Phosphorus therapy intravenous

Gatchalian RA, Popli A, Ejaz A A, Leehey DJ, Kjellstrand CM, Ing TS. Management of hypophosphatemia induced by high-flux hemodiafiltration for the treatment of vancomycin toxicity intravenous phosphorus therapy versus use of a phosphorus-enriched dialysate. Am J Kidney Dis 2000 36(6) 1262-6. 

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

Vitamin D and its metabolites play an important role in the maintenance of extracellular calcium concentrations and in normal skeletal structure and mineralization. Vitamin D is necessary for the optimal absorption of calcium and phosphorus. On a worldwide basis, the most common cause of hypocalcemia is nutritional vitamin D deficiency. In malnourished populations, manifestations include rickets and osteomalacia. Nutritional vitamin D deficiency is uncommon in Western societies because of the fortification of miUc with ergocalciferol. " The most common cause of vitamin D deficiency in Western societies is gastrointestinal disease. Gastric surgery, chronic pancreatitis, small-bowel disease, intestinal resection, and bypass surgery are associated with decreased concentrations of vitamin D and its metabolites. Vitamin D replacement therapy may need to be administered by the intravenous route if poor oral bioavailability is noted. Decreased production of 1,25-dihydroxyvitamin D3 may occur as a result of a hereditary defect resulting in vitamin D-dependent rickets. It also can occur secondary to chronic renal insufficiency if there is insufficient production of the 1 -a -hydroxylase enzyme for the... 

Medications are another cause of hyperphosphatemia. Excessive intravenous or oral administration of phosphorus is an obvious potential cause of elevated serum phosphate concentrations. Phosphate-containing enemas increase concentrations, especially in those with renal insufficiency. Intravenous or oral vitamin D therapy can increase absorption of phosphorus in the gastrointestinal tract by up to 50%. Bisphosphonate therapy is associated with increased serum phosphate concentrations. Acute phosphorus poisoning as a result of ingestion of laundry detergents is a rare and often unrecognized cause of elevated phosphate concentrations. 

Parenteral phosphorus supplementation is associated with risks of hyperphosphatemia, metastatic soft tissue deposition of calcium-phosphate product, hypomagnesemia, hypocalcemia, and hyperkalemia or hypernatremia (caused by intravenous phosphorus salt) (Table 49-9). Inappropriate administration of large doses of parenteral phosphorus over relatively short time periods has resulted in symptomatic hypocalcemia and soft-tissue calcification. The rate of infusion and choice of initial dosage should therefore be based on severity of hypophosphatemia, presence of symptoms, and coexistent medical conditions. Patients should be closely monitored with frequent (every 6 hours) serum phosphorus determinations for 48 to 72 hours after starting intravenous therapy. It may be necessary to continue administration of intravenous phosphorus for several days in some patients, while other patients may be able to tolerate an... 

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