CAUSES:

Poor Nutrition
Chronic Alcoholism
Diarrhoea
Beta 2 Agonists
Insulin Acetazolamide
Hemodialysis
Hyperparathyroidism

EFFECTS

Irritability
Confusion
Metabolic encephalopathy
Coma
Muscle weakness
Respiratory failure
Failure to wean from ventilator
Dysphagia
Ileus
cardiac arrhythmias and cardiomyopathy.
ODC shift to left

TREATMENT

Asymptomatic mild-to-moderate hypophosphatemia (1-2.5 mg/dL) can be treated with oral phosphate supplementation if the gastrointestinal tract is intact.

Symptomatic or severe hypophosphatemia (< 1.0 mg/dL) should be treated with intravenous phosphate.

Oral supplementation : 2.5 to 3.5 g (80 to 110 mmol) per day, divided over two to three doses.

Intravenous:

The required dose of initial intravenous phosphate may vary from 2.5 to 19.8 mg/kg.
Typically, 2-5 mg/kg of inorganic phosphate dissolved in 0.45% saline is given over 6-12 hours and repeated as needed.

Rapid or large infusions are dangerous : Large intravenous doses of phosphate may result in hyperphosphatemia, hypomagnesemia, hypocalcemia, and hypotension.

Hyperkalemia is prevented by using sodium phosphate instead of potassium phosphate in patients with potassium levels >4 mmol/L.

Do not mix with Calcium or Magnesium

Daily Phosphate level monitoring should be done

〰NEW INSIGHTS〰

FGF23 recently identified as a physiological regulator of phosphate and vitamin D metabolism

 FGF23 plays a central role in the pathogenesis of altered mineral metabolism and secondary hyperparathyroidism in CKD patients and post-transplant hypophosphatemia in kidney transplant recipients.

FGF23 can be used not only as a biomarker for assessing phosphate retention but also as a predictor of mortality and future development of re- fractory hyperparathyroidism.