Hepatic and pancreatic gross and histopathologic features. Enlarged liver with yellow discoloration and incidental benign bile duct adenoma (arrow) (A); extensive hepatic steatosis (hematoxylin-eosin, original magnification ×200) (B); marked acinar atrophy with fatty replacement of pancreas and fibrosis (hematoxylin-eosin, original magnification ×25) (C); and pancreas with fibrosis, acinar atrophy and preservation of islets (hematoxylin-eosin, original magnification ×100) (D).
Wade AN, Dolan JM, Cambor CL, Boullata JI, Rickels MR. Fatal Malnutrition 6 Years After Gastric Bypass Surgery. Arch Intern Med. 2010;170(11):993–995. doi:10.1001/archinternmed.2010.164
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Gastric bypass procedures are the most effective weight loss surgical treatments.1 The Roux-en-Y procedure, the most commonly performed bypass technique in the United States, restricts gastric volume and bypasses absorption from most of the proximal small intestine. Bypass of the duodenum impairs mixing of ingested nutrients with bile acids and pancreatic enzymes leading to maldigestion. The combination of malabsorption and maldigestion, while resulting in significant weight loss, predisposes to malnutrition.
A 48-year-old woman was seen at the endocrinology clinic for generalized weakness 6 years after Roux-en-Y gastric bypass for morbid obesity (preoperative height, 1.63 m; weight 113.4 kg; and body mass index [BMI], 42.7 [calculated as weight in kilograms divided by height in meters squared]). After an initial postoperative weight loss, her weight plateaued, but 2 years prior to presentation, she developed chronic, oily diarrhea accompanied by new, gradual weight loss. Gastrointestinal evaluation including upper and lower endoscopies had been unremarkable, and her symptoms failed to improve after a trial of antibiotics for presumed bacterial overgrowth; pancreatic enzymes were not tolerated because of worsening gastrointestinal symptoms. She also reported 6 months of weakness climbing stairs and carrying objects, which limited her activity. On examination, she weighed 49.8 kg (BMI, 18.9) and bilateral upper and lower proximal muscle weakness was present. On evaluation, her laboratory values were 2.2 g/dL for albumin (to convert to grams per liter, multiply by 10); 3 mg/dL for serum urea nitrogen (to convert to millimoles per liter, multiply by 0.357); and 18 U/L for amylase, 12 U/L for lipase, 27 U/L for creatine kinase, 50 U/L for alanine transaminase, and 62 U/L for aspartate transaminase (to convert to microkatals per liter, multiply by 0.0167). Oral supplementation with high-protein liquids, vitamins A and D, and a multivitamin was initiated.
Findings from a repeated gastrointestinal evaluation 6 weeks later were notable for increased qualitative fecal fat on a random sample. Magnetic resonance imaging revealed hepatic steatosis and ascites, and findings from endoscopy with jejunal biopsy were normal. Laboratory evaluation indicated worsening malnutrition and decreased muscle mass despite supplementation (albumin level, 1.6 g/dL, and creatinine kinase level, 19 U/L).
When she returned to the clinic 1 week later, she had developed nausea and vomiting and was too weak to ambulate. She weighed 56.2 kg and had a blood pressure of 80/60 mm Hg, with a pulse of 110/min. Pitting edema was present up to her abdomen, and a petechial eruption was present on her flanks and extremities. She was admitted to the hospital for intravenous thiamine and parenteral nutrition. The following day, she developed shock and required vasopressor and mechanical ventilator support. There was no evidence of sepsis or adrenal insufficiency. Despite maximal intervention, she developed multiorgan failure. Supportive measures were withdrawn at the request of her family and she died.
Postmortem examination revealed extensive hepatic steatosis and fatty replacement of the exocrine pancreas with nonspecific cardiac myocyte hypertrophy and atrophy (Figure).
Our patient presented with severe protein calorie malnutrition, which contributed to her death. Protein calorie malnutrition is uncommon after Roux-en-Y bypass, with an incidence of 4.7% in one small series.2 Its etiology is multifactorial—patients often have postoperative intolerance to protein-rich foods and protein digestion is impaired by reduced mixing with pancreatic enzymes, which results both from mechanical factors and, as in our patient, exocrine pancreatic insufficiency. The pathogenesis of the protean clinical manifestations of protein calorie malnutrition remains unclear, but increased oxidative stress and slower protein catabolism leading to reduced amino acid availability have been proposed.3 Hepatic steatosis and pancreatic atrophy with fatty replacement, likely due to disordered metabolism of free fatty acids, have both been described in malnourished children,4,5 but to our knowledge, this is the first report of fatty pancreatic replacement in an adult patient after gastric bypass.
Potentially fatal protein calorie malnutrition can occur after gastric bypass. Health care providers should ensure that patients undergo thorough, scheduled surveillance for nutritional deficiencies, which should be aggressively treated early in their course to prevent life-threatening complications.
Correspondence: Dr Wade, Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, 415 Curie Blvd, 700 Clinical Research Bldg, Philadelphia, PA 19104-6149 (email@example.com).
Author Contributions:Study concept and design: Wade and Rickels. Acquisition of data: Wade, Cambor, and Rickels. Analysis and interpretation of data: Wade, Dolan, Cambor, Boullata, and Rickels. Drafting of the manuscript: Wade. Critical revision of the manuscript for important intellectual content: Wade, Dolan, Cambor, Boullata, and Rickels. Administrative, technical, and material support: Wade, Dolan, Boullata, and Rickels. Study supervision: Rickels.
Financial Disclosure: None reported.