Dumping syndrome is a frequent complication of cancer and non-cancer oesophageal and gastric surgery, as well as bariatric surgery (also known as metabolic surgery). These interventions change gastric anatomy and innervation, which can enable a considerable amount of undigested food to reach the small intestine too rapidly 1-4. Dumping syndrome comprises a constellation of symptoms that can be subdivided into early and late dumping syndrome symptoms, which can occur jointly or separately 1-8. Typically, symptoms of early dumping syndrome occur within the first hour after a meal and include gastrointestinal symptoms (abdominal pain, bloating, borborygmi, nausea and diarrhoea) and vasomotor symptoms (flushing, palpitations, perspiration, tachycardia, hypotension, fatigue, desire to lie down and, rarely, syncope) 1,2. The underlying mechanisms might involve osmotic effects, peptide hormone release and autonomic neural responses 1. Symptoms of late dumping syndrome usually occur between 1 and 3 h after a meal and are primarily the manifestations of hypoglycaemia, which mainly results from an incretin-driven hyperinsulinaemic response after carbohydrate ingestion. Hypoglycaemia-related symptoms are attributable to neuroglycopenia (which is indicated by fatigue, weakness, confusion, hunger and syncope) and to vagal and sympathetic activation (indicated by perspiration, palpitations, tremor and irritability) 1,2. The literature has referred to late dumping syndrome as 'reactive hypoglycaemia' or, after bariatric surgery, as 'postbariatric hypoglycaemia'. However, on the basis of a common pathophysiology of rapid exposure of the small intestine to nutrients, which is also seen in early dumping syndrome (see subsequent discussion), we refer to this phenomenon as 'late dumping syndrome'. The prevalence of dumping syndrome depends on the type and extent of surgery, and on the criteria used to diagnose dumping syndrome. Dumping syndrome occurs in approximately 20% of patients undergoing

Anatomic and physiologic changes introduced by gastric surgery result in clinically significant dumping syndrome in approximately 10% of patients. Dumping is the effect of alteration in the motor functions of the stomach, including disturbances in the gastric reservoir and transporting function. Gastrointestinal hormones play an important role in dumping by mediating responses to surgical resection. Treatment options of dumping syndrome include diet, medications, and surgical revision. Poor nutrition status can be anticipated in patients who fail conservative therapy. Management of refractory dumping syndrome can be a challenge. This review highlights current knowledge about the mechanisms of dumping syndrome and available therapy.

This is the largest study to evaluate the outcome of endoscopic dilatations of GJ strictures after RYGB. Endoscopic balloon dilation is a safe and effective treatment for anastomotic strictures. However, it carries a small risk of perforation. Further case studies are needed to determine risk factors for perforation and if the patients can be managed conservatively in this setting.

Despite a high prevalence of esophageal dysmotility in our morbidly obese study population, there was a conspicuous absence of symptoms. Although the patients in this study were not directly questioned with regard to esophageal symptoms, several studies in the literature support our conclusion.

The American Society for Parenteral and Enteral Nutrition defines standards as benchmarks representing a range of performance of competent care that should be provided to assure safe and efficacious nutrition care in most circumstances. Standards are documents that define the structure needed to provide competent care. These Standards for Nutrition Support for Adult Hospitalized Patients are an update of the 2010 Standards. These practice-based standards are intended for use by healthcare professionals charged with the care of adult hospitalized patients receiving nutrition support therapy in any hospital with or without a formal nutrition support service or team. These Standards address professional responsibilities as they relate to patient assessment,

Morbid obesity is a serious disease resulting in considerable morbidity. Bariatric surgery is an important treatment modality of morbid obesity. It appears to be safe and effective in reduction of excess weight in carefully selected patients. However, it carries a risk of many short- and long-term complications, some of them unique to bariatric surgery. Knowledge of possible postoperative complications and their management will allow the achievement of the best results. Despite many types of bariatric procedures developed, only a few are currently performed. Since the number of bariatric procedures performed annually increases, primary care physicians and gastroenterologists will be increasingly challenged by post-bariatric surgery patients. Hence, better understanding of the anatomy and adaptive changes in bariatric patients allows for a more efficient evaluation and management of post-bariatric surgery problems. This article reviews common complications in post-bariatric surgery patients and provides guidelines for their evaluation and management.

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Gastroparesis (GP) is a common disease seen in gastroenterology practice particularly in western countries, and it may be underdiagnosed. The available drug therapies for this condition are quite disappointing. Botulinum toxin type A (BT) has been found to be effective therapy in various spastic disorders of smooth muscle of gastrointestinal tract. However, the benefits of BT injections in GP have been unclear. Several retrospective and open label studies have shown clinical advantages of intrapyloric Botulinum toxin type A injections, while two small randomized trials did not show positive results. Therefore, the available published studies yielded conflicting results leading to fading out of botox therapy for GP. We recognize possible clinical benefit of BT injections without any disadvantages of this treatment. We are calling for revisiting the endoscopy guided botox therapy in refractory GP. In this review we discuss important features of these studies pointing out differences in results among them. Differences in patient selection, doses and method of administration of botox toxin in the prior studies may be the cause of conflicting results. The mechanism of action, indications, efficacy and side-effects of BT are reviewed. Finally, we recognize limited evidence to recommend BT in GP and calling attention for future research in this field since no advances in drug management had been made in the last two decades.