Evaluation and Management of Hepatic Encephalopathy: Current Status and Future Directions

Abstract

Hepatic encephalopathy is a spectrum of neurocognitive manifestations often seen in patients with liver injury or rarely in patients with portosystemic shunting without liver injury. It can be divided into minimal (covert) hepatic encephalopathy and overt hepatic encephalopathy, depending on the severity. Patients with hepatic encephalopathy have compromised clinical outcomes, decreased quality of life, and increased healthcare utilization, often resulting in a heavy financial and personal burden on caregivers. The diagnosis remains largely clinical, with the exclusion of possible other causes for the altered mental status. Current treatment strategies include nonabsorbable disaccharides and antibiotics. This review will focus on the diagnosis, management and clinical impact of hepatic encephalopathy.

The Direct Contribution of Astrocytes and Microglia to the Pathogenesis of Hepatic Encephalopathy

“…The neurological and cognitive manifestations that present in patients with liver disease or portosystemic shunting in the absence of liver disease is termed HE. 4 Two categories of HE exist: covert HE (also known as minimal HE) and overt HE; these are distinguished by the severity of the patient presentation. 5 Patients with minimal HE have abnormal results with psychometric testing and subtle personality changes that may be evident to caregivers or by those familiar with the patient.…”

Critical flicker frequency test for diagnosing minimal hepatic encephalopathy in patients with cirrhosis

“…Based on the hypothesis, retinal gliopathy could be used as a marker of HE. CFF significantly decreased in parallel with the HE severity (7).…”

“…During the test, subjects are administered light pulses with decreasing frequency (from ≤60 Hz to 25 Hz) and are requested to press a switch as soon as the feeling of a fused light changes to a flickering light (7,8).…”

Lactulose improves cognition, quality of life, and gut microbiota in minimal hepatic encephalopathy: A multicenter, randomized controlled trial

“…Ammonia, the key factor mediating the occurrence of HE, is mainly derived from urea breakdown by urease‐producing bacteria located in the large intestine . There is increasing evidence that gut microbiota plays an important role in the pathogenesis of HE .…”

“…3 Ammonia, the key factor mediating the occurrence of HE, is mainly derived from urea breakdown by urease-producing bacteria located in the large intestine. 4,5 There is increasing evidence that gut microbiota plays an important role in the pathogenesis of HE. 6,7 Fecal microbiota are altered with increasing Child-Turcotte-Pugh (CTP) scores and development of HE in cirrhotic patients.…”