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Delayed Neuropsychiatric Sequel Following Pediatric Carbon Monoxide Poisoning: A Case Report and Literature Review
Hila Gavrieli1, Iris Noyman2, Eli Hershkovitz1
1Department of Pediatrics, Soroka University Medical Center, Beersheba, Israel.
Insights
Carbon monoxide (CO) poisoning can cause delayed neuropsychiatric sequelae (DNPS) weeks after exposure, leading to severe neurological issues. This case highlights DNPS presenting as seizures, encephalopathy, and optic nerve damage in a young patient.
Area of Science:
- Neurology
- Toxicology
- Neuroscience
Background:
- Carbon monoxide (CO) poisoning is a significant public health concern.
- The primary mechanism involves hypoxia from carboxyhemoglobin (COHb) formation.
- Delayed neuropsychiatric sequelae (DNPS) can manifest days to weeks after initial CO exposure.
Observation:
- DNPS presents with diverse symptoms including mood disorders, encephalopathy, and seizures.
- The pathogenesis involves hypoxia, inflammation, and direct cellular damage.
- A case of a 13-year-old boy with DNPS, seizures, encephalopathy, and optic nerve damage is presented.
Findings:
- The case illustrates a severe presentation of DNPS in an adolescent.
- Optic nerve damage was a notable complication in this patient.
- The complex pathogenesis of DNPS remains incompletely understood.
Implications:
- Increased awareness of DNPS is crucial for timely diagnosis.
- Further research is needed to elucidate DNPS pathogenesis.
- Understanding DNPS can lead to improved treatment strategies for CO poisoning survivors.
Abstract:
Carbon monoxide (CO) poisoning is a serious health problem. The main pathophysiological mechanism of acute CO poisoning is hypoxia due to the formation of carboxyhemoglobin (COHb). Delayed neuropsychiatric sequel (DNPS) occurs following an interval of several days to several weeks post-CO exposure and can present in many different manifestations, ranging from behavioral and mood disorders to encephalopathy and seizures and cause long-term neuropsychiatric sequel. The pathogenesis of DNPS following CO poisoning is a complex one that encompasses hypoxia-induced encephalopathy as well as inflammation, direct cellular changes and damage. The incidence varies and treatment is debated. We display a case of a previously healthy 13-year-old boy suffering from DNPS, presenting with seizures and encephalopathy and later developing optic nerve damage. Increased awareness to this condition might help diagnose future patients and aid in the understanding of the pathogenesis and treatment options for this poorly understood condition.
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