AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Background

Carbon monoxide (CO) is colorless, odorless, tasteless, and highly poisonous. It is the most frequent agent of toxic exposure in North America. In 2002, United States poison centers received CO-related calls at a rate of 54.5 calls per million persons. Each year, approximately 40,000-50,000 visits to emergency departments involve documented exposure to CO, and about 500 people per year die from accidental exposure. As many as 34% of fatal injuries in children and adolescents younger than 16 years may be due to CO poisoning.

CO is produced from the incomplete combustion of organic matter, including fossil fuels. People who smoke cigarettes may have baseline levels of carboxyhemoglobin (HbCO or COHB) as high as 10%, and their susceptibility to toxic effects from inadvertent exposure to other sources of CO may be heightened. Toxic exposures to CO are most frequently the result of house fires or the use of fuel-burning heating appliances or poorly maintained generators. Intentional poisoning is far more often fatal than accidental exposure. According to the Centers for Disease Control and Prevention (CDC), suicide involving exhaust pipes are responsible for 2000 deaths a year in the United States alone.

CO intoxication may also result from inhaling methylene chloride, a volatile liquid found in degreasers, solvents, and paint removers. Most of the adsorbed vapors are exhaled unchanged, but up to one third is metabolized in the liver to CO. Because tissues can store methylene chloride, its gradual release and metabolism elevates CO levels more than twice as long as direct CO inhalation does. Prolonged exposure to methylene chloride (up to 8 h) can produce CO levels higher than 8%.

Acute CO toxicity may cause asphyxia, myocardial dysfunction, and a full spectrum of peripheral and CNS effects. Symptoms are generally nonspecific and protean. Therefore, if a history of exposure is not given or suspected, this disease is extremely difficult to diagnose. In fact, CO toxicity is frequently misdiagnosed as a simple headache or viral syndrome. A high index of suspicion must be maintained, particularly during the winter months, when faulty heating systems and enclosed spaces make CO poisoning more common than it is at other times.

Pathophysiology

CO exerts its toxic effects by means of a combination of tissue asphyxia and inflammatory activity. Hypoxia occurs from 3 primary mechanisms: CO diminishes the oxygen carrying capability of hemoglobin, it decreases the uptake of bound oxygen into tissues, and it impairs the mechanisms of cellular respiration.

CO readily crosses capillary membranes in the lungs and binds the heme moiety on the erythrocyte hemoglobin complex with an affinity 200-300 times greater than that of oxygen. This binding drastically decreases binding spots available for oxygen transport. The amount of oxygen bound to hemoglobin in the setting of CO exposure is proportional to the partial pressure of oxygen (PO₂) in respired air and can be increased by giving supplemental O₂.

CO also shifts the oxyhemoglobin dissociation curve to the left, inhibiting the release of bound oxygen to tissues. In addition, approximately 10-15% of absorbed CO binds to extravascular proteins. CO dissolved in plasma is known to cross capillary membranes and bind myoglobin, reduced cytochromes, guanylate cyclase, and nitric oxide (NO) synthase. This process decreases the number of binding sites available for oxygen in select tissues, further contributing to hypoxia. The interplay of all these effects causes tissues exposed to CO to have an oxygen tension lower than that due to simple hypoxia alone. Because of the high affinity of CO for hemoglobin, even low ambient levels of CO can lead to clinically significant toxicity over long exposures.

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, instead of making water and adenosine triphosphate (ATP), the mitochondria make destructive oxygen free radicals.

Tissue hypoxia and oxidative stress account for most of the pernicious effects of CO in the body. Hypoxic stress in patients with CO poisoning is increased because of its effects on mitochondrial electron transport and cellular respiration. Although the acutely toxic effects of CO are primarily due to hypoxia, activation of inflammatory processes plays a major role in CO poisoning, particularly in the development of neurologic damage.

Inflammatory and immune-mediated mechanisms contribute to the development of the systemic inflammatory response syndrome (SIRS) and delayed neurologic sequelae (DNS). Animal models demonstrated that CO causes perivascular changes in the CNS that cause neutrophil sequestration and activation in the brain. Reactive oxygen species released by these cells then cause brain lipid peroxidation. Byproducts of peroxidation alter myelin basic protein (MBP) in the presence of CO, altering immunologic recognition of MBP and starting a cascade of autoimmune activity against cerebral proteins.

