Hypophosphatemia

Hypophosphatemia is a decrease in phosphorus levels in the blood below 0.8 mmol / l The main causes are alcoholism, artificial diet without the addition of phosphate and ingestion of alkalising gastric acid ( antacids ). Consequences of hypophosphatemia are disturbances of mineral metabolism and supply the cells with energy and oxygen. Treatment consists of administration of vitamin D and phosphate.

Epidemiology

In the general population the hypophosphatemia is rare. In hospital patients, the incidence of hypophosphatemia about 3 %, in patients in intensive care units around 30%. In patients with blood poisoning (sepsis), the incidence may be as high as 80 % in alcoholics up to 30 %, with serious injuries to 75 % and in chronic obstructive pulmonary disease up to 20 %.

Etiology

Causes include decreased phosphate intake by an unbalanced diet (eg alcoholics ) or as part of an intravenous nutrition ( intensive care medicine ). Especially with pre-existing phosphate deficiency and malnutrition (eg anorexia nervosa ) may cause an inadequate phosphate intake as part of a diet therapy to treat severe phosphate deficiency. The administration of insulin leads to a decrease in phosphorus levels. The ingestion of large amounts of antacids in the stomach leads to the binding of phosphate of the drug, and thus to a reduced phosphate uptake. Chronic diarrhea can result on increased phosphate loss to hypophosphatemia. Several congenital diseases of the phosphate transport system in the kidney lead to loss of phosphate in the urine. Other causes of hypophosphatemia are vitamin D deficiency, respiratory alkalosis, hyperparathyroidism ( primary hyperparathyroidism ) and the syndrome of the hungry bone after surgical removal of the parathyroid glands. Another cause of the emergence of hypophosphatemia hemodialysis in patients with renal insufficiency should be mentioned, in which the blood among other things, phosphate is removed.

The lowering of the levels of phosphate in all cells leads to a decrease in the high energy phosphate adenosine triphosphate link. In the erythrocytes, the mirror drops of 2,3- bisphosphoglycerate; thereby oxygen delivery is hampered by the blood to the tissue.

A severe hypophosphatemia ( serum phosphate levels <0.3 mmol / l ) can cause destruction of red blood cells by haemolytic anemia and destruction of muscle cells to rhabdomyolysis. A pronounced chronic hypophosphataemia can lead to demineralization of the bone. In hospitalized patients, a moderate hypophosphatemia with increased complication rates associated in the disease process, possibly the low levels of phosphate, however, is not the cause of the complications, but a consequence of the severe course of the disease (see also surrogate markers ).

Therapy

An increased phosphate intake may be at moderate phosphate deficiency achieved through increased consumption of milk and dairy products. If this is insufficient, sodium or potassium phosphate can be taken. In intensive care patients, phosphate additives can also be administered intravenously. A phosphate overdosage should be avoided, this is expressed in kidney failure, drop in calcium levels ( hypocalcemia ), low blood pressure (hypotension) and ECG changes.