fat handling that leads to a shift in fat metabolism
from utilization to storage. Surgery, in contrast to diet-induced weight loss,

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has a positive impact on energy expenditure and neuro-hormonally mediated

satiety. Both diet- and surgery-induced weight loss create changes in fat
handling that resist weight loss and promote weight regain. Several lifestyle
and dietary interventions improve fat handling and energy expenditure and, if
included in the postoperative program, may have a beneficial impact on weight
loss success and long-term weight loss maintenance. These interventions
include: 1) regular physical activity, 2) reduced sitting and frequent interruptions
to time spent sitting, 3) a diet high in foods with anti-obesity actions, i.e. foods
high in fiber and nutrients, n-3 EFA, protein, dairy and foods high in dietary
calcium, 4) reduced intake of fat-promoting food, i.e. processed grains, foods
high in sugar and high fructose corn syrup, processed meat, trans fats, and high
intake of saturated fat, 5) micronutrient repletion, 6) adequate sleep, and 7)
reduced stress.
Figure 1.
Panel A. Compensatory Responses to Dietary Weight Loss.
A.
1. Energy Balance
Energy Expenditure
Energy Intake
2. Defects in Fat Handling
Fat Oxidation
Fat Trafficking to AT
Capacity for AT Expansion
B.
1. Energy Balance
Energy Expenditure
Energy Intake
2. Defects in Fat Handling
Fat Oxidation
Fat Trafficking to AT
Capacity for AT Expansion

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Panel B. Compensatory Responses to Dietary Weight Loss with Diet

(black arrows) and Surgery (white arrows).
Figure 2. Lifestyle/Diet Interventions Contributing to Weight Loss

Success.
Physical
Activity
Sitting
Anti-obesity
Foods
Weight Loss
Obesigenic
Foods Success
Vitamins
Minerals
Sleep
Stress

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37. Vettor R, Mingrone G, Manco M, et al. Reduced expression of uncoupling
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lipids more than shorter periods of moderate to vigorous exercise (cycling) in

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[review]

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Chapter VIII
Alcohol metabolism and potential health consequences
with bariatric surgery
Cynthia K. Buffington, Ph.D.*

Keith Kim, M.D.*
* Metabolic Medicine and Surgery Institute
Florida Hospital Celebration Health, USA
A reduced tolerance to alcohol is common among individuals who have had a

Roux-en-Y gastric bypass (RYGB). We found from an online survey1 that 84%
of more than 300 RYGB patients had experienced an increased sensitivity to
alcohol since their surgery. Nearly half of survey participants reported ‘feeling’
the effects of alcohol after having only a few sips of an alcoholic drink.
Approximately 5% of survey participants claimed they had been issued a
citation by legal authorities for driving under the influence of alcohol (DUI) after
drinking only one alcoholic beverage. Other researchers, likewise, reported
reduced alcohol tolerance in patients who have had a RYGB. Woodard et al.2
found that 100% of their post-operative RYGB study participants experienced
symptoms of intoxication (e.g., dizziness, warmth, double vision) following
ingestion of a 5 oz glass of wine. These findings, along with numerous patient
accounts of enhanced postoperative alcohol sensitivity, suggest that RYGB and
possibly other bariatric procedures alter alcohol pharmacokinetics.
The objectives of this chapter are: a) to examine why alcohol sensitivity is
increased by RYGB and, perhaps, other bariatric procedures, b) to identify
adverse health effects of alcohol consumption after surgery, and c) to
recommend guidelines to bariatric patients for the use of alcohol after surgery.
Causes for increased alcohol sensitivity with bariatric surgery: changes in

alcohol pharmacokinetics
• Gastric Metabolic and Alcohol Absorption

With normal gut anatomy, alcohol, when ingested, passes into the stomach
where a portion is oxidized prior to its absorption by the small intestines.3-4
Alcohol is metabolized in the stomach by gastric alcohol dehydrogenase (ADH)
in a process known as first pass metabolism.5,6 Conditions that inhibit or reduce
activities of gastric ADH increase blood alcohol content (BAC) and its

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intoxicating effects. These conditions include female gender, older age, and
certain medications such as H2 receptor antagonists, salicylic acid, and
acetaminophen.3-6
The length of time alcohol stays in the stomach also regulates blood alcohol
levels by increasing the amount of alcohol oxidized by gastric ADH and by
controlling the rate of alcohol absorption. Although a small portion of alcohol is
absorbed in the stomach, most of it is absorbed in the small intestines.3,4
Alcohol absorption is primarily regulated by the rate in which alcohol empties
into the intestines from the stomach. The longer alcohol remains in the stomach
the less is absorbed, and the blood alcohol content and risk for intoxication and
toxicity are lower. Food, by causing pyloric contraction, slows gastric emptying
and, consequently, reduces the rate of alcohol absorption. If, however, alcohol
is consumed by an empty stomach, gastric emptying and rates of absorption
are substantially enhanced, along with a concomitant increase in blood
alcohol.7,8
Changes in gastrointestinal anatomy with specific bariatric procedures may

affect gastric alcohol metabolism and absorption. With the RYGB, for instance,
more than 95% of the stomach is bypassed, including the pylorus, so that
alcohol passes directly from the stomach pouch into the intestines.
Consequently, with substantially less exposure of ethanol to ADH and with more
rapid gastric emptying, gastric oxidation of ethanol is negligible and the rate of
absorption in the small intestines is high. Under these conditions, alcohol would
rapidly enter the circulation at concentrations significantly higher than with
normal gastrointestinal anatomy.
Studies of RYGB alcohol pharmacokinetics found that blood alcohol levels peak
within 10 minutes9,10 following consumption of an alcoholic beverage in contrast
to 30 to 60 minutes without surgery.3,10 Steffen et al.9 reported an exceptionally
high rate of alcohol absorption in their RYGB study population (n=5) following
ingestion of 0.3 g/kg alcohol. In these studies, blood alcohol levels peaked
within 2 to 10 minutes (mean = 5.4 minutes) post-ingestion. Furthermore, peak
blood alcohol concentrations for all patients reached, or exceeded, 8mmol/L

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(0.08%), a concentration that would restrict an individual from legally operating

a motor vehicle in many countries and the United States.
Klockoff and associates10, likewise, found a rapid rate of absorption and peak
blood alcohol levels among their RYGB patients. In these studies, the alcohol
pharmacokinetics of 12 previously morbidly obese patients who were 3 or more
years out from surgery were compared to those of 12 weight- and age-matched
non-surgery controls. Following ingestion of 0.3g/kg alcohol, researchers
collected blood samples every 10 minutes for 3.5 hours. They found that blood
alcohol levels peaked at 10 minutes for the RYGB patients and at 30 minutes
for the controls. Furthermore, both peak and maximal blood alcohol
concentrations were significantly higher with RYGB.
Other researchers used a fixed dose of alcohol (i.e., 5 oz red wine, rather than a
weight-adjusted amount) to study alcohol pharmacokinetics with RYGB.2,11
Following ingestion of 5 oz of wine, Woodard et al.2 found that the peak breath
analyzer alcohol values of 19 RYGB patients at 6 months post-operatively were
3.5 times higher than preoperative values, i.e. 0.088% versus 0.024%, and
remained elevated for a considerably longer period of time. In similar studies,
Hagedorn et al.11 found that, following the ingestion of 5 oz of red wine, peak
breath analyzer values were higher and the time for clearance longer for RYGB
patients (n=19) than for a group of leaner controls (n=17).
Alcohol pharmacokinetics may also be altered by other bariatric procedures.
Frezza and associates12 reported a lack of gastric first pass metabolism (gastric
alcohol oxidation), elevated blood alcohol concentrations, and an increased
incidence of liver disease with gastrectomy. Maluenda et al.13 compared pre and
postoperative alcohol pharmacokinetics of 12 vertical sleeve gastrectomy (SG)
patients who had consumed 3.6 oz of red wine at 14%/L body water. They
found that the peak breath alcohol concentrations were considerably higher
after SG (2.3 month average) than before surgery (2.02 vs. 0.87 g/l,
respectively) and that the time for breath alcohol concentrations to return to 0%
after surgery was significantly longer. However, other researchers14 found no
postoperative changes (3 and 6 months) in alcohol pharmacokinetics with either
the SG (n=7) or the adjustable gastric band (n=9), when using a fixed dose of
alcohol (5 oz red wine).

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Based upon the findings of the studies described above, it is apparent that the
RYGB (and possibly the SG) change ethanol pharmacokinetics. RYGB
increases the rate and the amount of alcohol that is absorbed into the
circulation through anatomical alternations in gastrointestinal anatomy, thus
explaining, at least in part, why the RYGB patient may ‘feel’ the inebriating
effects of alcohol after having only a few sips of a drink. Furthermore, the
heightened blood alcohol levels of the RYGB patient would not only increase
the RYGB patient’s risk for intoxication and alcohol toxicity but may also have
serious ramifications with regard to safety in driving a motor vehicle or
performing other skilled tasks.
II. Alcohol Clearance

The increased blood alcohol concentrations with RYGB, and possibly the SG,
may result, in part, from a loss of first pass gastric alcohol metabolism or from
an unidentified effect the procedures have on alcohol clearance. Several
studies,2,11,13 but not all,10 have found that alcohol levels remain elevated for
longer periods after RYGB or SG than before, suggesting reduced alcohol
clearance.
Nearly all alcohol (> 90%) is cleared from the body by the liver via two major
oxidative pathways, the alcohol dehydrogenase (ADH) pathway and the
microsomal ethanol metabolizing system.3,4,15,16 In a healthy liver, alcohol is
oxidized at a rate of approximately 7 g of ethanol per hour. This is equivalent to
one standard alcoholic beverage per hour (i.e., 5 oz glass of wine, 12 oz mug of
beer, or 1.5 oz shot of 80 proof liquor). Drinking at a rate that exceeds this
amount or absorbing higher amounts of alcohol, as would be the case for the
RYGB patient, would further increase blood alcohol and its toxic effects.
The primary site of ethanol oxidation is the ADH pathway, accounting for 60 to
90% of hepatic alcohol metabolism.3,4,16 ADH is maximally activated by small
amounts of alcohol, but activity along the pathway can be reduced by an
accumulation of its end-products (e.g., NADH, acetaldehyde). Fasting and low
calorie intake, such as occurs in the early postoperative period, as well as
defects in hepatic mitochondrial function with obesity per se, may reduce the
metabolism of products of the ADH pathway and decrease hepatic alcohol

Blanca Ríos, MD
clearance.3,16,17 Furthermore, activities along the ADH pathway may be

impaired by steatosis and fatty liver disease,18 conditions that are relatively
common among individuals with morbid obesity. The gastric bypass patient,
therefore, may not only have higher rates of alcohol absorption but, at least in
the early postoperative period, also have reduced alcohol clearance through
suppression of activities along the ADH pathway.
The heightened blood alcohol levels of RYGB following alcohol ingestion, as
well as conditions associated with low calorie intake and rapid weight loss [e.g.,
free fatty acids (FFA) and ketones], induce and stimulate activity on the second
major hepatic pathway of alcohol clearance, the microsomal ethanol
metabolizing (MEM) system (particularly CYP2E1).3,4,15,16,19 The hepatic MEM
system, when induced, clears up to 30% of alcohol from the body. Unlike the
ADH pathway, the MEM system is not rate-limiting, meaning that the higher the
amount of alcohol in the circulation the more that is oxidized by this system.
Unfortunately, alcohol metabolism via this pathway substantially increases the
risk of liver damage from the products of the reaction, acetaldehyde and
oxidative free radicals. Furthermore, induction of this pathway increases the
conversion of numerous xenobiotics, including household solvents, industrial
pollutants, tobacco smoke and certain drugs such as acetaminophen to highly
toxic metabolites and chemical carcinogens.15
Adverse health effects of alcohol use post-surgery

The elevated blood alcohol concentrations with the RYGB (and possibly other
bariatric procedures) and metabolic by-products of ethanol metabolism not only
cause liver damage and liver disease but also have a negative impact on other
tissues.16,20 Alcohol produces inflammation of the gastrointestinal tract,
contributing to pancreatitis and gastritis. Additionally, alcohol stimulates gastric
secretion and relaxes the lower esophageal sphincter, resulting in gastric reflux
and the risk for esophageal cancer. Skeletal muscle is particularly susceptible
to alcohol toxicity, and alcohol reduces muscle mass and strength and produces
symptoms of cramps and myalgia. Alcohol is also toxic to the heart, causing
cardiomyopathy, myocarditis and cardiac arrhythmias with significant risk of
sudden death. The effects of alcohol on the brain include changes in behavior

Blanca Ríos, MD
and judgment, altered memory and neuromuscular function, blurred vision,

changes in body temperature, abnormal breathing and the risk of blackouts,
coma and death.
In addition to its direct effects, alcohol can indirectly cause irreversible brain and
nerve damage, coma and possible death by promoting deficiencies in important
vitamins, such as thiamin (vitamin B1) and cobalamin (vitamin B12). Alcohol
inhibits the absorption of thiamin and other B-complex vitamins, reduces
activation of certain vitamins, and stimulates the breakdown of vitamin A,
pyridoxine and folate.4,16 These vitamins may already be deficient in bariatric
patients because of nutrient restriction, malabsorption, or impartial digestion of
foods produced by the respective surgery.21 Alcohol use, then, could compound
the negative effects that bariatric surgery has on vitamin/mineral status and
increase the risk of associated health problems, including neuropathy, an
irreversible loss of cognitive functions, defects in metabolism, a decrease in the
ability of the body to heal, low immunity, fatigue and more.21
Hypoglycemia is not uncommon with alcohol use, and the risk for alcohol-
related hypoglycemia may be considerably higher for the postoperative RYGB
patient than for someone who has not had surgery. Low intake of carbohydrate,
depletion or reduction of glycogen stores, and increased insulin secretion,
with22,23 or without 24 an increase in islet mass, reduces glucose availability in
the bariatric patient and increases the risk for a hypoglycemic episode. Alcohol
consumption also reduces glucose availability through suppression of
gluconeogensis and glycogenesis.25-26 Furthermore, both alcohol intake27 and
bariatric surgery28 may blunt counterregulatory hormone responses to
hypoglycemia. As neural tissue requires glucose for fuel, a hypoglycemic
episode could adversely affect neuromuscular and cognitive functions, resulting
in loss of coordination and balance, slurred speech, poor vision, confusion,
unconsciousness and even death.
In addition to the numerous adverse health consequences of alcohol use after
surgery, there are also reports of an increased risk of alcohol abuse and
addiction. In our web-based study,1 21.4% of more than 300 RYGB patients
claimed to have problems controlling their use of alcohol, in comparison to only
4.5% of patients before surgery. Another retrospective research 29 among 51

Blanca Ríos, MD
bariatric patients found that 21.4% of the RYGB patients had symptoms of
alcohol abuse disorder (AUD) as compared to 0% of individuals who had an
AGB. Other retrospective studies, however, found either no change or a
reduction in AUD post-RYGB. Among 70 RYGB patients surveyed 6 to 10 years
after their RYGB procedure, Ertelt et al.30 found little difference in symptoms of
AUD before or after surgery. Using diagnostic interview to assess symptoms of
AUD, Mitchell and associates31 found among 78 RYGB patients who were 13 to
15 years out from surgery that 12.8% of them had symptoms of AUD before
surgery in comparison to 7.7% after surgery.
The conflicting findings of these retrospective studies regarding alcohol abuse

with bariatric surgery have prompted the performance of prospective AUD
analyses. In a recent study by King and associates,32 the prevalence of AUD
was studied in 1,145 bariatric patients before surgery and again at 3,6,12 and
24 months postoperatively. According to the study results, the prevalence of
AUD in patients having a RYGB was significantly increased (10.7%) above
preoperative values (7.0%) at 2 years post-surgery. However, there were no
significant changes in AUD prevalence in patients who underwent an AGB. In
another longitudinal study of substance abuse, Conason et al.33 found that with
RYGB, but not AGB, the frequency of alcohol use 2 years after surgery was
significantly greater than before surgery. Likewise, animal studies 34 have proved
that RYGB increases ethanol consumption among obese or lean rats. The
results of the prospective studies in animals and humans would suggest an
increased risk of alcohol use and abuse with RYGB.
Why the RYGB procedure increases the risk of alcohol abuse remains a
mystery although potential causes have been reviewed35,36 and studied.34 Some
researchers37 suggest that alcohol abuse with RYGB may involve a transfer of
addictions from food prior to surgery to alcohol postoperatively. There are
common neural pathways in the brain known to regulate both eating behavior
and alcohol/drug use,38 and recent rodent studies with RYGB found changes in
the patterns of gene expression in regions of the brain associated with reward,34
in connection with an increased desire for alcohol. The rapid absorption and
heightened peak alcohol concentrations with RYGB may offer yet another

Blanca Ríos, MD
explanation for the increased risk of alcohol abuse with the procedure,35 as
substances which reach their peak concentrations faster have greater addictive
potential.39,40 The RYGB population may, therefore, be vulnerable to alcohol
abuse for a multitude of reasons, underscoring the need to identify at-risk
patients prior to surgery and abuse prevention intervention.36,41
Altogether, RYGB and possibly other procedures including the SG cause
changes in alcohol pharmacokinetics that increase the amount and the rate of
alcohol that enter the circulation. The increased blood levels of alcohol with
these surgical procedures, along with metabolic changes associated with rapid
weight loss, may have an adverse effect on activities along the major pathways
of ethanol clearance, increasing the patient’s risk of liver damage and disease.
The effects of RYGB in ethanol pharmacokinetics may also increase ethanol
toxicity to extra-hepatic tissues, compound the risk for postoperative
deficiencies of vitamin and minerals, promote hypoglycemia, and alter neural
pathways that contribute to alcohol abuse.
Patient recommendations for the use of alcohol after surgery

Changes in alcohol metabolism and associated health consequences with
RYGB and possibly other procedures stress the importance of patient education
regarding the use of alcohol after surgery. The surgeon or bariatric educator
should explain to the candidate how surgery may affect their sensitivity to
alcohol, and the candidate (and postoperative patient) should be made well
aware of the many increased health risks associated with alcohol use after
surgery. The wise choice for the bariatric patient would be to abstain from
drinking alcohol. However, as abstinence is not likely to be the choice of most
bariatric patients, it is important that they have guidelines for alcohol use. The
following are our recommendations for alcohol consumption after surgery:
I. Do NOT consume alcohol during the rapid weight loss period.

