Encefalopatía hepática fulminante vinculada a hiperintensidad de la corteza cerebral en la resonancia magnética

background: the presence of manganese deposits in basal ganglia is an expression of chronic liver damage in neuroimaging, whereas diffuse edema of the white matter and hyperintensity of the internal capsule are seen in mri in acute decompensation. in fulminant encephalopathy, changes in intensity in the cerebral cortex have been described, suggesting different pathogenic aspects. purpose: to describe and try to interpret hyperintensities images of the cerebral cortex in fulminant hepatic encephalopathy. case report: a 42 years old woman, with history of hyperthyroidism treated with propylthiouracil developed abdominal pain, choluria and general malaise, without fever. at admission, she had jaundice, elevated liver enzymes, and hyperammronemia of 481 ug. she developed progressive impairment of consciousness falling into a non-reactive coma with intermediate size and poorly reactive pupils, absence of oculocephalic reflexes and diminished osteotendinous reflexes, with indifferent plantar reflexes. brain ct showed brain edema without focal lesions. the mri showed hyperintense signal abnormalities in the fronto-parietal cortex in t2 and flair with restriction in difussion sequency. she became brain dead. comment: these exceptional images on mri are considered an expression of cytotoxic damage, consistent with high levels of ammonium in fulminant hepatic encephalopathy. the swelling of astrocytes and cortical neurons is caused by the accumulation of intracellular glutamine, highly osmophilic, and explains the restriction on the difussion and lower values in the adc. interstitial edema would be part of the chronic forms by acquisition of compensatory mechanisms capable of preventing the accumulation of glutamine.