Frequency

United States

Estimates of the frequency of CO exposure vary widely. The scope of the problem is difficult to assess because patients with CO mild exposures may not seek medical attention and because CO poisoning is frequently misdiagnosed. The CDC estimates that 15,200 people per year were treated in US emergency rooms for accidental, non–fire-related CO exposures in 2001-2002. Most exposures occur during the winter months.

Mortality/Morbidity

Approximately 480 accidental deaths and 2000 suicides per year are due to CO poisoning in the United States.

• Certain groups are more susceptible than others to the toxic effects of CO. Morbidity and mortality risks are increased in fetuses; infants; young children; people older than 65 years; people who smoke; and patients with heart disease, pulmonary disease, or anemia.
• In 1 study, 37% of patients treated for moderate-to-severe CO poisoning with hyperbaric oxygen therapy nonetheless had acute myocardial injury (ECG changes and/or elevated biomarkers). Patients were relatively young (mean age 47.2 y), and rates of previous cardiovascular disease were low (6.5% for previous myocardial infarction, 2.6% for previous revascularization procedure, and 3% for a history of congestive heart failure [CHF]). About 38% of patients with acute myocardial infarction after CO poisoning died (24% overall) at a median follow-up of 7.6 years.
• Over one half of patients with severe CO poisoning develop encephalopathy within a month of injury.

Race

All races are equally susceptible to the physiologic effects of CO poisoning, but non–English-speaking immigrants and minority racial groups are at increased risk of accidental exposure.

• For example, the unintentional death rate related to CO is 20% higher among African Americans than Caucasians.
• The difference is primarily due to economic disparities among racial and ethnic groups in the United States. Members of economically disadvantaged social groups are most likely to be involved in house fires, to have malfunctioning or no CO detectors in the home, to have faulty indoor heating systems, and to work in high-risk settings.

Sex

CDC analysis of data from the National Vital Statistics Program and National Electronic Injury Surveillance System All Injury Statistics for 2001-2003 showed that male individuals and female individuals were equally likely to seek care in the emergency department for accidental, non–fire-related CO exposure and poisoning. However, male individuals were 2.7 times more likely than female individuals to die from CO toxicity, with a case fatality rate increased by 2.3 times (where the rate was defined as the number of CO deaths divided by the sum of CO exposures X 100). Reasons for this discrepancy are not clear.

Age

The very young and very old are most susceptible to both exposure and the pernicious effects of CO.

• The CDC reports that, in the United States in 2001-2003, children younger than 4 years had the highest incidence of accidental CO exposure but the lowest death rates from CO poisoning.
• In the CDC report (2005), the risk of death from CO poisoning increased with age. The case fatality rate for CO was 0.6% for children younger than 4 years, increasing to 5.5% in adults aged 55-64 years. In 2001-2003, 23% of all deaths from CO poisoning occurred in adults older than 65 years.
• Human and animal data suggest that CO is both teratogenic and highly associated with fetal death. Neonates and in utero fetuses are most vulnerable to CO poisoning, for a number of reasons. Fetal hemoglobin binds CO with greater affinity than does adult forms, resulting in increased tissue hypoxia at similar HbCO levels. The fetus also has a low baseline PO₂, and levels of HbCO at equilibration are 10-15% higher than maternal levels.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

History

CO has been called the great imitator because of the protean symptoms it produces. As a result, CO poisoning is frequently misdiagnosed.

• Patients may complain of any number of vague symptoms. In 1 series, headache was the most frequent complaint (37.5%), followed by dizziness (18%), nausea (17.3%), loss of consciousness (7.7%), shortness of breath (6.7%), and loss of muscle control (3.5%).
• Symptoms may be attributed to a viral syndrome, migraine or tension headache, anxiety attack, hyperventilation syndrome, or a nonspecific illness.
• Unless the patient is brought in from the scene of a fire, a high index of suspicion must be maintained to make the diagnosis. An important clue is the finding of similar complaints among people who work or live together, particularly during the winter months, when heaters are on and when windows tend to be closed.
• Anyone working with combustion engines or combustible gasses indoors should be considered to be at high risk. CO poisoning should also be considered in patients presenting with vague somatic complaints after a natural disaster, when generator use is common.
• If CO poisoning is suspected or diagnosed, attempt to determine the source, the duration of exposure, the amount of time elapsed since the patient was withdrawn from the source, and the occurrence of any neurologic symptoms (eg, syncope, seizure, altered mental status, vertigo, focal neurologic deficits).

