Carbon monoxide poisoning

Authors Peter F Clardy, MD Scott Manaker, MD, PhD Holly Perry, MD Section Editors Stephen J Traub, MD Michele Burns Ewald, MD Deputy Editor Jonathan Grayzel, MD, FAAEM

Last literature review version 19.1: January 2011 | This topic last updated: October 28, 2010 (More)

INTRODUCTION Carbon monoxide (CO) is an odorless, tasteless, colorless, nonirritating gas formed by hydrocarbon combustion. The atmospheric concentration of CO is generally below 0.001 percent, but it may be higher in urban areas or enclosed environments. CO binds to hemoglobin with much greater affinity than oxygen, forming carboxyhemoglobin (COHb) and resulting in impaired oxygen transport and utilization. CO can also precipitate an inflammatory cascade that results in CNS lipid peroxidation and delayed neurologic sequelae.

CO poisoning will be reviewed here. A summary table to facilitate emergent management is provided (table 1). Related topics including smoke inhalation and hyperbaric oxygen therapy are presented separately. (See "Smoke inhalation" and "Hyperbaric oxygen therapy".)

EPIDEMIOLOGY Carbon monoxide (CO) poisoning is responsible for up to 40,000 emergency department visits and 5000 to 6000 deaths per year, making it one of the leading causes of poisoning death in the United States [1-3]. Inadvertent CO poisoning likely causes around 500 deaths annually; the

number of intentional CO poisonings is perhaps 10 times higher [1,4,5]. The overall case-fatality rate for CO poisoning ranges from 0 to 31 percent [3,6,7].

Unlike intentional poisoning, unintended poisoning demonstrates both seasonal and regional variation, and it is most common during the winter months in cold climates [5]. Morbidity, which is primarily related to late neurocognitive impairment, persists beyond initial stabilization in up to 40 percent of victims [3,6].

Smoke inhalation is responsible for most inadvertent cases of CO poisoning. Other potential sources of CO include poorly functioning heating systems, improperly vented fuel-burning devices (eg, kerosene heaters, charcoal grills, camping stoves [8], gasoline-powered electrical generators [9]), and motor vehicles operating in poorly ventilated areas (eg, ice rinks, warehouses, parking garages). CO poisonings following open air exposure to motorboat exhaust have also been reported [10]. In addition, underground electrical cable fires produce large amounts of CO, which can seep into adjacent buildings and homes [11]. An increase in carbon monoxide exposures has been reported to occur in the immediate aftermath of hurricanes [9,12,13].

Methylene chloride (dichloromethane) is an industrial solvent and a component of paint remover. Inhaled or ingested methylene chloride is metabolized to CO by the liver, causing CO toxicity in the absence of ambient CO [1,14]. The US Occupational Safety and Health Administration lowered the workplace exposure limit for methylene chloride from 500 to 25 parts per million (ppm) based on concerns over the chronic effects of carboxyhemoglobinemia [15]. (See "Overview of occupational and environmental health".)

PATHOPHYSIOLOGY Carbon monoxide (CO) diffuses rapidly across the pulmonary capillary membrane and binds to the iron moiety of heme (and other porphyrins) with approximately 240 times the affinity of oxygen. The degree of carboxyhemoglobinemia (COHb) is a function of the relative amounts of CO and oxygen in the environment, duration of exposure, and minute ventilation. (See "Oxygen delivery and consumption".)

Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline; smokers may have levels of 10 to 15 percent [1]. Severe chronic obstructive pulmonary disease can cause a modest but significant elevation in carboxyhemoglobin levels, even among patients without exposure to tobacco smoke. The mechanism and clinical significance of this finding is unclear [16].

Once CO binds to the heme moiety of hemoglobin, an allosteric change occurs that greatly diminishes the ability of the other three oxygen binding sites to off-load oxygen to peripheral tissues. This results in a deformation and leftward shift of the oxyhemoglobin dissociation curve, and compounds the impairment in tissue oxygen delivery (figure 1).

