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JOURNAL READING WITH REFLECTION

TITLE: Hepatic encephalopathy: current challenges and future prospects

AUTHOR: Irashini Swaminathan, Mark Alexander Ellul, Timothy

DATE PUBLISHED: March 22, 2018

Hepatic encephalopathy (HE) is a hallmark of liver failure and affects up to 40% of patients with liver
cirrhosis.1 It is defined as a multifactorial neuropsychiatric disorder presenting with a broad spectrum of cognitive impairment
and neuromuscular dysfunction.1 HE is a significant contributor to repeated hospitalizations for patients with liver cirrhosis and
severely impacts on the quality of life of both patients and caregivers.2 It is a marker of poor prognosis in cirrhotic patients,
with reported rates of survival of only 36% at 1 year from its first presentation.3
Chronic liver disease is the fifth most common cause of death in the UK, with the mortality expected to rise due to increase in
cirrhosis caused by alcohol-related liver disease, chronic hepatitis C and nonalcoholic fatty liver disease. 4,5 Patients commonly
present to primary and secondary care services with complications such as HE with or without a prior diagnosis of chronic
liver disease. A milder form of the disorder, covert hepatic encephalopathy (CHE) or covert encephalopathy with subtle
alterations of cognitive function, also exists.6 Although less severe, patients with CHE are at significant risk of interference
with their quality of life, including increased falls, hospitalizations and progression to overt HE. 6–8
HE can be classified as three separate clinical entities. Type A HE is due to acute liver failure, Type B due to
portosystemic shunting (e.g., transjugular intrahepatic portosystemic shunting procedures) and Type C results as a
complication of liver cirrhosis.9
Type A HE is associated with an increased intracranial pressure that progresses rapidly and may lead to brain
herniation. The pathophysiology of Type B and C HE is complex and remains under investigation. The main hypothesis
involves the limited ability of the liver to effectively remove nitrogenous waste products, resulting in their accumulation and
the deleterious effects on the brain due to portosystemic shunting.10,11 The key substrates implicated are ammonia and
glutamine. Several studies have demonstrated that cirrhotic patients who had or were experiencing significant neuropsychiatric
symptoms had elevated blood ammonia concentration.12,13 However, the levels were not predictive or consistent with the
severity of HE.14,15 The exception is in type A HE, where Bernal et al have shown that a cut-off level of ammonia >200
µmol/L16 is predictive of raised intracranial pressure and death.16,17

Source: https://www.dovepress.com/hepatic-encephalopathy-current-challenges-and-future-prospects-
peer-reviewed-fulltext-article-HMER

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