Medic 57 and Engine 57 were dispatched to a single-family dwelling for an unresponsive 72-year-old male. The patient’s wife had come home from running errands when she found her husband unresponsive in the garage. EMS arrived, proceeded to the garage and immediately noted the odor of fuel in the garage with the patient unresponsive on the garage floor. The patient’s wife told paramedics that the patient often worked on his truck in the garage and usually kept a side door open when the truck was running for prolonged periods of time. She estimated that she was not gone from the home for more than 20 minutes, and he had been awake and alert with the side garage door open until the time she left. It was a particularly windy day and when she arrived home, the door was closed and her husband was unconscious on the floor. Due to the overwhelming smell of fuel, she was unable to enter the garage. There was no suspected foul play.
The engine arrived with the ambulance and opened the garage door and side door. Firefighters removed the patient from the garage to the driveway where the EMS stretcher was prepared. Paramedics were then able to quickly begin patient care. Meanwhile, firefighters had a portable carbon monoxide (CO) detector, which had a reading of 450 ppm after venting of the garage.
On initial assessment, paramedics found the patient had no spontaneous respirations. His respirations were supported with a bag valve mask with 100% supplemental oxygen. The patient was also noted to have no carotid pulse and was in a pulseless electrical activity (PEA) rhythm with a rate in the 30s, so CPR was initiated. A King airway was placed with continued 100% oxygen and a right proximal tibial intraosseous infusion (IO) was placed. The patient received a total of three doses of 1mg epinephrine. There was no evidence of trauma. The patient was transported to the closest hospital.
While en route, the patient was noted to have a rhythm change to a sinus tachycardia with a palpable carotid pulse. He had no spontaneous movement. Intravenous access was obtained. His blood pressure was 86/40 mmHg and intravenous fluids were initiated. The patient arrived at the ED hypotensive and tachycardic, with an oxygen saturation of 99% on continued 100% oxygen delivery.
Once in the ED, the patient received several doses of push-dose vasopressors and was intubated with ketamine and succinylcholine, as he had a clenched jaw. Given the history of CO exposure, FiO2 of 100% was continued through the endotracheal tube. After intubation and push-dose vasopressors, the patient remained hypotensive to 68/40 mmHg. He was also hypothermic with an initial temperature of 92 degrees F and tachycardic in the 120s BPM. An ECG revealed sinus tachycardia with no evidence of acute ischemia. An external warming device was applied and an emergent central venous catheter and arterial line were placed.
Central vasopressors were initiated with improvement in blood pressure to the 90/60s mmHg and with IV fluids, the patient’s tachycardia also improved. He continued to have no spontaneous movements. Laboratory studies were sent, including a carboxyhemoglobin level given the concern for carbon monoxide exposure. A chest X-ray revealed the endotracheal tube in adequate position with no evidence of acute findings and a head CT scan revealed no acute abnormalities.
Shortly after sending the blood work, the patient’s treatment team was informed that his carboxyhemoglobin level was 45%. The patient was deemed to be a candidate for hyperbaric oxygen therapy. He was transferred via helicopter to the regional hyperbaric chamber. He remained on FiO2 of 100% throughout the transfer.
On arrival, the patient went immediately to the hyperbaric chamber. He was then admitted to the intensive care unit where his clinical condition improved. He was weaned off of his vasopressors and his hypothermia resolved. The patient began moving all four extremities and an MRI of the brain revealed no evidence of anoxic brain injury. He was extubated on the fourth day of admission and the following week was discharged to a rehabilitation facility for physical and occupational therapy.
Early recognition and treatment of patients with carbon monoxide exposure can be life-saving. Early recognition can also protect responding crews from becoming patients themselves.
