What is included in emergency department (ED) care for carbon monoxide (CO) toxicity?

Updated: Sep 18, 2018
  • Author: Guy N Shochat, MD; Chief Editor: Gil Z Shlamovitz, MD, FACEP  more...
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Answer

Considerations in emergency department (ED) care include the following:

  • Cardiac monitor: Sudden death has occurred in patients with severe arteriosclerotic disease at HbCO levels of only 20%.

  • Pulse oximetry: HbCO absorbs light almost identically to that of oxyhemoglobin. Although a linear drop in oxyhemoglobin occurs as HbCO level rises, pulse oximetry will not reflect it. Pulse oximetry gap, the difference between the saturation as measured by pulse oximetry and one measured directly, is equal to the HbCO level. [33] However, pulse CO-oximetry units are available that can screen for CO toxicity at the bedside.

  • Oxygen therapy is usually provided via a non-rebreather mask. However, Roth et al describe effective use of noninvasive continuous positive airway pressure (CPAP) ventilation using a tight mask and an inspired fraction of oxygen (FiO2) of 100%. These authors provide case reports of simultaneous CO toxicity in a couple, in which HbCO levels fell from 21% at admission to 6% within 1 hour and 3% after 90 minutes in the patient treated with CPAP. In the spouse, who was treated with conventional oxygen therapy, reduction of HbCO from the admission level of 21% to 3% took 6 hours. [34]

  • Continue 100% oxygen therapy until the patient is asymptomatic and HbCO levels are below 10%. In patients with cardiovascular or pulmonary compromise, lower thresholds of 2% have been suggested.

  • Calculate a gross estimate of the necessary duration of therapy using the initial level and half-life of 30-90 minutes at 100% oxygen.

  • In uncomplicated intoxications, venous HbCO levels and oxygen therapy are likely sufficient. Evaluate patients with significant cardiovascular disease and initial HbCO levels above 15% for myocardial ischemia and infarction.

  • Consider immediate transfer of patients with levels above 40% or cardiovascular or neurologic impairment to a hyperbaric facility, if feasible. Persistent impairment after 4 hours of normobaric oxygen therapy necessitates transfer to a hyperbaric center. Pregnant patients should be considered for hyperbaric treatment at lower carboxyhemoglobin levels (above 15%). Complicated issues of treatment of fetomaternal poisoning are discussed in Special Concerns.

  • Serial neurologic examinations, including funduscopy, CT scans, and, possibly, MRI, are important in detecting the development of cerebral edema. Cerebral edema requires intracranial pressure (ICP) and invasive blood pressure monitoring to further guide therapy. Head elevation, mannitol, and moderate hyperventilation to 28-30 mm Hg PCO2 are indicated in the initial absence of ICP monitoring. Glucocorticoids have not been proven efficacious, yet the negative aspects of their use in severe cases are limited.

  • Do not aggressively treat acidosis with a pH above 7.15 because it results in a rightward shift in the oxyhemoglobin dissociation curve, increasing tissue oxygen availability. Acidosis generally improves with oxygen therapy.

  • In patients who fail to improve clinically, consider other toxic inhalants or thermal inhalation injury as contributing factors. Be aware that the nitrites used in cyanide kits cause methemoglobinemia, shifting the dissociation curve leftward and further inhibiting oxygen delivery at the tissue level. Combined intoxications of cyanide and CO may be treated with sodium thiosulfate 12.5 g intravenously to prevent the leftward shift.
  • Admit patients to a monitored setting and evaluate acid-base status if HbCO levels are 30-40% or above 25% with associated symptoms.

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