- Pathophysiology
- Occurs in severely malnourished patients (e.g., anorexia nervosa, chronic alcoholism, cancer cachexia) upon re-initiation of nutritional support.
- Introduction of carbohydrates (esp. glucose) → ↑ insulin secretion.
- Insulin surge drives key electrolytes (phosphate, potassium, magnesium) from the extracellular to the intracellular space to be used for glycolysis and ATP production.
- This abrupt intracellular shift leads to a profound depletion of serum electrolytes.
- Simultaneously, ↑ insulin promotes sodium and water retention.
- Clinical Features
- Onset: Typically 2-5 days after refeeding begins.
- Manifestations are due to electrolyte abnormalities and fluid shifts:
- Hypophosphatemia (hallmark): Leads to ATP depletion.
- Cardiopulmonary: Arrhythmias, heart failure, respiratory muscle weakness.
- Musculoskeletal: Muscle weakness, rhabdomyolysis.
- Neurologic: Seizures, paresthesias, delirium.
- Hypokalemia: Muscle weakness, paralysis, arrhythmias (e.g., Torsades de pointes).
- Hypomagnesemia: Co-exists with hypokalemia; causes neuromuscular excitability (tetany, tremor) and arrhythmias.
- Thiamine (B1) Deficiency: Can be unmasked or worsened. Refeeding utilizes thiamine as a cofactor for carbohydrate metabolism. Lack of thiamine can precipitate Wernicke encephalopathy.
- Fluid Overload: Pulmonary and peripheral edema due to sodium/water retention.
- Management & Prevention
- Identify at-risk patients before starting nutrition.
- Check baseline electrolytes (phosphate, K+, Mg2+) and replete them before initiating feeding.
- Administer thiamine supplementation before providing carbohydrates.
- Start nutrition slowly: “Start low and go slow.” Begin at 10-15 kcal/kg/day and advance gradually over several days.
- Monitor electrolytes and fluid status closely (daily or more frequently) during the first week of refeeding.
- Replete electrolytes aggressively as needed.