Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1002_Библиотеки_им_академика_М_И_Перельмана

Bypassing the intestine comes with the substantial risk of increased bowel move­ments, atulence, anal rectal pathology, micronutrient and divalent cation decien­cies, and hypoproteinemia. Preserving 300 cm of small bowel, proper patient education, diet compliance, and nutritional supplementation mitigates the risk of these complications. Long-term follow-up with regular blood work checking protein, iron, calcium, fat-soluble vitamins, and parathyroid hormone (PTH) is mandatory. Morbidly obese patients are commonly nutrient decient secondary to years of abusing food with limited nutritional value [26]. Following SADS, gastric volume is reduced and the proximal half of the small intestine bypassed, a combination that predisposes patients to further malnutrition. Exacerbating the issue, poor intake leads to edema, reducing the absorptive capacity of the sleeved stomach. Following any bariatric pro­cedures that contain a malabsorptive element, complaints of weakness and fatigue must be investigated thoroughly. One critical deciency is thiamine secondary to poor intake and/or increased emesis. The human body has limited reserves of thiamine and the half-life is only 7days [27]. Deciency is potentiated by an impulse for consump­tion of high dextrose, high osmotic solutions (i.e., sports drinks). Thiamine promotes glucose utilization and should be administered prior to dextrose rich solutions [27]. Acute thiamine deciency can manifest with Wernicke’s syndrome and irreversible neurological damage. Additional factors that predispose SADS patients to malabsorp­tion include altered pH of gastric contents, bypassed duodenum, and the site of chole­cyctokinin (CCK) stimulation and small intestinal bacterial overgrowth (SIBO).

Output issues present later in the postoperative course. Laboratory abnormalities can occur, however this is not always the case. For patients with normal nutritional parameters despite frequent bowel movements, management is focused on control of diarrhea. As mentioned previously, carbohydrate abuse is often the etiology of diarrhea. Small intestinal bacterial overgrowth (SIBO) should be ruled out by a breath test. Treatment involves alteration of diet, the use of motility agents such as imodium and lomotil. An H2 blocker and PPI should be prescribed. Dietary modi­cation with minimization of carbohydrate and fat is necessary (the so-called FODMAP diet). Fiber and probiotics should be encouraged through diet and sup­plemented. Cholestyramine, a bile acid binding agent, is often effective but poorly tolerated by many patients. Other medications include clonidine, octreotide, and GLP-1 agonists. GLP-1 agonists delay gastric emptying. The GLP-2 analogue tele­glutitide is rarely used following bariatric surgery. Although its use leads to short­term gut hypertrophy, it is expensive and must be used regularly or the effect dissipates. If surgical revision is practical to reduce output it is often necessary given the paucity of alternatives.

If chronic diarrhea and poor nutritional parameters persist, liver failure may occur. Although more common following jejunoileal bypass in the past, liver failure can occur following modern bariatric surgery when the majority of usable calories are via simple sugars. Liver failure can be accelerated if bacterial overgrowth is present. Consideration should be given to surgical reconstruction following nutri­tional repletion whenever malnutrition is present. The primary goal of surgery is to increase the length of bowel taking part in absorption. Insertion of a jejunal feeding tube to augment postoperative oral feeding at the time of reconstruction should be considered.

B12 is a water-soluble vitamin, absorbed primarily in the ileum. Absorption of B12 requires the presence of intrinsic factor. Intrinsic factor activity is dependent on gastric acid levels, which are decreased following SADS.If bacterial overgrowth is present, bacteria compete for B12 further decreasing absorption. B12 deciency can present with megaloblastic anemia and neurologic symptoms. Supplementation is best given nasally, sublingually, or intradermally.

Another sequelae of malabsorption is nephrolithiasis, exacerbated by increased oxalate intake. Fat malabsorption leads to hypocalcemia secondary to calcium bind­ing to free fatty acids. Subsequently, free oxalate is absorbed via the colon. Oxalate in the bloodstream is ltered by the kidney and binds calcium within the urinary tract. Calcium oxalate crystals precipitate causing nephrolithiasis. Management includes a low oxalate diet, increased calcium, and adequate hydration.

For patients with severe esophagitis following SADS, conversion to an RYGB is a viable option. To accomplish this, the sleeved stomach is divided to form a pouch and the roux limb constructed from the previous BP limb. The distal sleeve is resected and an entero-enterostomy is performed where to loop was to prevent distal obstruction. This procedure is also indicated if chronic stricture or asymmetry of the sleeve is the etiology of GERD symptoms.

The purpose of this review article was to highlight our experience with the SADS.Bariatric surgery is an imperfect method to treat a fatal and debilitating dis­ease that works by creating a controlled abnormality. With proper technique, patient selection and education, and early detection of complications, SADS is an excellent weight loss option.