Protein-Energy Malnutrition & Refeeding Syndrome
Too little protein, too few calories, and the danger of feeding too fast
Energy and nitrogen balance
Energy yield. Multiply grams by these factors to estimate calories. Alcohol is a large hidden energy source: 14 g of ethanol supplies about 98 kcal before any carbohydrate in the drink is counted.
Nitrogen balance. Nitrogen balance is nitrogen intake minus nitrogen losses, most of which leave as urinary urea. Protein is about 16% nitrogen, so dividing grams of protein by 6.25 gives grams of nitrogen. Balance is positive when the body is building protein (growth, pregnancy, recovery from illness) and negative when it is breaking protein down (starvation, burns, sepsis, trauma, uncontrolled diabetes, glucocorticoid excess). A diet missing even one essential amino acid also produces negative balance, because protein synthesis stalls and the other amino acids are catabolized.
Kwashiorkor and marasmus
Kwashiorkor. Protein intake is inadequate while calories, mostly from starch, are relatively preserved. The classic patient is a toddler weaned onto a starchy, protein-poor diet; the name comes from a Ghanaian (Ga) word for the illness of a child displaced from the breast by a newborn sibling. Low albumin synthesis reduces plasma oncotic pressure, causing pitting edema that can mask weight loss. The liver cannot make enough apolipoproteins (especially apoB-100), so triglycerides cannot leave as VLDL and accumulate as a fatty, enlarged liver. The abdomen protrudes, and anemia and apathy or irritability are typical.
Skin and hair. Dark, cracked patches peel like old paint (flaky-paint dermatosis), leaving pale, raw skin. Hair becomes sparse, brittle, easily plucked and depigmented; alternating pale and dark bands (the flag sign) record periods of poor and better nutrition.
Marasmus. Total energy intake is inadequate, so the body burns fat and then muscle. The child shows severe muscle and subcutaneous fat wasting, loose skin folds, a wizened "old man" face from loss of buccal fat, and growth failure, but no edema, and albumin is near normal.
| Feature | Kwashiorkor | Marasmus |
|---|---|---|
| Deficit | Protein (calories relatively preserved) | Total calories |
| Typical patient | Toddler after weaning | Often an infant |
| Edema | Pitting edema | Absent |
| Albumin | Low | Near normal |
| Liver | Fatty, enlarged | Not fatty |
| Look | Flaky-paint skin, flag-sign hair, protuberant abdomen | Wasted muscle and fat, "old man" face, loose skin |
Shared dangers. Both forms cause thymic atrophy and impaired T-cell immunity, so infections are the main cause of death; hypoglycemia and hypothermia are common early threats. Feeding is restarted cautiously, and iron is withheld until the rehabilitation phase.
Essential fatty acid deficiency
Which fats are essential. Humans cannot insert double bonds beyond carbon 9 of a fatty acid chain, so linoleic acid (ω-6) and α-linolenic acid (ω-3) must come from the diet. Arachidonic acid is made from linoleic acid.
Causes and signs. Deficiency develops within weeks of fat-free TPN, especially in infants, and with severe fat malabsorption. It causes dry, scaly dermatitis, alopecia, thrombocytopenia, poor wound healing and growth failure in children. Without linoleic acid the body makes Mead acid (a triene) instead of arachidonic acid (a tetraene), so the triene:tetraene ratio rises. IV lipid emulsion prevents and treats it.
Refeeding syndrome
Who is at risk. Anorexia nervosa, chronic alcohol use, prolonged fasting or NPO status, cancer cachexia, kwashiorkor or marasmus, BMI below 16, or more than 15% unintentional weight loss over the preceding months. Total-body phosphate, K+ and Mg2+ are depleted even when serum levels look normal.
- Carbohydrate is givenOral, enteral or IV, after a period of starvation
- Insulin surgesThe body switches from catabolism to anabolism
- Phosphate, K+ and Mg2+ move into cellsPhosphate is consumed to make ATP and phosphorylated intermediates
- Serum levels plungeUsually within the first 2–5 days of feeding
| Deficit | Consequence |
|---|---|
| Phosphate (hallmark) | Low ATP: respiratory muscle failure, heart failure, rhabdomyolysis, seizures, confusion; low 2,3-BPG left-shifts the O2 curve |
| Potassium, magnesium | Arrhythmias and weakness; low Mg2+ makes hypokalemia refractory |
| Thiamine | Wernicke encephalopathy, lactic acidosis, wet beriberi |
| Sodium and water retention | Insulin retains sodium; edema and heart failure in an atrophied heart |
Thiamine. Thiamine pyrophosphate is the cofactor for pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and transketolase. A carbohydrate load uses up scant stores, so glucose given without thiamine can precipitate Wernicke encephalopathy (confusion, ophthalmoplegia or nystagmus, ataxia). Only a minority of patients show all three signs, so treat on suspicion.
Give thiamine before or with glucose in anyone malnourished or alcohol-dependent.
Prevention. Give thiamine before feeding, check and replete phosphate, K+ and Mg2+, start at about 10–20 kcal/kg/day, advance over 4–7 days, and check electrolytes daily for the first days.