CO exposure can be accidental or intentional as part of a suicide attempt. Refresh your memory about carbon monoxide poisoning.
Carbon Monoxide Poisoning
InBrief
Cheng-Hung Tai, MD and
Exposure to carbon monoxide (CO), a colorless, odorless gas, can cause significant toxicity and is the most common cause of fatal poisoning in the United States. Exposure can be accidental or intentional as part of a suicide attempt.
Carbon monoxide (CO) poisoning occurs after exposure to high levels of this gas. Common, nonspecific, presenting symptoms include headache, nausea/vomiting, dizziness, confusion, malaise, and loss of consciousness Changes in mental status are initially a brief confused/delirious state, but poisoning can progress to coma and even death. The classic description of "cherry-red lips" in acute CO poisoning is neither sensitive nor specific.
CO, the byproduct of hydrocarbon combustion, is present in automobile and heating system exhaust. This gas binds to hemoglobin much more avidly than does oxygen. The resulting compound, carboxyhemoglobin, replaces oxyhemoglobin and diminishes oxygen transport, resulting in poor oxygen delivery in the body and, ultimately, tissue hypoxia. Myocardial ischemia, arrhythmias, and delayed neurologic sequelae (cognitive/neurologic deficits, personality changes, other movement disorders) are commonly noted after significant CO poisoning.
Signs and Symptoms
As CO poisoning can present subtly, a high level of suspicion and good history-taking may help make the diagnosis. This is particularly true in mild cases where presentation is nonspecific and the cause is not obvious. A history of other people or pets having similar symptoms or a history of using devices that produce CO can be helpful.
Mild CO poisoning can present with headache, flu-like symptoms without fever, or nausea/vomiting.
Chronic CO poisoning may cause more insidious symptoms, such as trouble concentrating, personality changes, or memory loss. More severe intoxication can cause chest pain, ataxia, seizures, syncope, focal neurologic deficits, confusion, visual disturbances, retinal hemorrhages, bullous skin lesions, dyspnea, coma, and respiratory or cardiac arrest.
CO poisoning should be considered in comatose patients with an unexplained elevated anion gap metabolic acidosis or lactic acidosis. If the patient has been in a fire and has lactate levels >10 mmol/L, coexisting cyanide poisoning should be considered.
The cherry-red color change of skin and oral mucosa classically described for CO poisoning is rarely seen in living patients.
Causes and Risk Factors
CO is produced during house or building fires; use of wood/charcoal/propane/gas heaters or stoves, natural gas-powered motors, generators and furnaces, gasoline powered generators and motors, and industrial equipment; and from car and boat exhaust.
CO poisoning typically occurs indoors in a poorly ventilated space. However, a leaky or clogged exhaust system on a vehicle or boat can produce symptoms outdoors.
Methylene chloride is a substance used in Christmas bubble lights, varnishes, and paint strippers. It is converted by the liver to CO and can cause prolonged toxicity when inhaled or ingested.
Diagnostic Evaluation
A careful history and physical examination is critical in diagnosing CO poisoning. Pulse oximetery can not distinguish between carboxyhemoglobin and oxyhemoglobin and is not reliable in detecting patients exposed to CO. If CO poisoning is suspected after history and physical, an arterial blood sample should be checked for an elevated carboxyhemoglobin level; testing of venous blood is less reliable.
The American College of Emergency Physicians (ACEP) poisoning policy recommends an electrocardiogram and cardiac biomarker levels to identify acute myocardial injury.
Lactate levels have been found to correlate to symptom severity in CO poisoning.
Pulse oximetry is unreliable in diagnosing CO poisoning. The wavelengths for COHb and oxyhemoglobin are similar, and standard pulse oximetry cannot differentiate between them. As a result in CO poisoning, even if the patient is severely hypoxemic, a pulse oximetry oxygen saturation reading may be falsely normal.
There are noninvasive portable pulse CO oximetry monitors that can measure COHb levels. A study of one model found a false-positive rate of 9%; although underpowered to detect the true false-negative rate, the sample had an 18% false-negative rate. ACEP guidelines recommend not using noninvasive pulse CO oximetry to diagnose CO toxicity in patients with suspected acute CO poisoning; blood COHb testing should be the standard.
In arterial blood gas testing, the partial pressure of oxygen that reflects dissolved oxygen in the blood may be normal in CO poisoning. In some blood gas machines, the oxyhemoglobin level is calculated but not measured and may be inaccurately reported as normal in CO poisoning. Directly measured COHb levels should be ordered. There is good correlation between arterial and venous COHb levels; therefore, venous blood can be used for that testing.
COHb levels will frequently correlate with the symptoms; however, treatment decisions should be based on the clinical picture in conjunction with the CO level. If a patient has received 100% oxygen, or a significant time has passed between exposure and arriving at the hospital, COHb levels may be lowered by the time the blood level is drawn and may not reflect the severity of the exposure.
In the case of patients exhibiting significant neurologic sequelae, a computed tomography scan of the head to rule out other causes may be considered.
