PRES in Alcoholic Hepatitis: Hepatic Encephalopathy a Common Theme

Abstract

Posterior reversible encephalopathy syndrome (PRES) is documented in patients with renal failure, labile blood pressure, cytotoxic drugs, and autoimmune disorders. This is the first reported case of PRES in severe alcoholic hepatitis and hepatic encephalopathy. A 40-year-old female presented with altered mental status, fever, jaundice, tender hepatomegaly, WBC 14.1 thousand/ul, and a discriminant function of 99. Clinical and radiographic features were suggestive of chronic liver disease. Due to persistent headaches despite a slow and steady improvement of the encephalopathy on lactulose and rifaximin, an MRI was obtained. Although a limited study, bilateral temporal parietal restriction was described, raising concern for PRES. There was no evidence of seizure activity on sixtyminute electroencephalography (EEG), and her mild intermittent headaches were stable without neurologic deficits. She was discharged, but was readmitted after a witnessed tonic-clonic seizure the next day. Labs were all relatively unchanged from her discharge labs. Urine drug screen was negative and alcohol level was undetectable. A repeat MRI showed PRES (Figure 1). EEG showed high focal epileptogenic potential in the temporal-parietal area. She was started on seizure prophylaxis and continued on lactulose and rifaximin. Fluconazole was switched to itraconazole to minimize interactions with her seizure threshold. Prior to discharge, her neurologic deficits and headaches had completely resolved. While the pathogenesis of PRES is not fully understood, two prevailing hypotheses have been proposed. The more popular theory purports that severe and rapidly developing hypertension can devastate auto-regulation resulting in hyperperfusion with endothelial injury/vasogenic edema. The pathophysiology of hepatic encephalopathy is not completely understood, but ammonia has been recognized as a pivotal player in the process. As the brain has no inherent cycle of urea metabolism, ammonia reaching the astrocytes are detoxified by glutamine synthetase in the presence of glutamate to form glutamine, which promotes swelling of astrocytes. This vasogenic edema is a culprit in PRES pathophysiology. This is the first reported case of acute alcoholic hepatitis with hepatic encephalopathy developing PRES in the absence of known risk factors such as hypotension, ischemia, and blood pressure fluctuations.Figure 1