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a. There are no nociceptors in the brain [1], therefore damage in brain tissue does not cause pain.That’s why many open-brain surgeries can take place, while the patient is wide awake and chatting with the doctors! In fact, when first introduced, awake surgery was considered a pioneering and extremely helpful method, as it allowed surgeons to ensure they were destroying only epileptogenic or tumour tissue, without harming surrounding functional and vital areas [2].b. Taste receptors are not restricted to the tongue, but are found throughout the body; in the nasal epithelium, the trachea, the stomach, the bile duct, the intestines, aaand the brain [3]. It seems that the brain can “taste” how sweet or bitter the blood is, as certain areas known to influence glucose homeostasis, contain neurons expressing functional glucoreceptors [4], while neural cells in other areas express bitter taste receptors [5], whose functional role remains, as of yet, undetermined. Hmmm, “food for thought”…c. Starvation induces brain cell cannibalism.When energy sources in the brain are scarce, a pathway called “autophagy” (greek word for self-eating) is activated in the hypothalamus, resulting in the release of hunger signals that prompt foraging and eating [6].d. Certain microorganisms can creep in your brain and alter your behavior and personality, e.g making you disobey the rules.Many parasites alter the behaviour of intermediate hosts to increase predation risk, so that they complete their life cycle from the intermediate hosts in the final hosts [7]. For instance, a protozoon named Toxoplasma gondii lives in the cells that line the intestine of a feline. Its oocysts, when excreted with the feline’s feces to the soil, can infect a wide range of warm-blooded vertebrates, most notably rodents but also including humans [8]T. gondii then encysts the brain and other tissues of the intermediary host (typically rodent), until this host is consumed by the final (feline) host, within which it can reproduce. It is of great interest for sneaky little T. gondii that the rodent is eaten as fast as possible by a nearby cat, so this parasite has been selected to modify the rat’s behavior in a way that makes it more likely to be eaten. Indeed, rodents infected by this parasite have higher exploratory behavior, are first to enter traps and their strong innate aversion to cats is reversed into an attraction, luring them into the jaws of their No. 1 predator [9]. Although humans are a dead-end host for T. gondii, as currently cats rarely ever eat humans, infection with this parasite seems to alter human behavior as well. Infected male subjects become more suspicious, introverted, more oblivious to other people’s opinions of them, and more inclined to disregard rules [10]. There are also reports that the reflexes of infected drivers deteriorate and they are more likely to be involved in car accidents [11].What’s more is that it is highly unlikely that T.gondii is the only microscopic puppeteer able to pull our strings. It would be plausible to assume that there are dozens of other tiny brain manipulatos, such as the rabies virus, or parasites we haven’t even heard of. A case of wild, bizarre neurobiology…e. You may be able to lead a normal life with almost your entire brain missing.This case of a 44-year old, hydrocephalus man in France might be the most astonishing example of the plastic brain’s gigantic capacity for adaptation. This patient went to the doctor because of weakness in his left leg. When doctors examined his MRI scans they were shocked. Most of his skull cavity was filled with cerebrospinal fluid, while only a thin layer of gray matter was lining the interior surface of the skull (see that sobering MRI scan below!) [12]Despite the fact that only the bare minimum of his brain was retained, this man leads a normal life; he is a married father of two children and works as a civil service worker. Other impressive cases of extreme brain plasticity are patients who undergo hemispherectomy in young age, as a means of eliminating intractable seizures. This operation results in removal of an entire hemisphere of the brain. The most incredible fact about this process is that memory, speech and personality develop normally after hemispherectomies, and children's academic performances often improve after the surgery [13].It should be noted, though, that cases like the above are rare, and deficits of this extent can only be compensated, if the damage occurs at a pre- or early postnatal developmental stage, when the brain is maximally plastic.f. There is an ongoing battle going on in your brain – a battle for cortical real estate.The scientific, and more civilized term for this battle is “competitive plasticity”, and its outcome is dictated by the central “neural Darwinism” principle; survival of the busiest.In other words, brain regions dedicated to different functions, compete with each other, resulting in the less active areas being taken over by the more active areas. For example, sensory cortices of individuals who are congenitally deprived of a sense exhibit considerable plasticity and can be recruited to process information from other modalities that remain intact.To better illustrate this consider the study of Almeida et al.; In the brains of congenitally deaf individuals (but not in the brains of hearing participants), certain parameters of visual stimuli were represented in the auditory cortex. That is, the lack of auditory stimulation caused the respective processing area to be functionally “swallowed up” by the consistently activated visual processing areas [14].It truly is a “use it or lose it” brain.g. Memory works like a video recorder.The mind can literally “replay” and “fast forward” experiences you had during the day, while you are sleeping. In particular, animal experiments have shown that, during periods of deep sleep, brain areas involved in the encoding and retrieval of recent experiences can show similar patterns of activation (firing of the same neurons in the same sequence) to those observed during active behavior, a process called “coordinated replay”. This reactivation occurs at a much faster time scale than the actual experience, so in a sense it is a “fast forward” representation of the original event, and it is believed to be the neural correlate of storing experiences into memory [15]. Remember the good old “sleeping is good for your memory”?An even cooler finding, is that induced, artificial replay during sleep can implant false memories into the brains of mice. Using electrodes to directly stimulate