Phosphate

Phosphate is a major intracellular anion important for intracellular metabolism of proteins, fats and carbohydrates and is a major component in phospholipid membranes and phosphoproteins.

It also regulates enzymatic activity vital for energy transfer. About 4 mEq/g of nitrogen is needed for anabolism. 85% of total body phosphates are combined with calcium in the bones and teeth. Factors affecting calcium homeostasis also affect phosphate homeostasis, movement is the opposite of calcium.

•	Increased renal excretion due to glycosuria, hypokalemia, hypomagnesemia, and thiazide diuretics.

•	Decreased GI absorption due to antacid use (phosphate binding in the GI tract).

•	Intracellular shifting due to administration of concentrated glucose solutions (i.e., TPN) which increases insulin production which in turn causes phosphorus to shift into the cells. Intracellular shifts may also be caused by respiratory alkalosis.

Hypophosphatemia decreases GI motility which may lead to ileus. Severe hypophosphatemia is usually associated with muscle weakness, paresthesia, hemolysis, platelet dysfunction, and cardiac and respiratory failure. CNS effects often include encephalopathy, confusion, seizures, and, ultimately, coma.

Serum phosphorus levels below 2.5 mg/dL. Decreased potassium and magnesium levels may also occur.

Eliminate the cause of deficit. Discontinue phosphorus-binding antacids. If deficit is mild to moderate deficit give oral supplements. If deficit is more severe administer intravenous sodium phosphate or potassium phosphate.

Increase the phosphate content of the TPN solution to a maximum of 20mM per liter. The total daily phosphate dosage should not exceed 60 mM.

•	Decreased phosphate excretion due to renal disease.

•	Excess intake due to phosphate-containing laxatives or phosphate supplements.

•	Hyperphosphatemia may be caused by phosphate shifts from cells as a result of cell breakdown from trauma, burns or hemolysis. Respiratory acidosis (pH < 7.35 and paCO2 > 45 mm Hg) may also cause intracellular to extracellular shifts.

•	Other causes include catabolism, leukemia, lymphoma, Cushing's syndrome and acromegaly.

No direct symptoms are related to phosphorus excess, most are related to hypocalcemia and include neuromuscular abnormalities (numbness and tingling of extremities, tetany and convulsion), muscle cramps, brittle nails and dry skin and hair. Renal failure may occur if hyperphosphatemia is left untreated.

Discontinue the current TPN infusion if it contains phosphate and begin an infusion of D10NS at the current TPN infusion rate. Reorder a TPN solution without phosphate and continue to hold phosphate from the TPN solution and all other intravenous fluids until the serum phosphorous returns to normal.