II. Remember when drinking that small amounts of alcohol can cause intoxication
or result in low blood sugar, loss of consciousness and even death.
III. Do NOT drive or operate heavy equipment after drinking alcohol, even SMALL
amounts.

Blanca Ríos, MD
IV. Eat food immediately prior to drinking (or even with your drink).
V. Take your vitamin and mineral supplements regularly and maintain proper
hydration and nutrient status.
VI. Know the health hazards of alcohol use post-surgery:
- Liver damage and disease
- Behavioral changes
- Irreversible brain and nerve damage from the direct or indirect effects of
alcohol
- Hypoglycemia and neurological consequences
-Vitamin and mineral depletion and associated health issues
-Muscle loss, heart disease, gastritis, pancreatitis, GERD, cancer
-Risk of alcohol abuse and dependency
1. Buffington CK. Alcohol use and health risks: Survey results. Bariatric
Times. 2007;4:21-23.
2. Woodard GA, Downey J, Hernandez-Boussard T, et al. Impaired alcohol
metabolism after gastric bypass surgery: A case-crossover trial. J Am
Coll Surg. 2011;212:209-14.
3. Cederbaum AL. Alcohol metabolism. Clin Liver Dis. 2012;16:667-85.
4. Lieber CSW. Metabolism of alcohol. Clin Liver Dis. 2005;9:1-35.
5. Lieber CS, Gentry RT, Baraona E. First pass metabolism of ethanol.
Alcohol Alcohol. 1994 Suppl;2:163-69.
6. Palmer RH, Frank WO, Nambi P, et al. Effects of various concomitant
medications on gastric alcohol dehydrogenase and the first-pass
metabolism of ethanol. Am J Gastroenterol. 1991;86:1749-55.
7. Jones AW, Jonsson KA, Neri A. Peak blood-ethanol concentration and
the time of its occurrence after rapid drinking on an empty stomach. J
Forensic Sci. 1991;36:376-85.
8. Hahn RG, Norberg A, Jones AW. ‘Overshoot’ of ethanol in the blood after
drinking on an empty stomach. Alcohol Alcohol. 1997;32:501-05.
9. Steffen KJ, Engel SG, Pollert GA, et al. Blood alcohol concentrations rise
rapidly and dramatically after Roux-en-Y gastric bypass. Surg Obes
Relat Dis. 2013. [in press]
10. Klockhoff H, Naslund I, Jones AW. Faster absorption of ethanol and
higher peak concentration in women after gastric bypass surgery. Br J
Clin Pharmacol. 2002;54:587-91.
11. Hagedorn JC, Encarnacion B, Brat GA, et al. Does gastric bypass alter
alcohol metabolism? Surg Obes Relat Dis. 2007;3:543-48.

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12. Frezza M, Buda A, Terpin MM, et al. Gastrectomy, lack of gastric first
pass metabolism of ethanol and alcohol liver disease. Results of a
multicenter study. Ital J Gastroenterol Hepatol. 1997;29:243-48.
13. Maluenda F, Csendes A, De Aretxabala X, et al. Alcohol absorption
modification after laparoscopic sleeve gastrectomy due to obesity. Obes
Surg. 2010;20:744-48.
14. Changchien EM, Woodard GA, Hernandez-Boussard T. Normal alcohol
metabolism after gastric banding and sleeve gastrectomy: A case-cross-
over trial. J Am Coll Surg. 2012;215:475-79.
15. Lieber CS. The discovery of the microsomal ethanol oxidizing system
and its physiologic and pathologic role. Drug Metab Rev. 2004;36:511-
29.
16. Lieber CS. Alcohol and the liver: Metabolism of alcohol and its role in
hepatic and extrahepatic disease. Mt Sinai J Med. 2000;67:84-94.
17. Li J, Feuers RJ, Desai VG, et al. Surgical caloric restriction ameloriates
mitochondrial electron transport dysfunction in obese females. Obes
Surg. 2007;17:804-12.
18. Zorzano A, Ruiz del Arbol L, Herrera E. Effect of liver disorders on
ethanol elimination and alcohol and aldehyde dehydrogenase activities in
liver and erythrocytes. Clin Sci. 1989;76:51-57.
19. O’Shea D, Davis SN, Kim RB, et al. Effect of fasting and obesity in
humans on the 6-hydroxylation of chlorzoxazone: A putative probe of
CYP2E1 activity. Clin Pharmacol Ther. 1994;56:359-67.
20. National Institute on Alcohol Abuse and Alcoholism (NIAAA).
Understanding the impact of alcohol on the body. Available from:
http://www.niaaa.nih.gov/alcohol-health/alcohols-effects-body. Accessed
April, 2013.
21. Aills L, Blankenship J, Buffington C, et al. Bariatric nutition: Suggestions
for the surgical weight loss patient. Surg Obes Related Dis. 2008;4:S73-
108.
22. Patti ME, McMahon G, Mun EC, et al. Severe hypoglycemia post-gastric
bypass requiring pancreatectomy: Evidence of inappropriate insulin
secretion and pancreatic islet hyperplasia. Diabetololgia. 2005;48;2236-
40.
23. Service GJ, Thompson GB, Service FJ, et al. Hyperinsulinemic
hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl
J Med. 2005;353:249-54.
24. Meier JJ, Butler AE, Galasso R, et al. Hyerinsulinemic hypoglycemia
after gastric bypass is not accompanied by islet hyperplasia or increased
beta-cell turnover. Diabetes Care. 2006;29:1554-59.
25. Mokuda O, Tanaka H, Hayashi T, et al. Ethanol stimulates
glycogenolysis and inhibits glycogenesis via gluconeogenesis and from
exogenous glucose in perfused rat liver. Ann Nutr Metab. 2004;48:276-
80.
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26. Wiler SQ, Neese RA, Christiansen MP, et al. The inhibition of
gluconeogenesis following alcohol in humans. Am J Physiol.
1998;275:E897-907.
27. Rasmussen BM, Orskov L, Schmitz O, et al. Alcohol and glucose
counterregulation during acute insulin-induced hypoglycemia.
Metabolism. 2001;50:451-57.
28. Guldstrand M, Ahren B, Wredling R, et al. Alteration of the
counterregulatory response to insulin-induced hypoglycemia and of
cognitive function after massive weight reduction in severely obese
subjects. Metabolism. 2003;52:900-07.
29. Suzuki J, Haimovici F, Chang G. Alcohol use disorders after bariatric
surgery. Obes Surg. 2012;22:201-07.
30. Ertelt TM, Mitchell JE, Lancaster K, et al. Alcohol abuse and dependence
before and after bariatric surgery: A review of the literature and report of
a new data set. Surg Obes Relat Dis. 2008;4:647-50.
31. Mitchell JA, Lancaster KI, Burgard MA, et al. Long-term follow-up of
patients’ status after gastric bypass. Obes Surg. 2001;11:464-68.
32. King WC, Chen JY, Mitchell JE, et al. Prevalence of alcohol use
disorders before and after bariatric surgery. JAMA. 2012;307:2516-25.
33. Conason A, Teixeira J, Hsu C-H, et al. Substance use following bariatric
weight loss surgery. JAMA Surg. 2013;148:145-50.
34. Davis JF, Tracy AL, Schurdak JD, et al. Roux en Y gastric bypass
increases ethanol intake in the rat. Obes Surg (published online: 2013
February 26th).
35. Sogg S. Alcohol misuse after bariatric surgery: epiphenomenon or
“Oprah” phenomenon? Surg Obes Rel Dis. 2007;3:366-68.
36. Heinberg L, Ashton K, Coughlin J. Alcohol and bariatric surgery: review
and suggested recommendations for assessment and management.
Surg Obes Relat Dis. 2012;8:357-63.
37. Moorehead M. Transfer of addiction and considerations for preventative
measures in bariatric surgery. Bariatric Times. 2007; April 26th.
38. Simansky KJ. NIH symposium series: Ingestive mechanisms in obesity,
substance abuse and mental disorders. Physiol Behav. 2005;86:1-4.
39. Weaver M, Schnoll S. Stimulants: Amphetamines and cocaine. In:
McCrady BS, Epstein EE, editors: Addictions: A comprehensive
guidebook. New York: Oxford University Press; 1999:106-20.
40. Longo LP, Johnson B. Addiction: Part 1. Benzodiazepines – side effects,
abuse risk and alternatives. Am Fam Physician. 2000;61:2121-28.
41. Ashton K, Heinberg L, Merrell J, et al. Pilot evaluation of a substance
abuse prevention group intervention for at-risk bariatric surgery
candidates. Surg Obes Relat Dis. 2013. [in press]

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Chapter IX
Management of special conditions after bariatric surgery:
dumping syndrome
Dr. Poonam S. Shah M.D.*

Dr. Shashank S.Shah, M.S.*
*Laparo-Obeso Centre
Pune, India.
The dumping syndrome is an iatrogenic condition which can occur after partial
resection of the stomach, whatever the reason [e.g., peptic ulcer, gastric
cancer, fundoplication or bariatric surgery (weight loss procedure)]. Therefore, it
is known as a ‘post-gastrectomy’ syndrome.
This phenomenon has first been described in 1913 by Hertz AF,1 though the
term “dumping” was first used by Wyllys et al.2 in 1920 to describe a
radiographic observation of rapid gastric emptying of contrast, in patients with
typical (dumping) symptoms after gastrectomy. The syndrome has gained new
significance after the advent of bariatric surgeries that include partial
gastrectomy with or without intestinal anastomosis [e.g., gastric bypass (GBP),
biliopancreatic diversion (BPD), duodenal switch (BPD-DS), mini-gastric bypass
(MGB), sleeve gastrectomy (SG)].
Over the last century, many studies have been done in order to understand the
pathophysiology, effects and treatment of post-gastrectomy syndrome.3-6
However, there are very few studies on dumping related to post-bariatric
surgeries.7-12
Pathogenesis
The functions of the normal stomach are:
-To store the ingested food,
-Initiate digestive processes with the help of acid,
-Churn the food and makes it into a paste called ‘chyme’,
-Release the ‘chyme’ into the duodenum in a controlled cyclical fashion,
-Initiate a hunger signal via the ghrelin hormone, when empty.

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The movements of the stomach are regulated by the autonomic nervous system
which in turn is influenced by the central nervous system and various circulating
hormones.13-15
The ‘dumping’ syndrome is therefore the effect of change in the stomach’s
storage capacity and function, as well as in its motility (contractility, movements)
after a gastrectomy. The rate of gastric empting is faster and earlier than the
normal cycle. Normally the stomach empties its solid contents by movements of
antrum and relaxation of pylorus. Therefore, removal or bypass of the pylorus
makes the contents in the stomach to directly and suddenly enter the jejunum.
However, an increase in the rate of gastric empting is not the only mechanism
responsible for the dumping, but also many other factors.16 The resection of the
fundus and partial vagotomy limits the stomach distensibility and volume. The
negative feedback effect by presence of the chyme in the duodenum is also
lost, contributing to the faster rate of gastric empting. Loss of the pressure
gradient between the duodenum and stomach gives rise to earlier empting of
liquids.
Types of ‘dumping’ phenomenon

Depending upon the time of its occurrence after eating, the ‘dumping’ has been
described by Adlerberg and Hammerschlag in 1947 to be of two types: early
and late.17
Early dumping syndrome. Symptoms appear either while eating or soon after
the meal (within 30 minutes). Patients experience prominently gastrointestinal
symptoms.
Late dumping syndrome. Symptoms appear between one and three hours
after eating. Patients experience predominantly vasomotor symptoms.
Symptoms of the dumping Syndrome18,19

There are two types of symptoms experienced by the patient when ‘dumping’
occurs:
i) Gastrointestinal (GI) symptoms, and ii) vasomotor (VM) symptoms.

Blanca Ríos, MD
The type and severity of symptoms vary from individual to individual. Most
patients with ‘early’ dumping have both GI & VM symptoms, while ‘late’ dumping
patients have mostly VM symptoms.
The entry of the hyperosmolar chyme into the jejunum causes intestinal
distension and increased contractility. There is shift of fluid into the jejunum to
dilute the chyme. This causes the GI symptoms of abdominal distention,
cramping pain, flatulence, nausea, and watery diarrhea.5 The fluid shift also
causes a decrease in intravascular volume with a peripheral vascular
dilatation.20, 21 This causes the VM symptoms of hypotension, tachycardia
(palpitations), giddiness, flushing, sweating and an intense desire to lie down. 22
Changes in blood volume cause renal and cardiovascular alterations as well. 23
Mediators of the dumping syndrome and its symptoms

Various gut hormones and peptides (incretins) are mediators of the dumping
syndrome and its symptoms.24,25 Vasoactive gut hormones are released in
response to fluid shifts, giving rise to vasomotor symptoms and signs. The
hyperosmolar chyme stimulates the inappropriate release of gut hormones like
bradikinin, enteroglucagon, motilin, serotonin, vasoactive intestinal peptide
(VIP), pancreatic poypeptide (PP), petide YY, gastric inhibitory polypeptide
(GIP), neurotensin, etc.5,26-28 The late dumping is mainly seen when a high
carbohydrate content meal is delivered to the lower intestine causing a rapid
and excessive release of incretins like GLP in response to the high blood
glucose levels.8,22,29 The insulin released in response to the rapid rise of
incretins rapidly decreases the glucose to abnormally low levels, thus causing
the appearance of the symptoms and signs of hypoglycemia (e.g., sweating,
tremors, and hunger).
Diagnosis of the dumping syndrome

The diagnosis of the dumping syndrome is more of a diagnosis of exclusion
(Table 1). Sigstad, in 1970, developed a clinical diagnostic index for the
diagnosis of the dumping syndrome30 (Table 2). It is a useful scoring system in
which vasomotor symptoms and signs have more importance for diagnosis of
dumping than other symptoms. For example, many post-bariatric surgery
patients have vomiting as a common complaint; as found in the index, other

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causes are indicated aside from dumping if vomiting is the predominant

symptom.
The oral glucose provocation test31, 32 (after 10 hours of fasting) using just
50gms of glucose, for eliciting signs of dumping and hypoglycemia, remains a
simple test with simultaneous measurement of glucose, insulin and c. peptide
levels. It is important to look for signs of neuroglycemia for those rule out late
dumping and warrant other tests33 (see below). The Visick test should be
applied during the OGTT using 50gms, which is 100% sensitive and 92%
specific for early dumping, if heart rate is increased by 10 beats/min in the first
hour.19,23 The Electrocardiogram during the test may show changes like
lengthening of the QT interval, flattening of Q wave, elevation or depression of
the ST segment, etc.23
A positive result of the hydrogen breath test after ingestion of glucose is 100%
sensitive19. A gastric emptying study using Tm99 may be done to document
rapid gastric emptying.34 An endoscopy or a barium study and abdominal
imaging studies should be done when in doubt to rule out other causes.
----------------------------------------------------------------------------------------------------------
Table: 1. Dumping: a diagnosis of exclusion
----------------------------------------------------------------------------------------------------------
*Typical symptoms in patients who have undergone gastric surgery with or
without bypass of the pylorus- GBP, BPD, BPD-DS, MGB, SG.
*Absence of neuroglycemia symptoms in spite of low Glucose < 40-50 mg%
and the above signs of hypoglycemia.
*Typical signs and symptoms can be elicited with an oral glucose challenge
(OGTT) –of 50 gms.
-Visick test- OGTT 50 gm –Increase in H.R by 10 beats/min in the first hour-
100% sensitive, 92% specific for early dumping.
-Certain ECG changes observed during the test.
*Sigstad diagnostic index- >7- diagnostic (table 2).
*A positive result from a hydrogen breath test after ingestion of glucose–100%
sensitive.
*A gastric emptying study –Tm99 may be helpful to document rapid gastric
emptying.
*An endoscopy or a barium study to rule out other causes.