activity in the medial forebrain bundle (a component of the reward circuitry) paired with stimulation of certain “place cells” of the hippocampus (which are normally activated when an animal explores or navigates within an environment) neuroscientists made mice believe they had a pleasant, rewarding experience at a special location, when in reality this had never happened [16]h. More precisely: Memory works as a defective/creative video recorder.Our brains do not exactly “record” events we experience, but in reality they store rather inaccurate and malleable versions of past episodes. Memory is highly prone to a large array of distorting influences, including emotion, motivation, cues, suggestion, context and frequency of use [17]. Under certain conditions, even imagining events that never took place may create false memories of those events [18].i. Our visual system cannot perceive the present.Sensory receptors in our eyes receive physical stimuli in the form of light. These stimuli are then converted into electrical signals and sent to the brain, which interprets the signals as images. This process takes around 100 ms [19], meaning that due to that delay we would only be able to perceive snapshots of the recent past.However, according to modern science our brain seems to be “aware” of its inherent limitation and trying to compensate for it! It has been hypothesized that our visual system predicts how the world most probably looks like at the time the visual stimulus is delivered to the brain, and generates a percept of its own prediction, rather than an image of the recent past [20]. This “latency correction” is proposed to underlie some classical visual illusions [21], like the Flash-lag effect, in which a flash shown in alignment with a moving object is perceived to lag the moving object.Check out this flash-lag illusion video: Flash-lag Effect: Visual Illusion 3Dj. The brain located in your skull is not your only one (don’t smirk…).There is a second brain located in your intestines amounting to an impressive total of ~200-600 million neurons (as many as in the spinal cord), called the “enteric nervous system” (ENS) [22].It works in concert with the brain to control digestive function. However, it does not require the brain to function, but it can stand as an integrative neural system alone (making our intestine the only bodily organ that can circumvent the authority of the brain). When the vagus nerve is severed, ENS is capable of organizing and initiating its own reflexes for digestion [23], which is why people who have suffered complete spinal cord injury are still able to defecate, even though voluntary control over this activity is lost.An even more interesting fact, is that the gut sends neuroendocrine signals to the brain, where they are converted into emotions, like hunger or satiety, nausea, discomfort, and fatique [24]. And even if it goes against your gut feelings, the ENS produces ~90% of all serotonin (which we could simplistically describe as the “happiness neurotransmitter”) in the body [25], along with around 30 other types of neurotransmitters [26], and even expresses opiate receptors [27].1. Woolf, C., et. al. (2007) Nociceptors—Noxious Stimulus Detectors. Neuron, Volume 55, Issue 3, Pages 353-3642. Watch What It's Like to Be Awake During Brain Surgery3. Trivedi B.P (2012), Hardwired for taste, Nature Neuroscience; 486, S7–S9: doi:10.1038/486S7a4. Y. Oomura, T. Ono, H. Ooyama &M.J. Wayner (1969), Glucose and osmosensitive neurones of the rat hypothalamus, Nature; 222: 282–284.5. Singh N., Vrontakis M., Parkinson F. & Chelikani P. (2011), Functional bitter taste receptors are expressed in brain cells, Biochemical and Biophysical Research Communications; 406: 146-151.6. Kaushik S, Rodriguez-Navarro J.A. , Arias E.,et al. (2011), Autophagy in Hypothalamic AgRP Neurons Regulates Food Intake and Energy Balance. Cell Metabolism; 14(2), 173-183, doi: 10.1016/j.cmet.2011.06.0087. Webster J.P (2001). Rats, cats, people and parasites: the impact of latent toxoplasmosis on behaviour. Microbes Infect.;3:1037–1045.8. Beverley J.K.A. Toxoplasmosis in animals. Vet. Rec. 1976;99:123–1279. Berdoy M, Webster J.P, Macdonald D.W. (2000), Fatal attraction in rats infected with Toxoplasma gondii. Proc. R. Soc. B.;267:1591–1594.10. Flegr J. (2007), Effects of Toxoplasma on Human Behavior, Schizophr Bull; 33(3): 757–760.11. Kocazeybek B., Oner Y.A., Turksoy R., et al. (2009), Higher prevalence of toxoplasmosis in victims of traffic accidents suggest increased risk of traffic accident in Toxoplasma-infected inhabitants of Istanbul and its suburbs., Forensic Sci Int.;187(1-3):103-108.12. Feuillet L., Dufour H. & Pelletier J., (2007), Brain of a white-collar worker, The Lancet, 370 (9583): 262.13. Lew S.M. (2014), Hemispherectomy in the treatment of seizures: a review, Transl Pediatr; 3(3): 208–217..14. Almeida J., He D., Chen Q., et al. (2015), Decoding Visual Location From Neural Patterns in the Auditory Cortex of the Congenitally Deaf, Psychol Sci.; 26(11): 1771–1782.15. Van Dongen E.V., Takashima A. et al. (2012), Memory stabilization with targeted reactivation during human slow-wave sleep, PNAS; 109 (26): 10575–10580.16. de Lavilléon, G., Lacroix M.M. Rondi-Reig L. & Benchenane K., (2015). Explicit memory creation during sleep demonstrates a causal role of place cells in navigation., Nat. Neurosci., 18(4):493-495.17. Schacter D. L. (2012)., Constructive memory: past and future., Dialogues Clin. Neurosci. 14: 7–1818. Hyman IE. & Jr. Pentland J. (1996), The role of mental imagery in the creation of false childhood memories., J Mem Lang.;35:101–117.19. Liu, H., Agam, Y., Madsen, J. R., & Kreiman, G. (2009). Timing, timing, timing: Fast decoding of object information from intracranial field potentials in human visual cortex. Neuron; 62(2): 281–290.20. Changizi M.A., (2001), 'Perceiving the present' as a framework for ecological explanations of the misperception of projected angle and angular size., Perception; 30(2):195-208.21. Changizi M.A. & Widders D.M, (2002), Latency Correction Explains the Classical Geometrical Illusions, Perception; 31(10): 1241-1262.22. Furenss J.B., Callaghan B.P., Rivera L.R. & Cho H.J., The enteric nervous system and gastrointestinal innervation: integrated local and central control., Adv Exp Med Biol.;817:39-71.23. Ying L. & Chung O. (2003). "Musings on the Wanderer: What's New in Our Understanding of Vago-Vagal Reflexes? V. Remodeling of vagus and enteric neural circuitry after vagal injury". American Journal of Physiology. Gastrointestinal and Liver Physiology. 285 (3): 461-469.24. Mayer, E. A. (2011)., Gut feelings: the emerging biology of gut–brain communication. Nature Reviews. Neuroscience, 12(8), 10.1038/nrn3071. http://doi.org/10.1038/nrn307125. Jenkins, T. A., Nguyen, J. C. D., Polglaze, K. E., & Bertrand, P. P. (2016). Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis. Nutrients; 8(1), 56. Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis26. McConalogu K. & Furness J.B. (1994), Gastrointestinal neurotransmitters, Baillieres Clin Endocrinol Metab.;8(1):51-76.27. Holzer P. (2004), Opioids and opioid receptors in the enteric nervous system: from a problem in opioid analgesia to a possible new prokinetic therapy in humans., Neurosci Lett.; 361(1-3):192-195.

