Sudarsh Ts, Sriram Balaji, Dharani K, Krithika S, Karthigeyan Ts, Yogesh Subramanian, Aarav J Paul, Sahasyaa Adalarasan, Jayaprakash N, Hariharan C
Hyperammonemic encephalopathy is an uncommon but potentially life-threatening and reversible cause of acute altered sensorium, most often associated with hepatic dysfunction but increasingly recognized in patients receiving chemotherapy. We report the case of a 50-year-old woman who developed progressive disorientation and reduced responsiveness one hour after completing her first cycle of FOLFOX-6 (5-fluorouracil, leucovorin, and oxaliplatin) following hemicolectomy for splenic flexure carcinoma. Initial neuroimaging and infectious workup were unremarkable. Despite correction of transient renal dysfunction, neurological status did not improve. Serum ammonia was markedly elevated, and a diagnosis of non-hepatic hyperammonemic encephalopathy secondary to chemotherapy was made. Prompt discontinuation of FOLFOX and initiation of lactulose resulted in rapid and complete clinical recovery. This case highlights the importance of early recognition of chemotherapy-induced metabolic encephalopathy, particularly fluoropyrimidine-associated toxicity, and emphasizes serum ammonia estimation in unexplained post-chemotherapy neurological deterioration to ensure timely management and favorable outcomes.