Hepatic Encephalopathy

Hepatic Encephalopathy in Children

“…The underlying mechanism of HE is not well-defined, but multiple theories have been proposed. One leading hypothesis surrounds gut-derived toxins and hyperammonemia, though other possibilities involve altered bile acids, cytokines, and chemokines [ 1 , 4 ]. Ammonia is a byproduct of bacterial metabolism of both proteins and other nitrogenous compounds in the large intestine and is also generated during glutamine metabolism in small bowel enterocytes.…”

“…A majority of ammonia is typically metabolized to an innocuous by-product (urea), during first-pass metabolism in the liver via the portal vein, which is then excreted [ 5 ]. As such, in the setting of liver disease which disrupts this natural blood flow, metabolism and excretion of ammonia is inhibited, leading to hyperammonemia and its increased passage across the blood-brain barrier [ 1 ]. In the brain, ammonia is postulated to cause cerebral edema by inducing swelling of type II astrocytes [ 1 ].…”

“…Hepatic encephalopathy (HE) is defined as neuropsychiatric impairment and mental status changes that present in patients with liver disease [ 1 , 2 ]. Patients with HE are at risk of developing cerebral edema, and its diagnosis and grading can be particularly challenging in pediatrics depending on a child’s age, developmental achievements, and easily confused symptoms.…”

“…Patients with acute liver failure or chronic liver disease may both be afflicted, though with slightly different presentations. Episodes of HE may be prompted by sepsis, upper gastrointestinal tract bleeding, dehydration, constipation, ileus, or small bowel obstruction, among other things [ 1 , 3 ]. Degree of HE can be exacerbated by a variety of mechanisms including oxidative stress, hyperinflammatory states, altered cerebral blood flow and metabolic derangements.…”

International normalized ratio and Model for End-stage Liver Disease score predict short-term outcome in cirrhotic patients after the resolution of hepatic encephalopathy

“…Liver transplantation should be considered for patients suffering from HE, particularly those who have suffered it twice in the past 6 mo, in case of no complications that hinder surgery[3]. However, “transplantation might not be feasible owing to contraindications or organ shortage”[4]; for one thing, the muscle volume usually decreases rapidly in patients who have HE with persistent or frequent relapse, and survival is not easy even for those who have experienced liver transplantation for another[5]. In addition, patients with HE may seek an artificial liver support system, which can reduce plasma ammonia, inflammatory cytokines, bilirubin, and other toxins[6], providing the liver with a chance of recovery and avoiding liver trans-plantation, or allowing patients to wait for transplantation.…”