Hyperphosphatemia  in Critical Care




Hyperphosphatemia is caused by increased absorption, decreased loss (renal failure) or increased production (cell destruction).

Hyperphosphatemia causes hypocalcemia and ectopic calcification

The treatment is phosphate binding agents

Hyperphosphatemia is caused by increased absorption, decreased loss or increased production. Increased intake can occur as a result of excessive intravenous administration or oral supplementation or Vitamin-D intoxication. Occasionally hyperphosphatemia results from recurrent administration of phosphate-containing enemas. There is reduced excretion in renal failure, hypoparathyroidism and magnesium deficiency. Increased production is secondary to increased cell destruction tumour lysis syndrome, rhabdomyolysis, bowel ischemia, hemolysis, acute acidosis and malignant hyperthermia. Pseudohyperphosphatemia (rather like pseudohyponatremia) may occur due to hypertriglyceridemia.

Causes of Hyperphosphataemia

Increased intake

Intravenous infusion

Oral supplementation
Vitamin D intoxication

Phosphate-containing enemas

Acute phosphorus poisoning

Increased Production

Tumour-lysis syndrome


Bowel infarction

Malignant hyperthermia


Acid-base disorders (lactic acidosis, diabetic ketoacidosis, respiratory


Reduced Loss

Renal failure



Tumoral calcinosis

Vitamin D intoxication

Bisphosphonate therapy

Magnesium deficiency


Multiple myeloma

Haemolysis in vitro


 Acute hyperphosphatemia causes few sudden problems (unlike, for example hyperkalemia and hypermagnesemia). The major effect is to cause hypocalcemia and tetany, if serum phosphate rises rapidly. Calcium can be deposited in the tissues (ectopic/metastatic calcification) in severe hyperphosphatemia, as can occur in renal failure.

The treatment for acute hyperphosphatemia is administration of phosphate binding salts calcium, magnesium and aluminum. The latter is avoided in renal failure, as aluminum can accumulate (calcium is preferred). 




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