Treatment of Severe Hypophosphatemia

Abstract

Aspects of phosphate biochemistry pertinent to therapy, the distribution of phosphorus in body compartments, therapeutic phosphorus preparations, prevention of hypophosphatemia, therapeutic guidelines, and side-effects of phosphorus therapy are reviewed. Severe hypophosphatemia (less than 0.32 mmol/litre or less than 1 mg/dl) can occur with normal or depleted body stores. Because a large amount of phosphorus may shift rapidly between the extracellular and intracellular or bone compartments, the size of a possible total body deficit cannot be estimated from the serum phosphorus level. Similar shifts may occur unpredictably during repair of hypophosphatemia. Therefore, correction of hypophosphatemia in any patient must be empiric and the response of serum levels to therapy should be followed closely. We discuss a method likely to correct hypophosphatemia while minimizing side-effects.

Phosphorus and Calcium

“…[61][62][63] There are several other published reports of fixed-dose phosphate supplementation in patients with normal renal function. [64][65][66][67][68][69][70] Based on these published reports, Table 2 provides one approach to IV P dosing for treating hypophosphatemia in patients with normal renal function. 14,61-70 Although there are no specific data or algorithms to guide P repletion in patients with impaired renal function receiving nutrition support who are not being treated with continuous renal replacement therapy (CRRT), consider administering ≤ 50% of the initial empiric P dose initially.…”

Treatment of electrolyte disorders in adult patients in the intensive care unit

“…phosphate for hypophosphatemia in patients with normal renal function. [129][130][131][132][133][134][135] In patients with impaired renal function who are not being treated with CRRT, we recommend administering ≤50% of the initial empirical phosphate dosage. Patients being treated with CRRT may require higher initial dosages (i.e., closer to empirical doses used for patients with normal renal function), depending on the severity of hypophosphatemia, the amount of phosphorus being removed with CRRT, and whether or not phosphorus is used in the dialysate or replacement fluid.…”

“…However, doses can be infused up to a rate of 7 mmol of phosphate per hour. 134,135 Phosphorus can quickly shift between compartments within the body and serum concentrations can fluctuate 24,28,129 ; therefore, a repeat serum phosphorus level should be checked two to four hours after administering a dose. Additional phosphate supplements should be given until the patient is asymptomatic and the serum phosphorus concentration is at least >2.0 mg/dL, with a final goal of returning the serum phosphorus levels to within normal range.…”

High serum aluminium levels and acute reversible encephalopathy in a 4-year-old boy with acute renal failure

“…It could be argued that initial acute renal failure itself, hypophosphoraemia and hyponatraemia may be responsible for neurological deterioration. However, the fact that urea and creatinine were only moderately elevated, serum sodium concentrations were well over values normally considered significant for the development of neurological complications [6], and serum phosphorus levels were over lmg/dl (0.38 mmol/1) [11] reaching normal values within 24 h despite persisting neurological deterioration, does not support this idea.…”