Physical

Although burns, singed facial hair, and oropharyngeal soot clearly suggest CO exposure, physical findings specific to CO poisoning are few.

• The classic cherry-red skin and retinal discoloration is seen only with the most severe cases of CO poisoning, and it is generally a postmortem finding. The skin is most likely to be pale, cyanotic, or mottled because of hypoxia and cardiac depression.
• Bright red retinal veins are a relatively sensitive and early but often overlooked finding in moderate-to-severe cases of CO poisoning. Ophthalmic examination may demonstrate flame-shaped retinal hemorrhages or papilledema.
• CO causes myocardial depression and dysrhythmias. Animal models suggest that shock, if present, is more likely due to vasodilation.
• Vital signs may reflect tachypnea, hypoxia, tachycardia, hypotension or hypertension, and mild hyperthermia. Pulse oximetry may remain in the normal range despite cyanosis and tissue hypoxia because the wavelengths produced by HbCO and oxyhemoglobin are read similarly by these machines. CO poisoning typically produces a pulse oximetry gap (the difference between the pulse oximeter reading and the spectrophotometrically measured oxyhemoglobin saturation).
• Rales may be a sign of noncardiogenic pulmonary edema.
• Neurologic and neuropsychologic symptoms frequently occur in the setting of acute CO toxicity and are the most frequent long-term consequence of poisoning. Severe cases of CO poisoning are often characterized by serious neurologic abnormalities including low Glasgow Coma Scale (GCS) scores and seizures.
• Overall, memory disturbances, including both anterograde and retrograde amnesia, are the most common neurologic abnormalities. Other signs include lethargy, stupor, coma, gait disturbance, movement disorders, apraxia, agnosia, tics, vestibular dysfunction, hearing and visual loss, rigidity, brisk reflexes, emotional lability, frank psychosis, and impaired judgment and cognitive function.

Causes

CO is produced by the incomplete combustion of organic matter and fuels (gas, oil, wood, charcoal). Therefore, fires are the major sources of exposure and toxicity.

• In 2004, the Consumer Product Safety Commission reported that about 64% of deaths from unintentional CO poisoning were due to exposures in the home.
• The most common cause of accidental, non–fire-related CO exposure is malfunctioning household heating appliances used in poorly ventilated rooms.
• The incidence of CO poisoning increases after environmental disasters in which heating and electrical systems are destroyed. For example, after hurricanes Katrina and Rita in 2005, 78 cases of nonfatal CO poisoning and 10 deaths were reported in affected counties in Alabama and Texas. Nearly all cases were due to gasoline-powered back-up generators being run outside but near the home's air conditioner, through which CO was drawn into the home.
• Workers with a high risk of exposure to CO include forklift operators, attendants of underground parking garages, and mechanics.
• Open-air exposure leading to CO toxicity is not uncommon among motor boat enthusiasts, and it has been reported in children riding in the back of pick-up trucks.
• Fatal CO poisonings due to cooking fumes are reported among climbers and polar explorers. An experimental study in Norway showed that a kerosene camping stove used inside a closed tent for 2 hours raised ambient CO levels enough to cause a mean HbCO level of 21.5% and clinically significant hypoxia in healthy volunteers.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Migraine
Vascular headache
Anxiety
Altered mental status
Stroke
Meningitis
Alcohol intoxication
Drug abuse
Drug overdose
Psychiatric conditions (eg, delirium, acute psychosis)
Acute chest syndrome
Pulmonary embolism
Cardiac arrhythmia
Viral syndrome
Acute abdomen
Sepsis
Shock lung
Cyanide toxicity
Hyperventilation Syndrome

