15: Approach to the Patient Requiring Nutritional Support

Thin, sparse (protein, zinc, biotin)
Flag sign (transverse pigmentation) (protein, copper)
Easy pluckability (protein)

Nails
Spoon-shaped (i.e. koilonychia) (iron)
No luster, transverse ridging (protein, energy)

Skin
Dry, scaling (i.e. xerosis) (vitamin A, zinc)
Seborrheic dermatitis (essential fatty acids, zinc, pyridoxine, biotin)
Flaky paint dermatosis (protein)
Follicular hyperkeratosis (vitamin A, vitamin C, essential fatty acids)
Nasolabial seborrhea (niacin, pyridoxine, riboflavin)
Petechiae, purpura (vitamins C, K, A)
Pigmentation, desquamation (niacin)
Pallor (folate, iron, cobalamin, copper, biotin)

Eyes
Angular palpebritis (riboflavin)
Blepharitis (B vitamins)
Corneal vascularization (riboflavin)
Dull, dry conjunctiva (vitamin A)
Bitot spot (vitamin A)
Keratomalacia (vitamin A)
Fundal capillary microaneurysms (vitamin C)
Ophthalmoplegia (Wernicke encephalopathy) (thiamine)

Mouth
Angular stomatitis (B vitamins, iron, protein)
Cheilosis (riboflavin, niacin, pyridoxine, protein)
Atrophic lingual papillae (niacin, iron, riboflavin, folate, cobalamin)
Glossitis (niacin, pyridoxine, riboflavin, folate, cobalamin)
Decreased taste and smell (vitamin A, zinc)
Swollen, bleeding gums (vitamin C)

Glands
Parotid enlargement (protein)
Sicca syndrome (vitamin C)
Thyroid enlargement (iodine)

Heart
Enlargement, tachycardia, high-output failure (i.e. beriberi) (thiamine)
Small heart, decreased output (protein, energy)
Cardiomyopathy (selenium)
Cardiac arrhythmias (magnesium, potassium)

Extremities
Edema (protein, thiamine)
Muscle weakness (protein, energy, selenium)
Bone and joint tenderness (vitamins C, A)
Osteopenia, bone pain (vitamin D, calcium, phosphorus, vitamin C)

Neurological
Confabulation, disorientation (i.e. Korsakoff psychosis) (thiamine)
Decreased position and vibration sense, ataxia (cobalamin, thiamine)
Decreased tendon reflexes (thiamine)
Weakness, paresthesias (cobalamin, pyridoxine, thiamine)
Mental disorders (cobalamin, niacin, thiamine, magnesium)

Other
Delayed wound healing (vitamin C, protein, zinc, essential fatty acids)
Hypogonadism, delayed puberty (zinc)
Glucose intolerance (chromium)

Other clinical conditions without impairment of food intake are associated with nutrient deficiencies. Malabsorptive conditions may produce profound nutrient deficiency, especially those that impair the effective small intestinal mucosal absorptive surface area (e.g. celiac disease, short bowel syndrome, Whipple disease). Affected patients also lose endogenous stores of minerals, vitamins, and proteins that are not reabsorbed from gastric, pancreaticobiliary, and small intestinal secretions. When steatorrhea is present, divalent cations (calcium, magnesium, zinc) are lost because they combine with unabsorbed fatty acids to form nonabsorbable soaps.

Drugs may induce malabsorption by several mechanisms. Cholestyramine binds fats and fat-soluble vitamins, whereas neomycin precipitates bile salts. Sulfasalazine inhibits folate absorption and colchicine inhibits enterocyte release of fat-soluble vitamins. In addition to suppressing appetite, chronic ingestion of large amounts of ethanol is toxic to intestinal enterocytes, causing decreased transport of glucose, amino acids, folate, and thiamine.

Protein-calorie malnutrition occurs in conditions with increased catabolism, such as Crohn’s disease or high-dose corticosteroid use. Likewise, increased caloric and fluid needs are observed with pregnancy, lactation, sepsis, trauma, and burns. Additional deficiencies in Crohn’s disease include those of calcium, vitamin D, iron, vitamin B₁₂, zinc, and potassium. Other causes of intestinal failure that result in malabsorption include radiation enteritis, intestinal pseudo-obstruction with bacterial overgrowth, chronic adhesive peritonitis, and mucosal diseases without effective treatment (collagenous sprue). Advanced liver disease may alter the plasma amino acid profile. Increased fluid and electrolyte losses occur in the absence of malabsorption in patients with diarrhea, vomiting, enterocutaneous fistulae, gastric suctioning, and renal wasting.

Mineral deficiency states

Major mineral deficiencies elicit a range of clinical manifestations. Sodium deficiency results from increased losses caused by vomiting, diarrhea, diuresis, salt-wasting renal disease, fistulae, or adrenal insufficiency. Among hospitalized patients, hyponatremia commonly results from excess free water caused by cardiac, renal, or hepatic insufficiency. Severe sodium depletion with dehydration produces nausea and vomiting, exhaustion, cramps, seizures, and cardiorespiratory collapse.

Pseudohyponatremia results from excess lipid, glucose, blood urea nitrogen, mannitol, or glycerin in the serum. Potassium depletion results from gastrointestinal or urinary losses (diuretics, alkalosis, mineralocorticoid excess, renal tubular acidosis). Hypokalemia also results from potassium shifts from the extracellular to the intracellular compartment during alkalosis, after insulin or glucose administration, or periodic paralysis. Symptoms of potassium depletion include confusion, lethargy, weakness, cramps, myalgias, cardiac arrhythmias, glucose intolerance, nausea, vomiting, diarrhea, ileus, and gastroparesis. Hypocalcemia is caused by vitamin D deficiency, failed vitamin D synthesis or action, hypoparathyroidism, hypomagnesemia, acute pancreatitis, osteoblastic malignancies, malabsorption, and medications (e.g. aminoglycosides, cisplatin, calcitonin, furosemide, phosphates, and anticonvulsants). Manifestations of hypocalcemia include a positive Chvostek or Trousseau sign, tetany, hyperreflexia, paresthesias, seizures, mental status changes, increased intracranial pressure, bradycardia, heart block, and choreoathetotic movements. Chronic calcium deficiency causes rickets in children and osteomalacia in adults. Eighty percent to 85% of phosphorus stores are in bone.

Hypophosphatemia occurs in 2–3% of hospitalized patients because of decreased intestinal absorption (antacids, malabsorption, vitamin D deficiency, hypoparathyroidism), increased renal excretion (proximal tubule disease, alkalosis, diuretics, hyperparathyroidism, burns, corticosteroids), and intracellular shifts (respiratory alkalosis, carbohydrate administration). Severe hypophosphatemia produces hemolysis, encephalopathy, seizures, paresthesias, muscle weakness, rhabdomyolysis, decreased glucose utilization, and reduced oxygen delivery. Similarly, 70% of magnesium stores are in bone. Magnesium absorption decreases in malabsorption syndromes. Excessive urinary loss results from hypercalcemia, volume expansion, tubular dysfunction, alcoholism, diabetes, hyperparathyroidism, hypophosphatemia, and medications (e.g. diuretics, aminoglycosides, cyclosporine, amphotericin, cisplatin, digoxin). Shifts into the intracellular space result from refeeding, treating diabetic ketoacidosis, pancreatitis, and correcting acidosis in renal failure. Patients with hypomagnesemia present with tremors, myoclonic jerks, ataxia, tetany, psychiatric disturbances, coma, ventricular arrhythmias, hypotension, or cardiac arrest.

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