Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients 3662664356, 9783662664353

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Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients Christine Stier Sonja Chiappetta Editors

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Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients

Christine Stier · Sonja Chiappetta Editors

Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients

Editors Christine Stier University Hospital Mannheim, Division of Interdisciplinary Endoscopy Mannheim, Germany

Sonja Chiappetta Bariatric and Metabolic Surgery Unit Ospedale Evangelico Betania Naples, Italy

ISBN 978-3-662-66435-3 ISBN 978-3-662-66436-0  (eBook) https://doi.org/10.1007/978-3-662-66436-0 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer-Verlag GmbH, DE, part of Springer Nature. The registered company address is: Heidelberger Platz 3, 14197 Berlin, Germany

Foreword

Obesity is a growing disease worldwide, not only increasing unabated in developed countries, but also affecting emerging countries particularly severely. It is a chronic disease that produces a variety of sequelae and illnesses. Today, we no longer speak of morbid obesity, because it is a disease per se. According to the WHO definition, every person with a body mass index of more than 30 kg/m2 is suffering from obesity. This disease leads to a shortening of life expectancy and a reduction in quality of life in the remaining years. There is no causal therapy for this multifactorial disease. Prevention is the only effective measure to avoid the spread of the disease. It would be a measure for society as a whole that will meet with a lot of resistance. Conservative treatment approaches fail in most cases and almost always when higher degrees of obesity are involved. The most effective treatment option currently available is surgical intervention, which is referred to as bariatric surgery and/or metabolic surgery. It leads to various changes in the body that are very complex and can also have side effects. Through intensive followup care, the therapeutic effects can be increased and negative side effects can be limited or even avoided. This special knowledge of follow-up care is important for all practicing physicians, because the number of operations will continue to rise in parallel with the increase in obesity. Obesity is more common as a disease than the very common diagnoses of high blood pressure or diabetes mellitus. Therefore, it is no longer a task for specialists but the daily task of all practicing physicians, especially of course for general practitioners and internists. Based on many years of experience in the leading obesity centers in Germany, the editors have compiled this necessary knowledge in the present work. It offers practical guidance for the follow-up care of patients who have undergone bariatric surgery, with or without disease symptoms. The joint activity in two leading obesity centers and the scientific processing of the questions in clinical studies have led to a comprehensive body of special knowledge that can serve as a practical guide for every interested physician. The follow-up care after surgery of patients with obesity requires special knowledge, because operations aimed at weight reduction and treatment of comorbidities generate V

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such diverse and complex physiological changes that can be better understood and treated in the case of illness after studying this book. The main goal always remains the avoidance of sequelae and complications. I would like to express my sincere thanks to the editors for this compilation. Professor Dr. Rudolf Weiner Founding Chair of CAADIP and IFSO President 2014–2015

Preface

The World Health Organization (WHO) recommended to European countries as early as 2006 that obesity should be recognized as a chronic disease. After a long struggle and much hesitation, this step was taken in 2020. And this was a significant step, because finally and in the foreseeable future, patients suffering from the chronic disease obesity will be able to receive effective therapeutic help more easily. So far it has been the case that many affected people who have appeared at an obesity center had already invested in diet products, always in the hope of overcoming their disease—they have received hardly any treatment on a scientific basis. For this reason, the „diet industry“ flourished. This may also be because even in the 1960s and 1970s, not much was known about nutrition, the regulation of hunger, appetite, and satiety, or the physiology of the gastrointestinal tract. Thin children were sent for cures to gain weight— these are often patients in obesity centers today— and fat children were sent for hunger cures. From today’s perspective, this is no longer comprehensible. The science of the topic has thus developed rapidly, not least under the enormous economic pressure of the worldwide increase in obesity. Today we speak about the gut–brain axis, incretins, an adipogenic environment, or genetic and epigenetic influences. However, the exponentially increasing prevalence of obesity would require a medical emergency plan and this not only from a socio-economic point of view. Obesity leads to an increase in the incidence of type 2 diabetes to such an extent that we already talk about a twin epidemic, so-called “Diabesity.” Obesity increases the cardiovascular risk and cardiovascular diseases, the risk of cancer, of infertility, of liver diseases, of gastrointestinal diseases such as reflux, of lung diseases, of orthopedic diseases, of gynecological and many other diseases. Not least, it severely restricts the quality of life of those affected. Nevertheless, obesity is still stubbornly often considered to be self-inflicted, a lack of discipline, as excess—it is even associated with stupidity. In short, patients with obesity are stigmatized and discriminated against. In ignorance of the pathogenesis, it is often postulated that simply eating less would be the easy way to improve.

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Knowledge means the conscious, objective dealing with and understanding of facts and circumstances. Prejudices, on the other hand, do not have these characteristics. They usually constitute an unshakeable opinion that is not based on facts and, at the same time, refuses to understand them. It is therefore up to us to provide information about obesity as a chronic disease, about its pathogenesis, accompanying diseases, their therapy, and the resulting treatment prospects and successes, possible complications, as well as the necessary follow-up and long-term care of patients treated surgically for obesity. This book should be a small contribution toward the creation of more knowledge. In summer 2023

Dr. med. Christine Stier PD Dr. med. habil. Sonja Chiappetta

Contents

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Obesity: To Eat or Not to Eat—A Hypothalamic Question? . . . . . . . . . . . . 1 Christine Stier

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History of Bariatric and Metabolic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . 9 Christine Stier

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Current Standard Procedures of Bariatric and Metabolic Surgery . . . . . . 21 Christine Stier

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Pathophysiology: Restriction, Duodenal Exclusion, Malabsorption. . . . . . 43 Christine Stier

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Follow-up Intervals and Priorities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Christine Stier

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Postoperative Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Christine Stier

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Postoperative Supplementation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69 Christine Stier

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Nutritional Deficiencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Christine Stier

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Early Postoperative Complaints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111 Sonja Chiappetta

10 Postoperative Gallstone Formation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117 Sonja Chiappetta 11 Postoperative Kidney Stone Formation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123 Christine Stier 12 Bone Metabolism and Osteoporosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 Sonja Chiappetta IX

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13 Dumping Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 Christine Stier 14 Postoperative Fertility Enhancement and Contraception After Bariatric and Metabolic Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 Ann-Cathrin Koschker 15 Pregnancy After Bariatric and Metabolic Surgery. . . . . . . . . . . . . . . . . . . . 161 Ann-Cathrin Koschker 16 Drug Absorption/Postoperative Adjustment of Chronic Medication. . . . . . 173 Sonja Chiappetta 17 Weight Regain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179 Sonja Chiappetta und Christine Stier 18 Malnutrition and Extreme Weight Loss. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185 Sonja Chiappetta 19 Addiction Transfer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191 Sonja Chiappetta 20 Endoscopic Postoperative Diagnosis and Endoscopic Bariatric Interventions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197 Christine Stier 21 Less Common Complications. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 Sonja Chiappetta und Christine Stier 22 Post-Bariatric Body Contouring. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223 Naja-Norina Pluto Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233

Authors

Sonja Chiappetta Head Bariatric and Metabolic Surgery Unit, Ospedale Evangelico Betania, Naples, Italy Ann-Cathrin Koschker  Division of Endocrinology and Diabetes at the Department of Internal Medicine, Univeristy of Würzburg, Würzburg, Germany Naja-Norina Pluto  Board-certified Plastic and Aesthetic Surgeon, Plastische Chirurgie im Medienhafen, Düsseldorf, Germany Christine Stier University Hospital Mannheim, Division of Interdisciplinary Endoscopy, Mannheim, Germany

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Obesity: To Eat or Not to Eat—A Hypothalamic Question? Christine Stier

Obesity is increasing in epidemic proportions in all industrialized countries. The easy availability of high-calorie foods and the reduced daily need for physical activity in the work environment is referred to as an adipogenic environment. Finally, weight gain develops from an imbalance between energy intake and energy expenditure (Fig. 1.1). However, the regulating pathophysiological mechanisms are extremely complex and are subject to hormonal and neuronal control. The actual homeostasis takes place mainly in the hypothalamus and is beyond voluntary influence. Homeostatic regulatory mechanisms apparently determine the individual weight of each person. Remarkably, these central homeostatic regulatory mechanisms keep the body weight of many people strikingly stable (Fig. 1.2), despite their exposure to the modern, adipogenic food environment. Thus, the question arises why food energy is consumed in the course of the development of the chronic disease obesity, even though energy expenditure does not exceed energy intake. Hypothetically, these homeostatic control mechanisms may be decoupled in the course of disease genesis. Obesity can therefore initially be considered as a neuroendocrine regulatory disorder. In addition, there are secondary forms and genetic syndromes that act as a singular genetic factor in this regulatory circuit and thus inevitably lead to secondary obesity.

C. Stier (*)  University Hospital Mannheim, Division of Interdisciplinary Endoscopy, Mannheim, Germany © The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 C. Stier and S. Chiappetta (eds.), Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients, https://doi.org/10.1007/978-3-662-66436-0_1

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Energy consumption

Energy supply

Body weight

Energy supply

Energy consumption Gain in body weight

Energy consumption

Energy supply Decrease in body weight

Fig. 1.1   Homeostasis model of body weight: 1.1. Balance of energy intake and energy expenditure keeps body weight stable. 1.2. Imbalance of energy intake and energy expenditure leads to weight gain or loss

Genetics Epigenetics Nutrition Move

1  Obesity: To Eat or Not to Eat—A Hypothalamic Question?

Individual phenotypic variance of body weight around the set point, which is also individual

Body weight

Genetics Epigenetics Nutrition Move

set point

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Timeline

Fig. 1.2   Set point theory of body weight in healthy individuals

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Obesity is a chronic disease and has been recognized by the WHO since 2000. In 2006, the WHO called on all European Member States to recognize obesity as such. The genesis of this chronic disease can be described as a neuroendocrine dysregulation.

1.1 Primary Obesity The causes of primary obesity are seen as a multifactorial event. The following established aspects are cited as the basis for the emergence and development, whose weighting in interaction is not yet entirely clear: genetics and epigenetics, nutrition, hormones and metabolism, physical activity, sleep, stress, immune system, and reward behavior. In addition, other external factors such as upbringing, occupation, lifestyle, socioeconomic status, food policy, and health care interfere. Our fast-paced society is also characterized by increasing demands in everyday life and, above all, by the lack of, but actually necessary, psychological and physical balance. The human being as a whole, with health of body, mind, and soul, obviously moves into the background, and emotional reactions, such as fears or stress as disease-causing factors, especially of obesity, are not perceived or taken into account. There is no causal therapy for obesity. There are also no convincing prevention measures and the currently known measures obviously fail so that worldwide currently 39% of adults are overweight and 13% are obese. In particular, the increase in obesity among children is taking on alarming proportions.

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Important  The prevalence of obesity is rising rapidly worldwide both in industrialized and in developing and emerging countries. It is responsible for up to 6% of national health expenditures in the countries of the WHO European Region. Overweight and obesity are responsible for 80% of all type 2 diabetes cases, 35% of ischemic and 55% of hypertensive heart diseases, as well as more than 1 million deaths and more than 12 million sick years of life per year among adults in the WHO European Region. Obesity affects the poorer population groups more strongly and thus impairs their chance of improving their socioeconomic status. Statements of the WHO 2006.

1.2 Central Regulation of Hunger, Appetite, and Satiety This central regulation of hunger, appetite, and satiety is complex and complicated and therefore the terms hunger (survival instinct) and appetite (pleasure, reward, hedonic eating) should be defined first.

1.2.1 Hedonic Eating A philosophical excursion to the ancient Greeks is intended to present the original concept of hedonism and illustrate the corresponding background. The Greek Aristippus of Cyrene (435–355 BC) is considered the founder of hedonism. He distinguished three states of the soul and compared them in an analogy with sea movements. In his doctrine, mental pain as a fundamentally unnatural state corresponds to a storm with tearing waves, whereas pleasure in enjoyment (hedonism) is equivalent to a gentle wave movement and thus, according to the theory, a fundamentally natural state. Hedonism was for Aristippus the transition to complete peace of mind, happiness (ataraxia). For the founder of this theory, there was no difference between the pleasures of enjoyment, which he assigned to a single quality, namely the natural state of man, and the avoidance of pain on the way to happiness. Aristippus countered the critics of his doctrine with the description of his own relationship to pleasure (hedonia): “I am their master and not their slave; for to command over the pleasure of enjoyment and not to succumb to it, that is truly praiseworthy, not to deny it to oneself” (Diog. Lart. II,8,75), and further, “If that were reprehensible, it would certainly not be permissible among the gods” (Diog. Laert. II,8,68). This seems to be not always so easy today, especially with regard to the consumption of food. The 6000-year-old doctrine of Chinese medicine also knows that appetite (hedonic eating) and hunger (survival instinct) are to be assigned to two completely different physical states (yin and yang).

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Today, scientifically, and here both Chinese medicine and the theory of Aristippus represent noteworthy analogies, one distinguishes between hedonic eating and, in contrast, eating from pure physical energy demand, metabolic eating—between appetite and hunger. Consequently, appetite arises from the pleasure of enjoying a food, or the reward and happiness effect that is generated in the brain by it. Hunger, on the other hand, represents a pure survival instinct, caused by an acute existing, physical energy deficiency (Berthoud HR et al. 2017). Accordingly, the perception of appetite and hunger also differ fundamentally. If one has appetite, one looks for exactly the desired taste and the energy content of the food does not seem to matter. Rather, it is about the enjoyment and the associated self-reward by a specific food. In the ancient Greek sense, hedonic eating can therefore be understood as an attempt of the “way to happiness,” and thus above all, to feel better (happier) and to reduce stress. This has already manifested in our language with beliefs such as “chocolate makes you happy.” Basically, in modern society, one not only eats when metabolic hunger exists, but often without hunger and despite existing fat reserves. In contrast, with metabolic hunger, survival by securing the energy balance is in absolute focus. Appetite and thus the selection of a certain taste or food do not play a role. In the extreme case of hedonic eating, some individuals apparently show an addictive-like behavior toward food, and parallels have been drawn to drug and alcohol dependence, because the same dopaminergic brain areas are affected in the mentioned dependencies. 