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----------------------------------------------------------------------------------------------------------
TABLE 2: Sigstad's diagnostic index : >7 diagnostic of Dumping .
----------------------------------------------------------------------------------------------------------
Sigstad's diagnostic index, indicating symptoms and the points assigned for
those symptoms:
a. Shock: +5
b. Almost fainting, syncope, unconsciousness: +4
c. Desire to lie or sit down: +4
d. Breathlessness, dyspnea: +3
e. Weakness, exhaustion: +3
f. Sleepiness, drowsiness, yawning, apathy, falling asleep: +3
g. Palpitation: +3
h. Restlessness: +2
i. Dizziness: +2
j. Headaches: +1
k. Feeling of warmth, sweating, pallor, clammy skin: +1
l. Nausea: +1
m. Fullness in the abdomen: +1
n. Borborygmus: +1
o. Eructation: -1
p. Vomiting: -4
Hyperinsulinemic hypoglycemic. It is different from the late dumping that is

described above.
In contrast to late dumping which usually disappears about 18 months after
surgery, the hyperinsulinemic hypoglycemia appears more than a year after
surgery. This phenomenon was first described by Service et al. in 2005 35 in
GBP patients and then reported by many other researchers.36-,41 The
differentiating factor is signs of neuroglucopenia which are generally absent in
late dumping. Therefore, a late onset of symptoms more than a year after
surgery, plus demonstration of severe hypoglycemia not prevented by usual
dietary changes but requiring glucose, as well as absence of vasomotor
symptoms, should warrant tests like abdominal imaging studies and selective
arterial calcium stimulation tests to rule out other causes like insulinoma. The

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patients in the study by Service et al. had pancreatic nesidioblastosis and one
had multiple insulinomas. Distal pancreatectomy relieved all patients of the
hypoglycemic episodes.
Mechanism of hypoglycemia post bariatric surgery

A study of a large number of GBP patients over 21 years by Merck et al. in
2010,42 showed the risk of hypoglycemia and related disorders as 2- to 7- fold
more in GBP patients. The possible mechanisms of hypoglycemia are proposed
to be an increase in the B-cells of the pancreas with heightening in their function
which, coupled with an exaggerated increase in the GLP-1 with GBP, would
cause excess insulin.14, 43 The decrease of ghrelin levels in the stomach after
surgery lessens its inhibitory effect on insulin action and also inhibits the
counter regulatory hormones, letting the insulin act unopposed.44
Dumping-like symptoms are also experienced after sleeve gastrectomy, even
though the pylorus is preserved and the duodenum is in continuation with the
stomach. An increased rate of gastric empting and rapid intestinal transit has
been demonstrated by Shah et al. in 2009 using Tm99.34 In 2012, Tzovaras et
al. demonstrated symptoms suggestive of dumping syndrome after provocation
following a laparoscopic sleeve gastrectomy, in a study of 31, non-DM, morbidly
obese patients of which 9 developed early dumping and 1 late dumping
symptoms. It was observed that the symptoms suggestive of dumping
syndrome after provocation still existed at 6 and 12 months in a significant
proportion of patients following LSG, including both early and late dumping.
These findings are consistent with the high incidence of hypoglycemia after
OGTT at 6 and 12 months after LSG. The number of patients with symptoms of
dumping and incidence of hypoglycemia were seen to have increased by the
end of the first year following the SG.12,45 Other additional changes which can
be responsible for dumping after SG are: decrease of the distensibility of the
stomach due to fundic resection; substantial reduction of food volume due to
resection, and reduced appetite on account of lesser ghrelin; partial vagotomy
affecting motility; decrease in acid and, consequently, chyme that is not properly
formed, etc.

Blanca Ríos, MD
Treatment of dumping syndrome:

In the majority of patients a change in dietary habits prevents/controls the
dumping syndrome and also hypoglycemia.
 Dietary Modifications
Patients should be advised to eat several (5 to 6) small meals a day. Meals
should be low in carbohydrates and fats, high in protein, and contain no simple
sugars. This prevents hyperglycemia and the subsequent hyperinsulinemic
hypoglycemia. Adding fiber-rich and pectin containing foods (e.g., oats, apples)
to meals, delays gastric emptying and reduces glucose and insulin peaks. They
should avoid drinking liquids with meals until 30 minutes after eating. Meals
should have more solid and less liquid content.
The majority of patients, especially those with early dumping, can be stabilized
by changing dietary habits. However, the advised diet is similar to the ideal
bariatric diet that all post-surgery patients should ideally follow.46,47
*Effect of posture: Some patients don’t feel like lying down; they consider that
standing and/or walking after eating decrease or prevent the dumping. Some
feel that lying down flat prevents or decreases the dumping.48
 Medications
Medication should be added if dietary changes fail at stabilizing the symptoms.
Several drugs (e.g., tolbutamide, propranolol, cyproheptadine, methysergide,
verapamil) have been tried in many small studies, of which only the last two
have shown good results.49-51
Octreotide, a synthetic analog of the hormone Somatostatin, has long been

used in the treatment of dumping syndrome. It inhibits GH secretion and has a
multitude of other endocrine and nonendocrine effects, including inhibition of
glucagon, VIP, and GI peptides.
The action mechanisms of octreotide are: delay in the accelerated initial gastric
emptying, delay in small intestinal transit time, inhibition of enteral hormone
release, inhibition of insulin release and splanchnic vasoconstriction with

Blanca Ríos, MD
inhibition of postprandial vasodilatation. It is effective for early and late dumping

in a dose of 50-150 mcg/day IV. The usual initial dose of octreotide is 50 mcg,
administered subcutaneously bid/tid 30 minutes prior to each meal.
Symptomatic relief is seen in about 90% of patients with severe dumping
refractory to other forms of medical intervention.52-54 Long-acting release of
octreotide is as effective in the long term as subcutaneous octreotide, and has
superior symptom control as assessed by the Gastrointestinal Specific Quality
of Life Index; in addition, it provides better maintenance of body weight and
higher quality of life.
Acarbose is an alpha-glycoside hydrolase inhibitor, which interferes with

carbohydrate absorption, and has been shown to help patients with late
dumping.51,55-58 It delays production of monosaccharides by inhibiting alpha-
glucosidases associated with the brush border of the intestine. These are the
enzymes responsible for digestion of complex polysaccharides and sucrose. A
decrease in the vasomotor symptoms has also been noted with acarbose
(50/100 mg t.i.d)
3. Surgical treatment
Surgery should be considered only in cases refractory to dietary changes and
medicines like acarbose and octreotide. Attempts have been made to slow
down the rate of gastric emptying by decreasing the stomal size, i.e., the
diameter of the connection between the stomach and the intestine; for instance,
Porter and Claman reported good results by narrowing the gastrojejunal
stoma.59 In 2008, Horber et al.60 observed that severe, disabling hypoglycemia
after GBP occurred only in patients with loss of restriction. Gastric restriction
was restored by surgical placement of a silastic ring (n = 8, the first two patients
with additional distal pancreatectomy), or an adjustable gastric band (n = 4)
around the pouch in 12 consecutive patients presenting severe hypoglycemia.
At 5 to 19 months monitoring, 11 patients presented no hypoglycemic episodes,
while one had recurrence of hypoglycemia and underwent distal
pancreatectomy.

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Hence, reversal of the bariatric procedure, GBP, BPD-DS, MGB, may be

needed 61-64 in extremely severe cases where the dumping cannot be controlled
or prevented by dietary changes and the use of medication, seeing that this
causes excessive weight loss, malnutrition and affects the quality of life.
Can dumping be beneficial?

The early transit of food to terminal ‘Ileum’ stimulates the release of hormones
like GLP 1, PYY, which induces satiety, suppresses hunger and increases
insulin secretion (incretinogenic action). Therefore, they have an anti-diabetic as
well as a weight loss action. For some patients this can be a ‘blessing in
disguise’, especially for diabetics and their bariatric team, since it helps patients
to adhere to the prescribed (bariatric) diet and avoid dumping. Thus, this can
help them to keep their health and weight loss goals on track.
1. Hertz AF. Cause and treatment of certain unfavorable after effect of

gastroenterostomy. Ann Surg. 1913;58:466-72.
2. Wyllys E, Andrews E, Mix CL. “Dumping stomach” and other results of
gastrojejunostomy: Operative cure by disconnecting old stoma. Surg Clin
Chicago. 1920;4:879-92.
3. Eagon JC, Miedema BW, Kelly KA. Postgastrectomy syndromes. Surg
Clin North Am. 1992;72:445-65.
4. Bufler P, Ehringhaus C, Koletzko S. Dumping syndrome: A common
problem following Nissen fundoplication in young children. Pediatr Surg
Int. 2001;17:351-55.
5. Jordan GLJ, Overton RC, De Bakey ME. The postgastrectomy
syndrome: Studies on pathogenesis. Ann Surg. 1957; 145:471-78.
6. Glasgow, RE, Mulvihill, SJ. Postgastrectomy syndromes. Probl General
Surgery. 1997;14:132.
7. Mallory GN, Macgregor AM, Rand CS. The influence of dumping on
weight loss after gastric restrictive surgery for morbid obesity. Obes
Surg. 1996;6:474-78
8. Korner J, et al. Exaggerated glucagon-like peptide-1 and blunted
glucose-dependent insulinotropic peptide secretion are associated with
Roux-en-Y gastric bypass but not adjustable gastric banding. Surg Obes
Relat Dis. 2007 Nov-Dec;3(6):597-601. [Epub 2007 Oct 23rd]
9. Scopinaro N, Gianetta E, et al. Biliopancreatic diversion for obesity at
eighteen years. Surgery. 1996;119:261-68.

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10. Hess DS, Hess DW. Biliopancreatic diversion with a duodenal switch.
Obes Surg. 1998;8:267-82.
11. Marceau P, Hould FS, Simard S, et al. Biliopancreatic diversion with
duodenal switch. World J Surg. 1998;22:947-54.
12. Tzovaras, et al. Symptoms suggestive of dumping syndrome after
provocation in patients after laparoscopic sleeve gastrectomy. Obes
Surg. 2012 Jan;22(1):23-28.
13. Schemann M, Rohn M, Miche K. Motor control of the stomach. European
Review for Medical and Pharmacological Sciences. 2008;12(Suppl 1):41-
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14. Daniel J. Drucker. The role of gut hormones in glucose homeostasis. J
Clin Invest. 2007;117(1):24-32. [doi:10.1172/JCI30076]
15. David E. Cummings, Joost Overduin. Gastrointestinal regulation of food
intake. J Clin Invest. 2007;117(1):13-23. [doi:10.1172/JCI30227]
16. Sigstad H. Post-gastrectomy radiology with a physiologic contrast
medium: comparison between dumpers and non-dumpers. Br J Radiol.
1971;44(517):37-43.
17. Adlersberg D, Hammerschlag E. The postgastrectomy síndrome.
Surgery. 1947;21:720.
18. Tack J, Arts J, Caenepeel P, et al. Pathophysiology, diagnosis and
management of postoperative dumping syndrome. Nat Rev
Gastroenterol Hepatol. 2009;6:583-90.
19. Ukleja A. Dumping syndrome: pathophysiology and treatment. Nutr Clin
Pract. 2005;20:517-25.
20. Hinshaw DB, Joergerson EJ, Davis HA. Peripheral blood flow and blood
volume studies in the dumping syndrome. Arch Surg. 1957;74:686-93.
21. Vecht J, Winter M, Chang PC, et al. Acute vasodilatation in early
dumping syndrome. Gastroenterol. 1996;110:A329.
22. Holst JJ. Glucagon-like peptide 1: A newly discovered gastrointestinal
hormone. Gastroenterology. 1994;107:1848-55.
23. George C, Morris Jr, Lazar J. et al. Physiologic considerations in the
dumping syndrome. Ann Surg. 1958:01304-92.
24. Lawaetz O, Blackburn AM, Bloom SR, et al. Gut hormone profile and
gastric emptying in the dumping syndrome. A hypothesis concerning the
pathogenesis. Scand J Gastroenterol. 1983;18:73-80.
25. Johnson LP, Jesseph JE. Evidence of a humoral etiology of the dumping
syndrome. Surg Forum. 1961;12:316-17.
26. Bloom SR, Royston CM, Thomson JP. Enteroglucagon release in the
dumping syndrome. Lancet. 1972;2:789-91.
27. Naslund E, Bogefors J, Skogar S, et al. GLP-1 slows solid gastric
emptying and inhibits insulin, glucagon, and PYY release in humans. Am
J Physiol. 1999;277:R910-R916.
28. Hedberg J, Hedenström H, Karlsson FA, et al. Gastric emptying and
postprandial PYY response after biliopancreatic diversion with duodenal
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switch. Obes Surg. 2011 May;21(5):609-15. [doi: 10.1007/s11695-010-

0288-7]
29. Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypass for
obesity: mechanisms of weight loss and diabetes resolution. J Clin
Endocrinol Metab. 2004;89:2608-15.
30. Sigstad H. A clinical diagnostic index in the diagnosis of the dumping
syndrome. Changes in plasma volume and blood sugar after a test meal.
Acta Med Scand. 1970;188:479-86.
31. Van der Kleij FG, Vecht J, Lamers CB, et al. Diagnostic value of dumping
provocation in patients after gastric surgery. Scand J Gastroenterol.
1996;31:1162-66.
32. Halperin F, Patti ME, Skow M, et al. Continuous glucose monitoring for
evaluation of glycemic excursions after gastric bypass. J Obes.
2011:869536. [article online]
33. Zagury L, Moreira RO, Guedes EP, et al. Insulinoma misdiagnosed as
dumping syndrome after bariatric surgery. Obes Surg. 2004;14:120-23.
34. S. Shah, et al. Prospective controlled study of effect of laparoscopic
sleeve gastrectomy on small bowel transit time and gastric emptying half-
time in morbidly obese patients with type 2 diabetes mellitus. SOARD.
2010 Mar:138-41.
35. Service GJ, Thompson GB, Service FJ, Andrews JC, Collazo-Clavell ML,
Lloyd RV: Hyperinsulinemic hypoglycemia with nesidioblastosis after
gastric-bypass surgery. N Engl J Med. 2005;353:249-54.
36. Alvarez GC, Faria EN, Beck M, et al. Laparoscopic spleen-preserving
distal pancreatectomy as treatment for nesidioblastosis after gastric
bypass surgery. Obes Surg. 2007;17:550-52.
37. Bantle JP, Ikramuddin S, Kellogg TA, et al. Hyperinsulinemic
hypoglycemia developing late after gastric bypass. Obesity Surg.
2007;17:592-94.
38. Clancy TE, Moore FD Jr, Zinner MJ. Post-gastric bypass hyperinsulinism
with nesidioblastosis: subtotal or total pancreatectomy may be needed to
prevent recurrent hypoglycemia. J Gastroenterol Surg. 2006;10:1116-19.
39. Carpenter T, Trautmann ME, Baron AD. Hyperinsulinemic hypoglycemia
with nesidioblastosis after gastric-bypass surgery. N Engl J Med.
2005;353:2192-94.
40. Patti ME, McMahon G, Mun EC, et al. Severe hypoglycaemia post-
gastric bypass requiring partial pancreatectomy: evidence for
inappropriate insulin secretion and pancreatic islet hyperplasia.
Diabetologia. 2005;48:2236-40.
41. Vella A, Service FJ. Incretin hypersecretion in post-gastric bypass
hypoglycemia: primary problem or red herring? J Clin Endocrinol Metab.
2007;92:4563-65.

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42. Marsk R, Jonas E, Rasmussen F, et al. Nationwide cohort study of post-

gastric bypass hypoglycaemia including 5,040 patients undergoing
surgery for obesity in 1986-2006 in Sweden. Diabetologia. 2010;53:2307-
11.
43. Cummings DE: Gastric bypass and nesidioblastosis: Too much of a good
thing for islets? N Engl J Med. 2005;353:300-02.
44. Cummings DE, Weigle DS, Frayo RS, et al. Plasma ghrelin levels after
diet-induced weight loss or gastric bypass surgery. N Engl J Med.
2002;346:1623-30.
45. Tzovaras, et al. Dumping symptoms and incidence of hypoglycaemia
after provocation test at 6 and 12 months after laparoscopic sleeve
gastrectomy. Obes Surg. 2012 Oct;22(10):1600-06.
46. Kellogg TA, Bantle JP, Leslie DB, et al. Postgastric bypass hyper-
insulinemic hypoglycemia syndrome: characterization and response to a
modified diet. Surg Obes Relat Dis. 2008;4:492-99.
47. Jenkins DJ, Gassull MA, Leeds AR, et al. Effect of dietary fiber on
complications of gastric surgery: prevention of postprandial
hypoglycemia by pectin. Gastroenterology. 1977;73:215-17.
48. Butler TJ, Capper WM. A clinical study of the early post-gastrectomy
syndrome, Br Med J. 1951:265
49. Sullivan MB Jr, Thomas B. Patton insulin, tolbutamide, terotonin and the
dumping reaction. Ann Surg. 1964 May;159(5):742-46.
50. González-González A, Delgado M, Fraga-Fuentes MD. Use of diazoxide
in management of severe postprandial hypoglycemia in patient after
Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2011.
51. Moreira RO, Moreira RB, Machado NA, et al. Post-prandial hypoglycemia
after bariatric surgery: pharmacological treatment with verapamil and
acarbose. Obes Surg. 2008;18:1618-21.
52. Vezzosi D, Bennet A, Courbon F, et al. Short and long-term somatostatin
analogue treatment in patients with hypoglycaemia related to
endogenous hyperinsulinism. Clin Endocrinol. 2008;68:904-11.
53. Gray JL, Debas HT, Mulvihill SJ. Control of dumping symptoms by
somatostatin analogue in patients after gastric surgery. Arch Surg.
1991;126:1231-35.
54. Hasler WL, Soudah HC, Owyang C. Mechanisms by which octreotide
ameliorates symptoms in the dumping syndrome. J Pharmacol Exp Ther.
1996;277:1359-65.
55. Valderas JP, Ahuad J, Rubio L, et al. Acarbose improves hypoglycaemia
following gastric bypass surgery without increasing glucagon-like peptide
1 levels. Obes Surg 22:582–586, 2012
56. Speth PA, Jansen JB, Lamers CB. Effect of acarbose, pectin, a
combination of acarbose with pectin, and placebo on postprandial
reactive hypoglycaemia after gastric surgery. Gut. 1983;24:798-802.

