Carbon Monoxide Toxicity

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Practice Essentials

Carbon monoxide (CO) is a colorless, odorless gas produced by incomplete combustion of carbonaceous material. Clinical presentation in patients with CO poisoning ranges from headache and dizziness to coma and death.[1] Hyperbaric oxygen therapy (see the image below) can significantly reduce the morbidity of CO poisoning, but a portion of survivors still suffer significant long-term neurologic and affective sequelae.[2]



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Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.

CO is formed as a by-product of burning organic compounds. Many cases of CO exposure occur in private residences.[3]  CO toxicity is especially common during power outages due to storms, as a result of the improper use of gasoline-powered portable generators to provide electricity and indoor use of charcoal briquettes for cooking and heating.[4, 5]  Exhaust from generators and propulsion engines on houseboats has also been linked to CO poisoning.[6]

Most fatalities from CO toxicity result from fires, but stoves, portable heaters, and automobile exhaust cause approximately one third of deaths. These often are associated with malfunctioning or obstructed exhaust systems and suicide attempts. Cigarette smoke is a significant source of CO. Natural gas contains no CO, but improperly vented gas water heaters, kerosene space heaters, charcoal grills, hibachis, and Sterno stoves all emit CO. Other sources of CO exposure include the following[7, 8] :

CO intoxication also occurs by inhalation of methylene chloride vapors, a volatile liquid found in degreasers, solvents, and paint removers. Dermal methylene chloride exposure may not result in significant systemic effects but can cause significant dermal burns. Rarely, methylene chloride is ingested and can result in delayed CO toxicity.

The liver metabolizes as much as one third of inhaled methylene chloride to CO. A significant percentage of methylene chloride is stored in the tissues, and continued release results in elevated CO levels for at least twice as long as with direct CO inhalation.

Children riding in the back of enclosed pickup trucks seem to be at particularly high risk of CO intoxication. Industrial workers at pulp mills, steel foundries, and plants producing formaldehyde or coke are at risk for exposure, as are personnel at fire scenes and individuals working indoors with combustion engines or combustible gases.

For patient education information on CO poisoning and prevention, see the US Centers for Disease Control and Prevention's (CDC's) Carbon Monoxide Poisoning Basics Web page.

Pathophysiology

CO toxicity causes impaired oxygen delivery and utilization at the cellular level. CO affects several different sites within the body but has its most profound impact on the organs (eg, brain, heart) with the highest oxygen requirement.

Cellular hypoxia from CO toxicity is caused by impedance of oxygen delivery. CO reversibly binds hemoglobin, resulting in relative functional anemia. Because it binds hemoglobin 230-270 times more avidly than oxygen, even small concentrations can result in significant levels of carboxyhemoglobin (HbCO).

An ambient CO level of 100 ppm produces an HbCO of 16% at equilibration, which is enough to produce clinical symptoms. Binding of CO to hemoglobin causes an increased binding of oxygen molecules at the three other oxygen-binding sites, resulting in a leftward shift in the oxyhemoglobin dissociation curve and decreasing the availability of oxygen to the already hypoxic tissues.

CO binds to cardiac myoglobin with an even greater affinity than to hemoglobin; the resulting myocardial depression and hypotension exacerbates the tissue hypoxia. Decrease in oxygen delivery is insufficient, however, to explain the extent of the CO toxicity. Clinical status often does not correlate well with HbCO level, leading some to postulate an additional impairment of cellular respiration.

CO can produce direct cellular changes involving immunologic or inflammatory damage by a variety of mechanisms, including the following[4] :

CO directly impairs aerobic metabolism in tissues by poisoning the mitochondrial electron-transport chain. It does so by binding mitochondrial cytochromes, preventing the binding and subsequent reduction of oxygen at the end of the cycle. The process of oxidative phosphorylation cannot be completed, and the mitochondria, instead of making water and adenosine triphosphate (ATP), make destructive oxygen free radicals.

