Meperidine-associated central nervous system (CNS) excitatory toxiciti
es are believed to be caused by accumulation of the active metabolite
normeperidine. Normeperidine is eliminated by the kidneys and accumula
tes in patients with renal insufficiency, sickle cell disease, and can
cer. In patients with cirrhosis, the metabolism of meperidine is decre
ased, leading to accumulation of the parent drug and possible CNS depr
essive effects similar to hepatic encephalopathy. Although the elimina
tion of normeperidine is decreased as well in these patients, the rati
o of normeperidine to meperidine is generally low, and the narcotic ef
fects of meperidine usually predominate. This is the first reported ca
se of CNS excitatory toxicities in a patient with alcoholic hepatitis
and cirrhosis, and normal renal function. Administration of multiple d
oses of meperidine in patients with hepatic disease should be discoura
ged.