Important  Dopamine (C8H11NO2) is a biogenic amine from the group of catecholamines. It is predominantly an excitatory neurotransmitter of the central nervous system.

A decisive difference, however, is that eating, unlike drugs and alcohol, is a daily necessity of life preservation. One cannot “withdraw” from eating. Nevertheless, obesity—although not fundamentally understood in the underlying regulation—continues to be stigmatized and judged as a character weakness and lack of discipline of the affected person. Alcoholism, in contrast, is medically and socially recognized as a disease. 

Important  The mesolimbic dopamine pathway plays a primary role in the reward system. Therefore, the mesolimbic system is equated with the reward system and consists of the main dopamine pathways of the brain. These include the ventral tegmental area (VTA) and the nucleus accumbens (associated with reward and attention, but also with addiction), which are connected by these dopamine pathways. The neurons of the nucleus accumbens project with their axons to the other structures of the limbic system, such as the amygdala. Hedonic eating (reward eating, appetite) is regulated by the mesolimbic dopamine pathway.

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1.2.2 Metabolic/Homeostatic Eating The so-called “homeostatic” model for the regulation of energy balance describes metabolic eating in the presence of energy deficiency and consequently not eating when there are energy reserves. Therefore, there is no need to actively “refrain” from eating, but rather there is satiety and therefore no metabolic incentive or drive to eat. In contrast to this, exclusively metabolically driven eating, any eating without hunger can be considered “non-homeostatic.” A more expressive term for “non-homeostatic” eating is “hedonic” eating. As described above, this also involves rewarding and thus emotional factors. This, at least initially, seems to be not regulated or compensated for by a metabolic-homeostatic feedback. Interestingly, however, the release of the hunger hormone ghrelin in the context of hedonic eating is higher than in metabolic eating, and the corresponding satiety response, mediated by cholecystokinin (CCK) is weaker (Monteleone P et al. 2013). Consequently, one can accordingly eat much more with appetite and it results in a rather delayed feeling of satiety. The homeostatic model cannot be applied alone in modern society. Rather, there is a mixture of hedonic and metabolic eating with an emphasis on hedonic eating. The corresponding flip side of the coin is anorexia nervosa, which in a pathological way can apparently significantly weaken or even switch off not only the hedonic but also the homeostatic eating drive and thus lead to life-threatening underweight. This is possibly also to be valued as a “neuroendocrine dysregulation” physical condition as opposed to obesity, which has so far been defined as a purely psychological disorder in the context of an eating disorder. This may do as little justice to this chronic disease as judging the cause of obesity to be a weakness of character (Zipfel S et al. 2015). In connection with obesity, many metabolic feedback signals and neuronal systems have already been identified, which are mainly located in the brainstem and the hypothalamus and represent a “homeostatic system” (Fig. 1.3). The balance between eating and not eating is therefore predominantly found in the part of the brain that cannot be influenced voluntarily. Hunger can therefore not generally be regulated by discipline, because together with thirst and breathlessness, it fundamentally represents a strong survival instinct. 

Important  Hedonic eating is regulated in the mesolimbic system, metabolic eating in the hypothalamus. Both systems are interconnected and only inadequately influenced by cognition.

This at the same time represents the biggest obstacle in diets that are supposed to lead to a significant weight reduction. In addition, excessive calorie consumption increases the basal metabolic rate, whereas fasting and a low-calorie diet reduce the basal metabolic rate (Molé PA 1990). The basal metabolic rate accounts for the main part of the daily energy expenditure and cannot be compensated for by increasing physical activity.

1  Obesity: To Eat or Not to Eat—A Hypothalamic Question? Satiety

7 Hunger

Glucose level  Insulin 

Glucose level  Glucagon 

Lipid level Leptin 

Lipid level  Adiponectin 

Incretin  (GLP-1; GIP)

Ghrelin

Hypothalamus

Fig. 1.3   Homeostasis model metabolic eating

A reduction by dietary calorie restriction therefore makes it difficult for overweight people to lose weight, but even more to stabilize the weight reduction. The weight regain, based on the described physiological regulatory mechanisms, is called the yo-yo effect. 

Practical tip  The sentence “You are too fat, just eat less” is not helpful in the therapy of the chronic disease obesity. People with obesity know with painful certainty that they are not slim and have in the overwhelming majority many unsuccessful and agonizing diets behind them. Currently, the only available sustainable therapy for obesity and its metabolic comorbidities is a surgical intervention with anatomical modification of the gastrointestinal tract and resulting altered neuronal and hormonal influence on the regulation of hunger and satiety. Summary

• Future insights into the interaction of the “metabolic” with the “hedonic” system will help to further elucidate the pathophysiology of obesity. Both systems regulate satiety, appetite, and hunger centrally in the subconscious. • With significant weight loss, the basal metabolic rate automatically decreases. • In the following chapters, the individual standard procedures and their historical development will be discussed in more detail.

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References Berthoud HR, Münzberg H, Morrison CD (2017) Blaming the brain for obesity: integration of hedonic and homeostatic mechanisms. Gastroenterology 152(7):1728–1738 Molé PA (1990) Impact of energy intake and exercise on resting metabolic rate. Sports Med 10(2):72–87 Monteleone P, Scognamiglio P, Monteleone AM, Perillo D, Canestrelli B, Maj M (2013) Gastroenteric hormone responses to hedonic eating in healthy humans. Psychoneuroendocrinology 38(8):1435–1441 Zipfel S, Giel KE, Bulik CM, Hay P, Schmidt U (2015) Anorexia nervosa: aetiology, assessment, and treatment. Lancet Psychiatry 2(12):1099–1111

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History of Bariatric and Metabolic Surgery Christine Stier

The causes of the “obesity epidemic” are still not fully understood. Obviously, in most cases—with the exception of monogenic syndromes—there is an individual multifactorial genesis, which includes a genetic predisposition as well as an individual, personal “obesogenic environment.” Even though obesity has been recognized as a chronic disease by the World Health Organization since 2000 and a resolution of the European Parliament from February 2006 called on its member states to officially recognize “obesity” as a chronic disease, there is still considerable stigmatization of patients. “Laziness,” “gluttony,” “excessiveness,” and “lack of discipline” are just a few of the discriminatory characteristics that are often attributed to patients with obesity. A connection through the influences of both a secular and a clerical centuries-long world view of “simple folk” who had to be frugal must remain open Nevertheless, there are deeply rooted prejudices regarding patients with obesity in our modern world today. 

Important  Owing to deeply rooted prejudices toward the affected patients, awareness of the chronic disease obesity is still very limited today. Self-blame is still assumed and thus the responsibility for therapy is passed back to the affected patients.

Similarly, the first surgeons who dealt with the surgical treatment of obesity were a fringe group within surgery. At that time, there was no effective conservative therapy and so-called “starvation diets,” even for children, were routinely applied therapy approaches

C. Stier (*)  University Hospital Mannheim, Division of Interdisciplinary Endoscopy, Mannheim, Germany

© The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 C. Stier and S. Chiappetta (eds.), Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients, https://doi.org/10.1007/978-3-662-66436-0_2

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in the 1960s and in the following years. These were notoriously largely unsuccessful and retrospectively represented a torturous ordeal. As early as the 1950s, the first surgical approaches to treating obesity came about. The idea of a possible mode of action was mechanically simple and knowledge about the physiology of the small intestine and especially the liver had not yet been gained. There were and are a variety of operative procedures that were used for surgically induced weight reduction. Therefore, a historical review up to the development of the current standard procedures should be done first. This and the following chapter are intended to describe the anatomical and surgical basis in detail, in order to contribute to the understanding of possible complications after bariatric surgery. 

Important  The first bariatric operations developed as early as the 1950s, because conservative therapies were not successful. The simplified mechanical idea at that time corresponded to the idea of being able to influence the quantity of nutrient absorption by a surgical modification of the gastrointestinal tract, to limit it, and thereby to achieve a weight reduction.

2.1 Historical Malabsorptive Procedures The discussion of surgical treatment options for obesity by altering the gastrointestinal tract—as opposed to removing subcutaneous, excess fat tissue—began as early as the early 1950s with the description of a small bowel resection of 105 cm with subsequent anastomosis by Viktor Henrikson of Gothenburg, Sweden (1952). This pioneering achievement preceded the publication of Kremers—who described an intestinal bypass as a surgical procedure—by 2 years. This was thus the first documented attempt at an abdominal surgery procedure with the aim of achieving weight loss, although it was unsuccessful in the long term as a therapy for obesity. Henrikson did not describe the exact location of the performed resection. However, he mentioned that the patient was 2 kg heavier 14 months after the operation than after the strict preoperative diet, which was discontinued owing to failure (Cowan 1994). Apparently, it corresponded to the idea at that time that the excessive food intake of patients with obesity (hyperphagia, hyperalimentation) could not be influenced surgically, and therefore rather a significant reduction of the absorption tract of the ingested food (malabsorption) in the small intestine had to lead to the desired therapeutic goal. Based on this idea, mainly so-called malabsorptive procedures in the form of a shortening of the small intestine by a bypass procedure (Fig. 2.1) (Kral 1987) developed over the years.

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Fig. 2.1   Jejuno-ileal bypass: Surgically induced short bowel syndrome to induce malabsorption. (From Elder KA, Wolfe BM. Bariatric surgery: a review of procedures and outcomes. Gastroenterology. 2007 May;132(6):2253–71)

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Important Hyperalimentation was considered not to be surgically or mechanically influenceable. Therefore, initially malabsorptive procedures were developed, which were supposed to quantitatively reduce the absorption of food energy in the small intestine.

Jejuno-ileal bypass Various variations of the jejuno-ileal bypass were first described in the 1960s. These procedures were applied more frequently in the late 1960s and early 1970s. As little as possible of the ingested food should be absorbed, in order to be able to reduce the weight, despite hypothetically persistent hyperalimentation. Variable intestinal lengths were excluded from the food passage, which often comprised up to 90–95% of the entire small intestine, with all the resulting pathophysiological consequences. At that time, the popularity of these interventions was based on the one hand on the fact that no other surgical procedures were available, and on the other hand on the fact that partly highly significant weight losses were achieved, albeit associated with considerable morbidity and mortality. The complications that these interventions generated included the entire picture of a manifest short bowel syndrome with electrolyte disturbances, fluid loss, an exudative enteropathy, kidney stone formation and failure, steatorrhea, and often also an often fatal liver failure (Gay and Peters 1980). In addition, these bariatric surgical procedures were still performed with open surgical access—laparoscopy had not yet been established. This also contributed significantly to the high morbidity of the operations. These complications finally ended the era of the jejuno-ileal bypass as a bariatric surgical concept, and at the same time the idea that a pronounced malabsorption represented the only approach to surgical therapy for obesity. This showed again that until the 1980s, there was not enough medical knowledge about the pathophysiology of the development of obesity, or about the physiology and pathophysiology of the gastrointestinal tract.

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Important  The jejuno-ileal small bowel bypass was a first but complication-prone surgical therapy approach to the treatment of obesity. A short bowel syndrome was created iatrogenically.

2.2 Historical Restrictive Procedures The high complication and mortality rate of the jejuno-ileal bypass led to new considerations. Now, turning away from the small intestine, the stomach became the target organ for surgery, and a number of new procedures developed, which were aimed at reducing the (functional) gastric volume as a therapeutic option. Gastric Partitioning With the so-called gastric partitioning, the stomach was supposed to be anatomically modified without resecting any organ parts (Pace et al. 1979). The purpose of this procedure was now rather to reduce the food intake itself, instead of limiting its absorption in the small intestine as before. For this purpose, a small gastric pouch (foregut) was formed above a transverse, two-row staple line. Since staplers with a prefabricated suture gap were not available at that time, three staples were removed from the available staplers (TA90 or TA 55 from Autosuture®) in the middle, in order to ensure a standardized passage from the gastric pouch to the rest of the stomach with 9 mm (18 French). This transverse staple line was performed above the vasa gastricae brevis (Fig. 2.2).

Fig. 2.2   Original images of gastric partitioning: removal of three staples (9-mm suture gap) from the TA90 and then transverse “stapling” of the stomach above the vasa gastricae brevis, leaving a 9-mm passage from the gastric pouch to the rest of the stomach. (From Pace WG, Martin EW Jr, Tetirick T, Fabri PJ, Carey LC. Gastric partitioning for morbid obesity. Ann Surg 1979; 190: 392–400)

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It quickly became apparent that this measure was very prone to failure owing to frequent staple-line ruptures and stretching of the separated gastric segments (gastric partitioning) and therefore did not lead to the desired therapeutic goal in a sustainable way. 

Important  Gastric partitioning was one of the first surgical procedures to achieve weight reduction by limiting food intake. For this purpose, the stomach was segmented transversely into a small upper (pouch) and a large lower part with a staple line, connected by a central, standardized passage in the staple row.

Vertical gastroplasty according to Mason The logical further development led to vertical gastroplasty with band reinforcement (vertical banded gastroplasty—VBG). In this procedure, a central punch-out of the gastric corpus was first performed with a circular stapler. From there, in a vertical direction, parallel to the lesser curvature, undivided staple lines were made cranially to the angle of His. Around the lesser curvature and by the passage of the circular stapler, a reinforcing band or alternatively a mesh could be inserted, in order to create an alloplastic stoma and effect reinforcement (Fig. 2.3), with the intention of counteracting a stoma dilation. The VBG, an obesity surgical procedure that was performed exclusively on the stomach, again with the aim of reducing the food energy intake (restriction), was mainly performed in the 1980s. However, this procedure also showed only insufficiently sustainable results regarding weight reduction and stabilization, or there was often a weight regain. Fig. 2.3   Vertical banded gastroplasty (VBG)—vertical gastroplasty with a band: four vertical staple lines with stoma modification at the lower end of the suture line and reinforcement by a band (or alternatively a Prolene mesh)

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Despite the four applied staple lines, frequent staple line ruptures occurred. The also not infrequently observed stenosis of the stoma—possibly triggered by the implanted foreign body—led to an increase in the intraluminal pressure in the gastric pouch and thus represented one of the possible causes of a staple line rupture (Fig. 2.4). 