Studies have indicated that CO may cause lipid peroxidation and leukocyte-mediated inflammatory changes in the brain, a process that may be inhibited by hyperbaric oxygen (HBO) therapy. Byproducts of peroxidation alter myelin basic protein (MBP) in the presence of CO, affecting immunologic recognition of MBP and starting a cascade of autoimmune activity against cerebral proteins.

Following severe intoxication, patients display central nervous system (CNS) pathology, including white matter demyelination. This leads to edema and focal areas of necrosis, typically of the bilateral globus pallidus. Interestingly, the pallidus lesions, as well as the other lesions, are watershed area tissues with relatively low oxygen demand, suggesting elements of hypoperfusion and hypoxia.[9]

Studies have demonstrated release of nitric oxide free radicals (implicated in the pathophysiology of atherosclerosis) from platelet and vascular endothelium, following exposure to CO concentrations of 100 ppm. One study suggests a direct toxicity of CO on myocardium that is separate from the effect of hypoxia.[10]

HbCO levels often do not reflect the clinical picture, yet symptoms typically begin with headaches at levels around 10%. Levels of 50-70% may result in seizure, coma, and fatality.

CO is eliminated through the lungs. The half-life of CO at room air temperature is 3-4 hours. Treatment with 100% oxygen reduces the half-life to 30-90 minutes; HBO at 2.5 atm with 100% oxygen reduces it to 15-23 minutes.

Etiology

Most unintentional CO fatalities occur in stationary vehicles from preventable causes such as malfunctioning exhaust systems, inadequately ventilated passenger compartments, operation in an enclosed space, and utilization of auxiliary fuel-burning heaters inside a car or camper.

Most unintentional automobile-related CO deaths in garages have occurred despite open garage doors or windows, demonstrating the inadequacy of passive ventilation in such situations.

Colorado state data from 1986-1991 revealed that leading sources of 1149 unintentional nonfatal CO poisonings were residential furnaces (40%), automobile exhaust (24%), and fires (12%); however, furnaces were responsible for only 10% of fatal poisonings[11]

In the setting of structure fires, CO presents greater risk than thermal injury or oxygen deprivation, both for firefighters and victims.[12]

In most developing countries, cooking or heating is often done with unvented cookstoves, wood, charcoal, animal dung, or agricultural waste, which has been linked with elevated HbCO levels.

Boats and houseboats represent a significant and underappreciated source of exposure, with multiple case reports and studies.[6]

Epidemiology

Frequency

United States

Unintentional, non–fire-related CO poisoning is responsible for approximately 15,000 emergency department visits annually in the United States. In 2000-2009, the exposure site was reported as residence in 77.6% of cases and workplace in 12%.[13] The most common source of CO exposure in the home is furnaces (18.5%), followed by motor vehicles, stoves, gas lines, water heaters, and generators.[14] During 1999–2012, deaths from unintentional non–fire-related CO poisoning in the US totaled 6136, an average of 438 deaths per year.[15]

From 2015 to 2021, total US deaths from CO poisoning decreased from 1253 to 1067. The overall decrease was due to a fall in the number of fatal intentional CO poisonings, which offset an increase in the number of deaths from accidental CO poisoning. This was the first time in four decades that deaths from accidental CO poisoning increased, and the first time in the US that deaths from accidental CO poisoning outnumbered deaths from intentional poisoning.[16]

In 2023, the American Association of Poison Control Centers reported 13,681 single exposures to CO, 352 of which were intentional. Major outcomes occurred in 372 cases, and 46 deaths were reported.[17]

International

Quantifying the global incidence of CO poisoning is impossible because of the transient duration of symptoms in mild intoxication, the ubiquitous and occult nature of exposure, and a tendency toward misdiagnosis. Nevertheless, a study published in 2020 reported the worldwide cumulative incidence of CO poisoning to be an estimated 137 cases per million population. The study further found that the worldwide incidence had remained stable during the previous 25 years, while the mortality rate had declined; annual mortality was estimated to be 4.6 deaths per million population.[18]  

One Australian study of suicidal poisonings indicated no decrease following significantly lowered CO emissions from 1970-1996 and revealed no difference between the HbCO levels of occupants in cars with and without catalytic converters.[19]

Race

All ages, ethnic populations, and social groups are affected, yet particular groups may be at higher risk.

