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Neurological Sequelae After Acute Carbon Monoxide Poisoning
Bhushan Sudhakar Wankhade1, Wasim Shabbir Shaikh1, Zeyad Faoor Alrais1
1Critical Care Medicine, Rashid Hospital, Dubai Academic Health Corporation, Dubai, ARE.
Delayed neurological sequel (DNS) can occur after carbon monoxide poisoning (COP). While normobaric oxygen therapy (NBO2) aided recovery in some, two patients developed DNS, highlighting the need for further research into effective prevention strategies.
Area of Science:
- Neurology
- Toxicology
- Emergency Medicine
Background:
- Carbon monoxide poisoning (COP) is a significant cause of poisoning deaths.
- Delayed neurological sequel (DNS) is a potential neurological dysfunction following COP.
- A mass casualty incident involving COP from a faulty ventilation system presented a unique case study.
Observation:
- Five patients with severe COP, including loss of consciousness and shock, were treated.
- Initial management involved intubation, mechanical ventilation, and normobaric oxygen therapy (NBO2).
- While three patients recovered well, two developed DNS, characterized by diverse neuropsychological deficits.
Findings:
- NBO2 rapidly reversed elevated carboxyhemoglobin levels in all patients.
- DNS manifested with a range of cognitive, psychiatric, and motor symptoms.
- Magnetic resonance imaging (MRI) with gadolinium contrast is the preferred diagnostic tool for DNS.
Implications:
- The efficacy and optimal parameters for hyperbaric oxygen therapy (HBO2) in preventing DNS remain debated.
- Early and effective oxygenation is crucial for managing COP and potentially preventing DNS.
- DNS contributes to increased patient morbidity and healthcare costs, underscoring the need for improved treatment and prevention strategies.
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