Important The vertical gastroplasty corresponds to a functional, partial sleeve

gastrectomy without resection of gastric parts. The lower end of the suture line was reinforced by a band or a mesh (alloplastic material). This operation was still mostly performed with open access. Adjustable gastric band A gastric band—placed in the area below the cardia of the otherwise surgically unchanged stomach—was another purely restrictive procedure. The first gastric band implantations were performed as early as the 1960s. In 1986, Kuzmak introduced the so-called adjustable gastric band into obesity therapy. The first laparoscopic implantation was performed in 1993 in Belgium by Belachew. In the 1990s and at the beginning of the 2000s, the adjustable gastric band had its heyday (Fig. 2.5). Initially, there was great enthusiasm, especially because of the low perioperative mortality (0.1%) and morbidity in combination with a significant achievable weight loss of an average of up to 22% (O’Brien et al. 1990). Today, the indication for gastric band implantation is rarely given. This is mainly because of a documented high rate of late complications. These include so-called slippage (displacement of the band) and migration (ingrowth of the band into the gastric wall). Both usually lead to its explantation. 

Important The adjustable gastric band had a low perioperative morbidity and mortality, but because of slippage and migration, a high rate of late complications. Overall, this procedure generated less weight loss than today’s standard procedures.

Fig. 2.4   Regular representation of a vertical gastroplasty (VBG) on a barium swallow X-ray (left). Stenosis of the stoma of a VBG (middle): pressure increase in the gastric pouch with dilation (threedimensional representation with computed tomography). Endoscopic retrograde view of a VBG (right)

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Fig. 2.5   Adjustable gastric band. Image: loan IFSO, Atlas of Bariatric and Metabolic Surgery. Placing the band just below the cardia of the stomach. Adjustability of the stoma diameter by filling (blocking) or emptying the silicone pads of the band via a subcutaneously placed port (b)

2.3 Historical Combined Procedures Combined procedures merge the effects of a volume reduction of the stomach (restriction) with the exclusion of the duodenum and varying lengths of the adjoining small intestine. Biliopancreatic diversions (BPD) A renewed relapse into a more pronounced, iatrogenically created malabsorption were the two biliopancreatic diversions. These operations were classified in a separate category. Nevertheless, they are in the broadest sense bypass procedures, because the gastric volume is reduced and the duodenum and a long adjoining small intestinal segment are excluded from the food passage by diversion (bypass). The two biliopancreatic operations differ mainly in the shape of the gastric pouch. The proximal duodenum was closed blindly and the stomach subtotally resected to a residual volume of about 200 ml (BPD according to Scopinaro), or alternatively shaped as a sleeve gastrectomy (BPD with duodenal switch, BP-DS). The reconstruction of the food passage is done in both cases according to Roux-en-Y (Fig. 2.6). A significant difference compared with the common bypass procedures is the technique of intraoperative measurement of the small intestine. Although the small intestine is always measured from the ligament of Treitz distally in the bypass procedures, this measurement is done distally—from the Bauhin’s valve—cranially in a biliopancreatic diversion. This alternative approach to measuring the intestine justified the independent procedure classification as BPD.

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Fig. 2.6   Biliopancreatic diversion according to Scopinaro—BPD (left), biliopancreatic diversion with duodenal switch—BPD-DS (right). Images: loan IFSO, Atlas of Bariatic and Metabolic Surgery.

Below the entero-enterostomy, food transported in the alimentary limb (intestinal segment from the stomach to the entero-enterostomy) meets the digestive juices transported in the biliopancreatic limb (intestinal segment from the duodenum to the entero-enterostomy). The small intestinal segment distal to this rendezvous point (distal anastomosis) is called the “common channel.” Only from here can fats, proteins, and complex carbohydrates be digested. This common channel measures 50 cm in the classic BPD Scopinaro and 75–100 cm in the BPD-DS. Technically, the position of this entero-entero-anastomosis in the area of the ileum is first marked with a thread. Then, the directly adjacent segment of the alimentary limb is further measured cranially, 200 cm in both procedures. Subsequently, the small intestine (common channel plus alimentary limb) is transected. The often very long biliopancreatic limb is not measured. Its length ultimately depends on the individual total small intestinal length. Both procedures are pronounced malabsorptive operations, often with the consequences and complications of an iatrogenically created short bowel syndrome. These procedures were initially performed with open surgical access, but later also with minimally invasive access after the establishment of laparoscopy. The biliopancreatic diversions differed mainly in the form of the reduced stomach. The fully absorbable small intestine (common channel) measures 50 cm in the BPD Scopinaro, 75–100 cm in the BPD -DS. Both procedures thus have a strong malabsorptive effect.

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Gastric bypass procedures Parallel to this, the so-called bypass procedures were developed. Here, a small pre-stomach (pouch) was first formed to achieve a reduction in food intake or an early feeling of satiety. Added to this restrictive part of the operation was a diversion of the food directly into deeper sections of the small intestine, bypassing the rest of the stomach, the duodenum (duodenal exclusion), and varying lengths of subsequent jejunum sections. The length of the biliopancreatic limb is measured from the ligament of Treitz (classically 50–60 cm). The small intestine is then transsected. After anastomosis of the gastro-jejunostomy (pouch-jejunostomy) the alimentary limb is measured from the stomach (classically 150 cm). In this position, the introduction (anastomosis) of the biliopancreatic limb takes place. A measurement of the common channel is not performed for bypass procedures. Today, these measurements are often applied inversely (alimentary limb 60 cm, biliopancreatic limb 150 cm). At that time, the shape of the gastric pouch (Fig. 2.7a) and the reconstruction following the formed gastric pouch (Fig. 2.7b) with the small intestine (Billroth II versus Roux-

Fig. 2.7   Development and different forms of the gastric bypass: a non-divided gastric bypass; b gastric bypass with transverse transsection of the stomach (according to Mason), c retrocolic reconstruction, d antecolic reconstruction

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en-Y reconstruction) (Mason 1967) were not standardized. The small intestine section that had to be pulled up for the reconstruction of the passage to the gastric pouch could also be led dorsal of the colon (retrocolic, Fig. 2.7c) or ventral of the colon (antecolic) upward (Fig. 2.7d). Today, an antecolic transposition of the small intestine is performed as standard. 

Practical tip  Of the historical procedures, one can still encounter a vertical gastroplasty and rarely also a biliopancreatic diversion. Knowledge of both procedures is therefore essential in the follow-up, as both interventions can lead to significant long-term complications. A VBG should be safely recognized endoscopically, as well as a possible staple-line rupture (weight regain) or a stoma stenosis (recurrent vomiting). Long-term complications of a BPD/ BPD-DS (iatrogenic short bowel syndrome) often appear as an almost unsolvable problem. More common, however, is a n implanted gastric band. Also, a migration (ingrowth into the gastric wall) or a slippage (sliding of the band, possibly with significant pressure on the gastric wall) should be classified.

2.4 Development of Guidelines A milestone from the historical procedures to modern bariatric surgery was set by Wittgrove, who performed a gastric bypass laparoscopically for the first time in 1994. This led to a fundamental reduction of morbidity in bariatric surgery by avoiding the complete opening of the abdomen in patients with obesity—a patient group with an already significantly increased intra- and perioperative risk (heat and fluid loss, wound-healing disorders, reduced intraoperative overview, pronounced comorbidities). Another turning point had already been reached in March 1991, when the National Institute of Health (NIH) convened an interdisciplinary consensus conference and drafted the first guidelines for the use of visceral surgical procedures in obesity therapy (Consensus Statement 1991), which largely still apply today: Overview

Summary of the NIH guidelines of 1991 • Patients who are seeking an effective therapy for severe obesity for the first time should first participate in a nonsurgical program that includes a dietary change, an exercise therapy, and a behavior modification. • Restrictive or bypass procedures “can be considered for well-informed and motivated patients, with acceptable operative risks.”

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• Candidates for surgical therapy should be examined by a multidisciplinary team. • The operation should be performed by an experienced surgeon in an appropriate clinical setting. • A lifelong medical follow-up after a surgical therapy is “a necessity.” • Specific criteria for a surgical intervention were patients with a body mass index (BMI) > 40 kg/m2 as well as patients with a BMI of 35–40 kg/m2 with comorbidities that result in a high risk, such as cardiopulmonary diseases, severe diabetes, or physical complaints that severely impair the patient’s life, or quality of life (e.g., employability, family, physical independence).

Comparing this consensus of 1991 with the indications of the current S3 guideline 2018: “Surgery of obesity and metabolic diseases of the German Society for General and Visceral Surgery” (DGAV 2018), shows how visionary the NIH consensus conference 1991 already was. Excerpt from the S3 guideline 2018: Surgery of obesity and metabolic diseases The indication for a bariatric surgical procedure is given under the following conditions: 1. In patients with a BMI ≥ 40 kg/m2 without comorbidities and without contraindications, a bariatric surgical operation is indicated after exhaustion of conservative therapy and comprehensive education. 2. Patients with a BMI ≥ 35  kg/m2 with one or more obesity-associated comorbidities such as type 2 diabetes mellitus, coronary heart disease, heart failure, hyperlipidemia, arterial hypertension, nephropathy, obstructive sleep apnea syndrome (OSAS), obesity hypoventilation syndrome, Pickwick syndrome, non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH), pseudotumor cerebri, gastroesophageal reflux disease (GERD), asthma, chronic venous insufficiency, urinary incontinence, immobilizing joint diseases, impairment of fertility, or polycystic ovarian syndrome should be offered a bariatric surgical operation if conservative therapy is exhausted. 3. Under certain circumstances, a primary indication for a bariatric surgical procedure can be made without prior conservative therapy success. The primary indication can be made if one of the following conditions is met: Patients with a BMI ≥ 50 kg/m2. Patients for whom a conservative therapy attempt was assessed by the multidisciplinary team as not promising or hopeless. Patients with particularly severe comorbidities and sequelae that do not allow a surgical procedure to be delayed.

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C. Stier Summary

• From initially purely malabsorptive procedures, bariatric surgical techniques historically developed toward pure restriction and finally to the combination of both principles. • Both the NIH guidelines of 1991 and the almost simultaneous introduction and establishment of laparoscopy led bariatric surgery to grow into the modern era. This ultimately led to the academic attention and recognition that this field had long been denied.

References Consens Statement (1991) Gastrointestinal surgery for severe obesity. 25–27;9(1):1–20 Cowan GSM (1994) Commentary on Henrikson, V. Can small bowel resection be defended as therapy for obesity? Obes Surg 4:54 Deutsche Gesellschaft für Allgemein- und Viszeralchirurgie (DGAV) (2018) S3-Leitlinie: Chirurgie der Adipositas und Metabolischer Erkrankungen Gay TR, Peters RL (1980) Death from hepatic failure as a late complication of jejunoileal by-pass. Am J Gastroenterol 73(2):150–153 Henrikson V (1952) Is small bowel resection justified as treatment for obesity? Nordisk Med 47:744 Kral JG (1987) Malabsorptive procedures in surgical treatment of morbid obesity. Gastroenterol Clin N Am 16:293–305 Mason EE, Ito C (1967) Gastric bypass in obesity. Stlrg Clin N Am 47:1345–1351 O’Brien PE, Hindle A, Brennan L, Skinner S, Burton P, Smith A, Crosthwaite G, Brown W (2019) Long-term outcomes after bariatric surgery: a systematic review and meta-analysis of weight loss at 10 or more years for all bariatric procedures and a single-centre review of 20-Year outcomes after adjustable gastric banding. Obes Surg 29:3–14 Pace WG, Martin EW Jr, Tetirick T, Fabri PJ, Carey LC (1979) Gastric partitioning for morbid obesity. Ann Surg 190:392–400

3

Current Standard Procedures of Bariatric and Metabolic Surgery Christine Stier

Despite the decades of experience and accumulated knowledge about the mode of action of bariatric and metabolic surgery, the original simplifying terms “restriction” and “malabsorption” have not been completely abandoned. Procedures are still classified according to these principles of action. Today, perhaps even more than ever, it has become clear that especially the loss of restriction (regain of gastric volume) inevitably leads to weight regain. The term malabsorption, on the other hand, is more difficult, as the physiology of the duodenum and the small intestine must be taken into account. The next chapter is mainly dedicated to this topic in detail. It is mentioned here, because currently in a few centers and in selected patients highly malabsorptive operations are still performed, which, however, cannot be included in the category of standard procedures applied today. Therefore, at the end, the procedure that is currently the most popular of these, the SADI-S—a new representative of the BPD—is presented. 

Important  Bariatric surgery is now mandatorily laparoscopic. A change to an open surgical approach is only done in an emergency.

Currently, three operations have emerged as the bariatric surgery standard: sleeve gastrectomy (SG), Roux-en-Y gastric bypass (RYGB) and one anastomosis/mini gastric bypass (OAGB/MGB), which will be discussed in more detail in the following sections.

C. Stier (*)  University Hospital Mannheim, Division of Interdisciplinary Endoscopy, Mannheim, Germany © The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 C. Stier and S. Chiappetta (eds.), Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients, https://doi.org/10.1007/978-3-662-66436-0_3

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3.1 Sleeve Gastrectomy (SG) The SG has evolved from being the first step of the biliopancreatic diversion with duodenal switch (BPD-DS) into an independent procedure (Fig 3.1). This major intervention (BPD-DS) was performed especially in patients with so-called super-obesity as a multistep procedure (two-time). Thus, first the restrictive SG was performed, and then, with an interval—after the patients had already lost weight quantitatively owing to the restriction on the stomach and thus could reduce their surgical risk quantitatively as well— the highly malabsorptive duodenal switch was performed. A particular proponent of the BPD-DS was Michel Gagner (Canada), who also engaged in the SG (Ren et al. 2000; Feng and Gagner 2002). Since then, the SG has embarked on worldwide triumph and has become established owing to the seemingly simple technical implementation and is currently the most fre-

Fig. 3.1   Sleeve gastrectomy (SG) is a resecting procedure; the largest part of the stomach is removed along its longitudinal axis. (Image: loan IFSO: Atlas of Bariatric and Metabolic Surgery)

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quently performed bariatric surgical procedure. As steep as the learning curve of the actual operation seems, the therapy of the resulting complications has proved just as complicated. Directly or indirectly, these operation-specific complications are mostly due to the increased intraluminal pressure in the gastric sleeve.  Important  The most frequently performed bariatric surgical procedure worldwide

is currently the sleeve gastrectomy.