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Lab Studies

• Arterial blood gas analysis with co-oximetry
• • The cornerstone of diagnosis is measurement of the HbCO level. However, levels are not correlated with extent of exposure, with the symptoms, or with morbidity and mortality. HbCO levels in the normal or undetectable range to do rule out exposure or poisoning.
  • Handheld, noninvasive monitors have been tested and appear to be generally accurate. Most measurements done in the hospital setting are based on direct spectrophotometric measurement of HbCO by using specific blood gas analyzers. Venous samples are adequate since venous HbCO accurately reflects arterial levels.
  • Infants with persistent fetal hemoglobin may have falsely elevated HbCO measurements. Fetal hemoglobin may remain as high as 30% of total hemoglobin at the age of 3 months.
  • The PO₂ should remain normal after CO exposure. However, oxygen saturation may be falsely elevated if it is calculated from the PO₂, as is common with many blood gas analyzers, rather than directly measured.
  • Arterial blood gases are also used to assess the patient's acid-base status and help in guiding resuscitation efforts. Lactate and base deficit may be correlated with duration of exposure and resultant cellular hypoxia. However, the authors know of no studies conducted to examine their prognostic values.
  • Unexplained metabolic acidosis suggests cyanide exposure. Measurement of methemoglobin levels is also indicated in the setting of cyanosis with a low oxygen saturation but normal PO₂.
• The CBC should be obtained to evaluate the hemoglobin level. Anemia further reduces total arterial oxygen content.
• A complete metabolic panel allows the clinician to calculate the anion gap in patients with acidosis and to assess renal function in moderate-to-severe cases that may be complicated by rhabdomyolysis.
• Urinalysis (UA) and a serum creatine kinase (CK) determination should be ordered to assess the extent of muscular damage and to rule out rhabdomyolysis.
• In addition to basic laboratory tests, cardiac enzyme measurements should be performed when patients have chest pain, risk factors for AMI, or notable CO exposures. The incidence of ischemic cardiac insult after CO poisoning is high, even in young, healthy patients.
• Baseline coagulation parameters should be evaluated in severely poisoned patients at risk for SIRS with multiorgan failure (MOF) and disseminated intravascular coagulation (DIC).
• Measurement of the ethanol level and urine toxicologic screening may be useful in ruling out other causes of altered mental status.

Imaging Studies

• Chest radiography
• • Patients with evidence of hypoxia or any respiratory embarrassment should undergo chest radiography to evaluate for other causes of respiratory impairment.
  • Changes, such as a ground-glass appearance, perihilar haze, peribronchial cuffing, and intra-alveolar edema, imply a worsened prognosis.
• CT scanning
• • Head CT may demonstrate hypoattenuation of the globus pallidus and white matter within hours of CO poisoning.
  • Positive CT findings are generally predictive of neurologic complications.
• MRI: MRI is more sensitive than CT but difficult to perform on an emergency basis. Neither CT nor MRI findings are specific for CO poisoning.
• Positron emission tomography (PET) and/or single photon emission CT (SPECT): These are the most sensitive tests for ischemic brain injury, but the findings are nonspecific, and the studies even more difficult to obtain than MRI.

Other Tests

• ECG should be performed in all patients with notable exposures or with risk factors for AMI.
• Sinus tachycardia is the most common abnormality. Arrhythmias may occur secondary to hypoxia, ischemia, or infarction.
• Acute myocardial infarction may occur, even with low levels of CO exposure in patients with cardiovascular disease. Myocardial infarction is common among patients with moderate-to-severe CO poisoning.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Medical Care