Effect of carboxyhemoglobinemia on oxygen content and delivery

Red curve demonstrates the normal relationship between arterial (A) and venous (V) oxygen content. In general, a difference in arterial and venous oxygen content of 5 mL per 100 mL blood is expected at rest. The green line depicts the effect of a 50 percent decrease in hemoglobin concentration, which decreases arterial (A') and venous (V'1) oxygen content but does not change the partial pressure at which

hemoglobin is 50 percent saturated (P50). The blue curve shows the effect of a 50 percent carboxyhemoglobinemia (COHb), which both decreases oxygen carrying capacity (A') and impairs peripheral unloading of oxygen from hemoglobin under conditions of low oxygen tension (V'2), shifting P50 to the left (P'50). These changes result in a profound reduction in both oxyhemoglobin saturation and delivery of oxygen to peripheral tissues. CO also interferes with peripheral oxygen utilization. Approximately 10 to 15 percent of CO is extravascular and bound to molecules such as myoglobin, cytochromes, and NADPH reductase, resulting in impairment of oxidative phosphorylation at the mitochondrial level [6,17]. The half-life of CO bound to these molecules is longer than that of COHb. The importance of these nonhemoglobin-mediated effects has been best documented in the heart, where mitochondrial dysfunction due to CO can produce myocardial stunning despite adequate oxygen delivery [18].

CO also interferes with peripheral oxygen utilization by inactivating cytochrome oxidase in a manner similar to, but clinically less important than, cyanide. CO and cyanide poisoning can occur simultaneously in patients following smoke inhalation, and their combined effects on oxygen transport and utilization appear to be synergistic [19,20]. (See "Smoke inhalation", section on 'Cyanide'.)

The effects of CO on oxygen delivery and utilization, however, cannot account for the delayed neurologic sequelae (DNS) that may occur after CO poisoning. The mechanism of DNS is incompletely understood, but it probably involves lipid peroxidation by toxic oxygen species generated by xanthine oxidase. Xanthine oxidase is produced in situ from xanthine dehydrogenase via enzymes released by white blood cells that adhere to damaged endothelial cells [21-25]. During recovery from CO exposure, events analogous to ischemia-reperfusion injury and exposure to hyperoxia may exacerbate the initial oxidative damage [2,26].

KINETICS Carbon monoxide (CO) is rapidly absorbed across the pulmonary endothelium. Elimination is dependent upon the degree of oxygenation and, to a lesser extent, minute ventilation. The half-life of CO while a patient is breathing room air is approximately 300 minutes, while breathing high-flow oxygen via a nonrebreathing face mask is about 90 minutes, and with 100 percent hyperbaric oxygen is approximately 30 minutes.

CLINICAL PRESENTATION

Symptoms and signs The clinical findings of carbon monoxide (CO) poisoning are highly variable and largely nonspecific [27,28] (table 1). Moderately or mildly CO-intoxicated patients often present with constitutional symptoms, including headache (the most common presenting symptom), malaise, nausea, and dizziness, and may be misdiagnosed with acute viral syndromes [26]. In addition to current symptoms, the clinician should specifically inquire (of the patient and/or witnesses) about loss of consciousness.

In the absence of concurrent trauma or burns, physical findings in CO poisoning are usually confined to alterations in mental status, so a careful neurologic examination is crucial. Patients may manifest symptoms ranging from mild confusion to coma. Specific cognitive testing, such as the Carbon Monoxide Neuropsychological Screening Battery, is usually not used in the acute setting and, in any event, is not universally endorsed due to its inability to discriminate between the effects of CO and those of other intoxicants [1,24]. Although some textbooks describe a "cherry red" appearance of the lips and skin as indicative of CO poisoning, this is an insensitive sign [27].

Severe CO toxicity can produce neurologic symptoms such as seizures, syncope, or coma, and also cardiovascular and metabolic manifestations such as myocardial ischemia, ventricular arrhythmias, pulmonary edema, and profound lactic acidosis.

