Refeeding Syndrome: An Approach to Recognition and Management of the Disorder

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LEARNING OBJECTIVES: 1. Recognize patients at risk for refeeding syndrome and screen appropriately. 2. Treat vitamin and electrolyte deficiencies while assessing for cardiac decompensation in the refeeding syndrome patient. CASE: A 34-year old male prisoner with paranoid schizophrenia was admitted with history of avoiding food for 56 days with 9-kg (16%) weight loss and intention to begin feeding again. Symptoms at presentation included nausea and vomiting for 2 days and symptoms of orthostasis. The patient’s physical examination revealed a malnourished, otherwise healthy oriented male, with weight of 49 kg (BMI 16.7). Vital signs showed hypotension in the supine position with tachycardia, but was otherwise within normal limits. Initial laboratory analysis revealed serum potassium 3.4 meq/l, phosphorus 4.3meq/l, magnesium 2.6meq/l, and albumin of 4.2g/dl. Due to concerns related to refeeding syndrome, thiamine was given intravenously, and oral repletion of phosphorus and potassium was instituted. Dextrose-containing fluids and a liberalized diet was given. The patient’s serum phosphorus level dropped to 0.5 meq/l at hospital day 2 without symptoms, requiring 50 millimoles of intravenous phosphorus over 2 days to replete his phosphorus to normal. His potassium and magnesium levels also dropped during refeeding, and were appropriately supplemented. Diarrhea developed during oral feeding, lasting 4 days but resolved by time of discharge. No volume overload was detected, and the patient’s tachycardia resolved by day 6. DISCUSSION: Since its first description following refeeding starving prisoners in World War II, the refeeding syndrome has been reported in patients with alcoholism, anorexia, short bowel syndrome receiving total parenteral nutrition and in prisoners undergoing prolonged voluntary fasts. Thiamine deficiency must be addressed before feeding is begun. Total body stores of phosphorous, potassium and magnesium are significantly depleted, however serum levels are initially normal to slightly low due to renal adjustments in excretion. Rapid, high-carbohydrate feeding, as seen in this case, causes intracellular shifts of glucose, phosphorous and potassium as a massive insulin secretion is stimulated. Severe hypophosphatemia can quickly develop and remain asymptomatic until causing acute myocardial dysfunction. This along with the antinatiuretic effect of insulin can precipitate acute heart failure and death. Very close monitoring of electrolytes with aggressive phosphorous repletion, and slow initiation of caloric intake can avert this iatrogenic hazard. Clinicians that care for patients that may have had prolonged calorie interruption should be aware how to recognize this syndrome and navigate its pitfalls.

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Journal of General Internal Medicine





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Presented at the 28th Society of General Internal Medicine Annual Meeting
May 11-14, 2005
New Orleans, LA

Open Access