3.1.1  SG—Specific Indications The SG is a predominantly restrictive operation that is performed exclusively on the stomach. There is no change in the intestinal tract and the stomach and duodenum are still endoscopically visible naturally. This results in an indication for patients with obesity whose gastrointestinal tract must remain endoscopically assessable, such as in the case of simultaneous Crohn’s disease or a significant familial (genetic) predisposition for gastric malignancy. Proponents of the SG postulate an equivalent remission of comorbid type 2 diabetes mellitus (Peterli et al. 2018). Indeed, this seems a question that may be answered with a talent for statistical calculation, as opponents found lower remission rates after SG than after RYGB (Peterli et al. 2018; Laferrère and Patou 2018; Baud et al. 2016; Diabetes Research Network 2012). In particular, after SG, the improvement of the glycemic metabolic situation seems to occur synchronously with the weight reduction. However, it is completely beyond question that the SG leads to a highly significant weight loss and thus, together with all bariatric surgical procedures, represents the most effective available therapy for comorbid type 2 diabetes mellitus.  Important  After an SG, an endoscopic intervention, e.g., as in the case of an

obstructing choledochus stone, is always possible naturally. In principle, gallstone formation is about 20% more common in the context of weight reduction, regardless of whether it was achieved by diet or by surgery.  Important  A significant weight reduction has a curative effect on obesity-associ-

ated comorbidities. A relative contraindication for the SG is gastroesophageal reflux disease (GERD). The drastic reduction of the diameter of the stomach leads to an increase in intraluminal pressure, which is also manometrically detectable, as well as the fact that the esophagus has to swallow against a much higher pressure postoperatively (Yehoshua et al. 2008). This led to the term “High Pressure System” for the SG. Nevertheless, there are a few authors who postulate a postoperative improvement of preoperative acid reflux, apparently due to the reduction of the acid-producing parietal cells (Stenard and Iannelli 2015). The vast

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majority of bariatric surgeons and long-term experience, however, confirm the relative contraindication of GERD (Melissas et al. 2015; Gagner et al. 2016).

3.1.2 SG—Procedure  Important  The indication for SG in patients with manifest gastroesophageal

reflux disease should only be made in absolutely exceptional cases and after meticulous patient education, such as in cases of pronounced abdominal adhesions or comorbid Crohn’s disease. First, the preparation of the left diaphragmatic crus is performed with transection of the suspension of the cardia in the His angle. The treatment of a coexisting hiatal hernia is recommended and can therefore (but does not have to be), done immediately (Samakar et al. 2016). Then, the greater curvature is dissected, starting opposite the incisura and cranially, cutting through the short gastric vessels and detaching from the spleen, up to the left diaphragmatic crus. The adhesions on the dorsal side of the stomach are also freed, so that the entire stomach is mobile from the right side. Then, the preparation is completed distally. Finally, before the actual resection, a thick gastric tube is inserted as a calibration bougie (usually 36–40 Charrière ≘ 12–13.33 mm) along the lesser curvature of the stomach up to the antrum. This is particularly aimed at ensuring that the tube is not too tight overall, but especially at the so-called angulus fold and at the esophagogastric junction, enough lumen remains. The actual resection then begins about 5–6 cm proximal to the pylorus with the stapler. Depending on the thickness of the gastric wall (thicker in the antrum), cartridges with different stapler heights are used. The most proximal and thus the last cartridge, which has to be placed between the diaphragmatic crus and the spleen, often poses a challenge. Depending on the surgeon and the school, an additional suture of the staple line may then be performed, or a staple line reinforcement may have been applied directly to the used stapler cartridges. In the context of an over-suturing, the dissected omentum can then also be fixed to the proximal sleeve gastrectomy as an omentoplasty. Here, opinions differ and discussion is still open as to which approach is most effective (Shikora and Mahoney 2015). Finally, the resected part of the stomach (80–90% of the original volume) is removed from the abdomen. Outside the surgical field, the filling of the resectate with saline is done to determine the removed volume. After releasing the capnoperitoneum, the trocar incision sites (depending on the technique) (Peterli et al. 2018; Laferrère and Patou 2018; Baud et al. 2016) are closed again (Fig. 3.1).

3.1.3  SG—Typical Specific Perioperative Risks The Achilles heel of the SG is found at the proximal end of the staple line in the area of the angle of His. If a staple line leakage occurs (Figs. 3.2 and 3.3), it is found here in over 85% of cases. Such an SG leakage can occur directly postoperatively, or somewhat

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Fig. 3.2   Endoscopic representation of a chronic sleeve gastrectomy leakage in the angle of His: Small insufficiency pore with underlying abscess

Fig. 3.3   Endoscopic representation of a chronic sleeve gastrectomy leakage in the angle of His: Large dehiscence with visible intraabdominal abscess cavity

delayed, so that depending on the timing of occurrence, early leakage within the first week and late leakage after the first postoperative week are defined. Early postoperative complications: Functional angulus stenosis and SG leakage It was shown as early as the early 2010s that the leakage rate depends on the diameter of the calibration bougie used intraoperatively, and thus ultimately on the remaining diameter of the sleeve gastrectomy (Aurora et al. 2012), and therefore indicates the pressure-induced genesis of the complication. A calibration bougie with a diameter of 40 Charrière led to a significantly lower rate of leaks of only 0.6% than thinner calibration probes with a corresponding leakage rate of 2.8%. In particular, there is a risk of generating a pointed reduction of the lumen diameter at the level of the angulus fold (Fig. 3.4). This would then possibly lead to a so-called functional angulus stenosis. A functional stenosis can be passable with the endoscope. Such an artificial constriction at the anatomically and functionally important transition

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Fig. 3.4   Endoscopic and three-dimensional CT-graphic representations of functional angulus stenoses

from the gastric corpus to the antrum leads to “pressure turbulence” between these two functional subunits of the stomach (Fig. 3.5). A brief excursion into the physiology of gastric emptying can underline the impact of such a narrowing in the area of the angulus fold. The pylorus determines and limits the amount of food per emptying portion that is delivered from the stomach to the duodenum. To transport back excess food volume (Excess Volume) that is to be returned from the prepyloric area to the corpus for further mixing, the antrum must be able to generate a strong retropulsion (Berry et al. 2016). It is suspected that a relative narrowing at the angulus fold with these retropulsive contractions creates a kind of chimney effect, whereby the resulting pressure gradient is directed proximally toward the angle of His (Berry et al. 2016) (Fig. 3.5). In this way, the intraluminally altered anatomy puts the proximal end of the staple line “enormously under pressure.” A possible additional impairment of blood supply in the area of the angle of His due to the greater curvature-

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Fig. 3.5   Model of the development of a sleeve gastrectomy leakage

Fig. 3.6   Endoscopic and three-dimensional CT-graphic image of a functional angulus stenosis with subsequent resulting (paraesophageal) hiatal hernia (arrows)

side vessel dissection may be another possible attribute (Gomes et al. 2009; Natoudi et al. 2014), so that finally the staples of the suture line give way and a leakage occurs. 

Important  Resulting symptoms of a functional stenosis or narrowing at the angulus fold vary from reflux and chronic vomiting, possible dysphagia, from the pressure-generated development of a hiatal hernia (Fig. 3.6) to the development of a sleeve gastrectomy leakage (incidence in Germany: 70 cm) in the Roux-Y reconstruction. In both bypass operations, the pyloric function, and thus the natural, muscular valve at the gastric outlet, is no longer to pass and function. Thus, with an Ω-loop reconstruction, at least hypothetically, a bile reflux proximally is not reliably prevented, because the afferent, and thus digestive secretion-transporting small intestinal loop, is anastomosed directly below the gastric construction and without a muscular valve mechanism. Opponents of the method attribute a potential carcinogenicity to the procedure in the case of quantitative bile reflux into the esophagus. However, this has not been proven to date. The OAGB/MGB, on the contrary, has in the mean time developed globally into the third most common obesity operation (Fig. 3.9), because it can be performed quickly and safely with only one anastomosis on a relatively long, tubular gastric pouch.

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Fig. 3.10   Combined procedure (restrictive and malabsorptive): Creation of a relatively long, tubular gastric pouch, elevation of a distal jejunal loop as a biliopancreatic limb (green) to the pouch, and creation of a pouch-jejunostomy (150–200 cm). Distal to the anastomosis, the remaining small intestine forms the so-called common channel (visceral surgical nomenclature: efferent loop). Food is mixed directly below the gastric pouch with digestive juices from the afferent loop. (Image: Courtesy of IFSO: Atlas of Bariatric and Metabolic Surgery)

3.3.1  OAGB/MGB—Specific Indications The OAGB/MGB acts with its long biliopancreatic loop (green; 150–200 cm) much more malabsorptively than the classic RYGB. In addition, only one singular anastomosis has to be performed on the gastric pouch in this operation. This already results in the first specific indication.

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In patients with super-obesity (BMI > 50 kg/m2), the performance of an RYGB is technically often extremely challenging, especially if there is a pronounced abdominal fat accumulation (android fat distribution type). As a result, the intraabdominal space is extremely limited by a strong omentum and mesentery and the usually encountered hepatomegaly. This makes the performance of an entero-enterostomy very difficult, as it naturally comes to lie in the left mid or lower abdomen in the RYGB.  Important  A significant technical simplification is offered in a cramped anatomi-

cal situation by the OAGB/MGB, as the surgery has to be performed only on the stomach in the upper abdomen. This is usually technically possible even with very limited space conditions in patients with hepatomegaly and high-volume omentum (super-obesity) with laparoscopic access. Before the OAGB/MGB, the only alternative surgical procedure under such conditions was the SG and a multi-step procedure with further interventions had to be planned initially.  Important  Owing to the more pronounced malabsorption of the OAGB/MGB,

many authors see an advantage in the more significant weight reduction that can be achieved with this intervention. Likewise, the described higher diabetes remission rates are assessed as advantageous (Ruiz-Tovar et al. 2019; Castro et al. 2020). This leads to the further specific indication—as already mentioned and analogous to the RYGB—namely the surgical treatment of patients with obesity and a comorbid type 2 diabetes mellitus in the sense of a metabolic operation. The OAGB/MGB, owing to the exclusion of the remnant stomach, as well as the RYGB, puts the pylorus out of action and thus also represents a so-called low-pressure system. Thus, gastroesophageal reflux is not a hard contraindication, because the acid formed in the pouch can theoretically flow unhindered into the small intestine. The second, more significant component of a GERD, however, is the incompetent function of the lower esophageal sphincter (LES), which is supposed to prevent the reflux of stomach contents into the esophagus. If an incompetent LES is present, one should at least carefully consider the indication of an OAGB/MGB to prevent bile reflux. Bile in the gastric pouch is unproblematic and is routinely observed. Ascending bile reflux into the esophagus, on the other hand, is assessed as being more problematic.  Important  A strict contraindication, on the other hand, is a lack of patient com-

pliance regarding the lifelong necessary vitamin and mineral supplementation (chapter X). Owing to the pronounced malabsorptive character of the operation, supplementation can never be discontinued without leading to pronounced, possibly life-threatening vitamin and mineral deficiencies.

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3.3.2 OAGB/MGB—Operative Procedure At a distance of 15 cm (versus 5 cm for RYGB) aborally from the esophago-gastric junction and below the lowest pes anserinus branch (crow’s foot), the entry into the omental bursa is performed on the lesser curvature side. Here, the stomach is then stapled off with a 45-mm cartridge (versus 30 mm for RYGB). The placement of the second cartridge is parallel to the greater curvature and in the direction of the spleen. Also for OAGB/MGB, the calibration of the pouch is performed in most cases with a 36 Charrière (1.2 cm) gastric tube. Parallel to this tube, completion is performed cranially until the complete separation from the remnant stomach, resulting in a tubular, approx. 50 ml (versus 25 ml for RYGB) gastric pouch. In the correct technique, the pouch formation of the OAGB uses as many staple cartridges as the SG. Subsequently, the distal end of the pouch is opened by approx. 1 cm. From the ligament of Treitz, the jejunum is then measured (150/200 cm). A corresponding, mobile jejunal loop is brought up tension-free antecolic and antegastric to the gastric pouch. The biliopancreatic limb (afferent limb) lies on the left and the common channel (efferent limb) on the right. In this position, the linear stapler anastomosis is performed with a 45-mm cartridge (additional anastomosis compared with RYGB). The calibration tube is now advanced into the small intestine and the anastomosis is completely closed ventrally by laparoscopic, continuous suture by hand.

3.3.3 OAGB/MGB—Typical Specific Perioperative Risks The specific perioperative risks are similar to those of RYGB, but the probability of a stricture is lower for OAGB/MGB than for RYGB owing to the wider anastomosis. A specific perioperative risk arises with the OAGB/MGB owing to the relatively distal opening of the omental bursa and the formation of the gastric pouch from here. Two cartridges are placed so that a slightly widened, wedge-shaped base results, which resembles the hood of a cobra and is therefore named after it—the so-called cobra head (Fig. 3.11). When placing these two cartridges in the area of the transition from gastric corpus to gastric antrum, care must be taken that the second cartridge is not pushed too close to the greater curvature and thus cause an outflow obstruction in the remnant stomach (Fig. 3.11). The resulting relatively rapid symptomatology would resemble that of a remnant stomach dilation in RYGB. This situation would require immediate surgical correction. In the early days of this surgical procedure, the pouch was often made too wide, resulting in a relatively large pouch volume with significant residual acid production. Anastomotic and small bowel ulcerations could therefore develop even in the perioperative phase. Today, with the defined, narrow and tubular pouch, this is a much less frequent event than 5–6 years ago.