Myocardial injury Acute myocardial injury is common among CO-poisoned patients and is associated with increased long-term mortality. A retrospective study of 230 patients with moderate or severe CO poisoning referred to a specialized center found evidence of myocardial ischemia (characteristic electrocardiographic changes or elevated serum cardiac biomarkers) in one-third of all cases [29].

Long-term follow-up (median 7.6 years) of this cohort noted a mortality rate of 24 percent among patients who sustained acute myocardial injury [30]. Mortality among patients with myocardial injury was more than twice that of poisoned patients without evidence of such injury, and was estimated to be triple that expected for a comparable unpoisoned cohort.

This study population was young (mean age 47 years) and had a low incidence of established cardiac disease or cardiac risk factors, other than smoking. It is probable that the incidence of myocardial ischemia among CO-poisoned patients with established cardiac disease is even higher.

Delayed neuropsychiatric syndrome In up to 40 percent of patients with significant CO exposure, a syndrome of delayed neurologic sequelae (DNS) can arise 3 to 240 days after apparent recovery [31-34]. Characterized by variable degrees of cognitive deficits, personality changes, movement disorders, and focal neurologic deficits, DNS generally occur within 20 days of CO poisoning, and deficits may persist for a year or longer.

The development of DNS correlates poorly with COHb levels, although the majority of cases are associated with loss of consciousness during acute intoxication [1,6,35]. The incidence and severity of DNS have become increasingly important clinical end points in studies of treatment for CO poisoning. (See 'Hyperbaric oxygen' below.)

DIAGNOSIS Acute carbon monoxide (CO) poisoning is usually suspected on the basis of a suggestive history, while the diagnosis of chronic CO intoxication is notoriously difficult [1,28] (table 1). Standard pulse oximetry CANNOT screen for CO exposure, as it does not differentiate carboxyhemoglobin from oxyhemoglobin (figure 2) [36,37]. Eight-wavelength pulse oximeters capable of measuring carboxyhemoglobin and methemoglobin are being developed, but need further study [38]. (See "Pulse oximetry", section on 'Abnormal hemoglobins'.)

Effect of carboxyhemoglobin on measured oxygen saturation by pulse oximetry

SpO2 and O2Hb versus carboxyhemoglobin (COHb) at FiO2=1.0. SpO2 consistently overestimates saturation in the presence of COHb. At COHb=70 percent, SpO2 is still roughly 90 percent, while O2Hb has fallen to 30 percent.

Redrawn from Barker, SJ, Tremper, KK, Anesthesiology 1987; 66:677.

The diagnosis of CO poisoning is based upon a compatible history and physical exam in conjunction with an elevated carboxyhemoglobin level measured by cooximetry of a blood gas sample. Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline; smokers may have levels of 10 to 15 percent. Levels above these respective values are consistent with CO poisoning.

Carboxyhemoglobin levels correlate imprecisely with the degree of poisoning and are not predictive of delayed neurologic sequelae (DNS). Venous samples may be used to determine the carboxyhemoglobin level, but they are less accurate in quantifying the associated acidosis. The main uses of venous carboxyhemoglobin are in screening large numbers of potential CO victims in a disaster situation, or in monitoring the change in carboxyhemoglobin level over time during treatment.

Noninvasive pulse cooximeters capable of photo spectroscopic measurements of carboxyhemoglobin are in development [39]. However, preliminary observational studies question their accuracy [40,41]. Until well-performed trials demonstrate that these devices provide consistently accurate measurements, we cannot recommend their routine clinical use.

Blood PO2 measurements tend to be normal because PO2 reflects O2 dissolved in blood, and this process is not affected by CO. In contrast, hemoglobin-bound O2 (which normally comprises 98 percent of arterial O2 content) is profoundly reduced in the presence of COHb. (See "Oxygen delivery and consumption".)

Once the diagnosis of CO intoxication is confirmed, we recommend obtaining an electrocardiogram (ECG); cardiac biomarker evaluation is warranted in patients with ECG evidence of ischemia or a history of cardiac disease [29].

