Cefepime neurotoxicity in elderly patient with renal impairment: a case report

While cefepime-induced neurotoxicity is a known complication of beta-lactam therapy in renal impairment, its diagnosis is uniquely challenging in patients with complex neurosurgical baselines. This case illustrates the risk of diagnostic anchoring where the presence of a ventriculoperitoneal shunt diverts clinical suspicion toward mechanical failure and obscures a reversible toxic etiology.

A 63-year-old female with subarachnoid hemorrhage, slit ventricle syndrome, and a ventriculoperitoneal shunt presented with septic shock and acute kidney injury. Following renal adjustment of cefepime for Pseudomonas bacteremia, she developed profound altered mental status. Initial evaluation prioritized shunt malfunction, yet computed tomography was confounded by chronic slit ventricle physiology. Electroencephalography revealed generalized triphasic waves characteristic of metabolic encephalopathy rather than structural dysfunction.

Cefepime-induced neurotoxicity (CIN) pathophysiology involves gamma-aminobutyric acid-A receptor inhibition amplified by reduced renal clearance and sepsis-induced blood-brain barrier disruption. Here, the clinical picture was masked by the overlap between toxic encephalopathy and insidious shunt failure symptoms. This necessitated distinguishing toxicity from nonconvulsive status epilepticus or hydrocephalus using electroencephalogram (EEG), defying the heuristic that neurological decline in shunted patients is mechanical until proven otherwise.

This case underscores that CIN can mimic mechanical shunt failure, which necessitates a high index of suspicion in patients with indwelling neurosurgical hardware. Early EEG utilization is critical to overcome diagnostic bias and ensure prompt antibiotic discontinuation rather than unnecessary neurosurgical intervention.