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Small-curvature-sided vascular supply "crow's foot"

Co d ea

aH

br

Fig. 3.11   OAGB/MGB with illustration of the dissection line, starting with the “cobra head” and the subsequent vertical suture line. The red arrow indicates the distance that must be observed to prevent outflow obstruction of the remnant stomach

Comparison of the three surgical procedures: diabetes remission (Laferrère and Patou 2018) SG (n = 83)

RYGB (n = 152)

OAGB/MGB (n = 123)

1 year

81.9%

83.6%

91.9%

2 years

79.5%

83.6%

91.9%

5 years

75.9%

80.3%

89.4%

Comparison of the three surgical procedures: BMI (Laferrère and Patou 2018) SG (n = 83)

RYGB (n = 152)

OAGB/MGB (n = 123)

Baseline BMI

43.5 ± 10.2

44.1 ± 11.6

42.1 ± 11

1 year

31.3 ± 7.2

30.4 ± 6.9

24.7 ± 5.8

2 years

29.4 ± 5.7

28.8 ± 5.2

24.8 ± 5.3

5 years

32.4 ± 5.7

30.9 ± 5.9

25.9 ± 5.9

3  Current Standard Procedures of Bariatric and Metabolic Surgery

39

3.4 SADI-S, a Malabsorptive Surgical Procedure: SingleAnastomosis Duodeno-Ileal Bypass with Sleeve Gastrectomy The SADI-S (Fig. 3.12) is by definition a biliopancreatic diversion. The classic BPD procedures were already presented in the chapter on historical procedures. In contrast to the two known BPDs, the SADI-S has a loop reconstruction (Ω-reconstruction) and the common channel is significantly longer. Initially, it was 200 cm. However, even with this

Fig. 3.12   SADI-S: Modification of the BPD-DS with postpyloric Billroth II (loop-) anastomosis. The common channel was initially 200 cm and is now recommended to be 300 cm. (Image: Courtesy of IFSO: Atlas of Bariatric and Metabolic Surgery)

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length, significant deficiencies could still be detected, so it was first extended to 250 cm and finally to 300 cm, in order to avoid symptoms of an iatrogenic short bowel syndrome (Felsenreich et al. 2021).

References Aurora AR, Khaitan L, Saber AA (2012) Sleeve gastrectomy and the risk of leak: a systematic analysis of 4,888 patients. Surg Endosc 26(6):1509–1515 Baud G, Daoudi M, Hubert T, Raverdy V, Pigeyre M, Hervieux E et al (2016) Bile diversion in Roux-en-Y gastric bypass modulates sodiumdependent glucose intestinal uptake. Cell Metab 23:547–553 Berry R, Miyagawa T, Paskaranandavadivel N et al (2016) Functional physiology of the human terminal antrum defined by high-resolution electrical mapping and computational modeling. Am J Physiol Gastrointest Liver Physiol 311(5):G895–G902 Burla L, Weibel P, Baum C, Huber M, Gürtler T, Weber M (2020) Linear versus circular stapler for gastrojejunal anastomosis in laparoscopic Roux-En-Y gastric bypass: an analysis of 211 cases. Surg Res Pract 30(2020):4090797 Castro MJ, Jimenez JM, Carbajo MA, Lopez M, Cao MJ, Garcia S, Ruiz-Tovar J (2020) Longterm weight loss results, remission of comorbidities and nutritional deficiencies of sleeve gastrectomy (SG), Roux-En-Y gastric bypass (RYGB) and one-anastomosis gastric bypass (OAGB) on type 2 diabetic (T2D) patients. Int J Environ Res Public Health 17(20):7644. https://doi.org/10.3390/ijerph17207644 Contival N, Menahem B, Gautier T, Le Roux Y, Alves A (2018) Guiding the non-bariatric surgeon through complications of bariatric surgery. J Visc Surg 155(1):27–40 De Luca M, Angrisani L, Himpens J, Busetto L, Scopinaro N, Weiner R, Sartori A, Stier C, Lakdawala M, Bhasker AG, Buchwald H, Dixon J, Chiappetta S, Kolberg HC, Frühbeck G, Sarwer DB, Suter M, Soricelli E, Blüher M, Vilallonga R, Sharma A, Shikora S (2016) Indications for surgery for obesity and weight-related diseases: position statements from the International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO). Obes Surg 26(8):1659– 1696 Diabetes Research Network (2012) National Institute for Health Research. Sgromo et al., Oxford University Felsenreich DM, Langer FB, Eichelter J et al (2021) Bariatric surgery- how much malabsorption do we need?—A review of various limb lengths in different bariatric procedure. J Clin Med 10(4):674 Feng JJ, Gagner M (2002) Laparoscopic biliopancreatic diversion with duodenal switch. Semin Laparoscop Surg 9(2):125–129 Gagner M, Hutchinson C, Rosenthal RJ (2016) Fifth international consensus conference: status of sleeve gastrectomy. Surg Obes Relat Dis 12(49):750–756 Gomes M, Ramacciotti E, Miranda F Jr et al (2009) Vascular flow of the gastric fundus after arterial devascularization: an experimental study. J Surg Res 152:128–134 Laferrère B, Pattou F (2018) Weight-independent mechanisms of glucose control after Roux-en-Y gastric bypass. Front Endocrinol (Lausanne) 10(9):530 Melissas J, Braghetto I, Molina JC et al (2015) Gastroesophageal reflux disease and sleeve gastrectomy. Obes Surg 25(12):2430–2435

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Meyer G, Stier C, Markovsky O (2009) Postoperative Komplikationen beim laparoskopischen Roux-Y-Magenbypass in der Adipositaschirurgie [Postoperative complications after laparoscopic Roux-en-Y gastric bypass in bariatric surgery]. Obes Facts 2 Suppl 1(Suppl 1):41–48 Natoudi M, Panousopoulos SG, Memos N, Menenakos E, Zografos G, Leandros E, Albanopoulos K (2014) Laparoscopic sleeve gastrectomy for morbid obesity and glucose metabolism: a new perspective. Surg Endosc 28(3):1027–1033 Peterli R, Wölnerhanssen BK, Peters T, Vetter D, Kröll D, Borbély Y, Schultes B, Beglinger C, Drewe J, Schiesser M, Nett P, Bueter M (2018) Effect of laparoscopic sleeve gastrectomy vs laparoscopic Roux-en-Y gastric bypass on weight loss in patients with morbid obesity: the SMBOSS randomized clinical trial. JAMA 319(3):255–265 Pories WJ, Swanson MS, MacDonald KG, Long SB, Morris PG, Brown BM, Barakat HA, deRamon RA, Israel G, Dolezal JM et al (1995) Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg 222(3):339–350; discussion 350–352 Ramos A, Kow L, Brown W, Welbourn R, Dixon J, Kinsman R, Walton P (2019) Fifth IFDO Global Registry Report. IFSO Global Registry Ren CJ, Patterson E, Gagner M (2000) Early results of laparoscopic biliopancreatic diversion with duodenal switch: a case series of 40 consecutive patients. Obes Surg 16(6):514–523 Ruiz-Tovar J, Carbajo MA, Jimenez JM, Castro MJ, Gonzalez G, Ortiz-de-Solorzano J, Zubiaga L (2019) Long-term follow-up after sleeve gastrectomy versus Roux-en-Y gastric bypass versus one-anastomosis gastric bypass: a prospective randomized comparative study of weight loss and remission of comorbidities. Surg Endosc 33(2):401–410 Samakar K, McKenzie TJ, Tavakkoli A et al (2016) The effect of laparoscopic sleeve gastrectomy with concomitant hiatal hernia repair on gastroesophageal reflux disease in the morbidly obese. Obes Surg 26(19):61–66 Shikora SA, Mahoney CB (2015) Clinical benefit of Gastric Staple Line Reinforcement (SLR) in gastrointestinal surgery: a meta-analysis. Obes Surg 25(7):1133–1141. https://doi.org/10.1007/ s11695-015-1703-x Stenard F, Iannelli A (2015) Laparoscopic sleeve gastrectomy and gastroesophageal reflux. World J Gastroenterol 21(36):10348–10357 Yehoshua RD, Eidelman LA, Stein M et al (2008) Laparoscopic sleeve gastrectomy—volume and pressure assessment. Obes Surg 18(9):1083–1108

4

Pathophysiology: Restriction, Duodenal Exclusion, Malabsorption Christine Stier

Initially, the mode of action of the operation in restriction and malabsorption was divided and these two principles were interpreted as a purely mechanical effect. However, the mode of action of bariatric surgery is actually multifactorial. Scientific findings showed that the modification of the anatomy leads rather to altered neuronal and hormonal signals, which mainly affect the central regulation of hunger and satiety. The actual weight reduction is ultimately based, even after the operation, on significant and lasting calorie reduction. This can be exclusively, effectively, and sustainably ensured by the surgical procedures, as treated patients do not feel hunger despite the significant food restriction and at the same time feel rapid satiety (Fig. 4.1). Thus, bariatric surgery today represents the most effective and sustainable therapy for morbid obesity, as it directly influences the hypothalamic balance between hunger and satiety. Through this central effect, the postoperative food preference is apparently changed too, as an indicator of an also assumed influence on the mesolimbic reward system (Clemmensen 2017). This is the successful prerequisite to achieve lasting weight reduction and to be able to stabilize the achieved weight afterward. The special role of the duodenum in the regulation of metabolism was recognized and meanwhile proven. Therefore, the duodenal exclusion is now considered as an independent mode of action. Nevertheless, the duodenal exclusion also corresponds to malabsorption by definition (see corresponding chapter).

C. Stier (*)  University Hospital Mannheim, Division of Interdisciplinary Endoscopy, Mannheim, Germany © The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 C. Stier and S. Chiappetta (eds.), Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients, https://doi.org/10.1007/978-3-662-66436-0_4

43

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Saturation

Hunger Reduced intake of food -> Weight reduction

Fig. 4.1   Postoperatively, significantly reduced hunger and rapid satiety/fullness lead to significantly reduced food intake and thus to weight reduction



Important  Bariatric surgery influences the so-called gut–brain axis in such a way that the gastrointestinal tract today is considered a comprehensive target organ of obesity therapy (Clemmensen 2017).

4.1 Restriction Restriction literally means limitation. In the context of bariatric surgery, restriction is defined as a significant volume reduction of the stomach. This principle underlies practically every modern obesity procedure. In the SG, the excess volume is resected along a calibration tube in the longitudinal axis, whereas in the bypass procedures the pouch is separated from the rest of the stomach. As a result, the SG leaves a remaining gastric volume of about 80–100 mL and the bypasses volumes of about 25–40 mL for the RYGB and about 60–70 mL for the OAGB/MGB. Owing to the resulting faster stretching of the wall of the now significantly smaller stomach, satiety or a feeling of fullness is conveyed very quickly. 

Important  Restriction is a basic principle of practically every modern bariatric surgical operation.

4  Pathophysiology: Restriction, Duodenal Exclusion, Malabsorption

45

The areas of the stomach where ghrelin—the hunger hormone—is produced in the parietal cells are removed (SG) or excluded from the food passage (bypass procedures). The idea of the early days of bariatric surgery that the hypothetical, obesity-associated hyperphagia (hyperalimentation) could not be influenced surgically has thus not been confirmed and has been refuted.  Important

A therapeutic modification toward very fast satiety despite small food volumes and the general reduction of the feeling of hunger can thus be indicated by reducing the gastric volume (restriction). The reduced gastric volume does not limit the food intake mechanically, but rather mediates satiety neurally and hormonally. Nevertheless, volume is not equal to volume, because the emptying speed from the stomach, or the residence time of the food in the stomach (gastric accommodation) also plays a significant role. The slower the stomach empties and the longer it remains filled (depot effect), the longer a lasting and sustainable feeling of satiety persists. The emptying speed and thus reciprocally the filling state, is determined in the natural stomach by the pylorus. In the sleeve gastrectomy, the pylorus remains functional and the gastric emptying remains sphincter controlled muscularly, even if it is generally accelerated compared with the natural stomach.  Important  Satiety has two aspects: It arises from stretching of the gastric wall

(feeling of fullness) and the residence time of the food in the stomach (depot effect). Different than the gastric bypass procedures, here, the emptying speed is determined by the width, and thus the resistance of the anastomosis, between the gastric pouch and the jejunum. Analogous to the physical principle, this can therefore rather be called an obstruction or obstructive effect of the anastomosis. If the anastomosis widens too much, there is a significantly accelerated emptying of the gastric pouch with faster loss of the feeling of satiety (loss of the depot effect of the stomach), and thus again increased hunger. This can result in a higher meal frequency with more frequent and increased intake of food energy. If the anastomosis is so widened that it leads to a sudden emptying of the gastric contents from the pouch—“nomen est omen”—this can cause the symptoms of a dumping syndrome (see the corresponding chapter).

4.2 Malabsorption Malabsorption and maldigestion can lead to nutritional deficiencies. Malabsorption is defined exclusively as the absorption capacity of the small intestine.

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 Important

Malabsorption: Refers to the lack or impairment of uptake of food substrates from the chyme (food pulp). Maldigestion: Is characterized by an insufficient breakdown of already absorbed food.  Important  In the context of bariatric surgery, the term malabsorption would there-

fore depend on the length of the small intestine segment that is excluded from the food passage, and inversely on the remaining, functionally intact absorption segment (food + digestive juices = common channel). The first, more or less standardized, bariatric surgical procedure in the late 1950s was, as already described, the jejuno-intestinal bypass. This was a highly malabsorptive procedure, which corresponds to a pronounced short bowel syndrome from today’s perspective. 90–95% of the small intestine was removed from the food passage. The anatomy of the stomach was not changed. First publications with descriptions of patients who had survived this condition (Johns Hopkins Hosp Rep 1896) were already found at the end of the nineteenth century in relation to short bowel syndrome, or the loss of large parts of the small intestine. Possible consequences and effects on metabolism were only vaguely described from 1925 onward (Wildegans 1925; Kunz 1928). The actual term “short bowel syndrome” was finally found for the first time in 1966 in a publication by Shepard in the journal “Annals of Surgery” in connection with a surgical therapy approach (Shepard 1966).  Memorandum

At the beginning of bariatric surgery in the 1950s, short bowel syndrome was still largely unknown as a disease entity. In this ignorance, the maximum shortening of the small intestine—and thus the absorption segment of food—was the surgical therapy goal. Only the length of the remaining absorptive segment of the small intestine, the already mentioned common channel, was measured in the performed operations, regardless of the functionality of the different small intestine segments. This measurement of the remaining absorption segment, starting from Bauhin’s valve, finally manifested, as already described, in a separate classification of surgical procedures, the biliopancreatic divisions (BPDs).  Memorandum  The specific functionality of the individual small intestine seg-

ments was also largely unknown at that time and explains the simplified, mechanical conception of the mode of action: “The shorter the remaining absorption segment of the small intestine, the more weight loss is achieved.”