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57. Hasegawa T, Yoneda M, Nakamura K, et al. Long-term effect of alpha-

glucosidase inhibitor on late dumping syndrome. J Gastroenterol
Hepatol. 1998;13:1201-06.
58. Lyons TJ, McLoughlin JC, Shaw C, et al. Effect of acarbose on
biochemical responses and clinical symptoms in dumping syndrome.
Digestion. 1985;31:89-96.
59. Porter HW, Claman ZB. A preliminary report on the advantages of a
small stoma in partial gastrectomy for ulcer. Annals of Surg.
1949;129:417.
60. Horber, et al. Severe recurrent hypoglycemia after gastric bypass
surgery. Epub. 2008 Aug;18(8):981-88.
61. Hammer HF. Medical complications of bariatric surgery: Focus on
malabsorption and dumping syndrome. Dig Dis. 2012;30(2):182-6. [doi:
10.1159/000336681. Epub 2012 Jun 20th]
62. Lin HC, Hasler WL. Disorders of gastric emptying. In:Yamada T, ed.
Textbook of gastroenterology, 2nd ed. Philadelphia: JB Lippincott,
1995:1318–46.
63. Zurita Mv LC, Tabari M, Hong D. Laparoscopic conversion of
laparoscopic Roux-en-Y gastric bypass to laparoscopic sleeve
gastrectomy for intractable dumping syndrome and excessive weight
loss. Surg Obes Relat Dis. 2012 Nov 30th.
64. Dapri G, Cadière GB, Himpens J. Laparoscopic reconversion of Roux-
en-Y gastric bypass to original anatomy: Technique and preliminary
outcomes. Obes Surg. 2011 Aug;21(8):1289-95.

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Chapter X
Physical activity in bariatric patients
Klga. MSc Johanna Pino Zúñiga*,**

Klga. MSc Mariela Olivares Galvez**
Prof. PhD. Jorge Cáncino López***
*
Center Obesity Treatment, Pontificia Universidad Católica de Chile
**
Physical Therapy , UDA Health Sciences, Pontificia Universidad Católica de Chile
***
Physical Therapy School, Universidad Mayor, Chile
In 1991, the National Institute of Health established guidelines for performing surgeries
currently known as bariatric surgery. The criteria are to be performed BMI > 40 kg/m 2
or> 35 kg/m 2 in the presence of comorbidities such as diabetes, hiprelipidemia,
hypertension and obstructive sleep apnea. Often diet, exercise, behavior modification
and drugs are not sufficient to achieve the desired weight loss and it is necessary to
perform surgery, which, as any surgery, entails risks. Despite this, the mortality rate for
bariatric surgery is low and the risks depend on variables that may not be modified.
The variables that can be modified are pre-surgical: obesity level, the patient's general
condition, and smoking; exercise can act beneficially in the first two cases. 1-3
Physical activity acts beneficially both in reducing body weight and abdominal fat, as
well as in the improvement of the general condition of the patient through reduction of
comorbidities commonly associated with obesity, such as hypertension, diabetes,
resistance insulin, dyslipidemia. On the other hand, physical activity also increases the
cardiovascular and respiratory capacities, which generally are low in these patients. It
has been shown that patients who take an exercise program at the preoperative stage
have a better surgical outcome, including weight loss, body composition, and fitness,
as well as less surgical complications. Exercise is also the most important predictor of
the maintenance of long-term weight.4,5
Exercise produces multisystem benefits, resulting in an improvement of the general

condition of the patient and reducing the risk of being subjected to a complicated
surgery. It is also essential in the postoperative stage to achieve a weight reduction
with minimal muscle loss. Weight loss produced by bariatric surgery is associated with
both loss of fat mass (FM), as fat-free mass (FFM), independent of the surgery type,
initial BMI and the magnitude of weight loss, which may be observed by different
techniques to measure body composition. This weight loss (FFM) is determined by the
mechanisms of surgery (surgery type, hormonal changes, etc.), and post-caloric

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restriction. The importance of FFM is crucial to the aspect of energy metabolism, and
for the proper functioning of the musculoskeletal system. 6-9
This chapter will describe the mechanisms by which exercise acts systemically, making
it indispensable in the comprehensive treatment of obesity and the long-term
management of this condition.
Effects of exercise on cardiovascular system

Obese people are at greater risk of developing vascular disease, sleep apnea,
pulmonary hypertension, strokes, coronary artery disease, congestive heart failure,
venous insufficiency, deep vein thrombosis, pulmonary embolism, arrhythmias, and
sudden death.10,11 Obese patients have an increased sympathetic activity, resulting in
elevated basal heart rate and, therefore, lower heart rate reserve. That is, the ability to
respond to a stressful event, such as surgery, is reduced. Numerous studies show that
the deterioration of functional capacity in these patients can be compared with people
who suffer heart failure.6
There are numerous studies that show the effects of exercise on the cardiovascular
system, especially with regard to the effects of endurance exercise (such as walking,
biking, swimming, etc). The American College of Sports Medicine recommends at least
30 minutes of moderate exercise a day to reduce the risk of cardiovascular events.
Moderate exercises correspond to those working at 64-75% of the theoretical
maximum heart rate; 46-63% of VO2 max; or whose Borg is 12-13 (i.e., a subjective
feeling of fatigue which goes from quite low to slightly difficult). 12,13
While performing aerobic endurance exercise, the cardiovascular system is constantly

pumping blood into large muscle groups on account of the effort required by the
muscle, which causes an increase in cardiac output and a function of oxygen uptake.
An elevation in heart rate and blood volume occurs. This generates a slight rise in
blood pressure and peripheral vasodilation, as well as a reduction in peripheral
vascular resistance; thus, the amount of blood and oxygen that goes to the muscles
increases in order to meet the demands of physical activity. 14,15
On the other hand, an increase occurs in the size of muscle fibers of the heart walls
causing the heart to pump blood more effectively (improved cardiac inotropy). This
allows a reduction of the resting heart rate without affecting cardiac output minute. The
metabolic stress of the heart can be quantified through the double product (DP). This

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indicator is obtained by multiplying heart rate by stroke volume and is indicative of

myocardial oxygen consumption. Thus, training in obese patients produces reduced
heart working frequencies, and therefore a reduction in myocardial work. 14
A level of cardiac circulation, an increased number and size of the coronary artery
occurs, so cardiac perfusion also becomes more efficient. 14
At peripheral level, aerobic training produces greater muscle capillarization so it

becomes more effective in transporting oxygen to the tissue. This also tends to slow
the heart rate, decreasing peripheral resistance and making the heart work more
efficiently. It is important to consider that the cardiovascular system aims to provide the
necessary blood flow to skeletal muscle, in order to perform the mechanical work
required by exercise. In that sense, the relation between the cardiovascular system and
the muscular system can be quantified by a parameter such as oxygen pulse, which
considers the amount of oxygen consumed by the body in each heartbeat. Thus, the
amount of oxygen consumed with each pulse increases as a result of organic training
adaptation, which means a reduction of cardiovascular stress for the same workload. 14
According to the American College of Sports Medicine, the benefits of aerobic exercise
regarding cardiovascular level, are:12
1. Increased peak oxygen consumption through central and Peripherals

adaptations.
2. Reduction in myocardial oxygen consumption.
3. Increased capillary density musculoskeletal level.
4. Heightening in the threshold of symptoms in patients with angina pectoris.
5. Pressure reduction of both systolic and diastolic rest.
6. Rise in HDL cholesterol and triglyceride lowering.
7. Reduction of total fat and abdominal fat, which manifests in a decrease of waist
circumference (an important indicator of cardiovascular risk).
8. Reduced platelet aggregation by an increase in the release of nitric oxide (a
strong vasodilator).
Effects of exercise on the respiratory system

Obesity causes alterations in mechanical ventilation due to a couple of factors: excess
fat, which produces a lower compliance of the chest wall; and a prominent abdomen,
which causes an elevation of the diaphragm (the main muscle of breathing). This leads

Blanca Ríos, MD
to a decrease in lung volume in relation to a person with normal weight (Figure 1). The
above mentioned conditions make the use of general anesthesia dangerous; intubation
and mechanical ventilation are more complex, and involve more adverse events and
procedures in comparison with normal-weight people.5
Figure 1: Comparison of patients’ volume and lung capacity with VS normal

weight obesity.
Extracted from Electronic Journal of intensive Medicine 2006; Article A 38, 6(2). (CPT: Total
lung capacity, CRF: Residual functional capacity; VR: Residual volume, VC: Tidal volume, CC:
Closing capacity).
The figure shows how the respiratory physiology is altered in patients with obesity. It
shows a decrease in total lung capacity, tidal volume and functional residual capacity.
All these changes mean that obese patients are more likely to have an altered gas
exchange with increased CO2 retention, risk of desaturation, and areas of atelectasis
and lung collapse. On the other hand, an obese patient candidate for bariatric surgery
will be under general anesthesia, which involves the introduction of a foreign element in
the airway (endotracheal tube); this increases the production of secretions, hence it is
essential to have a good handle on them to prevent infections in the airway. 5
Several authors have shown that aerobic training improves the strength of respiratory
muscles, allowing greater tidal reach. Training enhances respiratory muscles,
increases lung volume and capacity, and reduces respiratory rate. This makes gas
exchange more efficient, produces more homogeneous ventilation and increases the
activity of the cilia, thus facilitating the handling of secretions. Pulmonary ventilation
provides the body with oxygen to cover its needs; in addition, it plays an important role
in the acid-base balance. When doing low-intensity aerobic exercise in phase I, VO2
increases linearly to VCO2 for ventilation. There is a deviation of the saturation curve of
hemoglobin to the right, that is, the hemoglobin oxygen affinity is lost for it to be used.

Blanca Ríos, MD
However, in phase II, the increase in the production of hydrogen ions heightens
ventilatory demands which are higher than the metabolic requirement, consequently
the patient will begin to hyperventilate and experience a greater exertion. Muscle
oxidative capacity will increase as a result of systematic training, resulting in lower
production of hydrogen ions with similar aerobic workloads. This will allow the exercise
to be completed without the development of hyperventilation, even with higher
intensity. This is an important element in reducing the perception of effort that patients
experience as part of the adaptation to exercise.5,16,17
Effects of exercise on glycemic control

Obesity is strongly associated with diseases in which impaired glucose metabolism,
starting from insulin resistance, and impaired glucose tolerance to type 2 diabetes
mellitus occurs.
This disease has its genesis in the interference that produces intracellular excess fatty
acids which are esterified, interrupting the signal cascade of insulin in their primary
targets: liver and muscle. The insulin resistance is a major problem, since increases
the risk of type 2 diabetes and hypertension. Numerous studies discuss the benefits of
exercise at increasing insulin sensitivity in healthy subjects and in diabetics: this
increase is produced by both aerobic and resistance exercises. 18
With exercise we can improve the activity of the GLUT4 glucose transporter found
primarily in skeletal muscle. The low muscle activity in these patients has led to a
reduction in muscle oxidative capacity, decreasing the utilization of fatty acids as fuel
for muscular activity. As mentioned above, the intracellular accumulation of fats is one
of the triggering agents of the insulin resistance associated with obesity and physical
inactivity. Exercise causes an increase in muscle energy, which demands a greater
number of intracellular signals designed to mobilize energy resources for the
development of muscle activity. An increment in the levels of calcium, nitric oxide,
AMPK (AMP-activated protein kinase), and others, through different mechanisms,
causes an increase in expression of GLUT-4 transporter in the muscle membrane,
thereby enhancing muscle glucose uptake independently of insulin action.

glucagon
< insulin excess > insulin

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insulin
Figure 2: "Mechanisms of glucose uptake by the muscle associated to the action
glucagon
of insulin and muscle contraction.”19 PI3-Kinase, Phosphatidylinositol 3-kinase;
Fig. 4 Effects of exercise on plasma glucose levels.
GLUT-4 glucose transporter-4.
glucose
insulin
Cell membrane
insulin
receptor
Muscle
PI3-Kinase GLUT-4 AMP Kinase
muscle
contraction
Fig. 5 Mechanism of glucose uptake by muscle. GLUT-4, glucose transporter-4; PI3-kinase, phosphatidylinositol 3-kinase.
Effects of exercise on the musculoskeletal system

Obesity is a disease characterized by an excess of body fat, which proportionally
essary to exercise every other day. A simultaneous benefit classified as type I (slow twitch) and type II (fast twitch);
reduces
is the increase in muscle muscle
caused mass and
by resistance efficiency
training, andof
typephysical work.
II fibers are In classified
further addition,into
excess
type IIA,weight
type
whereby the capacity of glucose uptake is increased and IIB and type IIC fibers. Oxidative enzyme activity is
causes more wear of the bearing joints (hips, knees and ankles). Although it is
glucose metabolism improves4). higher in type I, IIA, and IIC fibers, whereas glycolytic
associated with a lesser degree ofenzyme osteoporosis, obese
activity is higher in people
type IIA, have
IIB, anda IIC
higher
fibers.risk of
Skeletal muscles are classified into two types: slow
Diabetes, exercisefalling,
and muscle
andfibers
therefore, of experiencing fractures.
muscle and fast muscle (Table 1). Slow muscles, e.g. the
Muscle fibers. Skeletal muscle comprises heterogeneous adductor longus and soleus muscles, exhibit activity of
types of fibers with different morphological, functional,
Exercise helps to improve muscle relatively mass and low intensity and long duration, which is re-
reduce articular overload; produces better
and metabolic properties5). Muscle fibers are generally quired for performing functions against gravity, such as
fixing of calcium in bones, through the axial load and traction generated by the insertion
of the muscle in the bone (situation that is very important in patients undergoing gastric
bypass);20 improves joint lubrication, which enhances physical abilities such as
balance, coordination, agility, etc.
Sudden weight loss necessarily leads to loss of muscle mass, as in the case of patients
undergoing bariatric surgery.8 Resistance exercise with large muscle groups attenuates
this loss, and therefore weight reduction is mainly achieved at the expense of excess
fat. In practice, an increase in protein synthesis, which aids in the retention of muscle
mass during weight loss, occurs. Muscle tension, especially in strength training
(overload) induces the increase of intracellular signals, which are mediated by
increased levels of mammalian target of rapamycin (mTOR), resulting in higher protein
synthesis and the expression of a new muscle phenotype. 21 Although exercise causes
a systemic effect, strength training is recognized to have a high component of autocrine

Blanca Ríos, MD
response, which is responsible for the specific adaptation of the muscle that is being
exercised. In the case of postoperative patients, a marked decrease in the dorsal
musculature, which has been associated with increased discomfort in the back area, is
observed.
Pre-participation testing for exercise prescription

The obese person has a number of comorbidities, upon which exercise has been
shown to exert a beneficial effect. However, exercise training is not without risks. This
is why it is necessary for the obese patient to take a preliminary assessment prior to
the incorporation of an exercise program.
The assessment includes: anamnesis, previous medical history, medication use,

previous attempts at exercise programs and causes of abandonment. Postural
evaluation, aerobic endurance and muscular strength should be included in the
evaluation. The purpose of the evaluation is to determine the most suitable exercise
program for the obese patient.
 Anamnesis
Before starting the implementation of physical activity, the obese patient should
undergo screening for different diseases which must be stabilized before starting the
exercise, including: blood count, lipid profile, HOMA (Homeostasis Model Assessment),
and liver function tests. For diabetics, HbA1c and microalbuminuria is also needed.
It is important to know which medication the patient is using and how this interacts with
exercise, beta blockers, insulin, etc.
A stress test should be recommended for patients with the following characteristics:
- Over 40 years old.
- With cardiovascular disease history
- Diabetics.
 Postural and musculoskeletal testing
Obesity causes multiple alterations in different systems (e.g., cardiovascular,

respiratory, digestive). The musculoskeletal is one of the affected by this disease with
alterations to body geometry. There is an increase in the mass and inertia of different
segments, and the functional limitations in daily activities may predispose to injuries.
Obesity causes a rise of the axial load of the skeleton, resulting in excessive bone

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wear. This causes an increase in joint damage, especially in the spine, hips, knees and
ankles.5,6
Obese individuals generally have swollen abdomen, resulting in anterior displacement

of the center of gravity due to increased lordosis lumbar and pelvic anteversion. The
increased thoracic kyphosis causes cervical lordosis with anterior projection of the
head. There is a medial rotation of the hip with genu valgus. In the foot, overweight
causes the lowering of the plantar arch.5
Obese patients heighten energy expenditure when performing biomechanical
adjustments necessary to maintain postural balance. Being overweight, in addition to
causing joint discomfort, increases the risk of falls. 5
People with obesity experience frequent postural changes; the greater the degree of
obesity, the more postural changes will occur. These alterations predispose obese
people to have multiple musculoskeletal pathologies, such as: backache, herniated
nucleus pulposus (both cervical and lumbar), and patellofemoral dysfunction.
Exercise should be adapted to each patient, avoiding high impact training, and should
help the obese patient to correct his or her posture. The bariatric patient, due to the
abrupt loss of body weight, must practice muscular strengthening exercises in order to
reduce musculoskeletal discomfort. Therefore, it is necessary to begin with early
muscle strengthening, so weight loss goes along with an adequate posture and less
aching.
Figure 3, extracted from Kinefilaxia and Health.

