Case Presentation: A 68 year old man with PMH of cerebral palsy, cognitive impairment, and chronic pain with intrathecal baclofen pump initially presented with sepsis due to baclofen pump pocket infection, and underwent explantation of baclofen pump. Intraoperative cultures grew pseudomonas, so on POD 3 cefepime was initiated. On POD 4, he developed encephalopathy, becoming somnolent, moaning in pain, and he was unable to answer questions appropriately. Imaging including CT head and MRI brain did not reveal an acute cause. EEG showed generalized seizure tendency including generalized periodic discharges with triphasic morphology. On POD 5, cefepime was switched to meropenem. By POD 7, his mental status had largely returned to his baseline, and EEG morphology exhibited decreased frequency of triphasic morphology. He was shortly after discharged back to his care facility in stable condition.

Discussion: Cefepime is a fourth-generation cephalosporin commonly used as empiric therapy due to its broad-spectrum coverage. Cefepime-induced neurotoxicity (CIN) is rare, and is mainly attributed to its ability to cross the blood–brain barrier and competitively bind to GABA class A receptors, inhibiting endogenous GABA neurotransmission, leading to central excitation. It is thought that a serum or plasma trough threshold of >20 mg/L is associated with higher risk of CIN. CIN has a varied presentation, and most commonly includes encephalopathy, myoclonus, and nonconvulsive status epilepticus, and may also include hallucinations and coma. Previous literature has stated a main risk factor being renal insufficiency. However, more recent research suggests that patients with normal renal function may also develop neurotoxicity. EEG classically demonstrates triphasic morphology in CIN (possibly in up to half of cases), though it is not commonly used. EEG may be a useful marker in making the diagnosis. The treatment for CIN is discontinuation of cefepime, and hemodialysis may be considered for severe cases. Anticonvulsants are not recommended unless there are convulsive seizures or definite nonconvulsive status epilepticus.

Conclusions: Clinicians should consider CIN in the differential diagnosis of encephalopathy even in patients with preserved renal function. EEG may be a useful tool in establishing a diagnosis.