Earlier data stated that, for unintentional fatalities, race-specific death rates were 20% higher for Blacks. Later data revealed non-Hispanic Whites and non-Hispanic Blacks to have equally high death rates, significantly above that of Hispanics and those classified as "other."[20]

Conversely, intentional fatalities demonstrate that race-specific rates for Blacks and other minority racial groups are 87% lower than for Whites, revealing a cultural partiality to this form of suicide.

Two North American studies, from the 1990s and 2005, examined the incidence of CO toxicity from indoor heating devices used during severe winter storms. Both studies identified a strong association between CO toxicity and US immigrants who were non–English speaking.[21] However, a study of acute, severe CO poisoning from portable electric generators in the US from August 1, 2008 to July 31, 2011 found that 96% of patients spoke English.[5]

Sex- and age-related demographics

Worldwide in 2021, nearly 70% of deaths from unintentional CO poisoning occurred in males, and the highest number of deaths was in persons aged 50-54 years of age. However, the highest mortality rate was in persons aged 85 years or older, with 1.96 deaths per 100,000 population.[22] On the other hand, nonfatal exposures are more common in older teens and young adults (aged 15-34 y) than in older adults and are most common in young children (aged 0-4 y).[20, 14]

Individuals with pulmonary and cardiovascular disease tolerate CO intoxication poorly; this is particularly evident in those with chronic obstructive pulmonary disease (COPD), who have the additional concern of ventilation-perfusion abnormalities and possible respiratory depressive response to 100% oxygen therapy.

Neonates and the in utero fetus are more vulnerable to CO toxicity because of the natural leftward shift of the dissociation curve of fetal hemoglobin, a lower baseline partial pressure of oxygen (PaO2), and levels of HbCO at equilibration that are 10-15% higher than maternal levels.

Climate and weather

Age-adjusted fatality rates are higher in cold and mountainous Midwestern and Western states and peak in the winter months. In addition, hurricanes and other natural disasters that result in power outages can lead to a spike in CO poisonings, as those affected turn to alternative sources of fuel or electricity.[23] For example, multiple incidents of CO poisoning were reported in southern US states following the Katrina and Rita hurricanes of 2005, in Northeastern states following Hurricane Sandy in 2012, and in Florida following Hurricane Irma in 2017.[24, 25, 26]

Prognosis

Considerations regarding prognosis include the following:

A study by Ahn et al using the National Health Insurance Service (NHIS) of Korea database found evidence for an association between CO poisoning and the development of internal malignancies. According to the investigators, the adjusted hazard ratio (aHR) for solid organ malignancies was 1.03 in persons with CO poisoning. More specifically, the aHRs for malignancies of the oral cavity, lungs, bones, cervix, and kidneys were, respectively, 1.33, 1.39, 1.68, 1.32, and 1.14. On the other hand, the internal malignancy risk was lower for the thorax, anus, uterus, ovaries, and prostate, and for Hodgkin lymphoma, non-Hodgkin lymphoma, and multiple myeloma. The risk of hematologic malignancies was also lower, with the aHR being 0.71. The mean follow-up time for the persons who suffered CO poisoning was 2350.91 days.[27]

A study by Hwang et al that also used the NHIS of Korea database indicated that CO poisoning is linked to the development of migraine headaches. The aHR for migraine was 1.37, with the risk being greater regardless of age, sex, or HBO therapy use. Mean follow-up for persons with CO poisoning was 5.9 years.[28]

An analysis of 331 pediatric patients with CO poisoning seen at a single-site emergency department found risk factors associated with severe disease course were a low Glasgow Coma Scale score, high leukocyte count, and high troponin T levels at presentation.[29]  Patients with myocardial injury from CO poisoning are at higher risk for short-term mortality, and survivors are at increased risk for neurocognitive sequelae and future myocardial infarction.[30]

Survivors of intentional CO poisoning are at extreme risk for subsequent completion of suicide.[4]

History

Carbon monoxide (CO) toxicity is often misdiagnosed because of the vagueness and broad spectrum of complaints; symptoms often are attributed to a viral illness. Specifically inquiring about possible exposures when considering the diagnosis is important.

