Hepatic Encephalopathy and Nutrition Influences: A Narrative Review

Abstract

Hepatic encephalopathy (HE) is a potentially reversible neurocognitive condition seen in patients with advanced liver disease. The overt form of HE has been reported in up to 45% of patients with cirrhosis. This debilitating condition is associated with increased morbidity and mortality and imposes a significant burden on the caregivers and healthcare system. After providing an overview of HE epidemiology and pathophysiology, this review focuses on the interaction of HE and frailty, nutrition requirements and recommendations in cirrhotic patients with HE, and current dietary and pharmacologic options for HE treatment. (Nutr Clin Pract. 2020;35:36-48)

Cirrhosis: Therapeutic Aspects and Outcome for Hospitalized Patients in Burkina Faso

“…Treatments aiming to modify the colonic bacterial flora and accelerate intestinal transit may prove efficacious. The most commonly used treatment is the lactulose or lactilol (non-absorbable disaccharide) [25] [26] [27]. In our study, this treatment was administered in 73.6% of the cases.…”

“…Hepatic encephalopathy with an unfavorable outcome as per the West Haven criteria [25] is associated with higher short-term mortality (within 90 days) [26].…”

“…The treatment of encephalopathy is primarily based on the treatment (if possible) of the triggering cause. In addition to nutrition, the use of disaccharides and non-absorbable antibiotics (rifaximin) are part of the therapeutic means [25].…”

Nutrition Assessment and Management in Patients with Cirrhosis and Cognitive Impairment: A Comprehensive Review of Literature

“…Because of the decreased ability to utilize glucose, lipid oxidation and gluconeogenesis are accelerated, leading to a higher incidence of post-prandial hyperglycaemia [ 6 ]. This condition is also due to insulin resistance; in fact, a significantly lower insulin sensitivity index after oral tolerance testing and increased pancreatic insulin synthesis have been demonstrated in several studies to compensate the lack of glucose clearance [ 7 ]. Up to 70% of cirrhotic patients have some degree of glucose intolerance or insulin resistance, whereas 14–46% have type II diabetes mellitus [ 8 ].…”

“…A low BCAA to AAA ratio has been shown to be associated with a worse prognosis and risk of developing HE [ 10 ]. When this ratio is <3, AAAs cross the blood–brain barrier and act as substrates for the synthesis of false neurotransmitters such as octopamine, tyramine and phenylethanolamine, which displace major neurotransmitters such as dopamine and norepinephrine [ 7 ].…”