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Related Concept Videos

Toxidromes: Clinical Features01:30

Toxidromes: Clinical Features

Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...
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Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
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CNS depressants include drugs from the category of barbiturates and benzodiazepines. They are valuable medications for managing anxiety disorders and insomnia. Barbiturates, once used to induce and maintain sleep, have been replaced mainly by benzodiazepines due to barbiturate's toxicity, tolerance, and overdose risks. They interact with GABAA receptors, leading to sedation at low doses and potentially coma and death at higher doses. Phenobarbital, a long-acting barbiturate, possesses...
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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...
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Pharmaceutical poisoning can occur through various channels, impacting an estimated 2 million hospitalized patients in the U.S. annually with serious adverse drug responses. These scenarios encompass both therapeutic uses, such as drug toxicity, where even standard dosages can lead to severe central nervous system depression, and non-therapeutic exposures, including accidental ingestion by children, and environmental and occupational exposures.Unintentional poisonings often involve exploratory...
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Related Experiment Video

Updated: May 25, 2026

Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy
05:03

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Published on: April 17, 2020

Baclofen overdose mimicking brain death.

Ross Sullivan1, Michael J Hodgman, Louise Kao

  • 1SUNY Upstate Medical University, Department of Emergency Medicine, Syracuse, USA. sullivar@upstate.edu

Clinical Toxicology (Philadelphia, Pa.)
|February 2, 2012
PubMed
Summary
This summary is machine-generated.

Baclofen overdose can cause prolonged coma mimicking brain death. A standard 5-half-life observation period is insufficient for baclofen intoxication, requiring cautious brain death determination in overdose patients.

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Last Updated: May 25, 2026

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Published on: April 17, 2020

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Area of Science:

  • Neurology
  • Toxicology
  • Critical Care Medicine

Background:

  • Brain death guidelines require careful application in drug intoxication cases.
  • A common recommendation is to observe patients for five half-lives of a drug after overdose.
  • Prolonged coma in overdose patients can complicate the assessment of brain death.

Observation:

  • Two cases of severe baclofen intoxication presented with profound coma and absent brainstem reflexes.
  • Despite initial concerns for brain death, patients exhibited delayed arousal days after overdose.
  • Standard neurological assessments, including EEG and apnea tests, were inconclusive in determining brain death.

Findings:

  • Baclofen intoxication can induce prolonged and deep coma, potentially mimicking brain death.
  • A fixed 5-half-life observation period is inadequate for baclofen overdose, leading to potential misdiagnosis.
  • Delayed neurological recovery was observed in patients with massive baclofen overdose.

Implications:

  • Physicians must exercise extreme caution when evaluating brain death in comatose patients with drug intoxication.
  • Extended observation periods are necessary to allow for adequate drug clearance and neurological recovery.
  • These findings highlight the need for revised protocols for assessing brain death in specific intoxication scenarios, like baclofen overdose.