For nonfatal, nonintentional, non–fire-related exposures, the most common symptom has been reported to be headache (37%), followed by dizziness (18%) and nausea (17%).[14] However, any of the following symptoms should alert suspicion in the winter months, especially when the patient has a history compatible with CO exposure and when more than one patient in a group or household presents with similar complaints:

Chronic exposure also produces the above symptoms; however, patients with chronic CO exposure may present with loss of dentition, gradual-onset neuropsychiatric symptoms, or, simply, recent impairment of cognitive ability.

Physical Examination

Physical examination is of limited value. Inhalation injury or burns should always alert the clinician to the possibility of CO exposure.

Vital signs may include the following:

Although so-called cherry-red skin has traditionally been considered a sign of CO poisoning (ie, "When you're cherry red, you're dead"), it is in fact rare.[4]  Pallor is present more often.

Ophthalmologic and other findings include the following:

Neurologic and/or neuropsychiatric findings may include the following;

Long-term exposures or severe acute exposures frequently result in long-term neuropsychiatric sequelae. Additionally, some individuals develop delayed neuropsychiatric symptoms, often after severe intoxications associated with coma.

After recovery from the initial incident, patients present several days to weeks later with neuropsychiatric symptoms such as those just described. Two thirds of patients eventually recover completely.

Laboratory Studies

The clinical diagnosis of acute CO poisoning should be confirmed by demonstrating an elevated level of HbCO. Either arterial or venous blood can be used for testing.[4]

Analysis of HbCO requires direct spectrophotometric measurement in specific blood gas analyzers. Bedside pulse CO oximetry is now available but requires a special unit and is not a component of routine pulse oximetry. A 2012 study showed that noninvasive pulse CO oximetry correlates with more rapid diagnosis and initiation of HBO therapy than laboratory CO oximetry. However, the impact on clinical outcome is still not proven.[31]  A 2017 clinical policy statement from the American College of Emergency Physicians (ACEP) recommends against using pulse CO oximetry to diagnose CO toxicity in patients with suspected acute CO poisoning (level B recommendation).[32]  

Elevated CO levels of at least 3-4% in nonsmokers and at least 10% in smokers are significant.[4] However, low levels do not rule out exposure, especially if the patient already has received 100% oxygen or if significant time has elapsed since exposure. HbCO levels in cigarette smokers typically range from 3-5% (but may be as high as 10% in some heavy smokers).[4] Presence of fetal hemoglobin, as high as 30% at 3 months, may be read as an elevation of HbCO level to 7%.[33] Symptoms may not correlate well with HbCO levels.

Findings on arterial blood gas measurement include the following:

The ACEP recommends obtaining an electrocardiogram and cardiac biomarker levels in emergency department patients with moderate to severe CO poisoning (level B recommendation).[32] Cardiac marker results include the following:

Other test results include the following:

Imaging Studies

Radiography

Obtain a chest radiograph in patients with significant intoxications, pulmonary symptoms, or evidence of hypoxia, or if HBO is to be used. Findings usually are normal. Changes such as the following imply a worse prognosis than do normal findings:

Computed tomography scanning

Obtain a CT scan of the head with severe intoxication or change in mental status that does not resolve rapidly. Assess cerebral edema and focal lesions; most are typically low-density lesions of the basal ganglia.[39]

Positive CT scan findings generally predict neurologic complications. In one study, 53% of patients hospitalized for acute CO intoxication had abnormal CT scan findings; all of these patients had neurologic sequelae. Of those patients with negative scan results, only 11% had neurologic sequelae.[39]

Serial CT scans may be necessary, especially with mental status deterioration. One report describes the evolution of acute hydrocephalus in a child poisoned with CO, documented by serial CT scans.[40]

Magnetic resonance imaging

MRI is more accurate than CT scanning for detection of focal lesions and white matter demyelination and is often used for follow-up care.[41] The progression from conventional MRI to diffusion-weighted imaging (DWI) and then diffusion tensor imaging (DTI) has enabled increasingly sensitive evaluation of damage from CO poisoning. DTI can visualize progressive pathologic changes in the early stage of CO toxicity, allowing prediction of chronic conditions.[9]

Positron emission tomography scanning

Positron emission tomography (PET) and single-photon emission CT (SPECT) scanning are the most sensitive tests for ischemic brain injury, but the findings are nonspecific, and the studies are even more difficult to perform than MRI.

