Refeeding syndrome

Refeeding syndrome

Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism

extended period of catabolism ends abruptly with switching to carbohydrate metabolism

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. The metabolic consequences include:

• hypophosphataemia
  Hypophosphataemia, hypokalaemia and hypomagnesaemia are the characteristic electrolyte disturbances seen in patients with refeeding syndrome
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  Importance: 64
  • this is the hallmark symptom of refeeding syndrome
  • may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)
• hypokalaemia
  Hypophosphataemia, hypokalaemia and hypomagnesaemia are the characteristic electrolyte disturbances seen in patients with refeeding syndrome
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  Importance: 64
• hypomagnesaemia
  Hypophosphataemia, hypokalaemia and hypomagnesaemia are the characteristic electrolyte disturbances seen in patients with refeeding syndrome
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  Importance: 64
  : may predispose to torsades de pointes
  Torsades-des-pointes secondary to hypomagnesaemia can result as a consequence of refeeding syndrome
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  Importance: 83
• abnormal fluid balance
  abnormal fluid balance
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Pathophysiology of Hypophosphatemia in Refeeding Syndrome:

• Shift from Fat to Carbohydrate Metabolism: In refeeding syndrome, the reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism. This switch activates insulin secretion, which in turn increases cellular uptake of glucose.
• Intracellular Movement of Phosphate: Insulin and increased glucose uptake stimulate the intracellular movement of phosphate, which is used in the synthesis of ATP and 2,3-diphosphoglycerate in erythrocytes. This intracellular shift reduces serum phosphate levels.
• Decreased Phosphate Stores: Patients with chronic malnutrition often have depleted phosphate stores, although their serum phosphate levels may initially be normal. When refeeding starts, the sudden demand for phosphate in anabolic processes exceeds the supply, leading to hypophosphatemia.

Clinical Consequences of Hypophosphatemia:

• Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.
• Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.
• Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.
• Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
• Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.

Prevention

NICE produced guidelines in 2006 on nutritional support. Refeeding syndrome may avoided by identifying patients at a high-risk of developing refeeding syndrome:

Patients are considered high-risk if one or more of the following:

• BMI < 16 kg/m²
• unintentional weight loss >15% over 3-6 months
  unintentional weight loss >15% over 3-6 months
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• little nutritional intake > 10 days
• hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:

• BMI < 18.5 kg/m²
• unintentional weight loss > 10% over 3-6 months
• little nutritional intake > 5 days
• history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

NICE recommend that if a patient hasn't eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.

+PassMedicine Notes

Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. The metabolic consequences include:

• hypophosphataemia
• this is the hallmark symptom of refeeding syndrome
• may result in significant muscle weakness, including myocardial muscle (--> cardiac failure) and the diaphragm (--> respiratory failure)
• hypokalaemia
• hypomagnesaemia: may predispose to torsades de pointes
• abnormal fluid balance

Pathophysiology of Hypophosphatemia in Refeeding Syndrome:

• Shift from Fat to Carbohydrate Metabolism: In refeeding syndrome, the reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism. This switch activates insulin secretion, which in turn increases cellular uptake of glucose.
• Intracellular Movement of Phosphate: Insulin and increased glucose uptake stimulate the intracellular movement of phosphate, which is used in the synthesis of ATP and 2,3-diphosphoglycerate in erythrocytes. This intracellular shift reduces serum phosphate levels.
• Decreased Phosphate Stores: Patients with chronic malnutrition often have depleted phosphate stores, although their serum phosphate levels may initially be normal. When refeeding starts, the sudden demand for phosphate in anabolic processes exceeds the supply, leading to hypophosphatemia.

Clinical Consequences of Hypophosphatemia:

• Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.
• Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.
• Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.
• Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
• Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.

Prevention

NICE produced guidelines in 2006 on nutritional support. Refeeding syndrome may avoided by identifying patients at a high-risk of developing refeeding syndrome:

Patients are considered high-risk if one or more of the following:

• BMI < 16 kg/m2
• unintentional weight loss >15% over 3-6 months
• little nutritional intake > 10 days
• hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:

• BMI < 18.5 kg/m2
• unintentional weight loss > 10% over 3-6 months
• little nutritional intake > 5 days
• history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

NICE recommend that if a patient hasn't eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.