Please explain what and when the procedure was performed. Has the patient been seen since surgery by the physician? What was the reason provided for not seeing the patient?There is a patient abandonment issue. The person doing the surgery should do follow up for any complication related to the procedure he/she performed. Is it because of noncompliance, schedule conflict, non-payment etc?[Edit: Per additional history provided in the Comments section. The article below addresses medical management after bariatric surgery. The physician has tried to work up surgical complications. This is the section regarding nausea and vomiting. The authors mention antiemetic unless there are other issues. I hesitate to second guess what the surgeon’s train of thought is. I do think there should be response to the patient’s communications. I understand the frustration and the cost of repeat emergency room visits. Someone here has suggested contacting the chief of surgery. Post bariatric surgery recuperation can be problematic and I hope the symptoms resolve in time.Nausea and vomitingNausea and vomiting can often be helped by antiemetic or prokinetic drugs, however, some patients have chronic functional nausea and/or vomiting that does not fit the pattern of cyclic vomiting syndrome or other gastrointestinal disorders, hence particular attention should be directed to potential psychosocial factors post bariatric surgery. Therefore, low dose antidepressant medications and psychotherapy should be addressed. On demand CT scan and Gastroscopy could be the gold standard investigations in chronic situations[39,40].]World J Gastrointest Surg. 2014 Nov 27; 6(11): 220–228.Published online 2014 Nov 27. doi: 10.4240/wjgs.v6.i11.220PMCID: PMC4241489Medical management of patients after bariatric surgery: Principles and guidelinesAbd Elrazek Mohammad Ali Abd Elrazek, Abduh Elsayed Mohamed Elbanna, and Shymaa E BilasyAuthor information ► Article notes ► Copyright and License information ►This article has been cited by other articles in PMC.Go to:AbstractObesity is a major and growing health care concern. Large epidemiologic studies that evaluated the relationship between obesity and mortality, observed that a higher body-mass index (BMI) is associated with increased rate of death from several causes, among them cardiovascular disease; which is particularly true for those with morbid obesity. Being overweight was also associated with decreased survival in several studies. Unfortunately, obese subjects are often exposed to public disapproval because of their fatness which significantly affects their psychosocial behavior. All obese patients (BMI ≥ 30 kg/m) should receive counseling on diet, lifestyle, exercise and goals for weight management. Individuals with BMI ≥ 40 kg/m and those with BMI > 35 kg/m with obesity-related comorbidities; who failed diet, exercise, and drug therapy, should be considered for bariatric surgery. In current review article, we will shed light on important medical principles that each surgeon/gastroenterologist needs to know about bariatric surgical procedure, with special concern to the early post operative period. Additionally, we will explain the common complications that usually follow bariatric surgery and elucidate medical guidelines in their management. For the first 24 h after the bariatric surgery, the postoperative priorities include pain management, leakage, nausea and vomiting, intravenous fluid management, pulmonary hygiene, and ambulation. Patients maintain a low calorie liquid diet for the first few postoperative days that is gradually changed to soft solid food diet within two or three weeks following the bariatric surgery. Later, patients should be monitored for postoperative complications. Hypertension, diabetes, dumping syndrome, gastrointestinal and psychosomatic disorders are among the most important medical conditions discussed in this review.Keywords: Obesity, Bariatric surgery, Postoperative care, Body-mass index, El bannaCore tip: Obesity is a growing health concern worldwide that impacts the life of individuals both physically and psychologically. There are several well-established health hazards associated with obesity. Additionally, obese subjects are often exposed to public disapproval because of their fatness which significantly affects their psychosocial behavior. Bariatric surgery is one of the definite solutions for obesity. In this review, we will briefly discuss the general guidelines that should be considered before bariatric surgery. Also, we discuss the protocols of patients’ postoperative care and the management of medical disorders that must be considered after bariatric surgery.Go to:INTRODUCTIONObesity is a chronic disease that impairs health-related quality of life in adolescents and children. In 2010, overweight and obesity were estimated to cause 3.4 million deaths, 3.9% of years of life loss, and 3.8% of disability-adjusted life-years worldwide. Obesity is increasing in prevalence, currently, the proportion of adults with a body-mass index (BMI) of 25 kg/m or greater is 36.9% in men and 38.0% in women worldwide[1]. Attempts to explain the large increase in obesity in the past 30 years focused on several potential contributors including increase in caloric intake, changes in the composition of diet, decrease in the levels of physical activity and changes in the gut microbiome. More than 50% of the obese individuals in the world are located in ten countries (listed in order of number of obese individuals): United States, China, India, Russia, Brazil, Mexico, Egypt, Germany, Pakistan and Indonesia. Although age-standardized rates were lower in developing than in developed countries overall, 62% of the world’s obese individuals live in developing countries. Recently, United States accounted for 13% of obese people worldwide, the prevalence of obesity was 31.7% and 33.9% among adult men and women, respectively. In Canada 21.9% of men and 20.5% of women are obese. Reported