Background: Carbon monoxide is a potentially deadly, colorless, odorless gas. It is produced by the incomplete burning of various fuels, including coal, wood, charcoal, oil, kerosene, propane and natural gas.1 Equipment powered by internal combustion engines such as portable generators, cars, lawn mowers, and power washers produce CO.1 Though CO itself is odorless, those exposed may smell burning fuel. CO is absorbed through the lungs and leads to hypoxic injury.2
Epidemiology: Carbon monoxide poisoning is the most common cause of injury and death due to poisoning worldwide.3 The Center for Disease Control and Prevention (CDC) reports that each year, more than 500 Americans die from unintentional carbon monoxide poisoning, and more than 2,000 commit suicide by intentional poisoning.4
Symptoms: Because CO is odorless and colorless, patients may not recognize that they have been exposed. The initial symptoms of smaller exposures of CO are nonspecific. They include headache, fatigue, shortness of breath, nausea and dizziness.5 Headache is the most common symptom of acute poisoning and is often described as dull, frontal and continuous.6 High level CO poisoning results in progressively more severe symptoms, including mental confusion, vomiting, loss of coordination, loss of consciousness and ultimately death.1 The classic “cherry red” skin color is typically seen post-mortem and is not reliable in making a diagnosis of carbon monoxide exposure.
Symptom severity is related to both the CO level and the duration of exposure. Slow, low level exposures may present with mild symptoms that are often misdiagnosed as viral illnesses.7 Providers should suspect carbon monoxide exposure in individuals with CO exposure risks that present with similar symptoms. For rapid, high level CO exposures as was seen in this case, victims can develop severe symptoms without first developing milder symptoms. These exposures can also rapidly progress to unresponsiveness and death.8
Pathophysiology: When CO is not ventilated adequately from the body, it binds to hemoglobin and produces carboxyhemoglobin. Carboxyhemoglobin decreases the oxygen-carrying capacity of the blood and inhibits the transport, delivery and utilization of oxygen. Carbon monoxide has a higher affinity for hemoglobin than oxygen does, so it preferentially binds to hemoglobin over oxygen. The affinity between hemoglobin and carbon monoxide is approximately 230 times stronger than the affinity between hemoglobin and oxygen.9 Hemoglobin is a tetramer with four oxygen binding sites. Once carbon monoxide binds to one of the four sites, the affinity at the other three sites increases so the hemoglobin molecule retains oxygen at the other three sites to a greater extent.10 This decreases the amount of oxygen delivered to the tissues, ultimately leading to hypoxic tissue injury.7
Diagnosis: Diagnosis of carbon monoxide exposure can be difficult. Pulse oximeters will often mistake carboxyhemoglobin for oxyhemoglobin, so a falsely high reading may be present.11 Equipment is available to detect carbon monoxide levels in the air and is reported in parts per million (ppm). Most people will not experience any symptoms from prolonged exposure to CO levels of approximately 1–70 ppm, but some patients with cardiac disease might experience an increase in chest pain. As CO levels increase and remain above 70 ppm, patients may develop mild to moderate symptoms. At sustained CO concentrations above 150– 200 ppm, disorientation, unconsciousness and death are possible.12
Once a patient arrives in the emergency department, carboxyhemoglobin levels can be measured rapidly in the blood. For the particular lab test used in our emergency department, typical blood levels of carboxyhemoglobin for non-smokers is < 2%, < 8% for smokers, and toxic levels occur at > 20%.
Treatment: Initial treatment of a patient with carbon monoxide poisoning includes removing the patient from the exposure as soon as safely possible. After removing patients from the source of the CO exposure, 100% oxygen via non-rebreather mask or advanced airway device should be initiated regardless of initial pulse oximeter reading. Administering 100% oxygen shortens the half-life of carbon monoxide from 320 minutes to 80 minutes.9
With carboxyhemoglobin levels greater than 20% or severe symptoms, hyperbaric oxygen therapy can be considered. Hyperbaric oxygen treatment at three times atmospheric pressure reduces the half-life of carbon monoxide to 23 minutes, compared to 80 minutes with 100% oxygen.13 Several trials have compared high flow oxygen therapy to hyperbaric oxygen therapy. There was some evidence that hyperbaric oxygen therapy may be of benefit in terms of long-term survival and neurologic outcomes, however, further research is needed.14–19
In pregnancy, hyperbaric oxygen therapy is considered at lower carboxyhemoglobin levels and even with only mild maternal symptoms because elimination of carbon monoxide is slower in the fetus.20 Additionally, fetal hemoglobin has a 10–15% higher affinity for carbon monoxide than adult hemoglobin, which causes more severe poisoning in the fetus than in the adult.21
In this case, early recognition of carbon monoxide poisoning and appropriate resuscitation by prehospital personnel allowed emergency department staff to further stabilize, rapidly diagnose and transfer the patient to definitive care. High suspicion and early testing for CO poisoning can be life-saving.