Author: Nicolas Robertone.
Figure 3 shows postural changes with increasing degrees of obesity.
1. Increasing of dorsal curvature level.

2. Head: anterior projection, hyperextension of the cervical area.

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3. Shoulders: anterior projection, decreased chest expansion.

4. Intensification of the lumbar curvature.
5. Hyperextension of the knees.
6. Reduction of the plantar arch.
All these alterations predispose obese people to be more easily injured during physical
activity. Hence, proper evaluation is essential before performing an exercise program.
 Evaluation of physical fitness in the obese patient.

o Evaluation of aerobic endurance
The evaluation component of aerobic fitness can be performed through the

assessment of aerobic capacity, which involves quantifying physiological or
performance indicators for the development of prolonged submaximal exercise
intensity. The assessment of lactate threshold, anaerobic threshold, and ventilatory
thresholds are used for such purposes.
Moreover, the assessment of maximal aerobic power or maximal oxygen consumption

is used as an indicator of the maximum functional capacity of a person. This parameter
is indicative of life expectancy in multiple chronic diseases. 22 Then, it is essential to
evaluate exercise prescription and compare the effectiveness of training.
The assessment of maximal oxygen uptake can be made directly through the analysis
of respiratory gases or indirectly through submaximal tests. In the latter, the maximum
oxygen consumption is extrapolated.
One should not forget that tests in which the patient must carry their body weight might
have worse outcomes compared to those performed on a cycle ergometer (no weight
bearing). That is why one should be aware that in the walk test a biomechanic
limitation, and not necessarily a cardiorespiratory limitation, could appear. From the
motivational point of view, the perception of better physical condition could be an
inspiration to practice exercise. The test in cycle ergometer is performed with a
progressive resistance, and the heart rate is evaluated with different loads.
The Physical work Capacity Maximum (Max PWC) is a test on a cycle ergometer which
can be used in obese patients. In this test the initial burden for women is 50 Watts, and
75 Watts for men. The charge increases by 25 Watts every two minutes. The test stops
when the patient reaches a heart rate higher than 85% of the theoretical maximum

Blanca Ríos, MD
heart rate (220-age), or when the patient stops being able to maintain the cadence
because of fatigue. With these data, it is possible to find the maximal aerobic power,
which can be extrapolated to maximal oxygen uptake (VO2 max). 14
o Evaluation of muscle strength
The indirect assessment 1 maximum strength (1RM) can be used to evaluate the
maximum dynamic force. The test is performed until reaching muscle fatigue (RFM)
and then, based on the linear equation of the relationship between RFM and the
percentage of 1RM (% RM), the value of 1 RM is obtained. 23
Base equation on linear relationship for 1RM:

%1RM= (100-n°RFM *2,5)
1RM= load lifted/(%1RM/100)
This evaluation can be performed on exercise machines or free weights. Exercises

commonly used for this evaluation, which are designed for upper extremities, lower
extremities, and trunk, are: biceps curl, pull pulley, chest press, leg press, hamstring,
legs extension. It is necessary to evaluate the work load of each exercise. Thus, the
patient must lift the load as many times as possible; the number of repetitions should
not be less than 10 or higher than 15, in order for the equation to be valid.
Physical exercise produces changes in the body, therefore it is useful to perform the
following measurements before starting a workout plan: 7
• Anthropometric measurements: mainly the circumference of the neck, waist,
and hip; as well as the waist-hip ratio.
• Body composition: mainly bioelectrical impedance and body folds nowadays.
Phase training by surgery

Pre-operative phase
All the procedures performed in this stage aim at reducing the risk of surgery and early
eating habit changes; this guarantees a more successful long-term surgery.
For these purposes, exercise has the following effects:
 Contributes to weight loss.

 Contributes to reduction of abdominal fat.
 Improves cardiorespiratory fitness.
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 Improves glycemic levels through increased insulin sensitivity.

 Lowers blood pressure levels.
 Decreases cholesterol levels.
The above mentioned effects contribute to improve the overall condition of the
patient, reducing thus the risk of surgery.
Changes should be expected after 1-2 months. The minimum frequency of physical
activity is 3 times a week, although we know some effects such as weight loss and fat
burning will increase with the repetition of physical activity. Aerobic exercise is the type
of training that should be practiced at this stage.
The intensity of an exercise is expressed as a percentage of maximum oxygen

consumption (VO2 max), which is the most accurate variable to know which substrate
is used. It has been proved that the optimal fat utilization is between 60-70% VO2
max;24 this percentage varies from individual to individual, and has shown to be lower in
obese and diabetic subjects.25 Therefore, the patient should be evaluated individually
to establish ranges and correlation with heart rate, which is the parameter to be
monitored during training sessions. The intensity of continuous aerobic exercise varies
between 50-70% VO2 max among these patients, which is equivalent to 60-80% of the
theoretical maximum heart rate (220-age), depending on their initial assessment. The
goal is to keep this type of exercise for at least 20 consecutive minutes in order to
optimize the utilization of fatty acids as energy substrate; it should be done at least 3
times a week. The World Health Organization recommends between 150 and 300
minutes per week of aerobic physical activity in subjects aged between 18 and 64
years.
Aerobic training conducted in high intensity intervals (HIIT) has shown to be beneficial
to improve physical fitness, use of post-exercise fat, and glycemic control.13 This type
of training is done in intervals (from 30 seconds to several minutes) of high intensity
(close to 90% VO2 max), followed by periods (1-5 minutes) of low intensity (50-60%
VO2 max ) or recovery. To achieve the benefits of exercise, the patient must complete
a total of 10 minutes/session of high intensity workout at least 3 times a week. This
option is attractive for the cost-effectiveness that represents, but is suggested for
sedentary individuals after 1 month of continuous aerobic exercise.26

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At this phase, it is also important to work postural control (lumbar and abdominal
muscles), for there are significant changes in posture associated with weight reduction
produced by bariatric surgery.
Post-operatory hospital phase

The length of this stage and the patient’s outcome depends on whether the procedure
was performed laparoscopically or openly (from the physical point of view, the recovery
is longer and slower in the latter case).
Respiratory mechanics suffer alterations on account of various reasons: respiratory

depression caused by anesthesia, pain or fear; increased respiratory secretions by
intubation, supine position, etc. For these reasons, respiratory complications may be
frequent.
Respiratory therapy is indispensable particularly in patients who had a laparotomy. The

purposes are to prevent respiratory and thromboembolic complications, as well as to
reintegrate patients back to their daily activities as soon as possible.
At this stage, breathing exercises are performed in different positions, with the following
objectives: to optimize lung volumes with emphasis on bases (atelectasis are frequent),
use of respiratory stimulants (Inspirex), permeabilization of the airway and assisted
cough; in addition, the patient should walk with assistance. A patient undergoing
bariatric surgery should be walking within a maximum of 24 hours and then have a
relative rest, with daily marches scheduled as tolerated. Bed rest should be in semi-
sitting position to decrease the risk of aspiration of gastric contents (vomiting or reflux).
During the post-operative phase, patients should perform daily activities more slowly
and adapt themselves to the new dietary intake, walk daily as tolerated and return to
their regular work.
Patients may perform physical activity about the second and fourth week after the
procedure; before that, caloric intake, tolerance to food, and hydration of the patient
must be evaluated. The patient, despite not being hungry, should eat in agreement with
the nutritionist indications, with emphasis on the consumption of dairy and protein.
Late post-operative phase

The objectives at this stage are to contribute to weight loss with minimal muscle loss.
Exercise contributes to weight loss through excessive fat maintaining lean mass. We
know it is very important to maintain muscle mass during weight loss. Musculature

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moves the body, stabilizes joints, maintains a higher basal metabolism, helps maintain
a better proportionality of the different body segments, etc.
Aerobic exercise must continue during the post-operative phase in proper conditions to
optimize the consumption of fats and incorporate strength workout with emphasis on
the large muscle groups of upper extremities, lower extremities, and trunk.
Muscle strength exercise aims to improve strength and hypertrophy, and ultimately to
produce changes in muscle metabolism in order to optimize the oxidative process that
occur at this level. To work the above mentioned variables, the patient must do sets of
12 to 15 repetitions with moderate loads (60-70% 1RM), as previously assessed.
Weight maintenance
A high level of physical activity is a good predictor for long-term weight maintenance
among patients undergoing bariatric surgery. When talking about a high level of
physical activity, we do not necessarily refer to sports or workout, but to changes in
daily life that lead to a greater demand of energy. 100000 steps a week represents an
adequate level of physical activity for weight maintenance in previously obese
individuals.27,28
Below, we present some examples of daily activities and the way to determine the
corresponding energy expenditure.
MET energy cost of daily activities:
Watch TV: 0.9 Basketball: 6.0
Slow walk: 2.2 Remove dust: 2.7
Fast walk: 5.5 Sweep: 3.0
Slow trot: 8.0 Bicycle: 5.0
Brisk walking: 5.5 Standing: 4.0
Activity Duration (min.) _____ * MET___/60 = X (increased caloric intake).
X MET hour * kg body weight = ______ Kcal (increased daily consumption).
By knowing the energy cost of activities we are able to calculate how many calories a
person expends in a day.
For instance, an individual who weights 90 Kg and runs slowly for 20 minutes should
increase his or her consumption of calories by 240 Kcal a day.
20 (min) * 8 (METS) / 60 = 2.66 * 90 (kg) = 240

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Convincing an obese patient to perform regular physical activity is not an easy task. It
is important to make progressions and targets individually, in order to avoid injury and
frustration, and therefore desertion on part of the patient. It is essential to always have
the support of a multidisciplinary team and constant communication with it, so as to
approach the patient in the most appropriate manner.
Preparing for change of habits

Even when obesity is a chronic disease, the patient learns how to manage their daily
behaviors regarding food and physical activity.
An individual who undergoes surgery without changing his or her eating habits has a
high risk of failure. In fact, studies show that one of the best predictors in long-term
weight maintenance is physical activity.27,28
Therefore, it is extremely important to change the attitude towards exercise before

surgery, since at that time the patient feels a great motivation for making changes.
The preparation of the patient of bariatric surgery concerning food, physical activity,
and change of habits, improves the patient's general condition (with respect to disease
control, improved cardiovascular and respiratory capacity, and weight loss), as the
process of change develops. This leads to a reduction of the risks of surgery, and also
of the risk of the long-term failure.
From the point of view of acquiring habits, obese patients are difficult to manage since
they have low adherence to exercise. Nevertheless, an approach centered on the
individual, setting goals, enjoying physical activity, and helping the patient to achieve
an everyday strategy, are predictors of success at maintaining good habits. 28
Bibliographic references
1. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery a systematic review

and meta-analysis. JAMA. 2004;292(14):1724-37.
2. Walter J, Pories W. Bariatric surgery: Risks and rewards. J Clin Endocrinol
Metab. 2008;93 (11 Suppl 1):S89–S96.
3. Keats AS. The ASA (American Society of Anesthesiologits) classification of
phisicaal status. A recapitulation. Anesthesiology. 1978;49:233-36.
4. King W, Bond D. The importance of pre and postoperative physical activity
counseling in bariatric surgery. Exerc Sport Sci Rev. 2013;41(1): 26-35.
5. Pino, J. Actividad física y kinesiología en el paciente sometido a cirugía
bariátrica. In: Burdiles P, Csendes A, Guzmán S, et al. editors. Obesidad y
cirugía bariátrica. V 1. Santiago de Chile: Mediterránea; 2012:138-48.

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6. Gallagher MJ, Franklin BA, Ehrman JK, et al. Comparative impact of morbid
obesity vs heart failure on cardiorespiratory fitness. Chest. 2005;127(6):2197-
203.
7. Chaston T, Dixon J, O’Brien P. Changes in fat-free mass during significant
weight loss: a systematic review. International Journal of Obesity.
2007;31(5):743-50.
8. Ciangura C, Bouillot JL, Lloret-Linares C, et al. Dynamics of change in total and
regional body composition after gastric bypass in obese patients. Obesity.
2010;18:760–65.
9. Levitt D, Beckman L, Mager J, et al. Comparison of DXA and water
measurements of body fat following gastric bypass surgery and a physiological
model of body water, fat, and muscle composition. J Appl Physiol.
2010;109(3):786-95.
10. Poirier P, Giles TD, Bray GA, et al. Obesity and cardiovascular disease. Current
Literature and Information for Pharmacists. 2006;10 (31):1-2.
11. Klein S, Burke LE, Bray GA, et al. Clinical implications of obesity with specific
focus on cardiovascular disease: A statement for professionals from the
American Heart Association Council on Nutrition, Physical Activity, and
Metabolism. Circulation. 2004;110 (18):2952-67.
12. Exercise rescription for patients with cardiovascular and cerebrovascular
disease. In: Guidelines for exercise testing and prescription. 9th ed.
Philadelphia: ACSM´s; 2014:236-56.
13. Golbidi S, Laher I. Exercise and the cardiovascular system. Cardiology
Research and Practice vol. 2012. Article ID 210852, 15 pages, 2012.
14. López Chicharro J, Rabadán Ruiz M, Serratosa L. Respuestas y adaptaciones
cardiovasculares al ejercicio. In: López Chicharro J, Fernández A. Fisiología del
ejercicio. Buenos Aires and Madrid: Editorial Médica Panamericana; 2006:321-
40.
15. Nobrega A, O´Leary D, Moreira B, et al. Neural regulation of cardiovascular
response to exercise: Role of central command and peripheral afferents.
Biomed Res Int. 2014. Article ID 478965, 20 pages, 2014.
16. López Chicharro J. Fundamentos de fisiología del ejercicio. In: Fisiología
clínica del ejercicio. Available from: http://media.axon.es/pdf/59703.pdf
17. López Chicharro J, Vicente Campos D, Cáncino López J. Fisiología del
entrenamiento aeróbico, una visión integrada. 1st ed. Editorial Médica
Panamericana. Madrid, 2013.
18. Ronald J, Glen P, David H, et al. Physical activity/ exercise and type 2 diabetes,
Diabetes Care. 2004 Oct (27);10:2518-39.
19. Qiu J, Maekawa K, Kitamura Y, et al. Stimulation of glucose uptake by
theasinensins through the AMP-activated protein kinase pathway in rat skeletal
muscle cells. Biochem Pharmacol. 2014 Jan 15;87(2):344-51.
20. Goode LR, Brolin RE, Chowdhury HA et al. Bone and gastric bypass surgery:
effects of dietary calcium and vitamin D. Obesity Research. 2004 Jan;12(1):40-
47.
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21. Goodman CA, Frey JW, Mabrey DM, et al. The role of skeletal muscle mTOR in
the regulation of mechanical load-induced growth. J Physiol. 2011 Nov
15;589(Pt 22):5485-501.
22. Erikssen G. Physical fitness and changes in mortality: The survival of the fittest. Sports
Med. 2001;31:571-76.
23. Beam, W, Adams, G. Exercise Physioloy. Laboratory manual. 6th ed. McGraw-
Hill; New York. 2011.
24. Lanzi S, Codecasa F, Cornacchia M, et al. Fat oxidation, hormonal, and plasma
metabolite kinects during a submaximal incremental test in lean and obese
adults. PLo S ONE. 2014 Feb 11;9(2).
25. Williams CB, Zelt JG, Castellani LN, et al. Changes in mechanisms proposed to
mediate fat loss following an acute bout of high-intensity interval and
endurance exercise. Appl Physiol Nutr Metab. 2013 Dec;38(12):1236-44.
26. Shiraev T, Barclay G. Evidence based exercise – clinical benefits of high intensity interval
training. Aust Fam Physician. 2012 Dec;41(12):960-62.
27. Evans RK, Bond DS, Wolfe LG, et al. Participation in 150 min/wk of moderate or higher
intensity phisical activity yields greater weigth loss alter gastric by pass surgery. Surg
Obes Relat Dis. 2007 Sep-Oct;3(5):526-30.
28. Wetch G, Wesolwski C, Piepul B, et al. Phisical activity predicts weight loss following
gastric bypass surgery: findings from a support group survey. Obes Surg. 2008
May;18(5):517-24.

