Causes of a decrease in phosphorus in the blood (hypophosphatemia)
Last reviewed: 20.11.2021
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Hypophosphatemia can occur due to impaired absorption of phosphate in the intestine, increasing its excretion by the kidneys or the transition into the cells. Severe hypophosphatemia (less than 1 mg% or less than 0.32 mmol / L) usually indicates a decrease in the total amount of phosphorus in the body and occurs when alcohol is abused, respiratory alkalosis, intestinal absorption, severe burns, treatment of diabetic ketoacidosis, admission means that bind phosphate.
Moderate hypophosphatemia (1-2.5 mg% or 0.32-0.80 mmol / L) is not always due to depletion of total phosphate stores. In addition to the causes listed above, it may be caused by glucose infusion; deficiency of vitamin D in food or a decrease in its absorption in the intestine; increased phosphate losses through the kidneys, which occurs with hyperparathyroidism, during the diuretic phase of acute tubular necrosis, after kidney transplantation, with hereditary hypophosphatemia linked to the X chromosome, with Fanconi syndrome, paraneoplastic osteomalacia, and with increasing extracellular fluid volume.
In the clinical practice of resuscitation, intravenous glucose infusions are the main cause of hypophosphataemia, and a decrease in the concentration of inorganic phosphorus occurs in a few days. The hypophosphatemic effect of glucose is caused by insulin, which facilitates the transport of glucose and phosphate through cell membranes in the liver and skeletal muscles.
Respiratory alkalosis, as the cause of hypophosphataemia, may be important in patients who are on artificial ventilation of the lungs. The mechanism of hypophosphatemia is caused by an increase in the pH within the cells, which stimulates glycolysis, and the enhancement of phosphorylation of glucose facilitates the transmembrane transfer of phosphate anions.
In patients with sepsis, the concentration of inorganic phosphate in the blood serum is reduced quite early, so the inexplicable decrease in the phosphate content in the blood should always cause the clinicians to have a certain alertness aimed at finding the infection.
Glucosuria increases the excretion of phosphate in the urine, therefore, in patients with diabetic ketoacidosis, their deficiency is observed, despite the normal or even elevated levels of inorganic phosphorus in the blood serum.
Clinical manifestations of hypophosphatemia are observed only when the total phosphate reserve in the body is depleted and the serum phosphate concentration drops below 1 mg% (less than 0.32 mmol / L). Violations of the muscular system include weakness, rhabdomyolysis, reduced diaphragm function, respiratory and congestive heart failure. Neurological disorders include paresthesia, dysarthria, confusion, stupor, convulsions and coma. Rarely, hemolysis, thrombocytopathy and metabolic acidosis are noted. With acute phosphate deficiency, the contractility of the heart muscle decreases, and chronic cardiomyopathy develops. Chronic hypophosphatemia causes rickets in children and osteomalacia in adults.