prevalence rates of obesity include: 27.5% of men and 29.8% of women in Australia, 24.5% of men and 25.4% of women in the United Kingdom, in Germany 21.9% of men and 22.5% of women, in Mexico 20.6% of men and 32.7% of women, in South Africa 13.5% of men and 42% of women, in Egypt 26.4% of men and 48.4% of women, in Saudi Arabia 30% of men and 44.4% of women and in Kuwait 43.4% of men and 58.6% of women Figure ​Figure11)[2].There are several well-established health hazards associated with obesity, e.g., nonalcoholic steatohepatitis (NASH), type 2 diabetes, heart disease, chronic kidney disease, gastroesophageal reflux disease, gastrointestinal motility disorders, sexual disorders, cerebrovascular stroke, certain cancers, osteoarthritis, depression and others[3-10]. The risk of development of such complications rises with the increase of adiposity, while weight loss can reduce the risk. Bariatric surgery could be the definitive clue in many situations[11-15]. Bariatric surgery is one of the fastest growing operative procedures performed worldwide, with an estimated > 340000 operations performed in 2011. While the absolute growth rate of bariatric surgery in Asia was 44.9% between 2005 and 2009, the numbers of procedures performed in the United States plateaued at approximately 200000 operations per year[16,17]. Starting in 2006, the Center for Medicare and Medicaid Services, United States, restricted the coverage of bariatric surgery to hospitals designated as “Centers of Excellence” by two major professional organizations[18]. Medical management and follow up of patients who have undergone bariatric surgery is a challenge due to post operative complications.GENERAL GUIDELINES FOR SURGEONS/GASTROENTEROLOGISTSA well skilled physician or a surgeon has to consider the followings:(1) as the prevalence of obesity increases so does the prevalence of the comorbidities associated with obesity. Losing weight means overcoming illness at the present, complications in future and alleviating the economic burden in the present and future;(2) Overweight; BMI between 25 and 30, technically refers to excessive body weight, whereas “obesity” BMI ≥ 30 kg/m refers excessive body fat, “Severe obesity”, BMI ≥ 35 kg/m, or “morbid obesity” refers to individuals with obesity-related comorbidities. Furthermore, severe obesity and morbid obesity groups who failed dietary and medical regimens are candidates for bariatric surgery;(3) Children obesity; refers to children with BMI > 95th percentile for their age and sex and “overweight” refers to children with BMI between the 85th and 95th percentile for their age and sex;(4) Patients undergoing a bariatric operation should have a nutritional assessment for deficiencies in macro and micronutrients, also with no contraindication for such a major operation;(5) Most of bariatric procedures are performed in women (> 80%) and approximately half of these (> 40% of all bariatric procedures) are performed in reproductive aged women, accordingly, pregnancy planning and contraception options should be discussed in details with women who will undergo bariatric procedures. Fertility improves soon after bariatric surgery, particularly in middle-aged women, who were anovulatory. Additionally, oral contraceptives may be less effective in women who have undergone malabsorptive bariatric procedure. Therefore, it is better to delay pregnancy for 6-12 mo following bariatric surgery. Risk of preeclampsia, gestational diabetes, and macrosomia significantly decrease post bariatric surgery, but the risk of intrauterine growth restriction/small infants for their gestational age may increase. Body contouring surgery is in high demand following bariatric surgery;(6) All bariatric operations are accompanied with restrictive and/or malabsorption maneuvers; less food intake and malabsorption concepts;(7) The most common types of bariatric surgeries performed worldwide are Sleeve gastrectomy (SG): This procedure involves the longitudinal excision of the stomach and thus shaping the remaining part of the stomach into a tube or a “sleeve” like structure. SG removes almost 85% of the stomach (Figure ​(Figure2);2); Roux-en-Y gastric bypass (RYGB): It reduces the size of the stomach to the size of a small pouch that is directly surgically attached to the lower part of the small intestine. In this procedure, most of the stomach and the duodenum are surgically stapled and therefore, bypassed (Figure ​(Figure3);3); The laparoscopic adjustable gastric band (AGB): This is one of the least invasive procedures, where the surgeon inserts an adjustable band around a portion of the stomach and therefore, patients feel fuller after eating smaller food portions (Figure ​(Figure4).4). Bariatric surgical procedures, particularly RYGB, plus medical therapy, are effective interventions for treating type 2 diabetes. Improvement in metabolic control is often evident within days to weeks following RYGB; and(8) Complications reported following bariatric surgery vary based upon the procedure performed. Cholilithiasis, renal stone formation and incisional hernia could be the delayed phase complications; on the other hand, bleeding, leaking, infection and pulmonary embolism could be the early phase complications following the bariatric procedure. The overall 30-d mortality for bariatric surgical procedures worldwide is less than 1%.Roux-in Y Gastrectomy, sleeve gastrectomy. and adjustable gastric band.POST OPERATIVE CARE AND FOLLOW UPEarly post operative period; (1-3) d post bariatric surgeryPatients undergoing a bariatric operation are admitted to the post-anesthesia care unit (PACU) immediately at the conclusion of the operation. Usually, on postoperative day (POD) one, we begin oral therapy in tablet or crushed-tablet and liquid form if there is a naso-gastric tube after the gastrografin leak test. A basic metabolic profile (e.g., complete blood count, electrolytes, renal function, liver function, prothrombin time and partial thromboplastin time) should be obtained every 12 h for the successive two PODs, then every 24 h for another 3 d. Oxygen is administered by nasal cannula and weaned thereafter. The likelihood that, early specific complication, will arise for a given patient is determined by the nature of the procedure, the anesthetic techniques used, and the patient’s preoperative diseases. Respiratory problems are common complication in the early postoperative period following bariatric surgery. Patients with significant comorbidities, particularly neuromuscular, pulmonary, or cardiac problems are at a higher risk for respiratory compromise, but any patient can develop hypoxemia