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Chapter XI
Anesthetic considerations for obese surgical
patients undergoing bariatric surgery
Carron M, MD, PhD

Department of Medicine,
Anesthesiology and Intensive Care
University of Padova, Italy
Obesity is a growing global health problem. Given the increasing incidence of

morbid obesity and the effectiveness of weight loss surgical approaches in
treating this condition, bariatric surgery will likely increase as well. Accordingly,
anesthesiologists will attend an increasing number of obese patients in their
clinical practice. Optimal management of these patients is required to minimize
the risk of perioperative complications that contribute to morbidity and mortality.
A comprehensive preoperative evaluation, knowledge of specific problems
associated with obesity (such as metabolic syndrome, obstructive sleep apnea,
pulmonary disease, and cardiovascular disease), and the use of an appropriate
anesthetic approach are important aspects while attending obese surgical
patients. This review highlights the anesthetic considerations for obese patients
undergoing bariatric surgery, to help clinicians to formulate a perioperative
management plan that optimizes the patient’s outcome.
The incidence and prevalence of obesity continues to increase globally.1

Obesity has received much attention from the medical profession and others
because of its association with an increased risk of morbidity and all-cause
mortality.1,2 Given the increasing incidence of morbid obesity1,2 and the
effectiveness of surgical approaches to reduce weight,2,3 anesthesiologists will
no doubt attend an increasing number of obese patients in the foreseeable
future and should be prepared to provide optimal management.1-3 An adequate
anesthesiological approach to obese patients undergoing bariatric surgery is
discussed on the basis of more recent evidences, highlighting the proper
strategy for a better outcome.

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Preoperative evaluation
Prior to surgery, all obese surgical patients should undergo preoperative
evaluation and pertinent laboratory and diagnostic testing.3,4 Standard minimum
preoperative laboratory testing should include a complete blood count, tests of
the coagulation cascade, and blood glucose levels within 6 months of surgery.3
Extensive preoperative laboratory testing is not indicated for every morbidly
obese patient undergoing surgery.3 Kidney function tests, liver function tests,
and a lipid profile are not cost-effective in asymptomatic obese patients;
however, they should be obtained for obese surgical patients with known or
suspected kidney disease, liver disease, or metabolic syndrome (MS),
respectively.
A preanesthesia evaluation should be performed within 1 month and at least

within 1 day of scheduled surgery.3 The possibility of obstructive sleep apnea
(OSA), pulmonary disease, and cardiovascular disease (CVD) must be carefully
evaluated by history, physical examination, and the appropriate diagnostic tests.
OSA is a syndrome characterized by repetitive episodes of cessation of

breathing or reduced tidal volume respiration (apnea or hypopnea, respectively)
during sleep, which are often associated with a reduction in blood oxygen
saturation.4-6 OSA may complicate anesthetic management.3,4 Patients with
OSA have a high risk of postoperative upper airway obstruction, which may lead
to severe cardiorespiratory adverse events, such as respiratory failure, cardiac
ischemia, and arrhythmias.7 OSA has also been associated with a increased
risk of unplanned intensive care unit (ICU) admission and prolonged hospital
stay.7 Overnight polysomnography is the gold standard for diagnosing OSA.3,4,7
However, this test is costly, involves several hours of monitoring, and is often
difficult to schedule, which may cause the surgery to be delayed.3 Preoperative
screening questionnaires have been used as an alternative to
polysomnography.3,7 The STOP-Bang questionnaire (Snoring, Tiredness,
Observed apneas, elevated blood Pressure, Body mass index >35 kg/m2, age
>50 years, neck circumference >40 cm, and male gender), developed and
validated by Chung et al.,8 is the most widely used tool to predict postoperative

Blanca Ríos, MD
complications, particularly those related to the respiratory system.3,7 Assigning 1

point for the presence of each factor and 0 point for the absence generates a
total core ranging between 0 and 8. A STOP-Bang score of 0-2, 3-4, or 5-8
identifies patients with low risk, intermediate risk (2.5-3 fold increased risk vs. 0-
2 score), or high risk (5-7 fold increased risk vs. 0-2 score) of OSA,
respectively.9 If a preoperative screening questionnaire is not available, pulse
oximetry may be used as a simple screening tool. An oxygen saturation (SpO2)
of 94% on room air in the absence of other causes is indicative of severe, long-
standing OSA.6 OSA is often improved with mask or nasal continuous positive
airway pressure (CPAP), and those receiving home CPAP should bring their
equipment to the hospital for continued use in the perioperative period.3 For
individuals with severe OSA who are not receiving home CPAP treatment,
beginning CPAP therapy may be considered as part of the preoperative
preparation.7
Restrictive lung disease is common in patients with moderate or severe obesity,

especially those with MS or OSA.3,4,10 Pulmonary function tests are useful to
quantify the degree of restriction and may also help detect coexisting chronic
obstructive pulmonary disease.3,4,10 However, pulmonary function tests have a
limited sensitivity for predicting postoperative pulmonary complications in obese
patients.10 Thus, routine preoperative spirometry is not recommended for
asymptomatic obese patients.3 Preoperative evaluation is more appropriately
directed toward diagnosing treatable respiratory conditions that may affect
postoperative recovery, such as pulmonary edema, asthma, bronchitis, or
pneumonia, by obtaining a chest X–ray.3,4 Preoperative arterial blood gas
analysis may also be considered for patients with severe cardiopulmonary
dysfunction, primarily to obtain baseline measurements to guide postoperative
care.4
Preoperative identification of potentially serious CVD is also recommended for

obese patients.3,4 Unstable coronary syndrome, a recent myocardial infarction,
decompensated heart failure, significant arrhythmias, and severe valvular heart
disease, are the major clinical predictors of increased perioperative

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cardiovascular risk for patients undergoing noncardiac surgery, regardless of

whether they are obese or not.11 Elective surgery should be delayed later than
4-6 weeks after a recent myocardial infarction and until the other factors have
been optimally treated.11 Patients with abnormalities on their resting
electrocardiogram, such as ST-segment elevation or depression, high-grade
atrioventricular conduction abnormalities, left or right bundle-branch block, and
supraventricular or ventricular arrhythmias, should be adequately investigated
under the direction of an internist or cardiologist.11 Other techniques, such as
resting and exercise echocardiography or exercise myocardial perfusion
imaging should be considered, particularly if the results of the tests may change
the anesthetic management.3,11 Hypertension is not an independent risk factor
for perioperative cardiovascular complications.11 However, control of blood
pressure preoperatively may help reduce the tendency to develop perioperative
ischemia, and treatment has been associated with decreased rates of adverse
events.11 For high-risk surgical procedures, such as prolonged bariatric surgery
with large fluid shifts and/or blood loss, surgery-specific cardiac risks should
also be considered.11
The possibility of MS, nonalcoholic steatohepatitis (NASH), and deep venous

thrombosis (DVT) should also be evaluated in obese patients.3,4,12 MS refers to
a constellation of findings, including obesity with a truncal distribution,
hypertension, low high density lipoprotein levels, high triglyceride levels,
hyperglycemia (insulin resistance).4 Compared to patients without MS, obese
patients with MS have an increased risk of perioperative cardiac adverse
events, venous thromboembolic events, stroke, respiratory failure, acute kidney
injury, and death.4,5
NASH resembles alcoholic liver disease, but occurs in people who drink little or
no alcohol. The major feature in NASH is fat deposition in the liver, associated
with inflammation and cellular damage. NASH may cause substantial hepatic
dysfunction and eventually lead to cirrhosis.12 NASH can have a major impact
on anesthetic drugs metabolized by the liver.13

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Venous stasis disorders, such as chronic leg edema, venous insufficiency, and
stasis dermatitis, should be identified, as they are associated with an increased
risk of deep venous thrombosis (DVT) and other perioperative venous
thromboembolic events in morbidly obese patients.4,14 Elective bariatric surgery
should be delayed for at least 1 month after the diagnosis of a DVT; if bariatric
surgical procedure cannot be postponed, prophylactic inferior vena cava filter
placement should be considered for DVTs involving the lower part of the
body.3,4
Preoperative therapy
Obese patients should be instructed to take their usual medications up to and
including the day of surgery, except for diabetic medications, for which
adjustments are usually necessary, based on the time and type of surgery.3,11,15
If patients are subsequently found to have not taken their cardiovascular
medications on the day of surgery, angiotensin converting enzyme inhibitors
and angiotensin receptor blockers should not be administered, as omitting these
drugs on the day of surgery reduces the risk of intraoperative hypotension,
without introducing adverse consequences.15
The role of β-blockers and calcium channel blockers administered immediately

prior to surgery in reducing perioperative cardiac events is debated.11,15 Obesity
alone is generally not considered to be an indication for preoperative β-
blockers.11,15 β-blocker therapy may be considered in obese patients with other
risk factors for cardiac adverse events and, if necessary, it should be started 2-4
weeks before surgery.11,15 There is little evidence that calcium channel blocker
therapy reduces major adverse cardiac events in the perioperative period.15
The 2011 American Society of Anesthesiologists (ASA) guidelines for fasting (2

hours or more for clearing liquids and 6 hours or more for solids and nonhuman
milk) before procedures requiring general anesthesia, should be followed by
obese patients.16 The ASA does not support routine chemical prophylaxis
before surgery for patients with no apparent increased risk of pulmonary
aspiration.16 Chemical prophylaxis should be administered to obese patients
with an increased risk of pulmonary aspiration (i.e., morbidly obese patient

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undergoing upper abdominal surgery).3,4,10 In this case, H2-receptor antagonists,

nonparticulate antacids, and/or proton pump inhibitors may be considered.3
Antibiotic prophylaxis should be recommended for open surgery and suggested
for laparoscopic bariatric surgical procedures.3,10
As obese patients have an increased risk of perioperative DVT and other

venous thromboembolic events, strategies to prevent thrombosis should be
considered for all patients undergoing bariatric surgery. These strategies
usually include mechanical devices, such as lower extremity compressive
devices, and/or low-dose heparin (or a fractionated heparin compound) and/or
early ambulation.3,10
Oral benzodiazepines for anxiolysis are generally appropriate, as they cause

little or no respiratory depression.3,10 Intravenous midazolam, as well as other
sedatives and opioids, may be used for preoperative anxiolysis and analgesia in
obese patients, but they should be administered in cautiously-titrated, small
doses and only under conditions during which the patients are closely
monitored and supplemental oxygen is readily available.10 These intravenous
drugs may cause upper airway collapse, respiratory depression, and reduced
respiratory response to hypercapnia and hypoxia.3,10 Dexmedetomidine may be
particularly useful for morbidly obese patients because it does not cause
significant respiratory depression, and the concomitant use of low-dose
ketamine potentiates dexmedetomidine’s analgesic effects and reduces its
adverse hemodynamic effects.3
Perioperative anesthetic management

1. Positioning
Operating tables of an adequate size are required for safe anesthesia during
bariatric surgery.3 In addition, it is important to ensure that obese patients are
adequately immobilized so they do not slip off the operating table during table
position changes.3 Similarly, it is essential to correctly position the extremities
and protect pressure areas to help prevent positioning-related neural injuries
(e.g., brachial plexus, ulnar nerve, and sciatic nerve), and pressure sores.3

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2. Monitoring
Oxygenation, ventilation, circulation, and temperature should be continually
monitored during anesthesia in all obese patients.3,10 The preferred placement
of a noninvasive blood pressure cuff is the upper arm. However, using an
inappropriate cuff can significantly distort blood pressure reading. The cuff
should have a bladder length of 80% and a width of at least 40% of arm
circumference (a length-to-width ratio of 2:1). Alternatively, other places may be
used if necessary, such as the forearm, wrist, or ankle.3 Invasive arterial blood
pressure and central venous pressure monitoring should be used if necessary,
primarily depending on the type of surgery (i.e., bariatric surgery with fluid shifts
and/or blood loss), and patient co-morbidities (i.e., cardiopulmonary disease).
The central venous catheter should be used to such purpose and/or in absence
of adequate peripheral intravenous access and, preferable, not for outpatient
anesthesia.3 Depth of anesthesia monitoring (such as bispectral index, spectral
entropy, or auditory evoked potentials) should be considered, as it improves
anesthetic dosing, reduces intraoperative recall, and facilitates post-anesthesia
recovery.17 Neuromuscular function should be monitored in case of
neuromuscular blocking agents’ administration during bariatric surgery;
acceleromyography is highly recommended to reduce the risk of postoperative
residual curarization.18
3. Drug dosing
Obesity is associated with important physiological and anthropometric changes
that alter the pharmacokinetic properties of anesthetic drugs.19 Knowledge of
their appropriate dosing scalars is necessary for safe and effective
administration of anesthesia in obese patients.19 With the exception of
neuromuscular blocking agents (for which ideal body weight might be
appropriate) and succinylcholine (for which real body weight is suggested), lean
body weight is a more appropriate dosing scalar than real body weight for the
commonly used anesthetic agents, including induction agents and opioids.19,20
Simplified equations for rapid and accurate determination of ideal body weight
and lean body weight in obese patients were recently published.20

Blanca Ríos, MD
4. Preinduction preparation
The 30° reverse Trendelenburg position more than the 30° back-up Fowler and
horizontal-supine positions, as well as preoxygenation, are strongly
recommended before induction of anesthesia in obese patients.3,10 Following
these recommendations will prolong the safe period of apnea, thus reducing the
risk of hypoxemia, and reducing the time for the SpO2 to normalize if it does
fall.3,10 Tidal volume breathing of 100% oxygen for approximately 3 minutes is
suggested to achieve maximal preoxygenation, yet minimizes the possibility of
atelectasis due to a high inspired oxygen concentration.3,10 Four vital capacity
breaths with 100% oxygen within 30 seconds, is an effective alternative in
obese patients.3 Application of positive pressure ventilation (PPV) during
preoxygenation decreases atelectasis formation and improves oxygenation.21
Futier et al. found that 5 minutes of noninvasive PPV [i.e., pressure support
over positive end-expiratory pressure (PEEP)] improves oxygenation and end-
expiratory lung volume in obese patients compared with conventional
preoxygenation, with beneficial effects extending past endotracheal intubation. 22
5. Airway management
Obesity is associated with various clinical features, including fat deposition in
tissues surrounding the upper airway, at the occipitus, and in the neck, that may
lead to difficulty with face mask ventilation, endotracheal intubation, or both. 23-25
The following are independent risk factors for difficult mask ventilation: male
sex, age >55 years, history of snoring, OSA, lack of teeth, presence of a beard,
Mallampati class ≥3, abnormal mandibular protrusion, and large neck
circumference.23,24 Appropriate positioning using the standard “sniffing” position
and elevating the head, neck, and chest above the abdomen enhances airway
patency and reduces the risk of difficult mask ventilation.3,10
Although obese patients are often considered to have an increased risk of

difficult endotracheal intubation, there isn’t clear evidence about obesity being
per se a risk factor for difficult endotracheal intubation.24,25 Independent risk
factors for difficult intubation include the following: Mallampati class ≥3, reduced
thyromental distance, reduced sternomental distance, reduced mouth opening,

Blanca Ríos, MD
and increased neck circumference (>40 cm).24,25 A neck circumference:

thyromental distance ratio >5.0 has been demonstrated to be a better predictor
of difficult intubation than the Mallampati score or neck circumference.25
Devices for assisting difficult intubation (e.g., a variety of laryngoscope blades,

video laryngoscopes, a gum elastic bougie, a Frova intubating introducer,
supraglottic airway devices, and a fiberoptic bronchoscope) should always be
immediately available during induction of obese patients.3,10,26,27 The Proseal
laryngeal mask airway (a supraglottic airway device) was found to be an
effective temporary ventilatory device before laryngoscope-guided tracheal
intubation and for airway rescue after failed intubation, and has been
successfully used as a dedicated airway/conduit to the trachea under
bronchoscope guidance. In the presence of a skilled team and selected
patients, it is also a safe and effective device for ventilation during surgery in
morbidly obese patients.28 Awake fiberoptic endotracheal intubation should be
considered as the first approach in patients with limited mandible protrusion,
reduced mouth opening, limited cranio-cervical mobility, and an increased neck
circumference, and as a secondary option after failed conventional
endotracheal intubation.3,10,27
6. Induction, maintenance and emergence from anesthesia

Rapid sequence induction (RSI) involves the prompt induction of general
anesthesia and subsequent endotracheal intubation to minimize the risk of
arterial desaturation. It is commonly recommended for morbidly obese
patients.3,10 Although succinylcholine has been traditionally considered the
neuromuscular blocking agent of choice for RSI because of its fast onset and
short duration,29 rocuronium may be a reasonable alternative. Similar intubating
conditions have been found with the use of rocuronium 1-1.2 mg/kg and
succinylcholine 1 mg/kg.27 Sugammadex, a selective neuromuscular reversal
drug, greatly enhances the speed of reversal of rocuronium-induced
neuromuscular blockade. Sorensen et al.30 found that spontaneous ventilation
was re-established earlier after rocuronium 1 mg/kg plus sugammadex 16
mg/kg, than after succinylcholine 1 mg/kg (216 vs. 406 seconds).

