Pregnancy Following Bariatric Surgery-Medical Complications and Management

Abstract

Bariatric surgery is most commonly carried out in women of childbearing age. Whilst fertility rates are improved, pregnancy following bariatric surgery poses several challenges. Whilst rates of many adverse maternal and foetal outcomes in obese women are reduced after bariatric surgery, pregnancy is best avoided for 12-24 months to reduce the potential risk of intrauterine growth retardation. Dumping syndromes are common after bariatric surgery and can present diagnostic and therapeutic challenges in pregnancy. Early dumping occurs due to osmotic fluid shifts resulting from rapid gastrointestinal food transit, whilst late dumping is characterized by a hyperinsulinemic response to rapid absorption of simple carbohydrates. Dietary measures are the mainstay of management of dumping syndromes but pharmacotherapy may sometimes become necessary. Acarbose is the least hazardous pharmacological option for the management of postprandial hypoglycemia in pregnancy. Nutrient deficiencies may vary depending on the type of surgery; it is important to optimize the nutritional status of women prior to and during pregnancy. Dietary management should include adequate protein and calorie intake and supplementation of vitamins and micronutrients. A high clinical index of suspicion is required for early diagnosis of surgical complications of prior weight loss procedures during pregnancy, including small bowel obstruction, internal hernias, gastric band erosion or migration and cholelithiasis.

Keywords: Bariatric surgery; Dumping syndrome; Obesity; Postabsorptive hypoglycemia; Pregnancy.

Fig. 1

Pathophysiology of dumping syndromes following gastric bypass surgery and mode of action of common therapeutic agents. Reduced gastric volume results in rapid gastric emptying (1) and rapid glucose absorption (2), which induces a hyperinsulinemic response (3), leading to reactive hypoglycemia 1–3 h after food (late dumping syndrome). Rapid delivery of hyperosmolar chyme to the upper small bowel (4) induces release of several vasoactive gut hormones (5), such as vasoactive intestinal peptide, neurotensin, glucagon-like peptide-1 (GLP-1) and glucagon-dependent insulinotropic peptide (GIP), which results in vasomotor symptoms 10–60 min after food (early dumping syndrome). Agents that increase meal viscosity, such as pectin or guar gum, may help to slow down gastric emptying. The α-glucosidase inhibitor, acarbose, can slow down the breakdown and absorption of food sugars. Diazoxide inhibits insulin release from β cells in the pancreatic islets and can attenuate the hyperinsulinemic response. The somatostatin analogue, octreotide, works at multiple levels in the upper gastrointestinal tract, including slowing of gastric emptying and inhibition of secretion and release of insulin and vasoactive gut hormones, and can be useful in the treatment of intractable symptoms of both types of dumping syndrome