Refeeding syndrome is a potentially fatal condition when the levels of fluids and electrolytes shift in malnourished patients who receive artificial refeeding. This can occur due to metabolic changes happening in the body and can result in serious medical complications (1).
These metabolic and hormonal changes take place during starvation when the body switches from carbohydrates to fat and protein as the main source of energy, which significantly decreases the basal metabolic rate to prevent protein and muscle breakdown. Particularly, muscle and other tissues reduce their use of ketone bodies and start using fatty acids as the main energy source. This causes the increased levels of ketone bodies in the blood and their use by the brain as its main energy source instead of glucose. To preserve muscle protein reserve, the rate of gluconeogenesis in the liver decreases as well.
Prolonged starvation results in the depletion of numerous intracellular minerals and reduction in renal excretion (1).Decreased secretion of glucagon and increased insulin levels stimulate glycogen, fat, and protein synthesis. This process can only occur in the presence of minerals like phosphate, magnesium and cofactor thiamine. Insulin triggers the absorption of potassium, sodium, magnesium and phosphate into the cells, so their serum levels decrease even more (1). Refeeding syndrome is characterized by hypophosphataemia – the most significant biochemical feature of the syndrome that can cause sudden death, rhabdomyolysis, and respiratory insufficiency.
Other changes in the body associated with the syndrome include abnormal sodium and fluid balance; changes in metabolism of protein, glucose, and fat, hypokalaemia and hypomagnesaemia, thiamine deficiency. In other words, the clinical manifestation of the refeeding syndrome is stipulated by the functional deficits of these electrolytes and the rapid change in basal metabolic rate (1).