4  Pathophysiology: Restriction, Duodenal Exclusion, Malabsorption

47

The surgical modification of the gastrointestinal tract in such a way that the hypothetical, obesity-related hyperphagia could have been limited was considered impossible. This led to the fatal conclusion that only the significant shortening of the absorption segment was a surgically feasible treatment option. It resulted mainly in a significant quantitative but also qualitative limitation of absorption. First descriptions of deaths due to malnutriti on-induced liver failure, especially due to protein deficiency, led to a rethink and thus gradually to the end of the phase of short bowel syndrome (malabsorption) as the sole surgical therapy goal (Nut Rev 1977; Whelan 1980). By definition, duodenal exclusion also corresponds to a malabsorption. Micro- and macronutrients are absorbed much more restrictedly than with the duodenum in the food passage. However, it does not correspond to the definition of the technical term of pronounced short bowel syndrome. This principle of combining restriction and malabsorption is found again in modern bariatric surgery in combined procedures. The duodenum is excluded from the food passage with different lengths of attached segments of the jejunum (biliopancreatic limb) to enhance the restriction of a bariatric surgical intervention functionally (hormonal modification). Depending on the length of the exclusion of the biliopancreatic limb, the intervention (e.g., OAGB/MGB or long-limb RYGB) has a more or less pronounced malabsorptive effect. 

Practical tip

The length of the biliopancreatic limb (excluded duodenum with different lengths of segments of the jejunum) can vary in the gastric bypass procedures. RYGB: From 50 cm (classic) to 200 cm (long-limb RYGB). OAGB/MGB: From 150 cm to 200 cm (classic), in rare cases also longer. The length of the biliopancreatic limb is an important indicator that must always be known in the follow-up care to estimate the malabsorptive effect of a procedure and the resulting possible deficiencies.

4.3 Duodenal Exclusion In the duodenal “C”, the pancreas fits snugly against the duodenum. The pancreatic duct opens together, or close to, the bile duct at the papilla vateri (Fig. 4.2). Here, the food pulp (chyme) is mixed with the digestive juices, and fats, proteins and complex carbohydrates can be broken down and made absorbable for the small intestine. At the same time, a hormonal feedback is given about the content of the food. A high intraluminal concentration of glucose, fat or amino acids in the small intestine triggers release of an incretin, the glucose-dependent insulinotropic hormone (GIP)—a gastrointestinal hormone from the K cells (entero-endocrine cells) of the duodenum. It stimulates the secretion of insulin from the pancreas. In addition, GIP has an insulin-sensitizing effect on

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C. Stier

Fig. 4.2   Spatially close relationship between the duodenum, pancreas, and bile duct

the fat cell (Zhou 2005; Campell 2013). Another gastrointestinal hormone, secretin, is released from the S cells at a pH 14 g/dL

500 mg

500 mg

8.2.3.2 Copper Copper is an essential trace element. Copper deficiency leads to oxidative stress. Transcuprein (specific Cu transport protein), albumin, and histidine transport copper via the portal vein to the liver. The liver is the central organ of copper metabolism. Chaperones transport copper finally to specific, subcellular compartments. There it is incorporated into copper-dependent enzymes, such as caeruloplasmin, cytochrome-c-oxidase, or superoxide dismutase.

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C. Stier

Hemoglobin represents the iron value

Transport iron: Transferrin Measured by transferrin saturation in %.

Iron stores: Ferritin Liver, spleen, bone marrow

Stored Iron Transport iron Hemoglobin

Ferritin pg/L

Standard findings

Iron deficiency

Iron Deficiency Anemia

Transferrin - Saturation (%) Hemoglobin (g/dL) The hemoglobin value represents the iron value in the serum. A determination of the serum iron is therefore unnecessary and too inaccurate, as it shows a circadian course.

Fig. 8.5   Diagnosis of iron deficiency

8.2.3.3 Zinc Zinc is an essential trace element. The serum level is subject to homeostasis and is therefore only of little significance even in the case of existing zinc deficiency. The serum level is mainly regulated by enteral excretion. Zinc (20–30 mg/kg BW) is one of the most important trace elements in terms of quantity, besides iron. The total stock is about 1.5–2.5 g. Zinc forms bonds with amino acids and proteins, in which it is present as a divalent cation. Vitamin C, citrate, and tryptophan promote zinc absorption. Zinc storage: • Muscle (60%, ~1500 mg) • Bone (20–30%, ~500–800 mg) • Liver, kidney, myocardium, bladder, iris, retina, Langerhans islets, hair, skin, nails, testes, prostate Zinc plasma concentration: 11–17 µmol/L (70–110 µg/dL) • • • •

57–65% albumin-bound zinc 32–40% macroglobulin-bound zinc (coeruloplasmin) 3% free amino acids-bound zinc Inflammatory reactions cause a shift of zinc to intracellular and can lower the serum level slightly

8  Nutritional Deficiencies

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8.2.3.4 Selenium Selenium is an essential trace element. The total stock is about 10–15 mg (0.15–0.2 mg/ kg BW). Serum level: 55–103 µg/L. Inorganic selenate: • Is actively absorbed and oxidized to selenite in the liver Inorganic selenite: • Is passively absorbed and reduced to selenide in the liver Selenide: • Is converted to selenophosphate and to selenocysteine at the tRNA, to be finally incorporated into proteins. All functionally relevant selenium-dependent proteins of the human organism contain selenocysteine Selenium storage • Skeletal muscle (40–50%) • Different concentrations in: liver, kidneys, heart, pancreas, spleen, brain, gonads, erythrocytes, and platelets (Biesalski 2004) (Table 8.4)

8.2.4 Fat-Soluble Vitamins  Definition  Vitamins are essential organic substances that the metabolism cannot synthesize (according to demand). The absorption of fat-soluble vitamins behaves in the gastrointestinal system according to all dietary fats and is bile acid-dependent. Therefore, longer lasting steatorrhea or the fundamental changes in the intraluminal bile acid composition lead to a modified or reduced absorption of fat-soluble vitamins.  Memorandum  After their absorption, the fat-soluble vitamins are transported in

the blood as chylomicrons. The vitamins A and K are stored in the liver, vitamin E in the adipose tissue, and vitamin D mainly in the fat and muscle tissue, with smaller amounts also in the liver. The absorption mechanism of fat-soluble vitamins requires special attention. All fat-soluble vitamins are absorbed in the upper small intestine as part of fat digestion, i.e., the presence of dietary fats as transport means of the lipophilic molecules, bile acids for sol-

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Table 8.4  Symptoms due to deficiency (deficiency symptoms) of trace elements Iron

Copper

Zinc

Selenium

Incidence (Stein 2014) (Shankar 2010)

Up to 55%

Up to 45%

Up to 33% Up to 90% (malabsorptive procedures)

Up to 22%

Heart

Palpitations Increased cardiac output Dyspnea Decreased exercise tolerance

Arrhythmias Tachycardia

Gastrointestinal tract

Burning tongue Angular cheilitis

Motility disorders Glossitis Diarrhea with irritable bowel-like symptoms Constipation Abdominal pain

Sensory organs

Acute cardiac muscle failure (Keshan disease)

Taste disorders Vision problems, dry eye Smell disorders Mucosal inflammation

Bones

Osteopenia

Developmental disorders Joint cartilage degeneration (Kashin-Beck disease)

Muscles

Restless legs

Muscle weakness

Myositis Muscle weakness Muscle cramps

Hematopoiesis and vascular system

Iron deficiency anemia

Copper deficiency anemia (normocytic, iron refractory) Change of aortic elastin

Anemia

Immune system

Increased susceptibility to infection Wound healingDisorders

Increased susceptibility to infection

(continued)

8  Nutritional Deficiencies

91

Table 8.4   (continued) Iron

Copper

Zinc

Thyroid

Selenium Dysfunction (Selenium is a cofactor in the formation of the peripheral hormones)

Central nervous system

Cold sensitivity Headaches Concentration problems Dizziness Forgetfulness Performance decline, fatigue Tinnitus

Hypothermia Mental deterioration Fatigue symptoms Posterolateral myopathy (Juhasz-Pocsine et al. 2007) Confusion Irritability

Lack of motivation Depression Concentration problems

Sleep disorders Memory problems Headaches

Skin and appendages

Pallor Severe hair loss

Impaired pigmentation (graying) Impaired keratinization White discolored finger beds

Significant hair loss Alopecia Dermatitis Acne Eczema Zinc deficiency Dermatitis

Impaired pigmentation (graying) Hair loss White discolorations of the nails

Reproduction

Infertility

ubilization and micelle formation as well as pancreatic esterases are necessary for optimal intestinal uptake (Fig. 8.6). The reabsorption behavior of the bile acids changes owing to the duodenal exclusion in the course of a bypass procedure (Fig. 8.6). In principle, bile acids also undergo a change in the intestinal lumen; they are converted by the microbiome from primary to secondary bile acids (dehydroxylation).  Memorandum

In the biliopancreatic limb, which is excluded from the food passage, bile salts are passively reabsorbed. This effect is more significant the less chyme (food) is present in the lumen (demand-based). This also changes the composition of the bile acids in the blood, an already illustratively described effect (Lutz 2014). In addition, a part of the already qualitatively changed and quantitatively reduced bile acids is no longer absorbed and steatorrhea may result.

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C. Stier Esophagus Remnant Stomach (Remnant Stomach)

Pouch

Biliopancreatic loop

Very limited production of IF & acid Jejunum

Alimentary loop

Bile acids: Passive reabsorption Bile acids: Passive reabsorption Bile acids: Passive reabsorption Bile acids: Passive reabsorption

Bile acids: Passive reabsorption

Bile acids: Passive reabsorption

Colon

Pancreatic and biliary juice

upper jejunum

Bile aciddependent absorption of dietary fat (fat-soluble vitamins)

Bile acids: Passive reabsorption

lleum

Modification of the microbiome by modified GS composition

Reduced absorption of fat-soluble vitamins (relative bile acid deficiency)

Altered composition of bile acids

Duodenum

Intrinsic factor (IF)

Fig. 8.6   Modified qualitative absorption of fat-soluble vitamins by duodenal exclusion. Fat-soluble vitamins are absorbed to a limited extent, as, in the biliopancreatic limb, owing to exclusion from the passage, bile acids are quantitatively passively reabsorbed. The reduced and changed bile acid composition also causes a modification of the commensal microbiome (bile acids serve as food for the bacteria and are dehydroxylated by them to secondary bile acids)

 = microbiome As no chyme is present in the biliopancreatic limb after a bypass procedure, it must be assumed that the significant reabsorption of the bile acids correlates with the length of the biliopancreatic limb. The length of the common channel, on the other hand, determines the totality of the inflowing bile acids (possible bile acid loss syndrome).  Memorandum

This results in a significantly changed composition of the bile acids at the rendezvous point with the food (end of the biliopancreatic limb), which corresponds to a functional deficiency of bile acids. The result is a reduced bile acid-dependent absorption of fat-soluble vitamins and other dietary fats (possible resulting in steatorrhea).

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A secondary effect is the change in the composition of the microbiome, which feeds on the present bile acids to some extent (commensals).

8.2.5 Vitamin D Vitamin D is formed in the skin by sun exposure. For this, a vitamin D precursor is formed in the liver from cholesterol, which is then transported to the skin. There it undergoes conversion by UVB radiation into the provitamin D, which is further converted by the heated skin into cholecalciferol. After its return transport to the liver, it is converted to 25-OH-vitamin D3. The more the skin is heated by the sun, the more vitamin D3 is formed. This step is self-limiting, if it gets too hot, the provitamin is converted into inactive degradation products; thus, an overdose by sun exposure is not possible (Fig. 8.7).  Memorandum

Calcium homeostasis = endocrine effect of calcitriol. Depending on the calcium level, the further conversion to the hormone calcitriol takes place in the kidney as needed. This corresponds to the calcium-dependent endocrine pathway for the regulation of calcium homeostasis.