Other Tests

On electrocardiography, sinus tachycardia is the most common abnormality. Arrhythmias may be secondary to hypoxia, ischemia, or infarction. Even low HbCO levels can have a severe impact on patients with cardiovascular disease.

Neuropsychologic testing

Formal neuropsychologic testing of concentration, fine motor function, and problem solving consistently reveal subtle deficits in even mildly poisoned patients.

Abridged versions of these tests are available that can be performed in about 30 minutes by a well-trained examiner. These are more applicable to the emergency department setting. These tests have been developed as a possible means to assess the risk for delayed neurologic sequelae, to assess the need for hyperbaric oxygen therapy, and to determine the success of hyperbaric therapy in preventing delayed sequelae. The tests are used in some institutions, but studies prospectively confirming the conclusions are lacking.

Research indicates a specific link to deficits in context-aided memory in CO poisoning. Use of such specific testing in the emergency department has been proposed, as a tool for measuring the severity of neurologic involvement.

Prehospital Care

Prehospital care for patients with CO toxicity includes the following:

Emergency Department Care

Considerations in emergency department care include the following:

Oxygen therapy is usually provided via a non-rebreather mask. However, Roth et al described effective use of noninvasive continuous positive airway pressure (CPAP) ventilation using a tight mask and an inspired fraction of oxygen (FiO2) of 100%. These authors provided case reports of simultaneous CO toxicity in a couple in which HbCO levels fell from 21% at admission to 6% within 1 hour and 3% after 90 minutes in the patient treated with CPAP. In the spouse, who was treated with conventional oxygen therapy, reduction of HbCO from the admission level of 21% to 3% took 6 hours.[43]

Continue 100% oxygen therapy until the patient is asymptomatic and HbCO levels are below 10%. In patients with cardiovascular or pulmonary compromise, lower thresholds of 2% have been suggested. Calculate a gross estimate of the necessary duration of therapy using the initial level and half-life of 30-90 minutes at 100% oxygen.

In uncomplicated intoxications, venous HbCO levels and oxygen therapy are likely sufficient. Evaluate patients with significant cardiovascular disease and initial HbCO levels above 15% for myocardial ischemia and infarction.

Consider immediate transfer of patients with levels above 40% or cardiovascular or neurologic impairment to a hyperbaric facility, if feasible. Persistent impairment after 4 hours of normobaric oxygen therapy necessitates transfer to a hyperbaric center. Pregnant patients should be considered for hyperbaric treatment at lower HbCO levels (above 15%). Because fetal hemoglobin has a greater affinity for CO than hemoglobin in the mother's red blood cells, the fetus acts as a sink for the CO, so HbCO levels will be higher in the fetus than in the mother.[44]

Serial neurologic examinations, including fundoscopy, CT scanning, and, possibly, MRI, are important in detecting the development of cerebral edema. Cerebral edema requires intracranial pressure (ICP) and invasive blood pressure monitoring to further guide therapy. Head elevation, mannitol, and moderate hyperventilation to 28-30 mm Hg PCO2 are indicated in the initial absence of ICP monitoring. Glucocorticoids have not been proven efficacious, yet the negative aspects of their use in severe cases are limited.

Do not aggressively treat acidosis with a pH above 7.15, because acidosis results in a rightward shift in the oxyhemoglobin dissociation curve, increasing tissue oxygen availability. Acidosis generally improves with oxygen therapy.