Blanca Ríos, MD
During bariatric surgery, mechanical ventilation should be initiated with a tidal

volume of approximately 8 mL/kg (range 6-10 mL/kg) ideal body weight.10 Either
pressure- or volume-controlled ventilation may be used; there is no substantial
difference between the two ventilation strategies when used intraoperatively in
obese patients.31 The inspired oxygen should be titrated to maintain an SpO2
>95% (PaO2 >80 mmHg) and the respiratory rate set to maintain
normocapnia.10 For hemodynamically stable patients, recruitment maneuvers
(i.e., three sighs, each generating a pressure plateau of 45 cmH2O) followed by
PEEP 10 cmH2O for 5 min should be performed after anesthesia induction and
before planned extubation to reduce the risk of hypoxemia and atelectasis.10
Although the superiority of inhalation or total intravenous technique for

maintenance of anesthesia has not been clearly established for morbidly obese
patients, inhalation anesthesia continues to be favored by many
anesthesiologists.3,32 Desflurane reduces the average extubation time by 25%
compared to sevoflurane, and by 21% compared to propofol.33,34 These
advantages have been observed in both non-obese and obese patients.32-34
Other benefits of desflurane include a reduced incidence of desaturation, faster
recovery of protective airway reflexes, and improved patient mobility in the
postoperative period.32 Because of their rapid elimination and amnesic
properties, nitrous oxide and xenon are potentially attractive choices for obese
patients, but the increased risk of postoperative nausea and vomiting (PONV)
with nitrous oxide, and the need for a high inspired oxygen concentration and
the high cost of xenon, limit their use in this patient population.3
Opioid administration is associated with respiratory depression and upper

airway obstruction that may lead to hypoxemia and respiratory failure in obese
patients. Remifentanil is generally the opioid of choice for these patients
because of its fast organ-independent elimination via rapid metabolism by
tissue and plasma esterases.3,32
During maintenance of general anesthesia in obese patients, it is generally

desirable to maintain full neuromuscular blockade to facilitate controlled
ventilation and surgical exposure. This is particularly important during

Blanca Ríos, MD
laparoscopic surgery, when ventilation may be impeded by the

pneumoperitoneum, and when poor relaxation can interfere with visualization
and safe manipulation of surgical instruments. Neuromuscular blockade should
be achieved by intermediate-acting neuromuscular blockers, such as
vecuronium, rocuronium, and cisatracurium. These agents have similar duration
of action, but rocuronium has a more rapid onset of action, which makes it
suitable for rapid induction of neuromuscular blockade. Furthermore, as noted
above, rocuronium- (and vecuronium-) induced neuromuscular blockade is
rapidly and effectively reversed by sugammadex.3,32 The organ-independent
(Hoffman) elimination of cistatracurium is a potential advantage for obese
patients with hepatic or renal dysfunction.3,10
Full recovery from neuromuscular blockade is mandatory in obese patients to

prevent postoperative residual curarization and its associated
consequences.18,32,35 Between neostigmine, a reversible acetylcholinesterase
inhibitor, and sugammadex, a rocuronium/vecuronium neuromuscular blockade
antagonist, only sugammadex allows quick, effective, and safe attainment of the
recommended train of four ratio of 1.0 or more from any level of rocuronium or
vecuronium neuromuscular blockade in obese patients.32,36,37
The ideal fluid administration strategy for obese surgical patients has not been
established.3 Restrictive intraoperative crystalloid administration may be
associated with low urine output and reduced incidence of postoperative
hypoxia due to pulmonary dysfunction. By contrast, liberal intraoperative
crystalloid administration may increase urine output and reduce the incidence of
postoperative thirst, dizziness, drowsiness, fatigue, and nausea. Liberal (40
mL/kg) intraoperative crystalloid administration has been demonstrated to
increase urine output more than the conservative approach (15 mL/kg) in
morbidly obese patients, without significantly modifying the incidence of
postoperative rhabdomyolysis.3
7. Postoperative pain and nausea/vomiting management

PONV and pain are among the major perioperative concerns of most surgical
patients and their anesthesiologists. Nonsteroidal anti-inflammatory drugs or

Blanca Ríos, MD
cyclo-oxygenase-2 inhibitors, alone or in combination with other nonopioid

analgesics (such as acetaminophen), are strongly recommended to improve
pain relief and to reduce opioid consumption, thus avoiding opioid-related upper
airway obstruction and respiratory depression in obese patients.3,10,32 The use of
a single injection or continuous epidural analgesia, peripheral nerve blocks
(under ultrasound guidance), and/or wound infiltration whenever possible, may
likewise reduce requirements for supplemental systemic opioids, and, therefore,
the incidence of opioid-induced side-effects.3,10
A multimodal approach to PONV prevention is preferable for obese surgical

patients, especially for those undergoing laparoscopic procedures.3,10,32,38 This
approach includes reducing risk factors for PONV, such as avoidance of nitrous
oxide; use of propofol; avoidance or minimization of opioids and neostigmine;
administering two or more antiemetics, such as dexamethasone, 5-HT3 receptor
antagonists, droperidol, and scopolamine; and using other measures, such as
anxiolysis with benzodiazepines, pre-hydration with oral carbohydrate,
adequate hydration, and acustimulation at the P 6 acupoint.3,38
Postoperative management
Obese patients often require supplemental oxygen in the postoperative period,
mainly due to residual effects of anesthetics and atelectasis.3,10 In this case,
current guidelines recommend the use of postoperative noninvasive PPV
therapy.3,9 In particular, it appears that the use of CPAP immediately after
surgery holds the best potential for improving gas exchange and decreasing
postoperative respiratory complications.7,10 If bariatric surgery is performed on
an outpatient basis, the ASA recommends that patients with OSA remain in the
hospital an extra 3 hours before discharge.7 Discharge should be delayed an
additional 7 hours if any episode of significant upper airway obstruction is
observed.7,10
All patients undergoing bariatric surgery should have a comprehensive

preoperative evaluation, particularly looking for the presence of OSA,
pulmonary disease, and CVD. The preoperative physical examination should
particularly focus on the upper airway, for risk stratification regarding the

Blanca Ríos, MD
possibility of difficult mask ventilation and endotracheal intubation. Obese

patients should also have a pertinent diagnostic work-up. Preoperative
therapies should be continued as usual until the day of surgery, with exception
of diabetic medications. Following published guidelines for fasting, aspiration
chemical prophylaxis, and antibiotic prophylaxis is suggested for the obese
surgical patient. Airway management requires proper preparation, equipment,
and training. Preoxygenation and the 30° reverse Trendelenburg position are
strongly recommended before anesthesia induction and endotracheal
intubation. Anesthetic agents should be administered on the basis of proper
dosing scalars, and the preference should be for those with a short half-life and
rapid elimination kinetics. Sugammadex should be considered to reverse
rocuronium/vecuronium-induced neuromuscular blockade. Adequate
postoperative monitoring is recommended for all obese patients, particularly
those with OSA or another condition predisposing to a high risk of respiratory
complications.
1. Ogden CL, Carroll MD, Kit BK, et al. Prevalence of obesity in the United States,
2009-2010. NCHS Data Brief. 2012 Jan;(82):1-8.
2. Berrington de Gonzalez A, Hartge P, Cerhan J, et al. Body-mass index and
mortality among 1.46 million white adults. N Engl J Med. 2010 Dec
2;363(23):2211-19.
3. Ogunnaike B. The morbidly obese patient undergoing outpatient surgery. Int
Anesthesiol Clin. 2013 Summer;51(3):113-35.
4. Tung A. Anaesthetic considerations with the metabolic syndrome. Br J Anaesth.
2010 Dec;105 Suppl 1:i24-33.
5. Glance LG, Wissler R, Mukamel DB, et al. Perioperative outcomes among
patients with the modified metabolic syndrome who are undergoing noncardiac
surgery. Anesthesiology. 2010 Oct;113(4):859-72.
6. Seet E, Chung F. Management of sleep apnea in adults – functional algorithms
for the perioperative period: Continuing professional development. Can J
Anaesth. 2010 Sep;57(9):849-64.
7. Adesanya AO, Lee W, Greilich NB, et al. Perioperative management of
obstructive sleep apnea. Chest. 2010 Dec;138(6):1489-98.
8. Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: A tool to screen
patients for obstructive sleep apnea. Anesthesiology. 2008 May;108(5):812-21.
9. Chung F, Subramanyam R, Liao P, et al. High STOP-bang score indicates a
high probability of obstructive sleep apnoea. Br J Anaesth. 2012
May;108(5):768-75.
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10. Pelosi P, Gregoretti C. Perioperative management of obese patients. Best Pract

Res Clin Anaesthesiol. 2010 Jun;24(2):211-25.
11. American College of Cardiology Foundation/American Heart Association Task
Force on Practice Guidelines, American Society of Echocardiography, American
Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular Angiography and Interventions,
Society for Vascular Medicine, Society for Vascular Surgery & Fleisher LA,
Beckman JA, Brown KA, et al. 2009 ACCF/AHA focused update on
perioperative beta blockade incorporated into the ACC/AHA 2007: Guidelines
on perioperative cardiovascular evaluation and care for noncardiac surgery. J
Am Coll Cardiol. 2009 Nov 24;54(22):e13-e118.
12. Krawczyk M, Bonfrate L, Portincasa P. Nonalcoholic fatty liver disease. Best
Pract Res Clin Gastroenterol. 2010 Oct;24(5):695-708.
13. Carron M, Parotto E, Ori C. Prolonged neuromuscular block associated to non-
alcoholic steatohepatitis in morbidly obese patient: neostigmine versus
sugammadex. Minerva Anestesiol. 2012 Jan;78(1):112-13.
14. Steffen LM, Cushman M, Peacock JM, et al. Metabolic syndrome and risk of
venous thromboembolism: Longitudinal investigation of thromboembolism
etiology. J Thromb Haemost. 2009 May;7(5):746-51.
15. Smith I, Jackson I. Beta-blockers, calcium channel blockers, angiotensin
converting enzyme inhibitors and angiotensin receptor blockers: Should they be
stopped or not before ambulatory anaesthesia? Curr Opin Anaesthesiol. 2010
Dec;23(6):687-90.
16. American Society of Anesthesiologists Committee. Practice guidelines for
preoperative fasting and the use of pharmacologic agents to reduce the risk of
pulmonary aspiration: Application to healthy patients undergoing elective
procedures: An updated report by the American Society of Anesthesiologists
Committee on Standards and Practice Parameters. Anesthesiology. 2011
Mar;114(3):495-511.
17. Freo U, Carron M, Innocente F, et al. Effects of A-line autoregression index
(AAI) monitoring on recovery after sevoflurane anesthesia for bariatric surgery.
Obes Surg. 2011 Jul;21(7):850-57.
18. Brull SJ, Murphy GS. Residual neuromuscular block: Lessons unlearned. Part
II: Methods to reduce the risk of residual weakness. Anesth Analg. 2010
Jul;111(1):129-40.
19. Ingrande J, Lemmens HJ. Dose adjustment of anaesthetics in the morbidly
obese. Br J Anaesth. 2010 Dec;105 Suppl 1:i16-23.
20. Carron M, Guzzinati S, Ori C. Simplified estimation of ideal and lean body
weights in morbidly obese patients. Br J Anaesth. 2012 Nov;109(5):829-30.
21. Delay JM, Sebbane M, Jung B, et al. The effectiveness of noninvasive positive
pressure ventilation to enhance preoxygenation in morbidly obese patients: a
randomized controlled study. Anesth Analg. 2008 Nov;107(5):1707-13.
22. Futier E, Constantin JM, Pelosi P, et al. Noninvasive ventilation and alveolar
recruitment maneuver improve respiratory function during and after intubation of
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morbidly obese patients: a randomized controlled study. Anesthesiology. 2011

Jun;114(6):1354-63.
23. Kheterpal S, Martin L, Shanks AM, et al. Prediction and outcomes of impossible
mask ventilation: a review of 50,000 anesthetics. Anesthesiology. 2009
Apr;110(4):891-97.
24. El-Orbany M, Woehlck HJ. Difficult mask ventilation. Anesth Analg. 2009
Dec;109(6):1870-80.
25. Kim WH, Ahn HJ, Lee CJ, et al. Neck circumference to thyromental distance
ratio: A new predictor of difficult intubation in obese patients. Br J Anaesth.
2011 May;106(5):743-48.
26. Carron M, Freo U, Ori C. Bronchoscope-guided intubation through a Laryngeal
Mask Airway Supreme in a patient with a difficult-to-manage airway. J Anesth.
2009;23(4):613-15.
27. Suzuki A, Terao M, Aizawa K, et al. Pentax-AWS airway scope as an
alternative for awake flexible fiberoptic intubation of a morbidly obese patient in
the semi-sitting position. J Anesth. 2009;23(1):162-63.
28. Carron M, Veronese S, Gomiero W, et al. Hemodynamic and hormonal stress
responses to endotracheal tube and ProSeal Laryngeal Mask Airway™ for
laparoscopic gastric banding. Anesthesiology. 2012 Aug;117(2):309-20.
29. Perry JJ, Lee JS, Sillberg VA, et al. Rocuronium versus succinylcholine for rapid
sequence induction intubation. Cochrane Database Syst Rev. 2008 Apr
16;(2):CD002788.
30. Sørensen MK, Bretlau C, Gätke MR, et al. Rapid sequence induction and
intubation with rocuronium-sugammadex compared with succinylcholine: a
randomized trial. Br J Anaesth. 2012 Apr;108(4):682-89.
31. Aldenkortt M, Lysakowski C, Elia N, et al. Ventilation strategies in obese
patients undergoing surgery: A quantitative systematic review and meta-
analysis. Br J Anaesth. 2012 Oct;109(4):493-502.
32. Carron M, Veronese S, Foletto M, et al. Sugammadex allows fast-track bariatric
surgery. Obes Surg. 2013 Mar 22. [Epub ahead of print]
33. Dexter F, Bayman EO, Epstein RH. Statistical modeling of average and
variability of time to extubation for meta-analysis comparing desflurane to
sevoflurane. Anesth Analg. 2010 Feb 1;110(2):570-80.
34. Wachtel RE, Dexter F, Epstein RH, et al. Meta-analysis of desflurane and
propofol average times and variability in times to extubation and following
commands. Can J Anaesth. 2011 Aug;58(8):714-24.
35. Carron M, Freo U, Ori C. Sugammadex for treatment of postoperative residual
curarization in a morbidly obese patient. Can J Anaesth. 2012 Aug;59(8):813-
14.
36. Gaszynski T, Szewczyk T, Gaszynski W. Randomized comparison of
sugammadex and neostigmine for reversal of rocuronium-induced muscle
relaxation in morbidly obese undergoing general anaesthesia. Br J Anaesth.
2012 Feb;108(2):236-39.

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37. Carron M, Parotto E, Ori C. The use of sugammadex in obese patients. Can J
Anaesth. 2012 Mar;59(3):321-22.
38. Chandrakantan A, Glass PS. Multimodal therapies for postoperative nausea
and vomiting, and pain. Br J Anaesth. 2011 Dec;107 Suppl 1:i27-40.