following bariatric surgery. For prophylaxis against Deep Venous Thrombosis (DVT) following bariatric surgeries, ultrasound evaluation is recommended for all patients, D-dimer test should be applied for suspected patients with DVT, especially after long operative time, repeat ultrasound or venography may be required for those with suspected calf vein DVT and a negative initial ultrasound investigation[19,20].Late post operative monitoringAfter the PACU period, most patients are transferred to the inpatient surgical postoperative unit. For the next 24-72 h, the postoperative priorities include ruling out an anastomotic leak following laparoscopic RYGB or laparoscopic SG. If no leak is observed, patients are allowed to start a clear liquid diet and soft drinks. The postoperative care team cares for the following: control of pain, care of the wound, continuous monitoring of blood pressure, intravenous fluid management, pulmonary hygiene, and ambulation. Post-bariatric nausea and vomiting is directly correlated with the length of the surgery; it also increases in females, non-smokers, and those patients with prior history of vomiting or motion sickness. Prophylaxis with pharmacologic treatment before the development of post operative nausea and vomiting significantly reduces its incidence after surgery[21-23].After hospital dischargeDiet: Usually patients are discharged 4-6 d after surgery. Most patients are typically discharged from the hospital on a full liquid diet, patients should be taught to keep monitoring their hydration and urine output. Approximately two-three weeks after surgery, the diet is gradually changed to soft, solid foods. The average caloric intake ranges from (400) to (800) kcal/d for the first month, and thus the daily glycemic load is greatly reduced. We encourage patients to consume a diet consisting of salads, fruits, vegetables and soft protein daily.To control the epigastric pain and vomiting, patients should be taught to eat slowly, to stop eating as soon as they reach satiety and not to consume food and beverages at the same time. For most patients suffering chronic vomiting, prokinetic therapy and proton-pump inhibitors (PPIs) should be considered. Patients, who underwent SG, LAGB or RYGB, benefit from a well-planned dietary advancement. Patients should understand that the surgery has changed their body but not the environment, they have to choose healthy foods, do not skip meals and to visit the dietitian regularly in the first 12 mo after surgery. However, if food intolerance develops, patients may choose a more vegetarian-based diet. Nevertheless, fresh fruits and vegetables are usually tolerated without a problem. The daily protein intake should be between 1.0 to 1.5 g/kg ideal body weight per day[24]. The biliopancreatic diversion/duodenal switch (BPD/DS) is a malabsorptive procedure for both macro- and micronutrients. Hence, we encourage higher protein intake of 1.5 g to 2.0 g of protein/kg ideal body weight per day, making the average protein requirement per day approximately 90 g/d[25,26]. Alcohol is better prevented in the first 6-12 mo after surgery[27].Monitoring: Patients should generally have their weight and blood pressure measured weekly until the rapid weight loss phase diminishes, usually within 4-6 mo, then again at 8, 10 and 12 mo, and annually thereafter. Patients with diabetes are encouraged to check their blood glucose daily. Glycemic control typically improves rapidly following bariatric surgery. Patients maintained on antihypertensive or diabetic medications at discharge should be monitored closely for hypotension and hypoglycemia, respectively, and medications should be adjusted accordingly. We recommend that the following laboratory tests be performed at three, six, nine months and annually thereafter: (1) Complete Blood Count; (2) Electrolytes; (3) Glucose and Glucose Tolerance test; (4) Complete iron studies; (5) Vitamin B12; (6) Aminotransferases, alkaline phosphatase, bilirubin, GGT; (7) Total protein and Albumin; (8) Complete lipid profile; (9) 25-hydroxyvitamin D, parathyroid hormone; (10)Thiamine; (11) Folate; (12) Zinc; and (13) Copper.Complications following the surgical treatment of severe obesity vary based upon the procedure performed. Secondary hyperparathyroidism, Hypocalcemia, Gastric remnant distension, Stomal stenosis/Obstruction, Marginal ulcerations, Cholilithiasis, Ventral incisional hernia, Internal hernia, Hiatus Hernia, Short bowel syndrome, Renal failure, Gastric prolapse, infection, Esophagitis, Reflux, Vomiting, Hepatic abnormalities and dumping syndrome are common late-phase complications after bariatric surgery. However, the clinician should aware of complications specific for every bariatric procedure[28,29]. Before therapy, the clinician should understand that the impact of various bariatric surgeries on drug absorption and metabolism are scarce. On the other hand, RYGB and other malabsorptive procedures that significantly exclude the proximal part of the small intestine, decrease the surface area where most drug absorption occurs and may result in a reduction in systemic bioavailability[30-32].Go to:COMMON MEDICAL CONDITIONS FOLLOWING BARIATRIC SURGERYHypertensionHypertension is not always related to obesity, and dietary interventions do not assure the normalization of blood pressure. However weight loss, whether by an intensive lifestyle medical modification program or by a bariatric operation, improves obesity-linked hypertension. Patients should be monitored weekly until the blood pressure has stabilized, and patients may need to resume antihypertensive medications, but often at adjusted doses[33].DiabetesPatients with diabetes should have frequent monitoring of blood glucose in the early postoperative period and should be managed with sliding scale insulin. Many diabetic patients have a decreased need for insulin and oral hypoglycemic agents after bariatric surgery. Oral sulfonylureas and meglitinides should be discontinued postoperatively as these medications can lead to hypoglycemia after bariatric surgery. Metformin is the safest oral drug in the postoperative period, since it is not associated with dramatic fluctuations in blood glucose. RYGB is associated with durable remission of type 2 diabetes in many, but not all, severely obese diabetic adults. However those who underwent LAGB generally exhibit a slower improvement in glucose metabolism and diabetes as they lose weight in a gradual fashion[34,35].RefluxMedications for gastroesophageal reflux disease (GERD) may be discontinued after RYGB and Laparoscopic AGB, however, SG has been associated with an increased