A severely malnourished patient is started on aggressive parenteral nutrition. On day 3, he develops severe hypophosphataemia, hypokalaemia, and hypomagnesaemia with cardiac arrhythmia. This presentation is consistent with refeeding syndrome. The underlying mechanism involves:
- A Insulin surge from glucose loading driving intracellular uptake of phosphate, potassium, and magnesium for anabolic processes ✓
- B Excessive phosphate excretion from hyperphosphataemia caused by glucose infusion
- C Direct cytotoxicity of glucose to renal tubules causing electrolyte wasting
- D Thiamine deficiency impairing glucose utilisation and causing lactate accumulation that chelates divalent cations
Explanation
In refeeding syndrome, reintroduction of carbohydrates after prolonged starvation triggers a surge in insulin secretion. Insulin activates Na+/K+-ATPase and stimulates cellular uptake of glucose, phosphate, potassium, and magnesium for anabolic processes (glycolysis requires phosphate as ATP, potassium follows glucose into cells). Despite total body depletion of these minerals during starvation, serum levels were maintained by catabolic release from tissues. The sudden insulin-driven intracellular shift reveals the total body deficit as severe extracellular hypophosphataemia (causing haemolytic anaemia, muscle weakness, cardiac dysfunction), hypokalaemia, and hypomagnesaemia. Thiamine deficiency is a related but separate complication.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.