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Carbon Monoxide Poisoning: Intensive Care Medicine Seminar Royal Victoria Hospital Belfast April 2007

This document discusses carbon monoxide poisoning, including its sources, pathophysiology, diagnosis, and treatment. Carbon monoxide binds to hemoglobin in red blood cells, preventing oxygen from binding and causing cellular hypoxia. It can also directly injure cells. Symptoms of acute poisoning include headache, dizziness, and nausea. Some patients later develop neurological or psychiatric issues. Diagnosis involves measuring carboxyhemoglobin levels in blood or breath. Treatment focuses on administering high concentrations of oxygen via masks or hyperbaric chambers to accelerate the removal of carbon monoxide from the bloodstream.

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39 views17 pages

Carbon Monoxide Poisoning: Intensive Care Medicine Seminar Royal Victoria Hospital Belfast April 2007

This document discusses carbon monoxide poisoning, including its sources, pathophysiology, diagnosis, and treatment. Carbon monoxide binds to hemoglobin in red blood cells, preventing oxygen from binding and causing cellular hypoxia. It can also directly injure cells. Symptoms of acute poisoning include headache, dizziness, and nausea. Some patients later develop neurological or psychiatric issues. Diagnosis involves measuring carboxyhemoglobin levels in blood or breath. Treatment focuses on administering high concentrations of oxygen via masks or hyperbaric chambers to accelerate the removal of carbon monoxide from the bloodstream.

Uploaded by

Devil King
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd
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Carbon monoxide poisoning

Intensive Care Medicine Seminar


Royal Victoria Hospital Belfast
April 2007
BBC NEWS | Corfu children ki
lled by gas leak
Introduction
– Carbon monoxide (CO) intoxication is one of the most
common causes of accidental and intentional poisoning
– Atmospheric composition <0.001%
– Blood carboxyhaemoglobin
• Nonsmokers 1-3%
• Smokers 10-15%
– Sources of CO
• Motor vehicle exhaust fumes
• Heating systems
• Inhaled smoke
• Propane-powered forklift trucks
• Methylene chloride
Pathophysiology
Pathophysiology
• CO is colourless, odourless, nonirritant toxic gas
• CO toxicity due to
– Cellular hypoxia
– Direct cellular injury
• Cellular hypoxia
– CO competes with O2 for binding to Hb
– Affinity of Hb for CO x 200-250 > affinity for O2
– O2-Hb dissociation curve shift to the left
– Impaired tissue release of O2 and cellular hypoxia
Oxygen-Hemoglobin Dissociation Curve

Ernst A and Zibrak J. N Engl J Med 1998;339:1603-1608


Pathophysiology
• Direct cellular injury
– CNS reoxygenation injury
– Lipid peroxygenation
– Free radical formation
• CO toxicity in pregnancy
– Risk of fetal injury
Acute Symptoms Reported by 196 Patients after Exposure to Carbon Monoxide

Ernst A and Zibrak J. N Engl J Med 1998;339:1603-1608


Delayed neuropsychiatric
syndrome
• Incidence 10 - 30% of victims 3 - 240 days after
exposure
– Cognitive changes
– Personality changes
– Parkinsominism
– Dementia
– Psychosis
• Recovery 50 - 75% within 12 months
Diagnosis
• High level of clinical suspicion
• Serum COHb level
• Exhaled breath COHb level
• Measured by spectrophotometry
• Pulse oximetry cannot distinguish between HbO2 and
COHb
• Comprehensive neurological and neuropsychological
assessment
• CO Neuropsychological Screening Battery
• CT brain to exclude other conditions
Monoplace Hyperbaric Chamber

Tibbles P and Edelsberg J. N Engl J Med 1996;334:1642-1648


Treatment
• High-flow, FiO2 ~100%, normobaric O2
• O2 shortens the half life of COHb
– 21% O2 = 4-6 hours
– 100% O2 = 40-80 minutes
– 100% O2 2.5atm = 15-30 minutes
• Continue O2 until COHb normal
• Beware concomitant smoke inhalation and burn injury
• Normobaric v Hyperbaric O2 therapy
– HBO hastens resolution of acute symptoms
– Unclear evidence for effect of HBO on late
complications and mortality
Suggested Indications for Hyperbaric-Oxygen Therapy in Patients with Carbon Monoxide
Poisoning

Ernst A and Zibrak J. N Engl J Med 1998;339:1603-1608

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