Avoiding refeeding syndrome in anorexia nervosa

Abstract

The term refeeding syndrome has been used to describe the adverse consequences that can occur in all malnourished patients in the early stages of nutrition repletion whether the method of refeeding is oral, enteral or parenteral. Those consequences include acute thiamine deficiency resulting in Wernicke's encephalopathy and Korsakoff syndrome, with the potential for permanent cognitive impairment; hypophosphatemia, hypokalemia, hypomagnesemia and fluid overload resulting in cardiac failure. Adaptive changes in metabolism occur during a period of starvation or fasting: levels of glucose fall within 24 to 72 hours, as response, glucagon levels rise and insulin concentrations decrease. Glucose levels are maintained by glycogenolysis at first and gluconeogenesis latter. The reintroduction of nutrition leads to a switch from fat to carbohydrate metabolism and an increase of insulin concentration. Insulin stimulates the movement of potassium, phosphate, and magnesium into the cell leading to its depletion in extracellular compartment. Reactivation of carbohydrate metabolism increases degradation of thiamine, a cofactor required for cellular enzymatic reactions in Kreb's cycle. Deficiency in all these nutrients can then occur. Patients with anorexia nervosa are at risk of suffering from refeeding syndrome. This psychiatric disorder causes potentially life-threatening, physical complications and has the highest mortality rate among psychiatric disorders. The purpose of this review is to clarify recommendations for prevention and treatment of refeeding syndrome in anorexia nervosa.

Disclosure of interest

The authors have not supplied their declaration of competing interest.