Related Experiment Video
Updated: Jul 11, 2025
08:51
Intra-cardiac Side-Firing Light Catheter for Monitoring Cellular Metabolism using Transmural Absorbance Spectroscopy of Perfused Mammalian Hearts
Published on: May 12, 2019
6.8K
Delayed presentation of transdermal cyanide poisoning.
Anaesthesia Reports
|November 8, 2023
Summary
Transdermal cyanide poisoning, a delayed consequence of fire exposure, can be effectively treated with hydroxocobalamin after decontamination. Early suspicion and prompt intervention are crucial for patient recovery.
Area of Science:
- Toxicology
- Emergency Medicine
- Environmental Health
Background:
- Warehouse fires involving burning plastics pose unique toxicological risks.
- Inhalational injury is a primary concern, but delayed metabolic effects can occur.
- Standard diagnostic approaches may not immediately identify certain toxic exposures.
Observation:
- A patient exposed to burning plastic without protective gear developed delayed metabolic acidosis and elevated lactate.
- Initial assessment for inhalational injury was negative, complicating diagnosis.
- A handheld detector indicated significant toxin levels on the patient's skin.
Findings:
- Transdermal cyanide poisoning was diagnosed based on delayed biochemical changes and toxin detection.
- Initial treatment with hydroxocobalamin without full decontamination yielded limited results.
- Complete decontamination followed by hydroxocobalamin administration led to rapid clinical and biochemical improvement.
Implications:
- Clinicians must consider transdermal cyanide poisoning in fire-exposed patients, even with normal initial respiratory assessments.
- Prompt and thorough decontamination is essential for effective treatment of transdermal toxin absorption.
- Hydroxocobalamin is a critical antidote for cyanide poisoning, requiring timely administration post-decontamination.
Keywords:
cyanide poisoning
Related Concept Videos
01:14Prevention of Further Absorption of Poison
831
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...
831
01:26Toxic Reactions: Overview
991
When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
991
01:18Drug Delivery: Enteral Route
468
The enteral drug administration involves three primary routes: oral, sublingual, and buccal. Oral ingestion is the most prevalent, safe, economical, and convenient method for drug administration. However, it has certain drawbacks, including limited absorption due to the drug's low water solubility or poor membrane permeability, possible emesis from GI mucosa irritation, destruction of drugs by digestive enzymes or low gastric pH, and irregular absorption along with food or other drugs.
468
01:19Depolarizing Blockers: Pharmocokinetics
330
Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
330
01:17Antidotes
658
Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...
658
01:19Phase II Reactions: Miscellaneous Conjugation Reactions
64
Phase II biotransformations are detoxification mechanisms that conjugate xenobiotics with endogenous substances, neutralizing their toxicity.
A key example involves the conjugation of cyanide ions, which impair cellular respiration and alter hemoglobin into non-oxygen-carrying cyanmethemoglobin. To neutralize this threat, a sulfur atom from thiosulphate is transferred to the cyanide ion, catalyzed by the enzyme rhodanese, resulting in an inactive compound called thiocyanate. The production of...
A key example involves the conjugation of cyanide ions, which impair cellular respiration and alter hemoglobin into non-oxygen-carrying cyanmethemoglobin. To neutralize this threat, a sulfur atom from thiosulphate is transferred to the cyanide ion, catalyzed by the enzyme rhodanese, resulting in an inactive compound called thiocyanate. The production of...
64