Blanca Ríos, MD
Chapter XII
Bariatric sensitivity training
ASMBS Integrated Health Clinical Issues Committee (2013-2014)

Karen Schultz, MSN
Rationale
Obesity remains one of the last socially acceptable forms of discrimination.
Often, healthcare clinicians are not aware of their own bias(es) and/or feelings
toward individuals affected by obesity. Bariatric sensitivity training is one way to
educate clinicians about the impact that behaviors, words and actions may have
on those affected by obesity. Guidelines are needed to provide a basis for
content and consistent training for those working with all individuals affected by
obesity – this includes not only the bariatric surgery patient but also any
individual of size and includes patients, visitors and staff.
Recommendations:
Frequency - All institutions with metabolic and bariatric surgery programs
should require employee sensitivity training at initial orientation and then at least
every three years thereafter. A combination of live and web-based
presentations are the preferred methods.
Format – live presentations are preferred; web-based, video or self-learning
modules are also acceptable formats, provided there is a method of contact for
questions.
Presenter - healthcare provider with direct clinical experience treating patients
with obesity and severe obesity; a bariatric coordinator, who may be a non-
clinician, would also be an appropriate presenter.
Target audience - entire facility with special emphasis on bariatric-specific
units. At minimum, staff in the following service units should receive sensitivity
training: all bariatric nursing units, OR, ER, ICU, Admitting, Radiology,
Transporters; Program Staff, Surgeons and Surgeon’s office staff.
Core content – to include, but is not limited to, definition of overweight, obesity,
severe obesity; obesity related co-morbidities; obesity trends; environmental,
genetic and biologic causes and contributing factors; quality of life; emotional
impact of the disease; stigma and discrimination associated with obesity; health

Blanca Ríos, MD
care provider bias; strategies to avoid; discussion of example situations of care

presented with and without bias; examples of inappropriate and appropriate
images in media and healthcare settings; handouts.
The RESPECT© Model (stands for rapport, environment, safety, privacy,
encouragement, caring, tact), adopted by the National Association of Bariatric
Nursing, is a collection of guiding principles that can be applied in all areas of
an institution to foster appropriate attitudes towards people who suffer from
obesity and its related conditions. For example: One form of insensitivity is
lack of consideration in the physical environment. The facility should be
evaluated for adequate availability of safe and size appropriate furniture and
equipment. This should include wheelchairs, stretchers, beds, bedside chairs,
gowns, blood pressure cuffs and all seating that could be used by the bariatric
patient in the outpatient and inpatient settings. Additional purchase of
equipment may be necessary, keeping in mind that the general patient
population may also have the need for this size appropriate equipment. All staff
should be aware of the capacity limits of all available furniture and equipment.
The capacity limits should be marked discretely on the equipment, such as with
color-coded tags or tape.
Topic areas included in training
Obesity discrimination
Ways to avoid insensitivity
Healthcare provider bias
RESPECT Model
Specific examples of weight bias

Examples of interactions with persons with severe obesity
Quotes from patients
Labeling of weight dependent equipment

See MBSAQIP guidelines for specific requirements
Overview of incidence of obesity

Obesity statistics
Co-morbid conditions
Surgical requirements for metabolic and bariatric surgery
Discussion of levels of BMI
Overview of metabolic and bariatric procedures
(optional) Pre-surgery evaluation (e.g., assessment)

Patient process from seminar to surgery
Role play

Blanca Ríos, MD
Additional discussion topics may include pre-surgery evaluation, the patient

process from seminar to surgery and role-play exercises. Documentation of
attendance should be recorded and include the date, attendees, department,
presenter and a copy of the material presented. A pre-test and post-test is an
option that should be left to the discretion of each program.
Resources
ASMBS IHCIGC sensitivity training presentation-available for member
download (release date TBA)
Rudd Center-Breaking through the weight bias in healthcare
http://www.yaleruddcenter.org/resources/upload/docs/what/bias/BreakingThrou
ghWeightBiasHealthcare10.09.pdf
Rudd Center-Weight bias in health care settings: implications for treatment
providershttp://www.yaleruddcenter.org/resources/upload/docs/what/bias/Weigh
tBiasInHealthCareSettings.pdf
Rudd Center-Weight bias in health care: implications for patients, providers, and
public
healthhttp://www.yaleruddcenter.org/resources/upload/docs/what/bias/Breaking
ThroughWeightBiasHealthcare10.09.pdf
OAC Understanding Obesity Stigma brochure
http://www.obesityaction.org/weight-bias-and-stigma/understanding-obesity-
stigma-brochure
MBSAQIP Guidelines - MBSAQIP.org

Blanca Ríos, MD
RESPECT® patient care model

R = Rapport (establish a foundation of trust, confidence &collaboration)
E = Environment/Equipment (appropriate size equipment, gowns, lifting
devices, etc…)
S = Safety (build a culture of safety & security)
P = Privacy (protect patient privacy & dignity)
E = Encouragement (offer support & reassurance)
C = Caring/Comparison (avoid blaming the victim)
T = Tact (be aware of nonverbal signs, body language, tone of voice, etc…)
National Association of Bariatric Nurses
Disclaimer.The American Society for Metabolic and Bariatric Surgery (ASMBS)

is established as an educational professional medical society. It is not intended
to be, nor should it be viewed as a credentialing body. The above
recommendations are based on members' experience and are offered only as
guidelines and are specifically not intended to establish a local, regional or
national standard of care for any gastric band adjustment procedure. While the
ASMBS views these Guidelines as being important to successful weight loss
outcomes and provision of safe patient care, it does not warrant, guarantee or
promise that compliance assures positive surgical outcomes for any single
procedure. It is the responsibility of the program to determine appropriate billing,
documentation, and supervision guidelines for the use of physician extenders.
1. Bejciy-Spring, A. R-E-S-P-E-C-T: A Model for the Sensitive Treatment of the

Bariatric Patient. Bariatric Nurs and Surg Care; 3(1): pp.47-56.
2. Bocquier, A., Verger, P., Basdevant, A., Andreotti, G., Baretege, J., &Villani, P.
et al. Overweight and obesity: Knowledge, attitudes, and practices of general
practitioners in France. Obes Res; 2005.13(4):pp.787-95.
3. Foster, G. D., Wadden, T. A., Makris, A. P., Davidson, D., Sanderson, R. S., &
Allison, D. B. et al. Primary care physicians’ attitudes about obesity and its
treatment. Obes Res;2003.11(10):pp.1168-77.
4. Harvey, E. L., & Hall, A. J. Health professionals’ views of overweight people and
smokers. Int Journal Obes;2001.25:pp.1253-61.

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5. Hebl, M. R., &Xu, J.Weighing the care: Physicians’ reactions to the size of a
patient. Int Journal Obes; 2001.25:pp.1246-52.
6. Sabin, J. A., M Marini, M., & Nosek, B. A. Implicit and explicit anti-fat bias
among a large sample of medical doctors by BMI, race/ethnicity and gender.
PLoS One,pp.7.
7. Schwartz, M. B., O’Neal-Chambliss, H., Brownell, K. D., Blair, S. N., &
Billington, C. (2003). Weight bias among health professionals specializing in
obesity. Obes Res, 2001.11, pp.1033-39.

Blanca Ríos, MD
Curriculum vitae of authors
Blanca Ríos, MD
Clinical Psychologist, Brief Therapy Specialitist. Master in Clinical Psychology and

Psychotherapy of Anáhuac University. Psychologist and Psychotherapy of Institute of
Obesity and Metabolic Syndrome of Hospital Ángeles Pedregal in México City. Director
of online courses in integrated health and bariatric surgery. (www.obesity.academy)
Coordinator of Integrated Health in IFSO LAC (2011-2013). Chairwoman of Integrated
Health Committee of IFSO (2012-2016). She have many papers about psychology and
obesity. blanca_rios@hotmail.com www.blancarios.com
Dr. Adriano Segal
PhD in Medicine from the department of Psychiatry at the School of Medicine of

the USP/SP (HCFMUSP/SP). Coordinator of the Obesity and Metabolic
Syndrome Outpatient Service of the Endocrinology and Metabolism Hospital of
the HCFMUSP/SP. President of the COESAS-SBCBM (Associated Specialties
Committee of the Brazilian Society of Bariatric and Metabolic Surgery). Director
of Psychiatry and Eating Disorders at ABESO (Brazilian Association of Obesity
and Metabolic Syndrome studies).Technical director of the Segal Clinic.
segal@uol.com.br
Dra. Débora K. Kussunoki
Residency in Psychiatry at the Hospital of Clinics of the School of Medicine of

the University of São Paulo (HCFMUSP/SP). Psychiatrist at the Obesity and
Metabolic Syndrome Outpatient Service of the Endocrinology and Metabolism
Hospital of the HCFMUSP/SP. Coordinator of the Psychiatry Subcommittee at
COESAS-SBCBM (Committee of Associated Specialties of the Brazilian Society
of Bariatric and Metabolic Surgery). Member of ABESO (Brazilian Association of
Obesity and Metabolic Syndrome Studies). Technical director of the Segal
Clinic. deborakk@uol.com.br
Psych. Isabel C.M. Paegle
Specialist in Clinical Psychology, eating disorders and obesity. Specialist in

eating disorders and obesity of Hospital de Clinicas, Faculty of Medicine,
University of São Paulo. Associate Member of the Board Specialties – SBCBM
(Brazilian Society of Metabolic and Bariatric Surgery) 2013-2014. Member of
Multidisciplinary Team in clinical GOC GASTRO OBESO CENTER. Associate
Member of IFSO. Associate Member of Specialties COESAS-SBCBM -
Brazilian Society of Metabolic and Bariatric Surgery. Master in Health
Psychology of UMESP- Methodist University of São Paulo.
icmpaegle@terra.com.br

Blanca Ríos, MD
Dr. Poonam S. Shah M.D.
Internal Medicine from Pune University, India. She is working as a ‘Bariatric

Physician’ in ‘Laparo-Obeso Centre’, since its inception in 2004, a certified
‘International Centre of Excellence’ by the ‘Surgical Review Board’ at two
institutes in Pune, India. She has attended the pre-congress training programs
conducted by IFSO and ASMBS on various Integrated Health topics like
Nutrition, Behavioral Health as well as for the Internist, to educate herself for
better patient care as well as to keep herself updated with the recent protocols.
She is involved in the pre-operative work up, education as well as the post-
operative follow-up, education of weight loss patients and their families. Also
conducts the didactic programs for Surgeons, Physicians, Nutritionists etc as
part of the Bariatric Training Programs conducted by the centre. She actively
conducts the monthly Support Group (Dream Slim Club) meetings for patient
and their families for their education and support.Monitors the data entry of
patient details in the centre’s own software to help facilitate good patient follow-
up and also present papers on the centre’s experience with various bariatric
procedures and its effect on metabolic syndrome and other co morbidities.
Author or co-author in the papers published in International Journals. Co-
investigator in the various clinical trials, including a recently conducted
RCT,taken up by the centre. Integrated Health. member is invited as faculty/
speaker to various bariatric conferences or to organize the Integrated Health
Symposium. Member of IFSO Integrated Health has contributed six chapters on
Bariatric Nutrition and Metabolic Health, soon to be published. Colony. India.
drpoonamshah@rediffmail.com
Luca Busetto. MD
Degree in Medicine (Maximum) at the University of Padova, 1987. PhD in

Experimental and Clinical Gerontology at the University of Padova, 1994. Post-
degree in Geriatrics at the University of Padova, 1995. Research Assistant at
the Center for the Study and the Integrated Treatment of the Obesity - Bariatric
Unit- Department of Medicine - University of Padova since 22 september 1998.
Author of 82 publications in peer-reviewed international journals. Most relevant
publications in: Obesity Research, International Journal of Obesity, Obesity
Surgery, Surgery for Obesity and Related Diseases, New England Journal of
Medicine, Annals of Internal Medicine, Chest, Journal of Pathology, Hormone
and Metabolic Research, Journal of Nutrition, Nutrition Metabolism and
Cardiovascular Diseases, Clinical Nutrition, Annals of Nutrition and Metabolism,
Health and Aging, Annals of Clinical and Laboratory Science. TOTAL IMPACT
FACTOR: 290.9. H-INDEX: 26.Member of the Editorial Board of for the
followings international journals: Surgery for Obesity and Related Diseases
(associate editor), Obesity Surgery, Eating and Weight Disorders,
Mediterranean Journal of Nutrition and Metabolism. Member of the National
Board of the Italian Obesity Society (SIO). Member of the Position
Statements/Standard Committee of the International Federation for the Surgery
of Obesity and Metabolic Disorders (IFSO). Former member of the National
Board of the Italian Society for Bariatric and Metabolic Surgery (SICOb).
luca.busetto@unipd.it

Blanca Ríos, MD
Cynthia K. Buffington, Ph.D.
Education in physiology (PhD) with postdoctoral fellowship in biochemistry and

endocrinology. Associate professor of medicine and served as Director of
Research at the University of TN Obesity Wellness Center at the University of
Tennessee Health Science Center. In 2000 joined US Bariatric in Ft.
Lauderdale, FL (which was the largest bariatric center in the world at that time)
served as Director of Research and Education. Moved to Florida Hospital
Celebration Health in 2007 where she currently serves as Director of Research
at the Metabolic Medicine and Surgery Institute. Member of ASMBS since 1990
and one of founding members of Integrative Health Award ASMBS Circle of
Excellence Award 2004 and a finalist for the ASMBS Foundation’s \Outstanding
Achievement Award in 2007. On the Board of Editors for both Obesity Surgery
and SOARD. Have written number of manuscripts, book chapters, newsletter
articles and given numerous local, national and international presentations on
research and topics that concern obesity and bariatric surgery.
cynthia.buffington@fihosp.org
Keith C. Kim, MD, FACS, FASMBS
Bariatric surgeon - Florida Hospital /Florida Hospital Medical Group, Medical

Director of Metabolic Medicine and Surgery Institute at Celebration Health,
Recertification in General Surgery – American Board of Surgery, Certification in
General Surgery - American Board of Surgery, Investigator initiated, She has
many papers about bariatric surgery, textbooks, Book Chapters, Peer-review
Manuscripts and Editorial boards of Journal of Robotic Surgery, Reviewer for
Obesity Surgery Journal, Obesity Surgery, Surgical Review Corporation Review
Board.
Kgla. Mariela Olivares
BSc in Physical Therapy, registered Physical Therapist. Universidad de Chile

BSc in Physical Education. Universidad Metropolitana de Ciencias de la
Educación MSc in Sports Medicine and Exercise Science. Universidad Mayor
Graduarte program Physical activity sciences, Universidad de Chile.
Kinesiologist of the Nutrition and metabolic diseases center, Clínica las Condes
Main development area: Evaluation and exercise prescription of patients with
obesity or overweight, and other metabolic diseases. malevox@gmail.com
Kgla. Johana Pino
Kinesiologist approved with maximum distinction, Universidad de

Chile. graduated program: Exercise, Nutrition and Health, Universidad de Chile.
Multidisciplinary management of obesity, Universidad de Chile Physical activity
sciences, Universidad de Chile. Master in Sports Medicine, Universidad Mayor.
Kinesiologist of the Nutrition and metabolic diseases center, Clínica las Condes
Main development area: Evaluation and exercise prescription of patients with
Blanca Ríos, MD
obesity or overweight, and other metabolic diseases.

Investigation area: Phyisical fitness and metabolic disorders.
johannakine@gmail.com
Dr. Jorge Cancino López
Teacher of Physical Education, Metropolitan University of Educational

Sciences. Doctor of Science of Physical Activity, University of Las Palmas
(Spain). Professor at the Faculty of Science, School of Kinesiology, University
Mayor. Director of Graduate Exercise Physiology at University Mayor. Head of
the Department of Sports Science, High Performance Center, CAR-Chile.
Author of the Book of aerobic training Physiology: An integrated vision. Editorial
Médica Panamericana. jorgecancinolopez@gmail.com
Michele Carron, MD, PhD
Academic Career (University of Padova). School of Medicine, University of

Padova, 1998. Residency program in Anesthesia, Resuscitation and Intensive
Care, 2003. Doctoral (PhD) School of Pharmacological Sciences, 2007.
Assistant Professor at Department of Medicine, Anesthesiology and Intensive
Care, 2010.Hospital Appointments. Staff Physician, Intensive Care, S. Antonio
Hospital of Padova, 2004-2006. Staff Physician, Institute of Anesthesiology and
Intensive Care, University Hospital of Padova, 2007. Licences and Board
Certifications. Italian Licence for Medical Practice, University of Padova,
1999.Italian Board of Anesthesiology and Intensive Care, University of Padova,
2003.Physician referral for bariatric anesthesia at Certified IFSO Center of
Excellence in Bariatric Surgery, University, Hospital of Padova.
micarron@libero.it

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Blanca Ríos, MD

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Copyright 2015, Blanca Patricia Ríos Martínez

Copyright 2015, Instituto de Investigación y Educación en

All rights reserved.

This publication may not be reproduced or transmitted or in

The articles in this book are the sole responsibility of the

1st Edition ISBN: 978-607-97283-0-4

Legal deposit: 03-2016-070111434000-01

Produced in Mexico by: IIECS

Instituto de Investigación y Educación en Ciencias de la Salud

Design and edition: www.bariatric.today

Continuing Education: www.obesity.academy

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Chapter I. Presurgical psychological evaluation

Chapter II. Psychiatry disorders and post-operative follow-up

Chapter IV. Preoperative preparation of patients posted for bariatric

Chapter V. Post-bariatric surgery

Chapter VI. Management of special conditions: Type 2 Diabetes mellitus

Chapter VII. Compensatory responses to weight loss that contribute to

Chapter VIII. Alcohol metabolism and potential health consequences with

Chapter IX. Dumping syndrome

Chapter X. Physical activity in bariatric patient

Chapter XI. Anesthetic considerations for obese surgical patients

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Cap XII. Bariatric Sensivity training

Curriculum vitae of authors

This electronic book was elaborate with Integrated Health Committee

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Rafael Álvarez Cordero MD, PhD, FACS

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

attention of many international bariatric experts, her lectures and publications

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Antonio J Torres García

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Blanca P. Ríos Martínez, MD

Obesity is a public health problem of global significance which has increased as

Moreover, extreme obesity is related to significant psychosocial stress.2-4

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Pre-surgical psychological evaluation

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

takes or accompanies the patient to the appointment, in order to learn who is

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

2. Initial history and evolution of obesity, evaluation of weight variation

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

4. Expectations, motivation, goals and objectives; we try to make patients

The interview describes different stages of change, which are:

 There is neither true will to change nor awareness of the problem.

 Serious thinking about change through the next six months.

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

 Preparation for acting within a month.

It is relevant to identify in which stage the patient is, and consequently

5. Familiar environment (nuclear family and of origin). We know that family

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Some types of families are:13

Contributor Saboteur Antagonistic Indifferent Competitive Watchful

Encourages They search There’s no Weight loss

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

Table 1. Types of eaters.

Types of eaters Description

INTEGRATED HEALTH IN BARIATRIC SURGERY 2015

during the day or at a special schedule.