• Prehospital Care
• • Patients should immediately be removed from the source of exposure and given supplemental high-flow oxygen by means of nonrebreather face mask.
  • Patients should be kept calm and still to avoid exertion. Increased oxygen demand exacerbates symptoms.
  • Comatose patients and patients with severely altered mental status should be intubated for airway protection.
  • Cardiac monitoring should be started as soon as possible because of the high incidence of dysrhythmias and cardiac arrest.
  • If possible, emergency medical system (EMS) personnel should try to estimate the total time of exposure and the time elapsed since the patient was removed from the source.
• Emergency department care
• • As always, attention to the A, B, C, D of resuscitation is the mainstay of emergency care for the patient with CO intoxication.
  • Obtunded, comatose, or severely hypoxic patients should be intubated for airway protection.
  • All patients with suspected or confirmed CO exposure should be given on 100% oxygen until they are asymptomatic and when HbCO levels are below at least 10%.
  • Cardiac monitoring should be started immediately, and a 12-lead ECG should be performed as soon as possible.
  • Pulse oximetry readings may be falsely elevated in the setting of HbCO because light absorption is nearly identical for HbCO and oxyhemoglobin. Arterial blood gas analysis with co-oximetry should be done to directly measure the HbCO level, to determine the degree of hypoxia, and to monitor the patient's acid-base status.
  • The half-life of HbCO is about 320 minutes (5.3 h) while the person is breathing room air. This decreases to 30-90 minutes with 100% oxygen, which decreases to 15-23 minutes at 2.5-2.8 atm with 100% oxygen. These numbers can be used to estimate the duration of treatment for particular patients.
  • If mild symptoms do not resolve or if severe symptoms are present, hyperbaric oxygen therapy should be strongly considered.
  • Hyperbaric therapy should also be strongly considered for pregnant patients because CO readily crosses the placenta, and fetal hemoglobin has greater affinity for CO than does normal hemoglobin.
  • Caution should be exercised in treating acidosis because low pH shifts the oxyhemoglobin dissociation curve to the right, increasing oxygen uploading to tissues. Acidosis should improve with oxygenation. Cyanide poisoning should be suspected in cases of severe or recalcitrant acidosis. If concomitant cyanide and CO toxicity is suspected, treat the patient with sodium thiosulfate alone. The methemoglobinemia produced by amyl nitrite also shifts the oxyhemoglobin curve to the left, worsening hypoxia at the tissue level.

Consultations

• Consultation for hyperbaric oxygen therapy may be warranted.
• • Good evidence suggests that hyperbaric oxygen therapy does improve long-term neurologic outcome (Weaver, 1996; Juurlink, 2005). If the patient has any mental status changes or a history of neurologic impairment, an immediate consultation for hyperbaric oxygen treatment should be made. This may require transport to another center after the patient's condition is stabilized.
  • Although the utility of hyperbaric oxygen therapy in preventing mortality from CO poisoning is still debated, it is now the standard of care for moderate-to-severe CO poisoning for patients with neurologic impairment, acidosis, severe hypoxia, myocardial dysfunction or SIRS; for pregnant patients with symptomatic poisoning; and for pregnant patients with asymptomatic poisoning with HbCO levels of more than 15%.
  • The nearest hyperbaric oxygen center can be located by calling the Divers Alert Network (DAN) at 1-800-446-2671 or 1-919-684-2948, Mon-Fri, 9am-5pm (Eastern time) or 1-919-684-2948 (nonemergency medical questions) or 1-919-684-8111 (emergencies).
• Patients with moderate-to-severe cases should be admitted to a medical intensive care unit.
• A cardiologist should be consulted when patients have evidence of cardiac compromise.
• A neurologist should be consulted at least for patient follow-up because delayed neurologic symptoms are relatively common.

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients should be admitted to the hospital if they have persistent mild symptoms, if they have any history of neurologic impairment (syncope, seizure, amnesia, unresponsiveness) after exposure, if they have risk factors for or evidence of acute coronary syndrome (ACS), or if admission is needed for other reasons.
• • Most patients requiring admission should be monitored in a telemetry or intensive care setting.
  • Asymptomatic pregnant patients may not require admission, but they should be observed for a period of fetal monitoring.
• Admitted patients should be watched for development of the following syndromes:
• • Rhabdomyolysis
  • Acute respiratory distress syndrome (ARDS)
  • Disseminated intravascular coagulation
  • SIRS and/or MOF
  • Acute tubular necrosis (ATN)
  • Interval CO syndrome, including leukoencephalopathy of the subcortical white matter with ischemic damage to basal ganglia and hippocampus
• Although severe CO poisoning may result in any of the postinjury syndromes listed above, patients with concomitant trauma, burns, intoxication, inhalation injury, or serious premorbid illness are at increased risk.