Computed tomography (CT) of the head is usually helpful only to rule out other causes of neurologic decompensation. Hemorrhagic infarction of the globus pallidus and, less frequently, the deep white matter have been reported following acute intoxication, but they are rare [42]. Imaging studies, including CT, magnetic resonance imaging (MRI), and positron-emission tomography (PET), suggest that abnormalities in the globus pallidus and deep white matter may be noted in the setting of DNS [32,4346].

MANAGEMENT

Initial treament and disposition Carbon monoxide (CO) is removed almost exclusively via the pulmonary circulation through competitive binding of hemoglobin by oxygen. The half-life of carboxyhemoglobin (COHb) in a patient breathing room air is approximately 300 minutes; this decreases to 90 minutes with high-flow oxygen via a nonrebreathing mask. Thus, the most important interventions in the management of a CO-poisoned patient are prompt removal from the source of CO and institution of high-flow oxygen by face mask. A summary table to facilitate emergent management is provided (table 1).

Comatose patients, or those with severely impaired mental status, should be intubated without delay and mechanically ventilated using 100 percent oxygen. For patients suffering from CO poisoning after smoke inhalation, it is important to consider concomitant cyanide toxicity, which can further impair tissue oxygen utilization and worsen the degree of cellular hypoxia [17,19]. (See "Smoke inhalation".)

Many patients can be managed in the emergency department, as most symptoms resolve with high-flow oxygen. Patients whose symptoms do not resolve, who demonstrate electrocardiogram (ECG) or laboratory evidence of severe poisoning, or who have other medical or social cause for concern should be hospitalized. Psychiatric assessment and determination of suicidality are crucial following intentional CO poisoning. (See "Suicidal ideation and behavior in adults".)

Many acute care hospitals lack the ability to measure carboxyhemoglobin concentrations [47]. Patients suspected of CO poisoning who are treated in hospitals without on-site cooximetry should be treated with 100 percent oxygen via nonrebreathing face mask. Clinicians at such hospitals should strongly consider the immediate transfer of patients at high risk for adverse outcomes (specifically those with acidemia, ischemic ECG changes, persistent chest pain, or altered mental status) to facilities capable of providing hyperbaric oxygen therapy.

Source identification is critical in cases of accidental poisoning, in order to limit the risk to others. Local fire departments or other emergency management personnel can assist with an assessment of CO level in the suspected environment and removal of victims [1].

Hyperbaric oxygen Hyperbaric oxygen therapy (HBO) involves exposing patients to 100 percent oxygen under supra-atmospheric conditions. This results in a decrease in the half-life of (carboxyhemoglobin) COHb, from approximately 90 minutes on 100 percent normobaric oxygen to approximately 30 minutes during HBO. The amount of oxygen dissolved in the blood also rises from approximately 0.3 to 6.0 mL per dL, which substantially increases the delivery of non-hemoglobin-bound oxygen to the peripheral tissues. (See "Hyperbaric oxygen therapy".)

Despite the uncertainty in identifying patients who will benefit from HBO treatment, a broad set of recommendations has been established for therapy of CO-intoxicated patients (figure 3). In addition to a COHb level above 25 percent (see below), criteria for treatment with HBO include: evidence of ongoing end-organ ischemia (eg, profound metabolic acidosis (pH <7.1), myocardial ischemia), loss of consciousness, or in pregnant women a COHb >20 percent or evidence of fetal distress [1,2,28,48]. Given the possibility of long-term neurologic impairment following CO poisoning and the absence of clear harm from HBO therapy, we suggest that any CO-intoxicated patient who meets these criteria be treated with HBO.

Algorithm for using normobaric and hyperbaric oxygen following carbon monoxide exposure

Adapted from O'Brien, C, Manaker, S. Carbon monoxide and smoke inhalation. The Intensive Care Manual. Hanson, Lanken, Manaker (Eds), WB Saunders, Philadelphia, 2001.

