Neuroimaging findings in hyperammonemic encephalopathy associated with sepsis-induced acute liver dysfunction: a pilot case series

Background. Hyperammonemic encephalopathy (HE) is a severe complication of acute liver dysfunction (ALD), often associated with sepsis. However, its neuroimaging manifestations remain poorly understood. The aim of this pilot case series is to describe the brain MRI findings in patients with sepsis and HE. Methods. We analysed brain MRI data from 15 consecutive patients with sepsis and clinically confirmed HE. Assessment of cerebral changes was performed using a standard MRI protocol. The following parameters were evaluated during the analysis: localization and signal intensity characteristics of the lesions on MRI, presence or absence of diffusion restriction, presence magnetic susceptibility artifacts, and reversibility on follow‑up were evaluated descriptively. No control group was included. Results. Pathological changes were observed in all 15 patients. Symmetrical involvement of the insular cortex and cingulate gyrus was the most frequent pattern (13/15, 86.7%), followed by basal ganglia lesions (1/15) and cortico‑subcortical hemispheric lesions (1/15). All lesions were hyperintense on T2‑WI and FLAIR, with diffusion restriction on DWI suggestive of cytotoxic oedema. Follow-up MRI was performed in all patients after treatment adjustment and renal replacement therapy, demonstrating marked regression of all noted changes, concurrent with normalization of serum ammonia, transaminases, lactate and sepsis markers. Conclusion. The bilateral insular‑cingulate pattern appears to be the most common MRI finding in sepsis‑related HE and shows reversibility upon correction of hyperammonaemia. These observations suggest that MRI may provide supportive evidence for early diagnosis, but the findings are preliminary and require validation in larger controlled studies.