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Carbon Monoxide Poisoning

Summary

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  • Carbon monoxide (CO) poisoning results from inhalation of CO gas, leading to tissue hypoxia
  • Clinical presentation ranges from mild symptoms to coma and death
  • Imaging findings are non-specific but may include hypodensities on CT and hyperintensities on MRI

Pathophysiology

  • CO binds to haemoglobin with 200-250 times greater affinity than oxygen
  • Forms carboxyhaemoglobin (COHb), reducing oxygen-carrying capacity of blood
  • Causes leftward shift of oxyhaemoglobin dissociation curve, impairing oxygen delivery to tissues
  • Direct cellular toxicity via inhibition of mitochondrial cytochrome c oxidase

Demographics

  • Most common cause of fatal poisoning in many countries
  • Higher incidence in winter months due to increased use of heating systems
  • Risk factors:
    • Faulty heating systems
    • Enclosed spaces with poor ventilation
    • Occupational exposure (e.g., firefighters, industrial workers)

Diagnosis

  • Based on clinical suspicion and history of exposure
  • Measurement of COHb levels in blood
    • Normal: <3% in non-smokers, <10% in smokers
    • Toxic levels: >10%
  • Arterial blood gas analysis may show metabolic acidosis
  • ECG may reveal ischaemic changes or arrhythmias

Imaging

  • Brain CT:
    • Acute: may be normal or show cerebral oedema
    • Delayed: bilateral hypodensities in basal ganglia, particularly globus pallidus
  • Brain MRI:
    • T2-weighted and FLAIR: hyperintensities in basal ganglia, cerebral white matter, and hippocampus
    • Diffusion-weighted imaging: restricted diffusion in affected areas
    • Susceptibility-weighted imaging: may show petechial haemorrhages
  • Chest radiograph:
    • May be normal or show pulmonary oedema in severe cases

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  • A 50-year-old patient with a history of carbon monoxide exposure and extensive neuropsyhchiatric history.
  • MRI showed gliosis and loss of volume of the globi pallidi bilaterally with a rim of susceptibility artefact, probably from siderosis.
  • The appearances were consistent with the chronic manifestations of necrosis secondary to carbon monoxide poisoning.

panels-1

  • A 50-year-old patient with a history of carbon monoxide exposure and extensive neuropsyhchiatric history.
  • MRI showed gliosis and loss of volume of the globi pallidi bilaterally with a rim of susceptibility artefact, probably from siderosis.
  • The appearances were consistent with the chronic manifestations of necrosis secondary to carbon monoxide poisoning.

Treatment

  • Immediate removal from source of exposure
  • High-flow oxygen therapy (100% oxygen via non-rebreather mask)
  • Hyperbaric oxygen therapy in severe cases or pregnant patients
  • Supportive care:
    • Airway management
    • Fluid resuscitation
    • Correction of metabolic acidosis
  • Monitoring for delayed neurological sequelae
  • Long-term follow-up for cognitive and neurological deficits

Differential diagnosis

Differential Diagnosis Differentiating Feature
Hypoxic-ischaemic injury Bilateral globus pallidus T2 hyperintensity with cortical and hippocampal involvement
Methanol toxicity Bilateral putaminal necrosis with haemorrhage and optic nerve involvement
Osmotic demyelination Central pontine T2 hyperintensity with extrapontine basal ganglia involvement
Japanese encephalitis Bilateral thalamic and substantia nigra T2 hyperintensity