Further Outpatient Care

• Asymptomatic patients with HbCO levels less 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.
• Follow-up must be ensured because delayed sequelae are relatively common.
• • All discharged patients must be warned that some patients with no symptoms and low CO levels may still have interval CO injury. Delayed neurologic symptoms are possible as long as 1 month after the initial exposure.
  • Improvement of neurologic function with hyperbaric oxygen therapy given as long as 20 days after injury has been reported.

Transfer

• Patients may need to be transferred for hyperbaric oxygen therapy.
• Indications are as listed in Consultations above.

Deterrence/Prevention

• Rates of both intentional and accidental CO poisoning have declined precipitously in the United States since the enactment of improved vehicle-emissions policies in the 1970s.
• Accidental CO exposure in the home is by far the most commonly reported cause of poisoning. Important precautions include the following:
• • CO detectors with audible alarms should be installed in all homes, and the batteries should be changed regularly.
  • Before one buys a CO alarm, check to ensure it is listed with Underwriter's Laboratories (UL) standard 2034 for Single and Multiple Station Carbon Monoxide Detectors, or check the package or owner's manual to ensure that the detector and alarm meets the requirements of the International Approval Services (IAS) 6-96 standard.
  • CO detectors and alarms are also available for boats and recreational vehicles. The Recreation Vehicle Industry Association requires CO detectors and alarms to be installed in motor homes and in recreational vehicles that have or that are outfitted for a generator.
  • All fuel-burning appliances should be properly installed, maintained, and operated. A qualified technician should inspect furnaces, water heaters, and gas pipes each year. Fireplace chimneys and flues should also be cleaned and checked yearly.
  • Unvented fuel-burning space heaters should be used only if someone is awake to monitor them and only if windows or doors are slightly opened to allow for ventilation of the space.
  • Automobile exhaust systems should be inspected regularly for defects, and tailpipes should be examined for blockages (which are especially common in the winter, when snow may accumulate and become impacted in them).
  • Vehicles or fuel-burning appliances should never be left running in an enclosed space or outside an open window where exhaust can be drawn into an enclosed space.
  • Never use a charcoal grill, hibachi, lantern, or camp stove inside a tent or camper.

Prognosis

• Variations in clinical severity, laboratory values, and outcomes all limit prognostic accuracy.
• Cardiac arrest, coma, metabolic acidosis, and extremely high HbCO levels are associated with poor outcomes.
• CT abnormalities are associated with persistent neurologic impairment.

Patient Education

• Patients who smoke should be counseled to avoid smoking for 1-2 weeks after exposure because additional CO from tobacco smoke may increase risk of toxicity and sequelae.
• Although exercise increases hypoxic stress in patients with acute CO poisoning, exposure to CO alone is not an indication for bed rest.
• See the National Capital Poison Center Web site.
• See the American Association of Poison Control Centers Web site.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to diagnose CO poisoning, and potentially allowing the patient to return to a source of toxic exposure, is the primary pitfall of care.
• Failure to explain the risk of delayed neurologic problems, even in cases of apparently mild or asymptomatic exposure, may be an issue.
• Failure to transfer a patient with moderate-to-severe CO poisoning or a history of neurologic impairment after exposure may be considered failure to meet the standard of care, even if the utility of hyperbaric oxygen therapy is controversial.

Special Concerns

• Particular caution must be exercised when one treats a pregnant patient with potential CO exposure. Although the mother may appear well, the developing fetus is at risk for hypoxia, even with nontoxic maternal HbCO levels.
• CO shifts the oxygen-hemoglobin dissociation curve to the left. The oxyhemoglobin dissociation curve lies even further to the left in fetuses compared with the curve for normal adult hemoglobin. In addition, fetal hemoglobin binds CO with more avidity that adult hemoglobin does, and normal PO₂ is lower in the fetal circulation than in adult circulation. These factors all make the fetus more vulnerable to hypoxia than children and adults.
• 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 wash-out with room air. Maternal supplementation with 100% normobaric oxygen reduces the half-life to 3-4 hours. The half-life of fetal HbCO during hyperbaric oxygen treatment is not known.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Sep 19, 2006