The clinical entity of refeeding syndrome was first described in U.S. POWs in Japan who had been starved for many months to years, then developed extreme electrolyte abnormalities upon the reintroduction of food.
The most common electrolyte abnormalities associated with refeeding syndrome are hypophosphatemia, hypomagnesemia, and hypokalemia. The mechanism is as follows: during starvation, the secretion of insulin is decreased in response to a reduced availability of carbohydrates, and in order to survive metabolism is shifted to using fat and protein stores. During this adaptation total-body phosphate, magnesium, and potassium stores are depleted, despite maintaining relatively normal serum concentrations of these electrolytes. When suddenly exposed to ample food (and in particular carbohydrates), there is a shift to a carbohydrate-based metabolism associated with a sudden surge in insulin secretion. As we all know, insulin stimulates a rapid intracellular shift of potassium and phosphate, which can lead to a profound decrease in this electrolytes. In particular hypophosphatemia can lead to catastrophic muscle dysfunction, including respiratory collapse, as phosphate is necessary to maintain ATP stores needed for muscle contraction. Hypokalemia is well-known to result in cardiac arrhyhthmias.
Patients with alcoholism, anorexia nervosa, prolonged hospitalizations, or cancer patients may also be subject to refeeding syndrome. It typically occurs within four days of refeeding. Either hyperglycemia or hypoglycemia may also be present. Careful monitoring of electrolytes in patients prone to refeeding syndrome, as well as searching for nutritional deficiencies which may go along with refeeding syndrome (e.g., thiamine deficiency) are the cornerstones of preventing this potentially dangerous complication.