incidence of GERD in some procedures. Recurrent GERD symptoms after RYGB, particularly when accompanied by weight regain, should raise the possibility of a gastrogastric fistula between the gastric pouch and remnant, and should be investigated by an upper GI contrast study or CT scan and referred to the bariatric surgeon. Upper endoscopy is the best investigation to exclude other esophagogastroduodenal disorders. GERD may be associated with esophageal complications including esophagitis, peptic stricture, Barrett’s metaplasia, esophageal cancer and other pulmonary complications. Failure of the PPI treatment to resolve GERD-related symptoms has become one of the most common complications of GERD after bariatric surgery. Most patients who fail PPI treatment have Non Erosive Reflux Disease and without pathological reflux on pH testing. In patients with persistent heartburn despite of medical therapy, it is reasonable to recommend avoidance of specific lifestyle activities that have been identified by patients or physicians to trigger GERD-related symptoms[36-38].Nausea and vomitingNausea and vomiting can often be helped by antiemetic or prokinetic drugs, however, some patients have chronic functional nausea and/or vomiting that does not fit the pattern of cyclic vomiting syndrome or other gastrointestinal disorders, hence particular attention should be directed to potential psychosocial factors post bariatric surgery. Therefore, low dose antidepressant medications and psychotherapy should be addressed. On demand CT scan and Gastroscopy could be the gold standard investigations in chronic situations[39,40].Marginal ulcerationDue to increased risk of ulcer formation from nonsteroidal anti-inflammatory drugs (NSAIDs), these medications should be discontinued postoperatively, especially after RYGB. NSAID use is associated with an increased risk of bleeding. If analgesic or anti-inflammatory treatment is needed, the use of acetaminophen is preferred in a dose of 1-2 g/daily[41-45]. Other factors associated with increased risk of ulcer formation are smoking, alcohol, spicy food, gastrogastric fistulas, ischemia at the site of surgical anastomosis, poor tissue perfusion due to tension, presence of foreign material, such as staples and/or Helicobacter pylori infection. Diagnosis is established by upper endoscopy. According to our strategy, all patients should undergo diagnostic upper endoscopy to exclude congenital or GI diseases prior to bariatric procedures. Medical management is usually successful and surgical intervention is rarely needed[46-48].Go to:DUMPING SYNDROMEDumping syndrome or rapid gastric emptying is a group of symptoms that most likely occur following bariatric bypass. It occurs when the undigested contents of the stomach move too rapidly into the small intestine. Many patients who underwent bariatric bypass experienced postprandial hypoglycemia. However, the dumping syndrome usually occurs early (within one hour) after eating and is not associated with hypoglycemia. It is presumed to be caused by contraction of the plasma volume due to fluid shifts into the gastrointestinal tract. Dumping syndrome may result in tachycardia, abdominal pain, diaphoresis, nausea, vomiting, diarrhea, and sometimes, hypoglycemia. The late dumping syndrome is a result of the hyperglycemia and the subsequent insulin response leading to hypoglycemia that occurs around 2-3 h after a meal. Dumping syndrome is a common problem that occurs in patients who have undergone RYGB and when high levels of simple carbohydrates are ingested. Accordingly, patients who have experienced postgastric bypass bariatric surgery should avoid foods that are high in simple sugar content and replace them with a diet consisting of high fiber and protein rich food. Eating vegetables and salad is encouraged; beverages and alcohol consumption are better avoided[49].Go to:PSYCHOSOMATIC DISORDERS/DEPRESSIONMany patients usually experience enhanced self esteem and improved situational depression following weight loss. Depression often requires continued treatment, specially that, many patients with severe obesity often use food for emotional reasons. Therefore, when those patients experience a small gastric pouch postoperatively they may grieve the loss of food. Many studies documented the relationship between eating disorder and anxiety disorder, depression or schizophrenia[50,51]. Displaced emotions can result in somatization with symptoms of depression and psychosomatic disorders. It is important that clinicians recognize the psychological aspect of food loss after bariatric surgery, and reassure patients that the symptoms are related to the small gastric pouch size. Antidepressants often help to decrease the anxiety related to grieving associated with food loss, although the use of antidepressants needs to be approached with an empathetic style. Behavioral and emotive therapies are reported to be very helpful[52,53].Go to:OUTCOMEBariatric surgery remains the only effective sustained weight loss option for morbidly obese patients. The American Society for Metabolic and Bariatric Surgery estimated that in 2008 alone, about 220000 patients in the United States underwent a weight loss operation. The optimal choice for type of bariatric procedure, i.e., RYGB, SG, AGB or the selected surgical approach, i.e., open versus laparoscopic depends upon each individualized goals, i.e., weight loss, glycemic control, surgical skills, center experience, patient preferences, personalized risk assessment and other medical facilities. Laparoscopic sleeve gastrectomy is the most common bariatric procedure. However weight re-gain after long-term follow-up was reported[54-58]. Prospective studies and reviews report a general tendency for patients with metabolic disorders to improve or normalize after bariatric surgery. However weight loss is highly variable following each procedure. Recent studies have evaluated the potential impact of obesity on outcomes in organ-transplant recipients, for example bariatric surgery may be an important bridge to transplantation for morbidly obese patients with severe heart failure[59-63].Go to:RECENT ADVANCES IN BARIATRIC SURGERYA modified intestinal bypass bariatric procedure (Elbanna operation), reported a novel surgical technique designed to maintain good digestion, better satiety, and selective absorption with less medical and surgical complications (Figure ​(Figure5).5). This procedure preserves the proximal duodenum and the terminal ileum and thus preserving the anatomical biliary drainage and enterohepatic circulation[64,65].Figure 5Novel ElBanna surgical procedure.Recently, a