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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Hepatic Encephalopathy in Critical Care
Rahul Rane1, Kevin Koch1, Tariq Cheema1
1Division of Pulmonary and Critical Care Medicine, Allegheny Health Network Medicine Institute, Pittsburgh, USA.
Abstract:
Hepatic encephalopathy (HE) is a complex neurocognitive disorder stemming from liver dysfunction, ranging from subtle cognitive impairments to profound coma. It develops when the liver's detoxification capacity is compromised, leading to an accumulation of neurotoxins like ammonia that disrupt brain function. From an intensivist's perspective, HE is more than mere confusion; it's a critical brain-liver syndrome demanding careful airway management, hemodynamic stability, and vigilance against cerebral edema and intracranial hypertension. HE is categorized into three types: Type A, associated with acute liver failure (ALF), poses the highest risk for rapid neurological decline and cerebral herniation, making it particularly relevant in critical care. Type C, prevalent in cirrhotic patients, is more common and often coexists with other organ failures. Type B HE, though less recognized, occurs with portosystemic shunting. For intensivists and anesthesiologists, prompt recognition and a structured management approach are paramount. This involves identifying and treating precipitating factors, stabilizing cardiorespiratory function, reducing ammonia levels, and preventing cerebral edema. Ongoing assessment of liver function and consideration for urgent liver transplantation, especially in Type A HE, are crucial. A deep understanding of HE's pathophysiology guides aggressive interventions such as continuous renal replacement therapy, plasma exchange, and intracranial pressure monitoring in select cases.
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