The management of CO toxicity begins with a thorough primary survey to evaluate the status of the patient’s airway, breathing, and circulation. Finally, time since exposure and any prior delivery of supplemental oxygen must be considered, as CO levels fall rapidly (especially on O2 therapy) with time and may not reflect cellular dysfunction that is already occurring or has occurred. Consider also factors such as anemia and residing at high altitude. Another important determinant of normal CO levels is a patient’s smoking status smokers may have a baseline CO level of up to 10%, while nonsmokers’ levels are typically closer to 1%.
Pediatric patients in particular can be more susceptible to hypoxic insult, with more metabolically active tissues and requirements that often make them more quickly symptomatic. With CO levels exceeding 60% (a marker of poor prognosis), patients may succumb to arrhythmias and cardiovascular collapse, seizures, coma, and death.īoth duration of CO exposure and associated levels, as well as patient-specific factors correlate with clinical presentation and prognosis. A classic descriptor of CO toxicity includes cherry red lips or oral mucosa, however this finding is very rare in actuality, and is usually only present on post-mortem examination.
As levels increase, symptoms ranging from headache (most common) and “flu-like” symptoms (fatigue, dizziness, nausea, and vomiting) develop, and can progress to neuro-cognitive impairment, with alterations in level of alertness, vision changes, memory impairment, and sensorimotor deficits. Symptoms from CO toxicity can start when levels are as low as 5%, with impaired judgment and fine motor skills. Other instances that should raise suspicion include those where fuel is being burned indoors or in poorly ventilated areas (including the backs of vehicles or boats), or if multiple other people in the child’s environment are having similar symptoms. The most pressing scenario is usually that of an indoor fire with patients presenting with associated burns and smoke inhalation injuries. For all these reasons, the diagnosis of CO toxicity requires careful evaluation of historical clues and high clinical suspicion. As such, CO levels should be assessed via direct measurement using co-oximetry (via either venous or arterial sampling). These readings, as well as a patient’s color and respiratory rate and effort may therefore be deceptive and lead the physician away from recognition of severe tissue hypoxia. A standard pulse-oximeter incorrectly detects the wavelength of carboxyhemoglobin as oxygenated hemoglobin, while the dissolved oxygen in blood is not affected by CO’s effect on hemoglobin. Another clinical conundrum exists as both oxygen saturation (SaO2) and partial pressure of oxygen measurements (PaO2) are likely to be normal.
Based on its broad array of presentations, diagnosis can be especially difficult in pre-verbal or younger pediatric patients. This tissue hypoxia not only causes a shift to anaerobic metabolism and consequently lactate production, but also increases cerebral blood flow and capillary permeability to cause cerebral edema in the most severe cases.ĬO toxicity presents with a wide range of symptoms and findings that are often vague and non-specific. When hemoglobin binds CO to form carboxyhemoglobin, it effectively reduces hemoglobin’s O2 carrying capacity (leftward shift of the oxyhemoglobin dissociation curve) and delivery of O2 to vital tissues. Hemoglobin’s affinity for CO is approximately 200-250 times stronger than that of oxygen. Most common implicated devices include furnaces, fireplaces, space heaters, stoves, and automobile or boats, especially in poorly ventilated areas or with faulty or blocked exhaust systems. This colorless, tasteless, and odorless gas is formed via the incomplete combustion of carbon-containing fuels. A major contributor to indoor fire-related incidents, it is responsible for up to 500 deaths per year in the US and has both significant short and long-term morbidity. It is still winter, and we are all trying to stay warm inside while awaiting warmer days to arrive! We thought this would be a fitting time to review CO toxicity, with some pearls and management tips.Ĭarbon monoxide (CO) is the true “silent” killer. Anthony Del Zotto, DO, Charleston Area Medical Center and Jaryd Zummer, MD, University of Kentuckyīetter late than never.
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