In patients who fail to improve clinically, consider other toxic inhalants or thermal inhalation injury as contributing factors. Be aware that the nitrites used in cyanide kits cause methemoglobinemia, shifting the dissociation curve leftward and further inhibiting oxygen delivery at the tissue level. Combined intoxications of cyanide and CO may be treated with sodium thiosulfate 12.5 g intravenously to prevent the leftward shift.

Admit patients to a monitored setting and evaluate acid-base status if HbCO levels are 30-40% or above 25% with associated symptoms. Admitted patients generally require monitored settings, telemetry beds, or cardiac care unit/medical intensive care unit (CCU/MICU) beds for more severe cases.

Patients with cerebral edema may be most appropriately treated in a neurosurgical ICU setting; this may dictate transfer to another facility. Admission or consult by toxicology service is helpful in these cases.

A cardiology referral may be indicated for assessment and management of cardiac injury. Evaluation in such cases may involve electrocardiography, echocardiography, CT scanning, and cardiac MRI.[45]

Special Concerns in Pregnancy

In the pregnant patient, the lag time for uptake and elimination of CO between the mother and the fetus is considerable. Fetal HbCO levels change little during the first hour of maternal intoxication, then increase slowly over the first 24 hours. Fetal HbCO levels may peak after maternal levels decline.

The half-life of fetal HbCO is 7-9 hours during washout with room air. Maternal supplementation with 100% normobaric oxygen reduces the half-life to 3-4 hours. The half-life of fetal HbCO during HBO treatment is not known.

Hyperbaric Oxygen Therapy

If mild symptoms do not resolve or if severe symptoms are present, HBO therapy should be strongly considered. Specific indications for HBO therapy include a history of seizure or syncope, coma, altered mental status or confusion, an abnormal neurologic examination (particularly if any cerebellar signs are present), an HbCO level higher than 25%, or fetal distress in pregnancy.

However, HBO therapy currently rests at the center of controversy surrounding management of CO poisoning. Increased elimination of HbCO clearly occurs. Certain studies proclaim major reductions in delayed neurologic sequelae, cerebral edema, and pathologic CNS changes, as well as reduced cytochrome oxidase impairment.

Despite these individual claims, systematic reviews have not revealed a clear reduction in neurologic sequelae with HBO.[46, 47] A 2017 clinical policy statement from the American College of Emergency Physicians (ACEP) concluded that it remains unclear whether HBO therapy is superior to normobaric oxygen therapy for improving long-term neurocognitive outcomes.[32]  

A study by Han et al, in which 224 patients with acute CO poisoning were followed for up to 6 months, found no difference in the incidence of delayed neuropsychiatric sequelae between patients receiving HBO (n=198) and those receiving normobaric oxygen (n=26).[48]  In contrast, a nationwide observational study from Japan reported that patients who received HBO therapy had significantly lower rates of depressed mental status and reduced activities of daily living at discharge compared with a control group. Similar benefits were seen in patients with non-severe CO poisoning. The study used one-to-one propensity score matching to pair 2034 patients who received HBO therapy within 1 day of admission with an equal number of patients who did not receive HBO.[49]

However, evidence of a mortality benefit with HBO therapy has emerged. A retrospective study by Rose et al that reviewed 1099 cases of CO poisoning in adults concluded that HBO therapy was associated with an absolute risk reduction of 2.1% in both inpatient and 1-year mortality.[50]  

Lower mortality with HBO therapy was also reported in a retrospective, nationwide, population-based cohort study from Taiwan that included 7278 patients who received HBO and 18,459 patients who did not. Overall, the adjusted hazard ratio [AHR] for death in HBO-treated patients was 0.74 (95% CI, 0.67-0.81). In patients younger than 20 years, the AHR was 0.45 (95% CI, 0.26-0.80) and for those with acute respiratory failure, the AHR was 0.43 (95% CI, 0.35-0.53). The lower mortality rate was noted for a period of 4 years.[51]  

Presently, universal treatment criteria do not exist; however, a survey of directors of North American HBO facilities (with 85% responding) demonstrates some consensus. The most common selection criteria (regardless of HbCO level) include the following:

Ninety-two percent of HBO facility directors use HBO for headache, nausea, and HbCO levels above 40%; yet only 62% have a specific minimum HbCO level in asymptomatic patients. One half of the centers place a time limit on delay of treatment in patients with transient loss of consciousness alone.

