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By James L. Lewis, III, MD

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Hypophosphatemia is a serum phosphate concentration < 2.5 mg/dL (0.81 mmol/L). Causes include alcoholism, burns, starvation, and diuretic use. Clinical features include muscle weakness, respiratory failure, and heart failure; seizures and coma can occur. Diagnosis is by serum phosphate concentration. Treatment consists of phosphate supplementation.

Hypophosphatemia occurs in 2% of hospitalized patients but is more prevalent in certain populations (eg, it occurs in up to 10% of hospitalized patients with alcoholism).


Hypophosphatemia has numerous causes but clinically significant acute hypophosphatemia occurs in relatively few clinical settings, including the following:

  • The recovery phase of diabetic ketoacidosis

  • Acute alcoholism

  • Severe burns

  • When receiving TPN

  • Refeeding after prolonged undernutrition

  • Severe respiratory alkalosis

Acute severe hypophosphatemia with serum phosphate < 1 mg/dL (< 0.32 mmol/L) is most often caused by transcellular shifts of phosphate often superimposed on chronic phosphate depletion.

Chronic hypophosphatemia usually is the result of decreased renal phosphate reabsorption. Causes include the following:

  • Increased parathyroid hormone levels, as in primary and secondary hyperparathyroidism

  • Other hormonal disturbances, such as Cushing syndrome and hypothyroidism

  • Vitamin D deficiency

  • Electrolyte disorders, such as hypomagnesemia and hypokalemia

  • Theophylline intoxication

  • Long-term diuretic use

Severe chronic hypophosphatemia usually results from a prolonged negative phosphate balance. Causes include

  • Chronic starvation or malabsorption, often in patients with alcoholism, especially when combined with vomiting or copious diarrhea

  • Long-term ingestion of large amounts of phosphate-binding aluminum, usually in the form of antacids

Patients with advanced chronic kidney disease (especially those on dialysis), often take phosphate binders with meals to reduce absorption of dietary phosphate. The prolonged use of these binders can cause hypophosphatemia in, particularly when combined with greatly decreased dietary intake of phosphate.

Symptoms and Signs

Although hypophosphatemia usually is asymptomatic, anorexia, muscle weakness, and osteomalacia can occur in severe chronic depletion. Serious neuromuscular disturbances may occur, including progressive encephalopathy, seizures, coma, and death. The muscle weakness of profound hypophosphatemia may be accompanied by rhabdomyolysis, especially in acute alcoholism. Hematologic disturbances of profound hypophosphatemia include hemolytic anemia, decreased release of oxygen from Hb, and impaired leukocyte and platelet function.


  • Serum phosphate levels

Hypophosphatemia is diagnosed by a serum phosphate concentration < 2.5 mg/dL (< 0.81 mmol/L). Most causes of hypophosphatemia (eg, diabetic ketoacidosis, burns, refeeding) are readily apparent. Testing to diagnose the cause is done when clinically indicated (eg, suggestive liver function test results or signs of cirrhosis in patients with suspected alcoholism).


  • Treat underlying disorder

  • Oral phosphate replacement

  • IV phosphate when serum phosphate is < 1 mg/dL (< 0.32 mmol/L) or symptoms are severe

Oral treatment

Treatment of the underlying disorder and oral phosphate replacement are usually adequate in asymptomatic patients, even when the serum concentration is very low. Phosphate can be given in doses up to about 1 g po tid in tablets containing sodium phosphate or potassium phosphate. Oral sodium phosphate or potassium phosphate may be poorly tolerated because of diarrhea. Ingestion of 1 L of low-fat or skim milk provides 1 g of phosphate and may be more acceptable. Removal of the cause of hypophosphatemia may include stopping phosphate-binding antacids or diuretics or correcting hypomagnesemia.

Parenteral treatment

Parenteral phosphate is usually given IV. It should be administered in any of the following circumstances:

  • When serum phosphate is < 1 mg/dL (< 0.32 mmol/L)

  • Rhabdomyolysis, hemolysis, or CNS symptoms are present

  • Oral replacement is not feasible due to underlying disorder

IV administration of potassium phosphate (as buffered mix of K2HPO4 and KH2PO4) is relatively safe when renal function is well preserved. Parenteral potassium phosphate contains 93 mg (3 mmol) phosphorus and 170 mg (4.4 mEq) potassium per mL. The usual dose is 0.5 mmol phosphorus/kg (0.17 mL/kg) IV over 6 h. Patients with alcoholism may require 1 g/day during TPN; supplemental phosphate is stopped when oral intake is resumed. If patients have impaired renal function or serum potassium > 4 mEq/L, sodium phosphate preparations generally should be used; these preparations also contain 3 mmol/mL of phosphorus and are thus given at the same dose.

Serum calcium and phosphate concentrations should be monitored during therapy, particularly when phosphate is given IV or to patients with impaired renal function. In most cases, no more than 7 mg/kg (about 500 mg for a 70-kg adult) of phosphate should be given over 6 h. Close monitoring is done and more rapid rates of phosphate administration should be avoided to prevent hypocalcemia, hyperphosphatemia, and metastatic calcification due to excessive calcium phosphate product.

Key Points

  • Acute hypophosphatemia most often occurs in the setting of alcoholism, burns, or starvation.

  • Acute severe hypophosphatemia can cause serious neuromuscular disturbances, rhabdomyolysis, seizures, coma, and death.

  • Chronic hypophosphatemia may be due to hormonal disorders (eg, hyperparathyroidism, Cushing syndrome, hypothyroidism), chronic diuretic use, or use of aluminum-containing antacids by patients with chronic kidney disease.

  • Hypophosphatemia is usually asymptomatic, but severe depletion can cause anorexia, muscle weakness, and osteomalacia.

  • Treat the underlying disorder, but some patients require oral, or rarely, IV phosphate replacement.

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