Cholesterol

kin

HEAT

HEAT

SKIN

es

Cholecalciferol (Vitamin D3)

s th

provitamin D

arm

Vitamin D precursor

nw

Su

rays

1, 25-OH vitamin D3 (calcidiol, prohormone)

UVB

KIDNEY

rays

25-OH Vitamin D3 (Calcidiol, prohormone

25-OH vitamin D3 (calcidiol, prohormone)

ay thw pa t ne fec cri ef do ic En lcem ca

25-OH vitamin D3 (calcidiol, prohormone)

UVB

Cholecalciferol (Vitamin D3)

rt po ns ra ety n t ari tei D v ro op min Lip Vita

LIVER

Vitamin D precursor 7-dehydroxyCholesterol

Provitamin D Cholecalciferol (Vitamin D3)

Fig. 8.7   Endocrine calcium-dependent pathway of calcitriol formation (vitamin D hormone). Formation of a vitamin D precursor from cholesterol in the liver, transport to the skin, conversion by UV radiation into the provitamin D, which is then converted by the skin heat into vitamin D (cholecalciferol). This is transported back, to be converted in the liver into 25-hydroxy-cholecalciferol (pro-hormone). The prohormone is finally converted in the kidney, depending on the calcium level, into calcitriol (1,25 hydroxy-cholecalciferol; hormone)

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 Memorandum

Gene regulation, immunity = paracrine, cellular effect of calcitriol. Calcitriol can be formed directly from cholecalciferol (vitamin D) in the cell, independently of calcium (Fig. 8.8). Here it acts cellularly via the paracrine pathway, which is calcium-independent. Calcitriol has a cellular immunomodulatory and gene-regulatory effect (Fig. 8.8). In countries north of the 40th latitude, sufficient vitamin D production is not possible from October to March (Chapuy 1997; Van Schoor 2011; Webb 1988), so vitamin D supplementation may be necessary in winter. The ability to produce vitamin D is inversely proportional to the sun sensitivity of the skin, lighter skin types produce faster and more vitamin D, darker skin types slower and less (Jablonski 2004). Sun protection also significantly reduces vitamin D production, which depends on the area of exposed skin. Cholecalciferol (vitamin D3) is mainly obtained by sun exposure, but can also be obtained from a fatty fish-rich diet (e.g., indigenous peoples in the northern polar region: cod liver oil-rich diet). An interesting evolutionary aspect is that the indigenous peoples in the northern polar region, despite the only marginal sun exposure in the Arctic central and eastern Canada—possibly because of their vitamin D-rich diet—have not experienced any climatic

Cholesterol

kin

HEAT

HEAT

SKIN

es

Cholecalciferol (Vitamin D3)

s th

1, 25-OH vitamin D3 Cholecalciferol (Vitamin D3)

Autocrine Path

arm

rays

CELL

nw

UVB

Vitamin D precursor Provitamin D

25-OH Vitamin D3 (Calcidiol, Prohormone)

Su

rays

25-OH vitamin D3 (calcidiol, prohormone)

UVB

Cholecalciferol (Vitamin D3)

rt po ns ra ety n t ari tei D v ro op min Lip Vita

LIVER

Vitamin D precursor 7-DehydroxyCholesterol

Provitamin D (Calcidiol, prohormone)

Fig. 8.8   Paracrine, non-calcemic pathway of calcitriol formation (vitamin D hormone). Formation of a vitamin D precursor from cholesterol in the liver, transport to the skin, conversion to the provitamin D by UV radiation, which is then converted to vitamin D (cholecalciferol) by the skin heat. Cholecalciferol is enzymatically converted to calcitriol (1,25 hydroxy-cholecalciferol; hormone) in the cell. Effect: immunity, gene regulation

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skin color adaptation, unlike other northern tribes that have to cover their vitamin D supply mainly through sun exposure. Prohormones of calcitriol (1,25-OH vitamin D3): vitamin D3 and vitamin D2 Cholecalciferol

Vitamin D3

Is formed by the sun in the skin

Prohormone

Animal foods (fatty fish) Ergocalciferol

Vitamin D2

Is synthesized in the body from plant sterin derivatives (mainly mushrooms)

Prohormone with significantly lower effectiveness

Obesity often correlates disproportionately with a vitamin D deficiency. There is a calculation that has estimated an increase in BMI by one unit with a 1.15% drop in serum levels of 25-(OH)-vitamin D3 (Vimaleswaran KS 2013). In doing so, patients with obesity expose themselves to the sun only very little with uncovered skin (Savastano 2017). The sequestration in the adipose tissue and the volumetric dilution of orally ingested or cutaneously synthesized vitamin D3 in correlation with the large fat mass of obese patients can represent another factor of this high incidence of vitamin D deficiency. It is already found in 26–69% of non-operated patients with obesity and can postoperatively rise to values of up to 80% (Stein et al. 2014).

8.2.6 Vitamin A The main source of vitamin A are plant provitamin-A carotenoids and especially retinyl esters (lipophilic) from animal products. Retinyl esters are enzymatically (pancreatic lipase) hydrolyzed to retinol and absorbed in the intestinal lumen. Carotenoids remain unprocessed and are partially converted to retinol in the cells. The ejection into the lymphatic system finally occurs as chylomicrons and after conversion to remnants further into the liver, where a receptor-mediated uptake takes place. There it can be bound in the parenchymal cells to the cellular retinol-binding protein (CPBP), or perisinusoidally re-esterified in the stellate cells to the storage form. The liver is the most important store of vitamin A storage (50–80%).  Memorandum

Forms with vitamin A activity are retinol (retinyl ester), retinal, and retinoic acid (Fig. 8.9). More than 90% of the retinol is bound in the blood to the retinol-binding protein (RPB). The different subforms of the vitamin can basically be converted into each other, but the oxidation of retinal to retinoic acid is irreversible. Each form has specific effects (Fig. 8.9).

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Carotenoids

(animal products) Vitamin A ester

Retinol

(transport form) Vitamin A1 (alcohol)

(of plant origin) Precursor of vitamin A

NADH Interchangeable NAD+

Retinol

Vitamin A aldehyde

Retinyl ester (storage form)

Peri-sinusoidal in the Liver: Stellate cells

Retinal

+ Opsin = Rhodopsin

Oxidation irreversible

Retinoic acid

(not re-transformable)

Proliferation Cell differentiation: respiratory epithelium, intestinal mucosa, skin, embryonic cells Inhibition of various tumor promoters

Fig. 8.9   Vitamin A subforms: retinol (alcohol)—retinyl ester—retinal (aldehyde)—retinoic acid

The biological effect of vitamin A is given in International Units (IU) or in Retinol Activity Equivalent (RAE): IU vitamin A corresponds to 0.3 µg retinol 1 μg RAE corresponds to [12]: • 1 µg retinol • 12 μg β-carotene • 24 μg other provitamin A carotenoids (DGE reference values). 

Take-home message  Retinal (aldehyde form) is involved in the visual process. It

is coupled to opsin and thus part of the rhodopsin in the retina. If there is a vitamin A deficiency, the first clinical symptom to develop is night blindness.

8.2.7 Vitamin K Vitamin K receives little attention as a vitamin, except in its function as a cofactor of the coagulation factors II, VII, IX, and X, which are vitamin K-dependent.

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Two subfractions of vitamin K

• Vitamin K1: Phylloquinone – Cofactor of the coagulation factors II, VII, IX, and X • Vitamin K2: Menaquinone – The formation of osteocalcin is induced by calcitriol. The glutamyl residues are vitamin K2-dependent and γ-carboxylated by gamma-glutamyl carboxylase. This enables osteocalcin to bind calcium actively in the bone (Cranenburg 2007; Vermeer 2012). – Activates the matrix-GLA protein (MGP): binds calcium in the vascular system and thus counteracts vascular calcification. The supplementation of vitamin K2 has already been investigated in connection with the reduction of the risk of coronary heart disease. – Activates Gas6 (Growth-arrest-specific gene-6). Through this pathway, it plays a significant role in cell division, cell differentiation, and cell migration. Studies on its effect in the application for prostate, hepatocellular, lung, and bladder carcinoma have been discussed (Nimptsch et al. 2008; Otsuka 2004; Yoshida 2003; Duan 2020). – Likewise, a possible positive effect on insulin resistance is postulated via the osteocalcin mechanism (Li 2017).

There are different subforms of menaquinone (MK4- MK13, depending on the number of side arms). Vitamin K2 production via intestinal bacteria makes a significant contribution to the supply of vitamin K2, but often is not sufficient (Conly 1994). A disturbed intestinal flora may impair this pathway and explain the more frequent deficiency compared with vitamin K1 (Sato 2012). In supplementation, a vitamin K2 (MK7), which is derived from soy, is most commonly used. It is readily bioavailable, with only the trans-form having biological activity.

8.2.8 Vitamin E Vitamin E is the term for all natural and synthetic tocopherol and tocotrienol derivatives that have the biological activity of alpha-tocopherol. Vitamin E synthesis occurs exclusively in plants. Green plant parts contain relatively much alpha-tocopherol, corresponding to their content of chloroplasts, while yellow plant tissues, stems, roots and fruits of green plants have a comparatively low concentration of vitamin E. In non-green plants, besides alpha-tocopherol mainly gamma-tocopherol occurs, whereby the vitamin E content is proportional to the concentration of the color-giving chromoplasts.

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In slowly growing and mature plants, the tocopherol content is higher than in rapidly growing and young plants (Pietrzik 2008). Vitamin E enters the animal organism via plant consumption and is therefore also detectable in animal foods, but with significantly lower tocopherol concentrations and depending on the type of husbandry. Basically, it is a highly effective fat-soluble vitamin with multiple cell membrane stabilizing, anti-oxidative and other non-anti-oxidative functions.  Memorandum  It is propagated that vitamin E prevents the oxidation of polyunsat-

urated fatty acids in the membrane of the red blood cells (RBCs) and thus inhibits the breakdown of premature erythrocyte s (Jilani 2011). In several clinical studies, vitamin E was therapeutically used as a potential erythropoietic agent to reduce the premature hemolysis of the erythrocytes, as it increases the stability of the erythrocytes. Thus, it could improve the hemoglobin and hematocrit values by supplementation in anemic subjects (Jilani 2011). 

Practical tip  Iron-refractory anemia should, after excluding vitamin B deficiency, always also make one think of a vitamin E deficiency.

Biological activity in percent and conversion factors for individual vitamin E forms based on RRR-alpha-tocopherol (DGE): 1 mg RRR-alpha-tocopherol = 100% corresponds to 1.00 mg alpha-TE = 1.49 IU (International Units) 1 mg

Vitamin E form

Activity equivalent

Unit equivalent

RRR-beta-tocopherol

50%

0.75 IU

1 mg

RRR-gamma-tocopherol

10%

0.15 IU

1 mg

RRR-delta-tocopherol

3%

0.05 IU

1 mg

RRR-alpha-tocopheryl acetate

91%

1.36 IU

1 mg

RRR-alpha-tocopheryl hydrogen succinate

81%

1.21 IU

1 mg

R-alpha-tocotrienol

30%

0.45 IU

Deficiency symptoms of fat-soluble vitamins Vitamin D Sensory organs

Bones

Vitamin A

Vitamin K

Night blindness Xerophthalmia Blindness Rickets Osteoporosis Osteomalacia

Osteomalacia Osteoporosis

Vitamin E

8  Nutritional Deficiencies Vitamin D Muscles

99 Vitamin A

Muscle weakness Muscle cramps

Vitamin K

Vitamin E

Increased insulin resistance

Heart

Increased risk of coronary heart disease

Hematopoietic system

Bleeding tendency Iron-refractory anemia

Immune system

Increased susceptibility to infection

Hair and appendages

Hair loss

Central nervous system

Neuromuscular hyperexcitability Depression Fatigue Mood swings “There’s no sunshine anymore”

Increased susceptibility to infection Increased oxidative stress

Lack of motivation Concentration problems

Symptoms that were marked as practical tips are highlighted

8.2.9 Water-Soluble Vitamins (Vitamin B1, B6, B12, Vitamin C) Absorption site of water-soluble vitamins Vitamin

Absorption site

Thiamine (vitamin B1)

Jejunum, duodenum, ileum

Riboflavin (vitamin B2)

Entire small intestine

Niacin (vitamin B3)

Stomach Entire small intestine

Pantothenic acid (vitamin B5)

Entire small intestine

Biotin (vitamin B7)

Jejunum Entire small intestine

Pyridoxine (vitamin B6)

Jejunum

Folate (vitamin B9)

Jejunum Entire small intestine

Cobalamin (vitamin 12)

Terminal ileum Entire small intestine

Vitamin C

Stomach Ileum Entire small intestine

The main absorption sites (mostly active absorption) are highlighted The clinically relevant B vitamins are presented in detail.

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8.2.10 Thiamine (Vitamin B1) Based on the observations of the Dutch physician Christiaan Eijkman, that chickens developed beriberi-like symptoms after being fed peeled, polished rice but not after being given whole-grain rice or rice bran, thiamine has since been referred to as the “antiberiberi vitamin” (Eijkman 1987). Phosphorylated vitamin B1 ingested through food is dephosphorylated by nonspecific phosphatases of the intestinal wall and thus converted into an absorbable state. The biologically active form is thiamine pyrophosphate (TPP).  Memorandum  The absorption of free thiamine is highest in the jejunum after the

duodenum and ileum. Physiological amounts of vitamin B below a concentration of 2 µmol/L are absorbed by an energy-dependent, saturable sodium-mediated carrier mechanism. Above a concentration of 2 µmol/L, passive diffusion also occurs. 

Practical tip

Alcohol leads to downregulation of the thiamine-specific transport proteins by inhibiting the Na-K adenosine triphosphatase in the basolateral cell membrane and the metabolism of the pyrophosphate kinase. Substitution of thiamine is therefore recommended if necessary.

Forty percent of the thiamine occurs in the muscle; a proper thiamine store does not exist; thus, 3–8 µg/g are stored in the heart muscle, 2–6 µg/g in the kidney, 2–8 µg/g in the liver, and 1–4 µg/g in the brain. The thiamine excretion is dose dependent. In about 25%, a renal elimination occurs; at high applied doses, the elimination is almost completely renal. Non-absorbed thiamine is excreted via the biliary system, with increasing thiamine content in the stool, which is called a renal overflow effect at saturation of the tubular reabsorption. 

Practical tip

With a half-life of 9–18 days and a storage capacity of only 25–35 mg and a high daily turnover, the store can be depleted very quickly and thus result in a thiamine deficiency. A pronounced deficiency symptomatology results (see Chap. 21). The recommended daily intake is 1.0 mg for women and 1.1 mg for men.

A thiamine deficiency can occur because of a combination of reduced food intake, malnutrition, malabsorption, and recurrent vomiting (Fig. 8.10). 

Memorandum  Thiamine plays an essential role as a co-enzyme in the citric acid cycle and thus in the production of energy (ATP) from food.

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Fats

Carbohydrates

Proteins

THIAMINE PP

-amino acids

Acetyl-CoA

Pyruvate

Citrate

Malate

Iso-Citrate Citrate cycle Energy gain:

10 molecules ATP

Fumarate

-ketoglutarate

Carbon decomposition

Recovery of the acceptor molecule

Oxaloacetate

THIAMINE PP

Succinyl-CoA Succinate

Fig. 8.10   Thiamine as an important co-enzyme of the citric acid cycle: energy production from food energy (carbohydrates, fat, protein). Thiamine is the co-factor in the conversion of carbohydrates to pyruvate and the degradation of the carbon skeleton (first half of the citric acid cycle) in the conversion of α-ketoglutarate to succinyl-CoA

The typical thiamine deficiency manifestation is beriberi syndrome, which is divided into a cardiac form with heart failure and resulting edema, a neurological form with muscle weakness and other neurological symptoms, and a central form with possible Wernicke encephalopathy and Korsakoff psychosis. A similar symptomatology is also found in the context of the refeeding syndrome, a severe electrolyte imbalance with acute consumption thiamine deficiency (see also Chap. 21).

