ESSENTIALS OF DIAGNOSIS
Severe hypophosphatemia may cause tissue hypoxia and rhabdomyolysis.
Renal loss of phosphate can be diagnosed by calculating the fractional excretion of phosphate (FEPO4).
PTH and FGF23 are the major factors that increase urine phosphate.
The leading causes of hypophosphatemia are listed in Table 21–10. Hypophosphatemia may occur in the presence of normal phosphate stores. Serious depletion of body phosphate stores may exist with low, normal, or high serum phosphate concentrations.
Table 21–10.Causes of hypophosphatemia. |Favorite Table|Download (.pdf) Table 21–10. Causes of hypophosphatemia.
Diminished supply or absorption
Parenteral alimentation with inadequate phosphate content
Malabsorption syndrome, small bowel bypass
Absorption blocked by oral antacids with aluminum or magnesium
Vitamin D–deficient and vitamin D–resistant osteomalacia
Phosphaturic drugs: theophylline, diuretics, bronchodilators, corticosteroids
Hyperparathyroidism (primary or secondary)
Renal tubular defects with excessive phosphaturia (congenital, Fanconi syndrome induced by monoclonal gammopathy, heavy metal poisoning), alcoholism
Inadequately controlled diabetes mellitus
Phosphatonins of oncogenic osteomalacia (eg, FGF23 production)
Intracellular shift of phosphorus
Administration of glucose
Anabolic steroids, estrogen, oral contraceptives, beta-adrenergic agonists, xanthine derivatives
Hungry bone syndrome
Abnormal losses followed by inadequate repletion
Diabetes mellitus with acidosis, particularly during aggressive therapy
Recovery from starvation or prolonged catabolic state
Chronic alcoholism, particularly during restoration of nutrition; associated with hypomagnesemia
Recovery from severe burns
Serum phosphate levels decrease transiently after food intake; thus, fasting samples are recommended for accuracy. Moderate hypophosphatemia (1.0–2.4 mg/dL [0.32–0.79 mmol/L]) occurs commonly in hospitalized patients and may not reflect decreased phosphate stores.
In severe hypophosphatemia (less than 1 mg/dL [0.32 mmol/L]), the affinity of hemoglobin for oxygen increases through a decrease in the erythrocyte 2,3-biphosphoglycerate concentration, impairing tissue oxygenation and cell metabolism and resulting in muscle weakness or even rhabdomyolysis. Severe hypophosphatemia is common and multifactorial in alcoholic patients. In acute alcohol withdrawal, increased plasma insulin and epinephrine along with respiratory alkalosis promote intracellular shift of phosphate. Vomiting, diarrhea, and poor dietary intake contribute to hypophosphatemia. Chronic alcohol use results in a decrease in the renal threshold of phosphate excretion. This renal tubular dysfunction reverses after a month of abstinence. Patients with chronic obstructive pulmonary disease and asthma commonly have hypophosphatemia, attributed to xanthine derivatives causing shifts of phosphate intracellularly and the phosphaturic effects of beta-adrenergic agonists, loop diuretics, xanthine derivatives, and corticosteroids. Refeeding or glucose administration to phosphate-depleted patients may cause fatal hypophosphatemia.
Acute, severe hypophosphatemia (less than 1.0 mg/dL [0.32 mmol/L]) can lead to rhabdomyolysis, paresthesias, and encephalopathy (irritability, confusion, dysarthria, seizures, and coma). Respiratory failure or failure to wean from mechanical ventilation may occur as a result of diaphragmatic weakness. Arrhythmias ...