Gastroparesis

Gastroparesis results in symptoms and objective findings of delayed emptying from the stomach in the absence of mechanical obstruction. Typical causes are diabetic, post-vagotomy, or idiopathic. The disorder typically represents abnormal extrinsic or intrinsic neural supply to the gastric smooth muscle. Gastroparesis may present with significant nutritional deficiencies [7], and attention to hydration and nutrition are essential for proper management of patients. The mainstays of treatment are dietary change (low fat, low nondigestible residue [fiber], small particle size supplement), prokinetics, and antiemetics. A randomized controlled trial demonstrated symptomatic benefit of a small size particle diet [8]. Other management strategies for gastroparesis and diabetic gastroparesis are detailed elsewhere [9, 10].

Bariatric Surgery

Bariatric surgery, such as Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy, and the less frequently performed biliopancreatic diversion with duodenal switch, is effective at inducing significant weight loss; dietetic counseling is mandatory during the first year to enhance the efficacy of the weight loss intervention. However, these operations can be associated with nutritional deficiencies and malnutrition. Preoperative nutritional assessment and correction of vitamin and micronutrient deficiencies, as well as long-term postoperative nutritional follow-up, are required. Bone mineral density, vitamin and micronutrient deficiencies (including thiamine, vitamins A, B12, and D, calcium, copper, etc.) need to be monitored in the long term [11].

Operations, such as RYGB (especially with a long Roux limb) and biliopancreatic diversion, may result in significant steatorrhea and lead to enteric hyperoxaluria (as in Crohn’s disease); this may be prevented by reduction of dietary oxalate (e.g., tea, spinach). Patients who have undergone such bariatric surgery may therefore show characteristic 24-h urine changes including low urine volume, low urinary pH, hypocitraturia, hyperoxaluria, and hyperuricosuria. Potassium citrate raises urinary pH, enhances the activity of stone inhibitors, reduces the supersaturation of calcium oxalate, corrects hypokalemia, and is useful in treating patients who develop renal calculi after bariatric surgery [12].

 
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