Burn management: carbon monoxide toxicity

Clinical - Respiratory/Pulmonary

Normal individuals will have up to 3% CO, and smokers may have up to 9% . Patients are generally asymptomatic if < 10%, with overt signs developing at ~ 15%.


The diagnosis of CO poisoning is made by a history of exposure (internal combustion engine exhaust, fire, improperly adjusted gas or oil heating, charcoal or gas grills, or exposure to paint stripper containing methylene chloride, which is metabolized by the liver to CO). Confirmation of the diagnosis is made by finding elevated COHb in either arterial or venous blood. The COHb concentration in anticoagulated blood samples is stable for several days. Therefore, if COHb determination is not available at a referring facility, the diagnosis can be confirmed with a blood sample obtained at the time of initial evaluation and transported with the patient. Fetal hemoglobin (hemoglobin F) can produce a falsely elevated reading for COHb on certain four-wavelength laboratory co-oximeters. In the first few weeks of life, blood from normal infants may therefore falsely indicate 7% to 8% COHb.

Actual COHb levels measured on arrival at the emergency department correlate poorly with clinical status and should not be used as the sole criterion to determine the need for treatment. Because of the lower intracellular PO2, elimination of CO from intracellular binding sites occurs more slowly. Significant mental obtundation, vomiting, and headache may remain even in the face of a normal COHb level.

Brain imaging may reveal a variety of abnormalities in patients with CO poisoning, including hypodensities in the globus pallidus and subcortical white matter, cerebral cortical lesions, cerebral edema, hippocampal lesions, loss of gray-white differentiation, and white matter hyperintensities.

Clinical effects include headache, nausea, vomiting, dizziness, myocardial ischemia, loss of consciousness, and, during pregnancy, fetal distress.

Clinical Features of CO Poisoning

  • CNS: headache, dizziness, loss of consciousness, hyperdensities of subcortical white matter
  • Cardiovascular: myocardial ischemia
  • GI: nausea, vomiting
  • (in pregnancy): fetal distress

 Mechanism of Injury

Initially, it was thought that the primary mechanisms for injury in CO poisoning were creation of a functional anemia and a left-shifted oxyhemoglobin curve . More recently, it has been suggested that CO binding to myoglobin, cytochrome aa3, and cytochrome oxidase, as well as the resultant oxidative stress, may also contribute to CO toxicity. In fact, it may be these latter mechanisms which are primarily affected by hyperbaric therapy.


Provide immediate oxygen via a 100 per cent non-rebreather face mask , which will both promote cellular respiration and reduce the elimination T 1/2 of COHb from 4-5 hours to 1-2 hours . Always make a blood glucose determination and correct if necessary – extremes of glucose have the potential to exacerbate neuronal cell death. Continue oxygen therapy until the patient is asymptomatic (usually COHb < 10 per cent).

Hyperbaric Oxygen (HBO)

In case of persistent severe symptoms or markers of severe toxicity, consideration should be given to treatment with HBO. Many researchers advocate HBO for definitive treatment of severe symptomatic CO poisoning. The most obvious benefit of HBO is enhanced elimination of COHb, with a half-life average of 20 minutes at 3 atmospheres absolute. However, in reality most dissociation of COHb occurs with administration of normal pressure oxygen before HBO treatment. Therefore, the real benefit of HBO may be in regeneration of cytochrome oxidase and inhibition of leukocyte adherence to the microvascular endothelium. All this prevents the cascade of events that leads to ischemic reperfusion injury, the process thought to be responsible for lipid peroxidation of the brain and delayed neurologic sequelae.

Clear indications include 1) any loss of consciousness and 2) seizures, coma, or altered mental status. HBO should be considered 1) in patients with persistent neurologic symptoms, 2) in pregnancy, and 3) in patients with persistent cardiac ischemia. There are ways to optimize HBO treatment for CO poisoning. The first is that treatment should be performed as early as possible. In the only clinical series that retrospectively examined this factor, both mortality and delayed neurologic sequelae were substantially less in patients treated within 6 hours of discovery . Two recent controlled studies showed no benefit of HBO in poisoned patients when the average time to treatment was 6 hours. In contrast to these findings, a recent randomized trial showed a reduction in delayed sequelae from 33 per cent to zero, when patients were treated within 6 hours with HBO as opposed to routine oxygen.

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