The COHb level at which HBO should be performed, independent of clinical status, is controversial. Many medical toxicologists routinely recommend HBO when the carboxyhemoglobin level is greater than 25 percent, whereas some societies use 40 percent as the appropriate threshold. There is no clear basis in the medical literature for choosing one level over the other. We routinely advocate HBO in patients with a COHb level greater than 25 percent, but recognize other clinicians may disagree based on their interpretation of existing studies.

The potential benefit of HBO is greater the more rapidly treatment is provided. Benefit for patients treated more than 12 hours after their CO exposure is unproven. Despite some positive studies, the use

of HBO in mild to moderate CO poisoning is not routine, and we do not recommend HBO for patients other than those in the high-risk groups listed above. The other indications, complications, and technique of HBO are discussed separately. (See "Hyperbaric oxygen therapy".)

HBO may be beneficial in preventing the late neurocognitive deficits associated with severe CO intoxication; however, the quality and results of clinical trials have varied widely [3,31,49-53]. Of several trials designed to assess the efficacy of HBO, the two most important, double-blinded trials that included all patients regardless of poisoning severity came to contradictory conclusions [53]. The first was a single-center, controlled trial that randomly assigned 152 patients within 24 hours of presentation to hyperbaric or normobaric oxygen therapy [49]. Treatment was administered during three sessions in a hyperbaric chamber, effectively blinding the therapy a patient was receiving. Six weeks after presentation, cognitive sequelae were more common in the group treated with normobaric oxygen (46 versus 25 percent). This advantage of hyperbaric therapy in terms of neurologic performance was maintained at six months and one year following initial presentation.

Discordant findings were noted in a randomized trial of 191 patients referred to a tertiary center with CO poisoning during a two-year period, which failed to document benefit for patients who received HBO [51]. Rather, delayed neurologic sequelae and poor performance on neuropsychiatric tests after one month were significantly more common among HBO-treated patients.

A systematic review of the HBO literature found methodological flaws in each of these studies [53]. The first, which found a benefit from HBO therapy, suffered from a disparity in the severity of toxicity between patients randomized to normobaric oxygen therapy (NBO), (mean CO exposure of 22 hours), and patients treated with HBO (mean CO exposure of 13 hours). The second study, which found no benefit to HBO treatment, lost to follow-up over 50 percent of the patients randomized to HBO, and provided continuous NBO treatment for three days to those not receiving HBO. Such methodological problems make it difficult to draw conclusions about the appropriate role of HBO in the treatment of CO intoxication.

All patients selected to receive HBO should have at least one treatment at 2.5 to 3.0 atm as soon as possible to reverse the acute effects of CO intoxication, with possible additional therapy directed toward limitation or prevention of DNS [1,19,29,54].

Approximately 1500 patients with CO poisoning are treated with HBO in the United States every year [34]. A major impediment to the wider application of HBO in the management of CO poisoning is limited

availability of hyperbaric chambers. In the United States, approximately 250 hyperbaric facilities offer either single occupant ("monoplace") or multiple occupant ("multiplace") chambers. Information regarding the location of hyperbaric facilities can be accessed through the Undersea and Hyperbaric Medical Society website (www.uhms.org) or via the Divers Alert Network Emergency Hotline (1-919684-8111) [1].

HBO during pregnancy The importance of pregnancy on the decision to initiate HBO is based on the greater affinity and longer half-life of CO bound to fetal hemoglobin, the inability to substantially increase placental perfusion, and the direct effects of hypoxemia and acidosis on the fetus. A prospective, multicenter study of fetal outcome following accidental CO poisoning found no physical or neurobehavioral deficits in 31 infants who were exposed to CO in utero when their mothers suffered mild to moderate CO poisoning [55]. Severe maternal poisoning, however, resulted in adverse outcomes in three of five patients treated with normobaric oxygen alone; HBO was used in two other cases, and those children did not demonstrate evidence of prenatal injury. Exposure to HBO does not seem to adversely affect the fetus, but the published experience is limited [56].

