carbonmonoxide poisioning and its management

17
Carbon Monoxide Poisoning Sunil Kumar Daha Janakpur , Nepal

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Page 1: Carbonmonoxide poisioning and Its management

Carbon Monoxide Poisoning

Sunil Kumar Daha

Janakpur, Nepal

Page 2: Carbonmonoxide poisioning and Its management

• 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,

Page 3: Carbonmonoxide poisioning and Its management

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

Page 4: Carbonmonoxide poisioning and Its management

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

Page 5: Carbonmonoxide poisioning and Its management

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

Page 6: Carbonmonoxide poisioning and Its management

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

Page 7: Carbonmonoxide poisioning and Its management

• Oxyhemoglobin(HbO2) dissociation curve

Page 8: Carbonmonoxide poisioning and Its management

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

Page 9: Carbonmonoxide poisioning and Its management

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

Page 10: Carbonmonoxide poisioning and Its management

Clinical Features of acute CO toxicity

•HistoryPotential exposure to COHeadacheVisual disturbancesVomitingChest pain

Page 11: Carbonmonoxide poisioning and Its management

Clinical Features contd..

•Physical ExaminationConfusionAtaxiaDyspnea/tachypneaSeizureECG changes/dysrhythmiasSyncopeRetinal hemorrhageBullousskin lesionsFocal neurologic deficit

Page 12: Carbonmonoxide poisioning and Its management

• 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

Page 13: Carbonmonoxide poisioning and Its management

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

Page 14: Carbonmonoxide poisioning and Its management

Treatment

•Resuscitation ABCDE•Supplemental oxygen in the highest concentrations available should be initiated immediately•Initiate hyperbaric oxygen (HBO) treatment as required

Page 15: Carbonmonoxide poisioning and Its management

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

Page 16: Carbonmonoxide poisioning and Its management

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.

Page 17: Carbonmonoxide poisioning and Its management

References

1. TintinallisEmergency Medicine A Comprehensive Study Guide 7th Ed (2014)