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Carbon Monoxide: The Other Silent Killer

Although there has been a significant decline in the number of deaths associated with unintentional and intentional CO toxicity, ED visits due to CO exposure remain a common presentation, especially during the winter months, and must be considered in the

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Case Presentations

Case 1: Smoke Inhalation (Carbon Monoxide and Cyanide)

A 50-year-old woman was pulled from the window of a burning building and found to be in cardiac arrest with pulseless electrical activity. Standard advanced cardiac life-support was started, and infusion of intra-osseous hydroxocobalamin (OHCob) was administered at the time of intubation because of the concern for cyanide (CN) gas exposure during smoke inhalation. Return of spontaneous circulation occurred before arrival at the hospital. 

Upon presentation to the ED, the patient’s vital signs were: initial blood pressure (BP), 92/47 mm Hg; heart rate (HR), 112 beats/min; respiratory rate (RR), 31 breaths/min; and temperature (T), 99.7°F. Following intubation, the patient’s oxygen saturation (SaO2) on pulse oximetry (POX) was 93%, and her fraction of inspired oxygen (FiO 2) was 100%.

On physical examination, the patient’s face was covered with soot. The lung sounds were equal and clear to auscultation bilaterally. The neurological examination was significant for a Glasgow Coma Scale of 3, without administered sedation, and there were no signs of dermal burns. Initial arterial blood gas (ABG) results were: pH, 7.06; carbon dioxide partial pressure (PCO2), 58 mm Hg; partial pressure of oxygen (PO 2), 152 mm Hg; bicarbonate (HCO 3), 17 mm Hg; SaO 2, 98% (after intubation); FiO 2, 100%; carboxyhemoglobin (COHb), 30%; and lactate, 14 mmol/L.

Case 2: Household Misadventure (Carbon Monoxide)

Several days after disabling the carbon monoxide (CO) detector in his home to silence the alarm that had continued to sound, a 67-year-old man developed weakness and called his local fire department. Upon arrival at the man’s home, the fire department confirmed an ambient air CO gas concentration over 200 ppm. Emergency medical services (EMS) promptly brought the patient to the local ED for evaluation and treatment. 

Shortly after arrival at the ED, the patient’s weakness had resolved. His vital signs at examination were: BP, 154/85 mm Hg; HR, 79 beats/min; RR, 15 breaths/min; and T, 98.8°F. The patient’s COHb level was 28% with administration of 100% oxygen (O 2) via a nonrebreather mask (NRBM).

Carbon Monoxide Toxicity

Carbon monoxide is a toxin of considerable importance to emergency physicians (EPs). The diagnosis at times can be challenging, the interpretation of COHb can be confusing, and the role of hyperbaric oxygen (HBO) therapy in the treatment of CO poisoning remains controversial.

Natural Sources

Carbon monoxide is formed from the incomplete combustion of organic (carbonaceous) fuels, such as charcoal, wood, petroleum distillates (gasoline, kerosene, diesel fuel), and natural gas. Though the majority of atmospheric CO comes from natural sources (eg, volcanoes, forest fires, marsh gases), poisoning exposures are primarily due to man-made CO. 

Man-Made Sources

Motor vehicle exhaust is the most abundant source of man-made CO, and exposures to exhaust fumes are common causes of both intentional and unintentional poisonings and death. Other frequent sources of CO poisoning include smoke inhalation from house fires; inadequate ventilation during use of kerosene space heaters; charcoal grills or hibachis; burning wood or charcoal; fuel-powered tools such as generators, fork lifts, and chain saws; or faulty (natural or bottled) gas appliances, such as stoves, furnaces, or water heaters ( Table 1 ). Though propane is known to burn more cleanly than natural gas (ie, less harmful to the environment), it still can produce CO. 

Table 1.

Though neither electrical appliances nor “gas leaks” are sources of CO, like CO, natural gas (mostly methane) and bottle gas (propane) are odorless, tasteless, and colorless. Utility companies add sulfur containing mercaptans to natural gas so that leaks can be detected, but CO is only formed when the fuel is burned in a gas-powered appliance.

Endogenous Carbon Monoxide

Endogenous CO production can occur from catabolism of heme or from hepatic metabolism of methylene chloride, but exposures to this solvent are unlikely to generate COHb concentrations above 10%. 

Epidemiology

The incidence of CO poisoning is likely more frequent than documented since many cases of minor exposures are unreported due to self-limiting effects and/or the vague, nonspecific nature of symptoms associated with minor exposures. In 2015, US Poison Control Centers reported over 14,000 cases of CO poisoning, only 43% of which were treated in a health care facility. 1 The vast majority of exposures (97%) were unintentional and resulted in 52 deaths (0.398%). 1 

Data from hospitalized patients in 2007 revealed that over 200,000 ED visits and 22,000 hospitalizations were possibly associated with unintentional, non-fire-related CO exposures. 2 Approximately 10% of the exposures in each of these populations were confirmed by specific International

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