Write a short note on nutritional support and refeeding syndrome.

Nutritional Support — Indications

Nutritional support is indicated when a patient is malnourished or at risk of becoming so — inadequate oral intake for more than 5–7 days, unintentional weight loss exceeding 10%, BMI below 18.5, or a catabolic state such as sepsis, burns, trauma or major surgery. Nutritional assessment uses history and dietary recall, anthropometry (BMI, mid-arm circumference, triceps skinfold), serum albumin and prealbumin (both confounded by inflammation), and validated screening tools.

Routes

"If the gut works, use it." Enteral feeding maintains mucosal integrity, preserves gut-associated lymphoid tissue, reduces bacterial translocation, is cheaper and has fewer complications than parenteral nutrition.

Nasogastric tube position must be confirmed before use — pH testing of the aspirate and, where doubt exists, a chest X-ray. Feeding into a misplaced tube is a recognised never-event.

Refeeding Syndrome — Definition

Refeeding syndrome is the constellation of potentially fatal fluid and electrolyte shifts that occur when nutrition is reintroduced to a starved or severely malnourished patient. The hallmark is hypophosphataemia.

Pathophysiology

During prolonged starvation the body switches from carbohydrate to fat and protein catabolism; insulin secretion falls, and intracellular stores of phosphate, potassium and magnesium are depleted even though serum levels may appear normal, because they shift out of cells.

On refeeding, the carbohydrate load causes a surge of insulin, which:

• Drives phosphate, potassium and magnesium rapidly into cells — producing severe hypophosphataemia, hypokalaemia and hypomagnesaemia.
• Increases demand for thiamine as a cofactor in carbohydrate metabolism, precipitating Wernicke's encephalopathy in the already depleted.
• Causes sodium and water retention, precipitating fluid overload and cardiac failure.

Phosphate depletion is the central problem, since ATP and 2,3-DPG synthesis fail, impairing every energy-dependent cellular process.

Clinical Consequences

• Cardiac: arrhythmia, cardiac failure, sudden death — the commonest cause of mortality.
• Respiratory: diaphragmatic weakness and respiratory failure.
• Neurological: confusion, seizures, paraesthesiae, Wernicke's encephalopathy, central pontine myelinolysis.
• Haematological: haemolysis, impaired leucocyte function, thrombocytopenia.
• Muscular: weakness, rhabdomyolysis.

Patients at Risk

• Anorexia nervosa and other eating disorders; prolonged fasting or starvation.
• Chronic alcohol misuse; malabsorption; chronic malnutrition.
• Prolonged vomiting, post-bariatric surgery, oncology patients, elderly with poor intake, and those with minimal intake for more than 5 days.
• Very low BMI, substantial unintentional weight loss, or low baseline potassium, phosphate or magnesium.

Prevention & Management

1. Identify high-risk patients before starting feeding — this is the entire preventive strategy.

2. Check baseline potassium, phosphate, magnesium, calcium and renal function, and correct deficiencies before or alongside starting feeds — but do not delay feeding solely to correct them.

3. Give thiamine and B-complex vitamins before feeding begins and for the first several days.

4. Start feeding at a low calorie rate and increase slowly over several days, rather than aiming for full requirement immediately.

5. Monitor electrolytes daily for the first several days, and replace phosphate, potassium and magnesium aggressively as they fall.

6. Monitor fluid balance, daily weight, pulse and for signs of cardiac failure; restrict sodium.

7. Involve a dietitian and nutrition support team from the outset.