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Carbon Monoxide Poisoning
Sunil Kumar Daha
Janakpur, Nepal
• Potential Sources of Inhalation
• Space heaters
• Wood-burning stoves
• Charcoal burning for heat
• Portable generators without adequate ventilation
• Burn in a closed space
• Methylenechloride, found in varnishes and paint strippers,
Pathophysiology
• CO is colorless, odorless gas
• Concentration in atmospheric air: 10ppm
• Toxicity begins at 100ppm
• Endogenously produced in the body during normal breakdown of heme
• Normal physiologic
• Blood carbon monoxide levels from this process are ~1% in healthy nonsmokers
Pathophysiology
• Binding affinity of normal adult hemoglobin for carbon monoxide is about 200 times that of oxygen
• Fetal hemoglobin has an even higher binding affinity potentially more severe fetal toxicity
• Approximately 85% of carbon monoxide is bound to hemoglobin and forms COHbRest is dissolved in plasma or bound intracellularly, often to Myoglobin
PathophysiologyHalf-lives of COHb on room air at normal atmospheric pressure: 249 -320 minutesOn 100% oxygen at atmospheric pressure: 74-80 minutesCOHb generated by methylenechloride exposure, which can have a half-life of up to 13 hours due to ongoing metabolism
Pathophysiology•COHb does not provide oxygen delivery to the cells•As COHb levels increase, relative anemia and hypoxia occurs•Carbon monoxide shifts the oxyhemoglobin dissociation curve to the left Impaired oxygen release to the tissues
• Oxyhemoglobin(HbO2) dissociation curve
Cellular effects of CO 1.Lactic acidosisCO inhibits intracellular cytochrome oxidaseinterference with cellular respiration and ATP generation relative uncoupling of oxidative phosphorylation lactic acidosis2.Endothelial dysfunction and vasodilatationDue to release of Guanylatecyclase and nitric oxide by COLeads to Hypotension
Cellular effects of CO
•The combination of relative hypoxia and hypotension can cause ischemia-reperfusion injury in : Cardiac myocytesNeuronal tissue•Results: RhabdomyolysisAcute myocardial infarctionNeuronal cell death( mostly Cells in the basal ganglia involved, seen as globuspallidus lesions in cranial CT
Clinical Features of acute CO toxicity
•HistoryPotential exposure to COHeadacheVisual disturbancesVomitingChest pain
Clinical Features contd..
•Physical ExaminationConfusionAtaxiaDyspnea/tachypneaSeizureECG changes/dysrhythmiasSyncopeRetinal hemorrhageBullousskin lesionsFocal neurologic deficit
• Diagnosis• Elevated carboxyhemoglobinlevel• Artificially elevated oxyhemoglobinsaturation using
pulse oximetry• Elevated lactate• Elevated anion gap metabolic acidosis• Elevated creatinephosphokinase• Elevated troponin• Variable ECG findings—ranges from normal to injury
pattern(ST elevation MI)• Bilateralglobuspalliduslesionson MRI
Caution!
•Standard pulse oximetry is unreliable in the diagnosis of CO poisoning•The wavelengths for COHbfall into the same range of those for oxyhemoglobin, which makes it difficult for standard pulse oximetry to differentiate the two reading•Thus pulse oximetry value of oxygen saturation will be higher than the saturation on the ABG
Treatment
•Resuscitation ABCDE•Supplemental oxygen in the highest concentrations available should be initiated immediately•Initiate hyperbaric oxygen (HBO) treatment as required
Indications for Hyperbarric Oxygen
• Treatment of CO poisioning• Syncope• Confusion/altered mental status• Seizure• Coma• Focal neurologic deficit• Pregnancy with carboxyhemoglobinlevel
>15%• Blood level >25%• Evidence of acute myocardial ischemia
SYMPTOM SEVERITY DISPOSITION COMMENTS
Minimal or no symptoms Home Assess risk factors
HeadacheVomitingElevated CO level
Home after symptom resolution
Administer 100% oxygen in ED•Observe 4 hrs•Assess safety issues
AtaxiaSeizureSyncope Chest painFocal neurologic deficitDyspneaECG changes
HospitalizeConsult with hyperbaric specialist
Administer 100% oxygen in ER•Carbon monoxide level Stability of the patient must be considered for transfer of hyperbaric oxygen.
References
1. TintinallisEmergency Medicine A Comprehensive Study Guide 7th Ed (2014)