Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Esophageal Varices-II: Clinical Features and Management01:28

Esophageal Varices-II: Clinical Features and Management

Esophageal varices often manifest as gastrointestinal bleeding episodes, presenting symptoms like hematemesis (vomiting of blood), hematochezia (passing fresh blood via the rectum), and melena (black, tarry stools). Other signs can include weight loss, anorexia, abdominal discomfort, jaundice, pruritus, altered mental status, and muscle cramps.
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol abuse, or...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Experimental models of hepatic encephalopathy: ISHEN guidelines.

Liver international : official journal of the International Association for the Study of the Liver·2009
Same author

Performance of the hepatic encephalopathy scoring algorithm in a clinical trial of patients with cirrhosis and severe hepatic encephalopathy.

The American journal of gastroenterology·2009
Same author

Melatonin arrhythmia is corrected after liver transplantation.

The American journal of gastroenterology·2009
Same author

The role of etiology in the hyperamylasemia of acute liver failure.

The American journal of gastroenterology·2009
Same author

Impact of preoperative overt hepatic encephalopathy on neurocognitive function after liver transplantation.

Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society·2009
Same author

Detection and diagnosis of herpes simplex virus infection in adults with acute liver failure.

Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society·2008

Related Experiment Video

Updated: Jul 7, 2026

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

Brain edema in acute liver failure.

Andres T Blei1

  • 1Division of Hepatology, Northwestern University Feinberg School of Medicine, Chicago, IL 60610, USA. a-blei@northwestern.edu

Critical Care Clinics
|February 5, 2008
PubMed
Summary

Acute liver failure (ALF) rapidly impairs liver function, affecting the brain. This review details ALF's neurologic consequences, focusing on hepatic encephalopathy and brain edema.

Area of Science:

  • Neurology
  • Hepatology
  • Internal Medicine

Background:

  • Acute liver failure (ALF) is a critical condition characterized by rapid liver function decline.
  • ALF presents with coagulopathy and encephalopathy in previously healthy individuals.
  • Neurologic complications are a major concern in ALF management.

Purpose of the Study:

  • To analyze the specific repercussions of ALF on the brain.
  • To discuss unique features of ALF relevant to neurologic interpretation.
  • To review hepatic encephalopathy and brain edema in ALF.

Main Methods:

  • Literature review and analysis of existing studies on ALF and its neurologic effects.
  • Discussion of pathogenesis, clinical presentation, and therapeutic strategies for brain edema in ALF.

More Related Videos

Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples
04:32

Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples

Published on: October 23, 2020

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke
12:19

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke

Published on: March 11, 2018

Related Experiment Videos

Last Updated: Jul 7, 2026

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples
04:32

Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples

Published on: October 23, 2020

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke
12:19

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke

Published on: March 11, 2018

  • Interpretation of neurologic findings in the context of ALF.

    • Main Results:

    • ALF significantly impacts brain function, leading to complex neurologic manifestations.
    • Hepatic encephalopathy is a key neurological complication of ALF.
    • Understanding brain edema pathogenesis is crucial for managing ALF patients.

    Conclusions:

    • ALF poses severe risks to brain health, necessitating specialized neurologic assessment.
    • Effective management of ALF requires addressing hepatic encephalopathy and brain edema.
    • Further research into ALF's neurotoxic mechanisms can improve patient outcomes.