Untreated pneumothorax is the only major contraindication for HBO therapy.[44]

HBO at 3 atm raises the amount of oxygen dissolved in the serum to 6.8%, enough to sustain cerebral metabolism. Elimination half-life is reduced to 15-23 minutes. Elimination half-life of CO from methylene chloride intoxication of 13 hours at room air temperature is reduced to 5.8 hours.

Chambers can be small monoplace hulls allowing space for a single patient in a supine position who can be viewed through a window at the head, or they can be acrylic walled and allow full visualization. Many of these monoplace chambers allow for care of critically ill patients, including intravenous lines, arterial lines, and ventilator. Others are large multiplace chambers that permit ventilation equipment and allow medical teams to accompany the patient. A monoplace chamber is shown below.



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Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.

Treatment regimens usually involve 100% oxygen at 2.4-3 atm for 90-120 minutes. Retreatment, although controversial, may be performed for acutely and chronically persistent symptoms. One study suggested that degree of metabolic acidosis can predict the need for retreatment.[52]

Complications of therapy include decompression sickness, sinus and middle ear barotrauma, seizure, progression of pneumothorax to tension pneumothorax, gas embolism, reversible visual refractive changes, and complications related to transport of unstable patients.

For treatment of complications from therapy, decongestants are useful, prophylactic myringotomy is common and a requirement for intubated patients, and chest tube placement is mandatory with pneumothorax. Exercise caution in patients who have experienced chest compressions, central venous catheterization, intubation, and positive pressure ventilation. Seizures are most often secondary to oxygen toxicity and do not mandate anticonvulsant therapy or discontinuation of HBO therapy.

In multiplace chambers, seizure therapy consists of removing the oxygen mask. In monoplace chambers, decompression lowers oxygen concentration. It is crucial not to do this during the tonic phase of the seizure, because it may cause pulmonary barotrauma secondary to gas expansion in the lungs.

A 10-year, retrospective study found that transfer to an HBO facility did not need to be delayed for concern of cardiac arrest, respiratory arrest, myocardial infarction, or worsening mental status if they had not occurred during initial resuscitation; however, hypotension, dysrhythmia, seizure, emesis, and agitation were of concern in transit as well as in initial resuscitation.[53]

Complications

Survivors of CO poisoning are at risk for a range of neurologic and psychiatric complications, including the following[54] :

Discuss the possibility of delayed neurologic complications, although they are much more common in patients with toxicity severe enough to require hospital admission.

Prevention

CO detectors

Home CO detectors with audible alarms are available and can limit CO toxicity.[56]  One study of 911 calls for suspected CO poisoning showed in 80% of calls for detector alarms, verifiable ambient CO levels were present in the home; the mean concentration of CO was 18.6 ppm in homes tested because of detector alarms but was 96.6 ppm in homes without alarms where calls were prompted by suspicious symptoms.[57]

Long-Term Monitoring

Asymptomatic patients with HbCO concentrations of lower than 10% may be discharged home after observation. Patients with only mild symptoms may be safely discharged home after 4 hours of treatment with 100% oxygen if their symptoms completely resolve in that time. A physician should reevaluate all discharged patients within 24-48 hours because symptoms may recur or be delayed.

In cases of accidental CO poisoning, patients should be followed up in 4-6 weeks to screen for cognitive sequelae. With intentional poisoning, psychiatric follow-up is mandatory, given the high rate of subsequent completed suicide.[4]

A nationwide, population-based study from Korea found that the risk of venous thromboembolism was significantly elevated in the first 90 days after CO poisoning (odds ratio [OR] 3.96; 95% confidence interval [CI] 2.50 to 6.25). Risk was especially high in the first 30 days for pulmonary embolism (OR 22.00; 95% CI 5.33 to 90.75) and deep venous thrombosis (OR 10.33; 95% CI 3.16 to 33.80). These researchers recommended monitoring patients for venous thromboembolism risk in the 3 months following CO poisoning.[58]