1. Choi IS (June 2001). Carbon monoxide poisoning: systemic manifestations and complications (free full text). Journal of Korean Medical Science. 16(3):253–261.
2. Ernst A, Zibrak JD (November 1998). Carbon monoxide poisoning. The New England Journal of Medicine. 339(22):1603–1608.
3. Thom SR (October 2002). Hyperbaric-oxygen therapy for acute carbon monoxide poisoning. The New England Journal of Medicine. 347(14):1105–1106.
4. Carbon Monoxide poisoning fact sheet (pdf). Centers for Disease Control and Prevention. July 2006. Retrieved 2008-12-16.
5. Hardy KR, Thom SR (1994). Pathophysiology and treatment of carbon monoxide poisoning. Journal of Toxicology: Clinical Toxicology. 32(6):613–629.
6. Hampson NB, Hampson LA (March 2002). Characteristics of headache associated with acute carbon monoxide poisoning. Headache 42(3): 220–223.
7. Goldfrank L, Flomenbaum N, Lewin N, et. al. (2002). Carbon Monoxide. Goldfrank’s Toxicologic Emergencies (7th ed.). New York: McGraw-Hill 1689–1704.
8. Weaver LK (March 2009). Clinical practice. Carbon monoxide poisoning. The New England Journal of Medicine. 360(12):1217–1225.
9. Haldane J (1895). The action of carbonic oxide on man (PDF). The Journal of Physiology. 18(5–6):430–462.
10. Gorman D, Drewry A, Huang YL, et. al. (May 2003). The clinical toxicology of carbon monoxide. Toxicology. 187(1):25–38.
11. Barker SJ, Tremper KK (May 1987). The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2. Anesthesiology. 66(5):677–679.
12. United States Consumer Product Safety Commission. (n.d.) Carbon monoxide questions and answers. Retrieved on March 15, 2016, from http://www.cpsc.gov/en/Safety-Education/Safety-Education-Centers/Carbon-Monoxide-Information-Center/Carbon-Monoxide-Questions-and-Answers-/
13. Raub JA, Mathieu-Nolf M, Hampson NB, et. al. (April 2000). Carbon monoxide poisoning—a public health perspective. Toxicology. 145(1):1–14.
14. Scheinkestel CD, Bailey M, Myles PS, et. al. (March 1999). Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial (Free full text). The Medical Journal of Australia. 170(5):203–210.
15. Thom SR, Taber RL, Mendiguren II, et. al. (April 1995). Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Annals of Emergency Medicine. 25(4):474–480.
16. Raphael JC, Elkharrat D, Jars-Guincestre MC, et. al. (August 1989). Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet. 2(8660):414–419.
17. Ducasse JL, Celsis P, Marc-Vergnes JP (March 1995). Non-comatose patients with acute carbon monoxide poisoning: hyperbaric or normobaric oxygenation? Undersea & Hyperbaric Medicine. 22(1):9–15.
18. Mathieu D, Mathieu-Nolf M, Durak C, et. al. (1996). Randomized prospective study comparing the effect of HBO vs 12 hours NBO in non-comatose CO-poisoned patients: results of the preliminary analysis. Undersea & Hyperbaric Medicine. 23:7.
19. Weaver LK, Hopkins RO, Chan KJ, et. al. (October 2002). Hyperbaric oxygen for acute carbon monoxide poisoning. The New England Journal of Medicine. 347(14):1057–1067.
20. Greingor JL, Tosi JM, Ruhlmann S, et. al. (September 2001). Acute carbon monoxide intoxication during pregnancy. One case report and review of the literature. Emergency Medicine Journal: EMJ. 18(5):399–401.
21. Omaye ST (Nov 2002). Metabolic modulation of carbon monoxide toxicity. Toxicology. 180(2):139–50.