Cefepime neurotoxicity can mimic postanoxic coma with myoclonic status epilepticus

Abstract

A 61-year-old woman admitted for operative treatment of aortic and mitral stenosis and coronary artery bypass grafting developed encephalopathy and abnormal movements postoperatively. The evening after surgery, she was hypoxic and hypotensive. The following day, she was awake and following commands without any obvious focal deficits. Over subsequent days her mental status worsened as she remained in shock. Hypoperfusion of the kidneys and liver resulted in acute tubular necrosis and transaminitis. On postoperative day 2 she was started empirically on cefepime and vancomycin for fever and leukocytosis of unknown origin. Her level of consciousness gradually declined and by the fifth postoperative day she was comatose and had developed repetitive involuntary movements of the face consisting of sudden opening of the eyes and opening and closing of the jaw. The movements of the mouth were forceful enough to damage 2 endotracheal tubes. She also had dystonic-like movements in the lower extremities. The movements had myoclonic features but at times appeared more dystonic and were strongly exacerbated by stimulation, particularly when applied to the feet (video). Dexmedetomidine was used to minimize the movements. When sedation was held the movements increased and her examination otherwise remained unchanged. The patient's eyes were partially open but she did not track light or moving objects. Brainstem reflexes were preserved but she had no motor response to pain in any of the extremities. A noncontrast CT scan of the brain showed no intracranial pathology. An EEG showed no electroencephalographic correlate to the movements. The background was diffusely slow in the range of 1-4 Hz with intermixed and ␤ activity and no reactivity was observed. The following day, the patient's antibiotic regimen was changed from cefepime to piperacillin/tazobactam for additional anaerobic coverage as fever and leukocytosis remained present and no source had been identified. On the sixth postoperative day, she had regained consciousness and could interact with family and examiners. She could answer questions by shaking and nodding her head and could follow commands in all extremities. The abnormal movements were much less prominent and did not require dexmedetomidine to prevent damage to the endotracheal tube; however, the presence of the tube clearly made the movements of the face more frequent. The following day she underwent tracheostomy placement with removal of the endotracheal tube after which the facial movements disappeared.

Usefulness of bilateral bispectral index (BIS) monitoring in a comatose patient with myoclonic status epilepticus secondary to cefepime

“…Indeed, in a retrospective study, it was reported that non‐epileptic events such as tremor‐like movements, multifocal myoclonic jerks without electrographic changes, and slow semi‐purposeful movements of the limbs or trunk, frequently mimic seizures in the ICU setting, and only bedside v‐EEG recordings may help in the differential diagnosis (Benbadis et al , 2010). Interestingly, similar movements to those described by Hocker and Rabinstein (2011) ( e.g. sudden and forceful opening and closing of the jaw) mimicking post‐anoxic coma may also be observed in the video reported here.…”

“…It is not unusual to doubt the existence of hypoxic or hypotensive complications in critically ill subjects. This point is crucial when one makes a decision regarding the aggressiveness of treatment and prognostication (Hocker and Rabinstein, 2011). It is widely known that the prognosis of acute MSE after cardiac arrest is poor, and intensive treatment does not modify outcome at all.…”

“…In addition, neurotoxic side effects due to cefepime include a broad spectrum of clinical manifestations such as myoclonus, dystonic movements, tremor, asterixis, and coma (Grill and Maganti, 2008). Recently, some authors have emphasized the importance to keep in mind the fact that cefepime neurotoxicity may clinically mimic post‐anoxic coma with myoclonic status epilepticus (MSE) (Hocker and Rabinstein, 2011).…”

“…In addition, neurotoxic side effects due to cefepime include a broad spectrum of clinical manifestations such as myoclonus, dystonic movements, tremor, asterixis, and coma (Grill and Maganti, 2008). Recently, some authors have emphasized the importance to keep in mind the fact that cefepime neurotoxicity may clinically mimic postanoxic coma with myoclonic status epilepticus (MSE) (Hocker and Rabinstein, 2011). To the best of our knowledge, we report the first video-electroencephalogram (v-EEG) study of a critically ill patient receiving treatment with cefepime who developed an episode of profound stupor associated with multifocal facial, trunk, and limb jerks, compatible with the diagnosis of confirmed symptomatic MSE (Foreman and Hirsch, 2012).…”