novel bariatric technique dedicated; Modified Elbanna technique in childhood bariatric, showed promising success in pediatric surgeries (non published data).Go to:CONCLUSIONThe rising prevalence of overweight and obesity in several countries has been described as a global pandemic. Obesity can be considered like the driving force towards the pre-mature deaths. It increases the like hood for the development of diabetes, hypertension and NASH. The American Heart Association identified obesity as an independent risk factor for the development of coronary heart disease. In order to minimize post-surgical cardiovascular risk, surgical weight loss may become a more frequently utilized option to address obesity. Currently, bariatric surgery passes through a plateau phase, hence medical management and follow up of patients who have undergone bariatric surgery is a challenge.Go to:FUTURE RECOMMENDATIONSChildren obesity has become one of the most important public health problems in many industrial countries. In the United States alone, 5% of children have severe obesity. It is imperative that health care providers should identify overweight and obese children so as to start early counseling and therapy. To establish a therapeutic relationship and enhance effectiveness, the communication and interventions should be supported by the entire family, society, school, public media and primary health care. Bariatric surgery could be considered in complicated cases that failed all other options.Go to:FootnotesP- Reviewer: Amiya E, Firstenberg MS, Narciso-Schiavon JL S- Editor: Tian YL L- Editor: A E- Editor: Lu YJGo to:References1. 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IntroductionDespite continuous advances in the medical world, obesity continues to remain a major worldwide health hazard with adult mortality as high as 2.8 million per year. The majority of chronic diseases like diabetes, hypertension, and heart disease are largely related to obesity which is usually a product of unhealthy lifestyle and poor dietary habits. Appropriately tailored diet regimens for weight reduction can help manage the obesity epidemic to some extent. One diet regimen that has proven to be very effective for rapid weight loss is a very-low-carbohydrate and high-fat ketogenic diet.FunctionA ketogenic diet primarily consists of high-fats, moderate-proteins, and very-low-carbohydrates. The dietary macronutrients are divided into approximately 55% to 60% fat, 30% to 35% protein and 5% to 10% carbohydrates. Specifically, in a 2000 kcal per day diet, carbohydrates amount up to 20 to 50 g per day.History and OriginRussel Wilder first used the ketogenic diet to treat epilepsy in 1921. He also coined the term "ketogenic diet." For almost a decade, the ketogenic diet enjoyed a place in the medical world as a therapeutic diet for pediatric epilepsy and was widely used until its popularity ceased with the introduction of antiepileptic agents. The resurgence of the ketogenic diet as a rapid weight loss formula is a relatively new concept the has shown to be quite effective, at least in the short run.Physiology and BiochemistryBasically, carbohydrates are the primary source of energy production in body tissues. When the body is deprived of carbohydrates due to reducing intake to less than 50g per day, insulin secretion is significantly reduced and the body enters a catabolic state. Glycogen stores deplete, forcing the body to go through certain metabolic changes. Two metabolic processes come into action when there is low carbohydrate availability in body tissues: gluconeogenesis and ketogenesis.Gluconeogenesis is the endogenous production of glucose in the body, especially in the liver primarily from lactic acid, glycerol, and the amino acids alanine and glutamine. When glucose availability drops further, the endogenous production of glucose is not able to keep up with the needs of the body and ketogenesis begins in order to provide an alternate source of energy in the form of ketone bodies. Ketone bodies replace glucose as a primary source of energy. During ketogenesis due to low blood glucose feedback, stimulus for insulin secretion is also low, which sharply reduces the stimulus for fat and glucose storage. Other hormonal changes may contribute to the increased breakdown of fats that result in fatty acids. Fatty acids are metabolized to acetoacetate which is later converted to beta-hydroxybutyrate and acetone. These are the basic ketone bodies that accumulate in the body as a ketogenic diet is sustained. This metabolic state is referred to as "nutritional ketosis." As long as the body is deprived of carbohydrates, metabolism remains in the ketotic state. The nutritional ketosis state is considered quite safe, as ketone bodies are produced in small concentrations without any alterations in blood pH. It greatly differs from ketoacidosis, a life-threatening condition where ketone bodies are produced in extremely larger concentrations, altering blood ph to acidotic a state.Ketone bodies synthesized in the body can be easily utilized for energy production by heart, muscle tissue, and the kidneys. Ketone bodies also can cross the blood-brain barrier to provide an alternative source of energy to the brain. RBCs and the liver do not utilize ketones due to lack of mitochondria and enzyme diaphorase respectively. Ketone body production depends on several factors such as resting basal metabolic rate (BMR), body mass index (BMI), and body fat percentage. Ketone bodies produce more adenosine triphosphate in comparison to glucose, sometimes aptly called a "super fuel." One hundred grams of acetoacetate generates 9400 grams of ATP, and 100 g of beta-hydroxybutyrate yields 10,500 grams of ATP; whereas, 100 grams of glucose produces only 8,700 grams of ATP. This allows the body to maintain efficient fuel production even during a caloric deficit. Ketone bodies also decrease free radical damage and enhance antioxidant capacity.Issues of ConcernAdverse EffectsThe short-term effects (up to 2 years) of the ketogenic diet are well reported and established. However, the long-term health implications are not well known due to limited literature.The most common and relatively minor short-term side effects of ketogenic diet include a collection of symptoms like nausea, vomiting, headache, fatigue, dizziness, insomnia, difficulty in exercise tolerance, and constipation, sometimes referred to as keto flu. These symptoms resolve in a few days to few weeks. Ensuring adequate fluid and electrolyte intake can help counter some of these symptoms. Long-term adverse effects include hepatic steatosis, hypoproteinemia, kidney