There is limited information on the characteristics of the fetal heart rate tracing of pregnant women with carbon monoxide poisoning in the third trimester. In the few cases with detailed reports, the initial tracing showed baseline fetal tachycardia of 160 to 190 beats per minute in three of four fetuses, and all four had minimal variability with no accelerations or decelerations [57,58]. After 60 to 90 minutes of maternal HBO therapy, all of the tracings became normal.

Isocapnic hyperpnea The elimination half-life of COHb is, in part, a function of minute ventilation. Isocapnic hyperpnea is a technique by which an intubated patient is hyperventilated with a normobaric mixture of oxygen and a small amount of CO2, maintaining a PaCO2 of approximately 40 mmHg despite a sixfold increase in minute ventilation. Application of this technique in an animal model more than doubled the rate of CO elimination compared with conventional ventilation with 100 percent oxygen [59]. Furthermore, the technology required for isocapnic hyperpnea is much less expensive and cumbersome than HBO. Adding CO2 to the respiratory circuit MUST be accompanied by assisted hyperventilation or respiratory acidosis may occur, compounding the metabolic acidosis produced by carboxyhemoglobin.

A conceptually similar approach has been tested experimentally in nonintubated patients. One study randomly assigned seven patients with COHb levels of 10 to 12 percent to receive either 100 percent oxygen via face mask or FiO2 >95 percent with 4.5 to 4.8 percent CO2, in order to maintain normocapnia with a minute ventilation two to six times baseline [60]. The half-life of COHb was significantly reduced

by the isocapnic hyperpnea approach (31 versus 78 minutes). Larger trials will be needed before this approach can be endorsed for all patients; however, the relative simplicity and low cost of this technique suggest that it might have a role in the early management of suspected CO poisoning.

PEDIATRIC CONSIDERATIONS In young children, signs of carbon monoxide poisoning may be more subtle and nonspecific than those in adults. Infants and toddlers may present with complaints such as fussiness and feeding difficulty as the sole manifestation of carbon monoxide poisoning [61]. Because of their higher oxygen utilization and higher minute ventilation, young children may develop signs and symptoms of carbon monoxide poisoning before older children and adults who experience the same exposure (eg, family members living in a house with a faulty furnace).

In contrast, older children have symptoms similar to adults as they are able to verbalize feelings of headache and nausea. The incidence of delayed neuropsychological sequelae in the pediatric population falls between 3 and 17 percent (lower than that reported in adults) [62-64].

Patient age does not alter the management of carbon monoxide poisoning. However, when hyperbaric oxygen therapy (HBO) is administered to young children, specific concerns must be addressed:

Myringotomy should be performed in children with active otitis media who are younger than five years or who are unable to equalize their middle ear pressure [65].It may be helpful to allow a family member to accompany a frightened child into the chamber.When HBO is administered to an infant, care must be taken to keep the infant warm: Children in this age group easily become hypothermic.Congenital abnormalities must also be taken in account:

A chest radiograph should be obtained to detect congenital anomalies such as lobar emphysema which could lead to a pneumothorax.Patients with unpalliated ductal dependent cardiac lesions should undergo HBO with caution as oxygen may precipitate duct closure. In most cases, such patients are poor candidates for HBO.

ADDITIONAL RESOURCES To obtain emergent consultation with a medical toxicologist, call the United States Poison Control Network at 1-800-222-1222, or access the World Health Organization's list of international poison centers (www.who.int/ipcs/poisons/centre/directory/en).

PREVENTION Home carbon monoxide (CO) monitors equipped with alarms are relatively inexpensive, widely available, and potentially life-saving. The US Consumer Product Safety Commission (CPSC) recommends that every home have a CO monitor equipped with an alarm; further information is available online www.cpsc.gov or via their hotline (1-800-638-2772).

