Hyperammonemic Encephalopathy due to Sepsis-Associated Liver Injury

Hyperammonemic encephalopathy (HE) arising in acute liver injury (ALI) represents an extremely severe yet potentially reversible complication associated with high mortality rates and persistent neurological deficits. Sepsis may act as a primary trigger of ALI, which is diagnosed in 46% of patients with septic processes. From a pathogenetic perspective, HE is characterized by a multifactorial nature, encompassing the direct neurotoxic effects of ammonia, systemic inflammatory response, oxidative stress, astrocytic dysfunction, and disruption of neurotransmitter homeostasis. The clinical spectrum ranges from subclinical cognitive impairment to deep coma and generalized seizure activity, which significantly complicates the differential diagnosis of this condition from other central nervous system lesions encountered in intensive care unit settings. Specific laboratory markers are absent; nevertheless, the detection of elevated plasma ammonia concentration serves as a key indicator. Magnetic resonance imaging plays a crucial role in confirming the diagnosis, with characteristic findings including bilateral symmetric lesions in the insular cortex and cingulate gyrus. A high level of clinical vigilance, a personalized management strategy, timely diagnostic verification, and early initiation of multimodal therapy contribute to improved prognosis and outcomes in this patient population. This report presents a clinical case of HE induced by ALI in the setting of abdominal sepsis in a 63-year-old patient.