8.2.11 Pyridoxine (Vitamin B6) Vitamin B6 is a collective term for all vitamin-active derivatives of 3-hydroxy-2-methylpyridine: pyridoxine, pyridoxol, pyridoxal, and pyridoxamine. It is ubiquitously available from plant and animal foods. The intake of dietary vitamin B6 occurs in the small intestine, whereby the absorption rate depends on the B6 form. In the colon, a passive uptake of bacterially produced vitamin B6 by the microbiome takes place. 

Practical tip  The daily requirement is 1.2 mg for women, 1.9 mg for pregnant and lactating women, and 1.4 to 1.6 mg for men.

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The deficiency symptoms are divided into neurological and non-neurological symptoms, whereby the effect of vitamin B6 is not limited to the nervous system but it also has important functions in erythrocyte formation, protein degradation, and antibody formation (Table 8.5 and Fig. 8.11).

Table 8.5  Symptoms of vitamin B6 (pyridoxine) deficiency Neurological symptoms

Non-neurological symptoms

Loss of concentration

Dermatitis

Aggression

Glossitis, stomatitis

Feeling of illness

Gastro-intestinal symptoms

Sleep disorders

Hair loss

Anxiety

Hypochromic, microcytic, iron-refractory anemia

Apathy

Hyper-homocysteinemia

Headaches, migraine

Hypercholesterolemia

Peripheral neuropathy Ataxia, paralysis, paresthesia Seizures Prodromal symptoms were highlighted

Fig. 8.11   Symptomatic vitamin B6 deficiency with massive hair loss, glossitis, and anxiety

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8.2.12 Folate (Vitamin B9) Folate is mainly absorbed in the duodenum and the upper jejunum. The storage capacity of 5–10 mg is sufficient for about 2–4 months. Naturally, only folates occur; folic acid on the other hand is artificially produced. Folic acid has the highest stability and oxidation state compared with the natural folate compounds and is almost completely absorbed as a pure substance. Folates are found in both animal and plant foods and have to be enzymatically hydrolyzed before absorption in the duodenum and the proximal jejunum. This is done by a γ-glutamyl-carboxy-peptidase at the brush border membrane of the enterocytes. The absorption of vitamin B9 is a pH-dependent process with maximum absorption at pH 6.0 (Pietrzik 2008).  Memorandum  The liver is the main storage organ (50%) and regulates the supply

of other organs. 

Practical tip  The daily requirement for adults is about 300 µg; for pregnant women it is 550 µg.

“Folium” means green leaf. Accordingly, folate is found in green leafy vegetables, legumes, and whole grain products. Through the food chain, folate is also found in animal products such as egg yolk and liver. The amount of folate excreted with the bile, about 10–90 µg per day, is subject to an enterohepatic circulation and is almost completely reabsorbed. Diseases of the small intestine or small intestine resections can impair the enteral reabsorption (Pietrzik 2008). The rapidly available, relatively high biliary folate concentration (folate pool) exceeds that of the blood plasma by 10-fold and regulates together with the comparatively small intracellular folate pool (liver and extrahepatic tissues) the folate homeostasis to maintain a constant folate serum level (Pietrzik 2008). The amount of folate that is excreted enterally is difficult to assess owing to the additional microbial synthesis of folates. It is postulated that feces have 5- to 10-fold higher folate concentrations than ingested food. Symptoms of folate deficiency Mucosal changes of the oral cavity Higher incidence of neural tube defects Higher incidence of cleft lip and palate High homocysteine levels (vascular damage) Megaloblastic anemia (vitamin B12 deficiency must be excluded)

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8.2.13 Cobalamin (Vitamin B12) The vitamin B12 synthesis is complex. Only microorganisms are capable of it. Thus, the bacterial synthesis by the microbiome contributes to the coverage of the vitamin B12 requirement in a species-specific way. Although synthesis by the microbiome is sufficient for herbivores, carnivores can additionally cover their needs through meat intake. For humans as carnivores, the microbiome-synthesized vitamin B12 is not sufficient, especially because the bacterial synthesis occurs below the terminal ileum and thus beyond the biological absorption mechanism. Since cobalamin is acid-sensitive, it is first bound to haptocorrin and thus protected from the acidic pH of the stomach. In the alkaline milieu of the duodenum, haptocorrin is then cleaved from vitamin B12 by proteases of the pancreas, which binds to the intrinsic factor (IF), formed in the parietal cells of the stomach. The stimulation of IF production is mediated by gastrin. When protein enters the stomach, gastrin is released. Circulating gastrin triggers the release of histamine and thus stimulates the parietal cells to produce via their H2 receptors. The complex formation between vitamin B12 and the IF is essential for its absorption, which is mediated by the cubam receptor complex in the terminal ileum (Kozyraki 2020). 

Practical tip The daily vitamin B12 requirement is 3 to 4 µg per day, the reserves last for about 2 years (half-life 3–5 years). Therefore, a subclinical vitamin B12 deficiency is not easy to detect in the laboratory.

About 1% of the dietary cobalamin is absorbed without prior binding to the IF by a nonspecific mechanism via the gastro-intestinal tract or mucous membranes (nose, mouth). The intrinsic factor-mediated vitamin B12 absorption is only a maximum of 1.5–2.0 µg per meal, as the capacity of the cubam receptor complex for the Cbl-IF complex is limited. With an oral vitamin B12 intake above the physiological dose of about 10 µg, the IFindependent, passive cobalamin absorption becomes increasingly important. Nevertheless, malabsorption of the IF-mediated vitamin B12 absorption can result from short-segment resections of the terminal ileum. In the context of bariatric surgery, the system is encroached upon from the other side and the production of IF is drastically reduced by the significant reduction of the gastric volume (Fig. 8.12).  Memorandum  The smaller the functionally remaining gastric pouch, the lower

the assumed production of IF. As a consequence, the volume reduction, and consequently that of the IF after bariatric surgical procedures (reduction of parietal cells by restriction), plays an influential role in

8  Nutritional Deficiencies Parietal cell of the gastric portion in the food passage (pouch): Acid and IF production

105 Parietal cell of the gastric portion that is not in food passage (Remnant Stomach): No or very little acid and IF production.

Fig. 8.12   Parietal cell: in the food passage and secreting; excluded from the food passage and not secreting (bypass procedure). IF = intrinsic factor

the uptake of vitamin B12. It can be assumed that the remnant stomach (the remaining stomach that is no longer in the passage) hardly produces IF, because the IF production of the parietal cells is no longer stimulated by histamine. However, there are no publications on this (PubMed). 

Practical tip

Correlating to the volume of the gastric portion remaining in the passage, the IF production is reduced, and therefore requires appropriate supplementation of vitamin B12. The smallest functional gastric pouch is after RYGB, followed by OAGB/MGB and SG.

It is clinically often difficult to detect a functional and often already symptomatic vitamin B12 deficiency, despite a normal total vitamin B12 serum level. This requires a differentiated clarification with determination of holo-transcobalamin (Holo-TC), methyl malonic acid (MMA), and homocysteine (Hcy), as shown in the following table. HoloTC, as the parameter of first choice, captures both the manifest vitamin B12 deficiency and the stage of storage depletion, when a negative vitamin B12 balance already prevails, but no functional deficiency is present. When there is a lack of vitamin B12, the concentration of MMA in the blood and urine increases. As there is only a single, vitamin B12-dependent metabolic pathway for

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Table 8.6  Laboratory values for the clarification of a vitamin B12 deficiency Vitamin B12

Total vitamin B12

Holo-TC

MMA

Normal value

196–900 ng/L

35–50 pmol/L

3–4 kg) BW, the fit and correct position of the diaphragm must be checked more frequently. Such a weight change is usually exceeded by a multiple in the first postoperative year, thus, this does not seem practicable during this period.

14.3.3 Oral Contraception An oral contraceptive in the form of a low-dose pill (combination of estrogen and progestin) always entails an increase in the risk of a thrombotic event (factor 3–6) (Gorenoi et al. 2007); thus, in patients after bariatric surgical therapy, especially before the significant postoperative weight reduction, there is a relative contraindication.

14  Postoperative Fertility Enhancement and Contraception …

159

 Memorandum  Patients who take an oral contraceptive before bariatric surgery

should stop it 4–6 weeks before surgery and switch to an alternative form of contraception. Also postoperatively, an oral contraceptive should be avoided for the first 6 weeks because of the perioperatively increased risk of thrombosis. In addition, postoperatively, depending on the chosen procedure, the question of the reliability and safety of the contraceptive effect of an oral preparation arises. The effect of a combined oral contraceptive should not be impaired in patients with a gastric band or SG (Ciangura et al. 2019), as long as there is no vomiting or diarrhea. For the SG, the consensus recommendation by Shawe et al. from the same year has already come to a slightly different result (Shawe et al. 2019). For the RYGB, the data situation is rather thin anyway; thus, it does not seem sensible to us to rely on it for such a medically and biographically important issue and we advise our patients—even after SG—against oral contraception. Owing to the even more pronounced malabsorption, patients undergoing procedures such as OAGB, SADI-S, and BPD-DS are clearly discouraged from oral contraception in the practice guidelines (Ciangura et al. 2019). Older data on the contraceptive oral intake of a purely progestin preparation show reduced absorption in the now no longer used procedure of a jejunoileal bypass. Summary

• Patients should be advised to use parenterally effective LARC after bariatric surgery. • Reliable contraception, also in the future long-term course after surgery, and the early involvement of the gynecologist are the best protection against an unwanted pregnancy. This requires clear communication and education of the patients before surgery. • In particular, the significant advantage of contraception—at least in the first postoperative year, the period of the strongest weight loss—should be addressed and clearly stated that otherwise the weight reduction may stagnate or even lead to weight regain.

References Balen AH, Rutherford AJ (2007) Managing anovulatory infertility and polycystic ovary syndrome. BMJ 335(7621):663–666. https://doi.org/10.1136/bmj.39335.462303.80 Best D, Avenell A, Bhattacharya S (2017) How effective are weight-loss interventions for improving fertility in women and men who are overweight or obese? A systematic review and metaanalysis of the evidence. Hum Reprod Update 23(6):681–705

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Ciangura C, Coupaye M, Deruelle P et al (2019) BARIA-MAT group clinical practice guidelines for childbearing female candidates for bariatric surgery, pregnancy, and post-partum management after bariatric surgery. Obes Surg 29(11):3722–3734 Fillo J, Levcikova M, Ondrusova M, Breza J, Labas P (2017) Importance of different grades of abdominal obesity on testosterone level, erectile dysfunction, and clinical coincidence. Am J Mens Health 11(2):240–245 Gorenoi V, Schönermark MP, Hagen A (2007) Nutzen und Risiken hormonaler Kontrazeptiva bei Frauen. DIMDI, Cologne Moxthe LC, Sauls R, Ruiz M, Stern M, Gonzalvo J, Gray HL (2020) Effects of bariatric surgeries on male and female fertility: a systematic review. J Reprod Infertil 21(2):71–86 Paasch U, Grunewald S, Kratzsch J, Glander HJ (2010) Obesity and age affect male fertility potential. Fertil Steril 94(7):2898–2901 Sermondade N, Huberlant S, Bourhis-Lefebvre V, Arbo E, Gallot V, Colombani M, Fréour T (2019) Female obesity is negatively associated with live birth rate following IVF: a systematic review and meta-analysis. Hum Reprod Update 25(4):439–451 Shawe J, Ceulemans D, Akhter Z et al (2019) Pregnancy after bariatric surgery: consensus recommendations for periconception, antenatal and postnatal care. Obes Rev 20(11):1507–1522 Silvestris E, de Pergola G, Rosania R, Loverro G (2018) Obesity as disruptor of the female fertility. Reprod Biol Endocrinol 16(1):22 Zeiss R, Schönfeldt-Lecuona C, Gahr M, Graf H (2020) Depressive disorder with panic attacks after replacement of an intrauterine device containing levonorgestrel: a case report. Front Psychiatry 28(11). https://doi.org/10.3389/fpsyt.2020.561685

Pregnancy After Bariatric and Metabolic Surgery

15

Ann-Cathrin Koschker

The majority of patients undergoing bariatric surgery are female and of reproductive age. It is not surprising, therefore, that pregnancies of bariatric surgery patients are an increasingly common event. In fact, the data on this topic are still rather scarce, especially the postpartum outcome of the mothers has so far received little attention, and the long-term somatic and cognitive development of the children has not been adequately investigated. The current recommendations are also based on partly inconsistent data, so the field is wide for future research (Shawe 2019). Depending on the guideline, it is recommended to use effective contraception for the first 12 (up to even 24 months) (Shawe 2019)) to allow and stabilize the maximum weight loss through the surgery before conception, to prevent any macro- and micronutrient deficiencies and electrolyte disorders (ACOG 2013).  Memorandum  In principle, it therefore seems sensible, for a planned pregnancy,

to wait for weight stabilization in addition to a certain minimum interval after the surgery, and to ensure adequate supplementation. This should be clearly communicated at the planning stage of bariatric surgery and be aware of a woman of childbearing age. Typical obesity-associated complications such as gestational diabetes, preeclampsia, macrosomia seem to occur less frequently after bariatric surgery, but other problems occur more often (Table 15.1). A.-C. Koschker (*)  Endokrinologie und Diabetologie, Universitätsklinikum Würzburg, Würzburg, Deutschlande-mail: [email protected] © The Author(s), under exclusive license to Springer-Verlag GmbH, DE, part of Springer Nature 2023 C. Stier and S. Chiappetta (eds.), Interdisciplinary Long-Term Treatment of Bariatric and Metabolic Surgery Patients, https://doi.org/10.1007/978-3-662-66436-0_15

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Table 15.1  Obstetric outcome after bariatric surgery. The control group was matched for the BMI that the women undergoing bariatric surgery had before their procedure (Johansson 2015) Complication (in %)

Bariatric surgery (n = 596)

Controls (n = 2356)

Odds Ratio (OR)

P value

GDMa

1.9

6.8

0.25 (0.12–0.47)