Hyperphosphatemia may be seen with increased phosphorus intake (abuse of phosphate laxatives or excessive potassium phosphate administration), decreased phosphorus excretion (renal insuffi-ciency), or massive cell lysis (following chemother-apy for lymphoma or leukemia).
Although hyperphosphatemia itself does not appear to be directly responsible for any functional disturbances, its secondary effect on plasma [Ca2+] can be important. Marked hyperphosphatemia is thought to lower plasma [Ca2+] by precipitation and deposition of calcium phosphate in bone and soft tissues.
Hyperphosphatemia is generally treated with phos-phate-binding antacids such as aluminum hydrox-ide or aluminum carbonate.
Although specific interactions between hyperphos-phatemia and anesthesia are generally not described, renal function should be carefully evaluated. Sec-ondary hypocalcemia should also be excluded.
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