Adverse effects
The affinity of hemoglobin for CO is 200 times that of oxygen. CO displaces oxygen from the hemoglobin molecule and binds to hemoglobin to form carboxyhemoglobin (COHb), resulting in hypoxemia. The half-life of COHb in room air averages 240-320 minutes and can vary depending on the amount of respiration. On 100% oxygen, the half-life is about 80 minutes. In methylene-chloride exposure, the half-life can be up to 13 hours due to continued CO production.
COHb shifts the oxygen dissociation curve to the left; hemoglobin will hold on to oxygen molecules more tightly than normal rather than delivering it to the tissues, which exacerbates the tissue hypoxemia already caused by the CO.
CO results in a relative uncoupling of oxidative phosphorylation and causes lactic acidosis. It also causes release of guanylate cyclase and nitric oxide, which can cause hypotension. A cellular inflammatory process involving white blood cells and release of free radicals can also occur. The hypoxia, hypotension, and inflammation can lead to cell injury or death. The basal ganglia and globus pallidus are extremely sensitive to the effects of CO toxicity.
In pregnant women, even mild CO poisoning can affect the fetus, potentially causing fetal demise or congenital malformations, since fetal hemoglobin has a stronger affinity for CO than does adult hemoglobin.
Adverse outcomes
Survivors of CO poisoning can suffer from long-term neurocognitive sequelae, including impaired memory, cognitive dysfunction, depression, anxiety, or vestibular and motor deficits.
About one-third of patients may have subtle memory deficits or show personality changes after CO poisoning.
Pearl to Know
CO is produced in the body during the normal breakdown of heme. Normal physiologic CO levels are about 1% in nonsmokers, whereas smokers can have levels up to 10%.
Treatment Options
The immediate treatment for CO poisoning is high-flow oxygen therapy, usually via face mask. For patients exposed to smoke inhalation, cyanide toxicity should also be considered. An electrocardiogram and cardiac enzyme determination should be obtained to rule out any myocardial ischemia. In the case of patients exhibiting significant neurologic sequelae, a computed tomography scan of the head to rule out other causes may be considered.
Initial treatment of CO toxicity consists of standard patient stabilization depending on severity of condition. There is some evidence that controlling hyperglycemia in severe CO poisoning may improve outcomes.
All suspected CO-toxicity patients should be treated with 100% oxygen, as it significantly decreases the half-life of COHb from an average of 240-320 minutes to < 80 minutes. Hyperbaric oxygen therapy reduces the COHb half-life to about 24 minutes.
History and the event should direct the initiation of treatment. COHb levels greater than 10% is abnormal in any person and COHb levels greater than 15% is significantly abnormal. High flow oxygen should be initiated.
In mild cases of CO poisoning, administration of 100% oxygen until symptoms abate and avoidance of repeated exposure to the source of the CO might be adequate therapy.
Hyperbaric therapy has been used in moderate-to-severe CO poisoning to try to prevent neurologic sequalae. However, a Cochrane review found conflicting and generally weak evidence on the usefulness of hyperbaric oxygen to prevent neurologic injury. The ACEP CO poisoning policy concluded that it is unclear whether hyperbaric therapy is superior to normobaric oxygen therapy for improving long-term neurocognitive outcomes. If used, hyperbaric oxygen therapy should be initiated within the first 6 hours after exposure.
The indications for hyperbaric oxygen therapy are as follows:
loss of consciousness.
confusion/altered mental status, seizure, or new focal neurologic deficit
carboxyhemoglobin level > 25%.
carboxyhemoglobin level > 15% (pregnant patients).
metabolic acidosis with pH < 7.10.
signs of end-organ damage (e.g. acute myocardial ischemia).
Extracorporeal membrane oxygenation (ECMO) has been used in CO poisoning with good results in several case reports and an animal study. It may be considered when hyperbaric therapy is not available, but further studies are needed to assess its actual effectiveness.
Patients with self-inflicted CO poisoning should undergo psychiatric evaluation prior to hospital discharge.
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Resources and further reading
Baran DA, Stelling K, McQueen D, Pearson M, Shah V. Pediatric veno-veno extracorporeal membrane oxygenation rescue from carbon monoxide poisoning, Pediatr Emerg Care. 2018 Apr 25 (epub ahead of print).
Baud F, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325:1761-1766.
Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011;(4):CD002041.
2: Carbon monoxide acute exposure guideline levels. In: National Research Council (US) Committee on Acute Exposure Guideline Levels. Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 8. Washington (DC): National Academies Press (US); 2010.
Maloney G. Carbon monoxide. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 8th edition. New York, NY: McGraw-Hill; 2016.
Moon JM, Shin MH, Chun BJ. The value of initial lactate in patients with carbon monoxide intoxication: in the emergency department. Hum Exp Toxicol. 2011;30:836-843.
Penney DG. Hyperglycemia exacerbates brain damage in acute severe carbon monoxide poisoning. Med Hypotheses. 1988;27:241-244.
Rose JJ, Wang L, Xu Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017;195:596–606.
Simonsen C, Magnusdottir SO, Andreasen JJ, Rohde MC, Kjærgaard B. ECMO improves survival following cardiogenic shock due to carbon monoxide poisoning - an experimental porcine model. Scand J Trauma Resusc Emerg Med. 2018;26:103.
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American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning; Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med. 217;69:98-107.
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