SUMMARY AND RECOMMENDATIONS Carbon monoxide (CO) poisoning is common, potentially fatal, and probably underdiagnosed because of its nonspecific clinical presentation. CO has profound effects on oxygen transport and, to a lesser degree, peripheral oxygen utilization. In addition to the extended summary below, a brief table to facilitate emergent management is provided (table 1).

CO poisoning is most common during winter in cold climates, but it may occur in all seasons and environments. Smoke inhalation is responsible for most accidental cases. Other potential sources of CO include poorly functioning heating systems, improperly vented fuel-burning devices (eg, kerosene heaters, charcoal grills, camping stoves, gasoline-powered electrical generators), and motor vehicles operating in poorly ventilated areas. (See 'Epidemiology' above.)CO diffuses rapidly across the pulmonary capillary membrane and binds to the iron moiety of heme with approximately 240 times the affinity of oxygen. The degree of carboxyhemoglobinemia (COHb) is a function of the relative amounts of CO and oxygen in the environment, duration of exposure, and minute ventilation. (See 'Pathophysiology' above.)The clinical findings of CO poisoning are highly variable and largely nonspecific. Mild to moderate CO-intoxicated patients often present with constitutional symptoms, including headache (most common), malaise, nausea, and dizziness, and may be misdiagnosed with acute viral syndromes. In the absence of concurrent trauma or burns, physical findings in CO poisoning are usually confined to alterations in mental status, ranging from mild confusion to seizures and coma. A careful neurologic examination is crucial. (See 'Clinical presentation' above.)Cardiac ischemia can occur. Once the diagnosis of CO intoxication is confirmed, we recommend obtaining an electrocardiogram (ECG); cardiac biomarker evaluation is warranted in patients with ECG evidence of ischemia, symptoms suggestive of ischemia, age greater than 65 years, or a history of cardiac disease or cardiac risk factors. (See 'Clinical presentation' above.)The diagnosis of CO poisoning is based upon a compatible history and physical examination in conjunction with an elevated carboxyhemoglobin level. Diagnosis requires quantification by cooximetry of a blood gas sample; pulse oximetry is unable to distinguish between oxyhemoglobin and COHb. Blood PO2 measurements tend to be normal because PO2 reflects O2 dissolved in blood, and this process is not affected by CO. (See 'Diagnosis' above.)Continual assessment and standard interventions to secure the airway, breathing, and circulation of the patient poisoned with CO are of paramount importance. We recommend that all comatose patients and those with severely impaired mental status be intubated without delay and mechanically ventilated (Grade 1B). (See 'Management' above.)The most important interventions in the management of a CO-poisoned patient are prompt removal from the source of CO and institution of 100 percent oxygen by nonrebreathing face mask or endotracheal tube. We recommend initial treatment with 100 percent normobaric oxygen for all suspected victims of CO poisoning, regardless of pulse oximetry or arterial PO2 (Grade 1B). (See 'Management' above.)In patients who have severe intoxication, there is controversy surrounding the ability of hyperbaric oxygen therapy (HBO) to decrease the incidence and severity of delayed neurocognitive deficits following CO poisoning. Expert guidelines regarding the judicious use of hyperbaric oxygen have been published (figure 3). We suggest treatment with HBO in the following circumstances (Grade 2B):

CO level >25 percentCO level >20 percent in pregnant patientLoss of consciousnessSevere metabolic acidosis (pH <7.1)Possible end-organ ischemia (eg, ECG changes, chest pain, altered mental status) (see 'Management' above)

Many patients with mild symptoms from an accidental poisoning can be managed in an emergency department and safely discharged. Patients whose symptoms do not resolve, who demonstrate ECG or laboratory evidence of severe poisoning, or who have other medical or social cause for concern should be hospitalized. Psychiatric evaluation must be obtained for all patients with self-inflicted CO poisoning. (See 'Management' above.)Determination of the mechanism of exposure is critical in cases of accidental poisoning in order to limit the risk to others. Local fire departments can assist with an assessment of CO level and removal of victims in the suspected environment. (See 'Management' above.)

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