Nutrition Following Gastric Operations for Morbid Obesity

Abstract

Nutritional status after 238 gastric operations designed to reduce caloric intake and body weight to within 30% of ideal was assessed by measuring body composition using the multiple isotope dilution technique. Body cell mass (BCM) and body fat were quantitated before and at 24 months after operation. Malnutrition was defined as a total exchangeable sodium (Nae) to total exchangeable potassium (Ke) ratio greater than 1.22. Data were collected on 96 patients. All had lost a mean of 26% of preoperative weight by 24 months. Significant malnutrition occurred in 47 patients whose Nae/Ke ratio ranged from 1.23 to 2.17 (1.45 +/- 0.03). There was a 34% reduction in body fat. The malnourished patients lost 10% more BCM by 24 months than did the normally nourished group. Malnutrition resolved as the stoma enlarged in 19 patients, and dietary counselling helped eight patients. Eighteen patients required reoperation to establish a larger orifice, and endoscopic dilatation was successful in two patients. Administration of a liquid diet via the gastrostomy was required for prolonged periods in some malnourished patients. Seventeen patients who had lost weight rapidly over a short time had low vitamin B12, thiamine, and serum and RBC folate levels. One patient had a markedly decreased serum thiamine level with neuropathy. Symptoms of weakness, easy fatigability, and lassitude were found in the malnourished patients. Low thiamine and serum folate levels were also seen in patients ingesting a liquid diet of 750 kcal with a standard multivitamin supplement. Malnutrition was not seen in these patients. In the 49 patients who remained well nourished, BCM decreased by 19%, but the Nae/Ke remained normal. Weight loss was well tolerated, and no patients required reoperation or supplemental liquid diet to increase caloric or protein intake. The degree of malnutrition in patients after gastric operations is as great as following intestinal bypass but is not associated with liver failure. Malnutrition with vitamin deficiency is a great potential hazard in patients who undergo intake-limiting operations, especially if the goal of the operation is to restore near-normal weight. Current operations are successfully designed to maintain a small orifice size, so that the risks of malnutrition are likely to increase in the future.

Weight loss and quality of life after bariatric surgery: a study of 200 patients after vertical gastroplasty or adjustable gastric banding

“…Iron deficiency has been less reported after AGB, but is the most frequent nutritional deficit induced by bariatric surgery overall. Folic acid deficiency is less frequent and is in direct relation to severe food intake reduction and fast loss of weight (MacLean et al, 1983). Thiamin deficiency, sometimes already present in obese people before bariatric surgery, has been described in VBGM (Seehra et al, 1996;Houdent et al, 2003), and in AGB procedures (Quar Bozbora et al, 2000).…”

Preoperative eating behavior, postoperative dietary adherence, and weight loss after gastric bypass surgery

“…Caloric intake often increases significantly during the postoperative course. 8,[14][15][16][17][18][19] In the Swedish Obese Subjects trial, 8 surgery patients consumed approximately 2900 kcal/ d prior to surgery. Their intake decreased to approximately 1500 kcal/d 6 months after surgery, but increased to approximately 2000 kcal/d 10 years later, when patients had regained approximately 10% of their maximum weight loss.…”

Genes and networks expressed in perioperative omental adipose tissue are correlated with weight loss from Roux-en-Y gastric bypass

“…8 Failure rates as high as 43% have been reported among patients with greater preoperative BMI. 9 This high degree of variability of the postoperative weight loss provides an opportunity for investigation into the mechanisms by which weight loss is achieved following RYGB. The traditional explanation for induction of weight loss post-RYGB has been a diminished nutrient/energy intake as a result of the gastric restriction created by the small gastric pouch as well as a variable component of malabsorption.…”