Electrolyte and acid-base abnormalities have been reported in acute NSAID overdoses. Alterations in serum electrolytes may occur secondary to decreased prostaglandin synthesis or from NSAID-induced renal failure. Sodium and water retention may lead to volume overload, with patients having preexisting renal failure, cirrhosis, or congestive heart failure. Hyperkalemia, hypocalcemia, and hypomagnesemia have been reported in NSAID overdoses complicated by acute renal failure.15
Increased anion-gap acidosis has been observed in large overdoses of the propionic acid NSAIDs ibuprofen and naproxen. Prostaglandin inhibition is not directly responsible for the anion-gap acidosis; rather, acidosis is likely to be related to lactic acidosis. Case reports of large overdoses suggest that the acidosis is related to large quantities of these mildly acidic NSAIDs and their metabolites in serum.16 However, these studies neither measured nor considered lactate as the possible mechanism. Concurrent lactic acidosis in the setting of NSAID-induced seizures may worsen the acidosis in some cases.
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