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Related Concept Videos

Prevention of Further Absorption of Poison01:14

Prevention of Further Absorption of Poison

In cases of acute poisoning, the primary objective is to prevent further absorption of the toxic substance into the body. Immediate interventions using various decontamination techniques targeting the gastrointestinal (GI) tract can achieve this. Decontamination is crucial to prevent poison from entering the systemic circulation, which involves washing affected areas with water and mild soap and removing contaminated clothing. Once external decontamination is done, attention must be turned to...
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Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
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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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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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Anticholinesterase Agents: Poisoning and Treatment

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.     
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...
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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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Delayed and prolonged coma after acute disulfiram overdose.

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Summary

Disulfiram overdose in a 35-year-old man caused prolonged coma and severe toxic encephalopathy. Symptoms included quadriparesis lasting beyond unconsciousness, highlighting disulfiram

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Area of Science:

  • Neuroscience
  • Toxicology
  • Pharmacology

Background:

  • Disulfiram is used to deter alcohol consumption.
  • Intentional overdose can lead to severe adverse effects.
  • Understanding disulfiram toxicity is crucial for clinical management.

Observation:

  • A 35-year-old man intentionally overdosed on disulfiram.
  • He experienced delayed and prolonged coma, toxic encephalopathy, and convulsions.
  • Quadriparesis persisted after the loss of consciousness.

Findings:

  • Disulfiram overdose can induce severe neurological impairment.
  • Symptoms include coma, seizures, and motor deficits.
  • The neurological effects may be prolonged and delayed.

Implications:

  • This case highlights the potential for severe neurotoxicity from disulfiram overdose.
  • Prompt recognition and management of disulfiram toxicity are essential.
  • Further research into the neurotoxic mechanisms of disulfiram is warranted.