Hepatic encephalopathy

Hepatic encephalopathy is a reversible, potentially life-threatening spectrum of neuropsychiatric and motor abnormalities caused by brain dysfunction secondary to severe hepatic insufficiency, portosystemic venous shunting, or both It primarily affects the central nervous system in patients with acute liver failure, advanced cirrhosis, or surgical and spontaneous portosystemic shunts Pathophysiologically, failing hepatic clearance allows neurotoxins—principally gut-derived ammonia—to cross the b...

Hepatic encephalopathy is a reversible, potentially life-threatening spectrum of neuropsychiatric and motor abnormalities caused by brain dysfunction secondary to severe hepatic insufficiency, portosystemic venous shunting, or both

Hepatic encephalopathy is a reversible, potentially life-threatening spectrum of neuropsychiatric and motor abnormalities caused by brain dysfunction secondary to severe hepatic insufficiency, portosystemic venous shunting, or both It primarily affects the central nervous system in patients with acute liver failure, advanced cirrhosis, or surgical and spontaneous portosystemic shunts Clinically, manifestations range along a continuum from subtle, subclinical neurocognitive deficits (minimal or c...

It primarily affects the central nervous system in patients with acute liver failure, advanced cirrhosis, or surgical and spontaneous portosystemic shunts

Pathophysiologically, failing hepatic clearance allows neurotoxins—principally gut-derived ammonia—to cross the blood-brain barrier, triggering astrocyte swelling, systemic and neuroinflammation, and altered neurotransmission Clinically, manifestations range along a continuum from subtle, subclinical neurocognitive deficits (minimal or covert disease) to overt disturbances characterized by inverted sleep-wake patterns, asterixis, confusion, somnolence, and progression to hepatic coma

Pathophysiologically, failing hepatic clearance allows neurotoxins—principally gut-derived ammonia—to cross the blood-brain barrier, triggering astrocyte swelling, systemic and neuroinflammation, and altered neurotransmission Clinically, manifestations range along a continuum from subtle, subclinical neurocognitive deficits (minimal or covert disease) to overt disturbances characterized by inverted sleep-wake patterns, asterixis, confusion, somnolence, and progression to hepatic coma