What is carbon monoxide (CO) toxicity?What are the most common causes of carbon monoxide (CO) toxicity?What is the role of methylene chloride vapors in carbon monoxide (CO) toxicity?Who are at high risk for carbon monoxide (CO) toxicity?What is the pathophysiology of carbon monoxide (CO) toxicity?What are the physiologic mechanisms of carbon monoxide (CO) toxicity?How does carbon monoxide (CO) cause harm to the brain?How is carbon monoxide (CO) eliminated from the body?How does the mortality rate from carbon monoxide (CO) toxicity differ between males and females?What is the incidence of carbon monoxide (CO) toxicity in the US?What is the global incidence of carbon monoxide (CO) toxicity?What are the racial predilections of carbon monoxide (CO) toxicity?How do fatality rates from carbon monoxide (CO) toxicity vary by age?Which risk factors for carbon monoxide (CO) toxicity are related to weather?Why is misdiagnosis of carbon monoxide (CO) toxicity common?What are symptoms of carbon monoxide (CO) toxicity?Which physical findings suggest carbon monoxide (CO) toxicity?Which ophthalmologic findings suggest carbon monoxide (CO) toxicity?Which neurologic findings suggest carbon monoxide (CO) toxicity?What are the causes of carbon monoxide (CO) toxicity?What are the differential diagnoses for Carbon Monoxide Toxicity?How is the clinical diagnosis of acute carbon monoxide (CO) toxicity confirmed?Which findings on arterial blood gas measurements suggest carbon monoxide (CO) toxicity?What are cardiac markers for carbon monoxide (CO) toxicity?What is the role of lab studies in the evaluation of carbon monoxide (CO) toxicity?What is the role of chest radiograph in the evaluation of carbon monoxide (CO) toxicity?What is the role of CT scanning in the evaluation of carbon monoxide (CO) toxicity?What is the role of MRI in the evaluation of carbon monoxide (CO) toxicity?What is the role of electrocardiography in the evaluation of carbon monoxide (CO) toxicity?What is the role of neuropsychologic testing in the evaluation of carbon monoxide (CO) toxicity?What is included in prehospital care for carbon monoxide (CO) toxicity?What is included in emergency department (ED) care for carbon monoxide (CO) toxicity?How can clinicians locate a hyperbaric oxygen center for treatment of a patient with carbon monoxide (CO) toxicity?What is the efficacy of hyperbaric oxygen therapy for treating carbon monoxide (CO) toxicity?When is hyperbaric oxygen therapy indicated for the treatment of carbon monoxide (CO) toxicity?How is hyperbaric oxygen therapy administered for carbon monoxide (CO) toxicity?What are possible complications of hyperbaric oxygen therapy for carbon monoxide (CO) toxicity?What are possible complications of carbon monoxide (CO) toxicity?

Author

Guy N Shochat, MD, Associate Clinical Professor of Emergency Medicine, University of California, San Francisco, School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Lucchesi, MD, Chair, Associate Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH, Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

Disclosure: Nothing to disclose.

Chief Editor

Gil Z Shlamovitz, MD, FACEP, FAMIA, Professor of Clinical Emergency Medicine, Keck School of Medicine of the University of Southern California; Chief Medical Information Officer, Keck Medicine of USC

Disclosure: Nothing to disclose.

Additional Contributors

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Christopher I Doty, MD, MAAEM, FAAEM, FACEP, Tenured Professor of Emergency Medicine, University of Kentucky College of Medicine; Vice Chair of Education, Department of Emergency Medicine, University of Kentucky Chandler Medical Center

Disclosure: Nothing to disclose.

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Disclosure: Nothing to disclose.

Samara Soghoian, MD, MA, Clinical Assistant Professor of Emergency Medicine, New York University School of Medicine, Bellevue Hospital Center

Disclosure: Nothing to disclose.

References

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Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.

Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.

Monoplace hyperbaric chamber. Courtesy JG Benitez, MD, MPH.