Background: Cefepime-induced neurotoxicity is reported in up to 15% of critically ill patients receiving the drug and approx. 80% of affected individuals demonstrating underlying renal dysfunction. However, approximately 20% of cases occur in patient with preserved renal function, as described by Payne et al. (2017)1 We report a case highlighting the possibility of Cefepime-induced encephalopathy as a cause of neurological deterioration in critically ill patient especially with preserved renal functions. Case description: A 76-year-old male patient with Chronic obstructive pulmonary disease, chronic hyponatremia (sodium 118 mEq/L), hypoalbuminemia (albumin 2.5 g/dL), reduced left ventricular ejection fraction (LVEF-40%), and recurrent multidrug-resistant infections developed progressive encephalopathy within 48 hours of initiating intravenous Cefepime–enmetazobactam combination (2.5gm IV every 8 hourly) having 2 gm of Cefepime and 500 mg of enmetazobactam in each vial. Patients Glasgow Coma Scale declined from 14/15 (E4V4M6) to 9/15(E2V3M4) over period of 48 hours. With detailed evaluation of the etiology of neurological deterioration almost ruled out all structural and metabolic causes for the same. Electroencephalography (EEG) demonstrated left fronto-temporal and right frontal epileptiform activity with diffuse cerebral dysfunction, consistent with type 1 antibiotic-associated encephalopathy pattern described by Bhattacharyya et al. (2026). Cefepime-induced neurotoxicity was kept as a strong possibility even with preserved renal functions. Serum creatinine remained within normal limits (0.4–0.6 mg/dL) all throughout. Discussion: Application of the Bradford Hill criteria supports a probable causal relationship of CIN. The EEG findings can be very specific and helps in making early diagnosis. Many non-renal risk factors such as advanced age, hypoalbuminemia, sepsis-related blood–brain barrier disruption, and chronic electrolyte disturbance should also be kept in mind while starting Cefepime in patients with such risk factors. Conclusion: Cefepime-induced neurotoxicity should be considered in any critically ill patient with unexplained neurological deterioration during Cefepime therapy, irrespective of renal function. Statement of clinical significance: This case demonstrates that CIN can occur despite preserved renal function when non-renal risk factors—advanced age, hypoalbuminemia, sepsis-related blood–brain barrier disruption, and chronic electrolyte disturbance—converge. Clinicians should maintain a high index of suspicion and obtain early EEG in at-risk patients receiving Cefepime, regardless of renal function status.
Soni* et al. (Mon,) studied this question.