NON CONVULSIVE STATUS EPILEPTICUS INDUCED BY CEFEPIME
Abstract number :
2.169
Submission category :
Year :
2004
Submission ID :
4691
Source :
www.aesnet.org
Presentation date :
12/2/2004 12:00:00 AM
Published date :
Dec 1, 2004, 06:00 AM
Authors :
1Helio van der Linden, 1Marcilia L. Martyn, 2Joaquina Q. Andrade, 1Luiz M. Castro, and 2Rosi M. Grossman
Non convulsive status epilepticus (NCSE) is underdiagnosed in critically ill patients, because decreased level of consciousness may be erroneously attributed to toxic-metabolic encephalopathy. Antibiotics, especially penicillins, cephalosporins, imipenem and quinolones have been implicated in seizures and NCSE. Recently, cefepime, a fourth generation cephalosporin, has been reported to induce NCSE, specially in association with renal failure. Case series, describing clinical and EEG findings in seven patients with NCSE treated with cefepime. Mean age of patients was 52 years (24 to 74 ), all were women. Six patients presented abnormal renal function while on cefepime treatment. Three were under dialysis, and the other, hepatic failure after liver transplant. Cefepime was started for sepsis in 3, pneumonia in 1, severe skin infection in 1 and fever of unknown origin in 3. Doses ranged from 2-4g/day. Two patients had neurological disease prior to introduction of cefepime. One patient had herpes encephalitis treated with acyclovir without consciousness impairment until cefepime was started. Another patient had an external ventricular shunt due to brain hemorrhage. When cefepime was started the patient was alert, with global aphasia. The interval between initiation of antibiotic therapy and first neurological signs (confusion, impaired level of consciousness in all patients, and myoclonic jerks in two) ranged from 24 to 96 hours. One patient had excessive drowsiness and brief staring periods. The EEG showed electrographic status epilepticus, characterized by continuous generalized sharp and slow waves in 6 patients. The EEG of the patient with milder clinical features (excessive drowsiness) showed diffuse background slowing and bursts of slow delta activity. All patients underwent CT scan and extensive metabolic and clinical work-up to rule out other causes of acute encephalopathy. Neurological improvement was observed 24 to 72 hours after discontinuation of cefepime, confirmed by repeat EEGs, showing resolution of electrical status epilepticus. One patient died of systemic complications several days after neurologic improvement. Cefepime is the possible culprit of nonconvulsive status in all cases in this series. Level of consciousness and responsiveness should be carefully monitored in patients receiving cefepime, specially in patients with renal failure. Early EEG diagnosis and cefepime withdrawal influence outcome in these cases.