stones, and vitamin and mineral deficiencies.Cautions and ContraindicationsPeople suffering from diabetes and taking insulin or oral hypoglycemic agents suffer severe hypoglycemia if the medications are not appropriately adjusted before initiating this diet. The ketogenic diet is contraindicated in patients with pancreatitis, liver failure, disorders of fat metabolism, primary carnitine deficiency, carnitine palmitoyltransferase deficiency, carnitine translocase deficiency, porphyrias, or pyruvate kinase deficiency. People on a ketogenic diet rarely can have a false positive breath alcohol test. Due to ketonemia, acetone in the body can sometimes be reduced to isopropanol by hepatic alcohol dehydrogenase which can give a false positive alcohol breath test result.Clinical SignificanceThe popular belief that high-fat diets cause obesity and several other diseases such as coronary heart disease, diabetes, and cancer has not been observed in recent epidemiological studies. Studies carried out in animals that were fed high-fat diets did not show a specific causal relationship between dietary fat and obesity. On the contrary, very-low-carbohydrate and high-fat diets such as the ketogenic diet have shown to beneficial to weight loss.Evidence Behind The Ketogenic DietIn relation to overall caloric intake, carbohydrates comprise around 55% of the typical American diet, ranging from 200 to 350 g/day. The vast potential of refined carbohydrates to cause harmful effects were relatively neglected until recently. A greater intake of sugar-laden food is associated with a 44% increased prevalence of metabolic syndrome and obesity and a 26% increase in the risk of developing diabetes mellitus. In a 2012 study of all cardiometabolic deaths (heart disease, stroke, and type 2 diabetes) in the United States, an estimated 45.4% were associated with suboptimal intakes of 10 dietary factors. The largest estimated mortality was associated with high sodium intake (9.5%), followed by low intake of nuts and seeds (8.5%), high intake of processed meats (8.2%), low intake of omega-3 fats (7.8%), low intake of vegetables 7.6%), low intake of fruits (7.5%), and high intake of artificially sweetened beverages (7.4%). The lowest estimated mortality was associated with low polyunsaturated fats (2.3%) and unprocessed red meats (0.4%). In addition to this direct harm, excess consumption of low-quality carbohydrates may displace and leave no room in the diet for healthier foods like nuts, unprocessed grains, fruits, and vegetables.A recent systemic review and meta-analysis of randomized controlled trials comparing the long-term effects (greater than 1 year) of dietary interventions on weight loss showed no sound evidence for recommending low-fat diets. In fact, low-carbohydrate diets led to significantly greater weight loss compared to low-fat interventions. It was observed that a carbohydrate-restricted diet is better than a low-fat diet for retaining an individual’s BMR. In other words, the quality of calories consumed may affect the number of calories burned. BMR dropped by more than 400 kcal/day on a low-fat diet when compared to a very low-carb diet.A well-formulated ketogenic diet, besides limiting carbohydrates, also limits protein intake moderately to less than 1g/lb body weight, unless individuals are performing heavy exercise involving weight training when the protein intake can be increased to 1.5g/lb body weight. This is to prevent the endogenous production of glucose in the body via gluconeogenesis. However, it does not restrict fat or overall daily calories. People on a ketogenic diet initially experience rapid weight loss up to 10 lbs in 2 weeks or less. This diet has a diuretic effect, and some early weight loss is due to water weight loss followed by a fat loss. Interestingly with this diet plan, lean body muscle is largely spared. As a nutritional ketosis state sustains, hunger pangs subside, and an overall reduction in caloric intake helps to further weight loss.Other IssuesLong-term compliance is low and can be a big issue with a ketogenic diet, but this is the case with any lifestyle change. Even though the ketogenic diet is significantly superior in the induction of weight loss in otherwise healthy patients with obesity and the induced weight loss is rapid, intense, and sustained until at least 2 year, the understanding of the clinical impacts, safety, tolerability, efficacy, duration of treatment, and prognosis after discontinuation of the diet is challenging and requires further studies to understand the disease-specific mechanisms.A ketogenic diet may be followed for a minimum of 2 to 3 weeks up to 6 to 12 months. Close monitoring of renal functions while on a ketogenic diet is imperative, and the transition from a ketogenic diet to a standard diet should be gradual and well controlled.Enhancing Healthcare Team OutcomesTo counter the obesity epidemic, some healthcare workers do recommend the ketogenic diet. However, the primary care provider, nurse practitioner, dietitian and internist need to be aware of a few facts.Overweight individuals with metabolic syndrome, insulin resistance, and type 2 diabetes are likely to see improvements in the clinical markers of disease risk with a well-formulated very-low-carbohydrate diet. Glucose control improves due to less glucose introduction and improved insulin sensitivity. In addition to reducing weight, especially truncal obesity and insulin resistance, low-carb diets also may help improve blood pressure, blood glucose regulation, triglycerides, and HDL cholesterol levels. However, LDL cholesterol may increase on this diet.Also, in various studies, the ketogenic diet has shown promising results in a variety of neurological disorders, like epilepsy, dementia, ALS, traumatic brain injury, acne, cancers, and metabolic disorders.Due to the complexity of the mechanism and lack of long-term studies, a general recommendation of the ketogenic diet for prevention of type 2 diabetes mellitus or cardiovascular disease may seem premature but is, however, not farfetched for primary weight loss.While in the short term the ketogenic diet may help one lose weight, this is not sustained over the long run. In addition, countless studies show that the diet is associated with many complications that often lead to emergency room visits and admissions for dehydration, electrolyte disturbances, and hypoglycemia.ReferencesJagadish S, Payne ET, Wong-Kisiel L, Nickels KC, Eckert S, Wirrell EC. The Ketogenic and Modified Atkins Diet Therapy for Children With Refractory Epilepsy of Genetic Etiology. Pediatr. Neurol. 2019 May;94:32-37.