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Carbon Monoxide Toxicity in Older Adults

Citation

Annals of Long-Term Care: Clinical Care and Aging. 2015;23(4):35-38.

Authors

Ijeoma M. Muo, MD, MPH 1; Steven R. Gambert, MD, MACP, AGSF 2

Affiliations: 1Department of Medicine, Division of Gerontology and Geriatric Medicine, University of Maryland School of Medicine, Baltimore, MD 2University of Maryland Medical Center and GRECC, Baltimore VA Medical Center, Baltimore, MD

Abstract: There is a scarcity of research that specifically examines acute carbon monoxide (CO) toxicity in the elderly, however, prevalence may be underestimated in this group. CO toxicity is associated with acute myocardial injury, which may lead to chest pain, myocardial infarction, arrhythmias, or congestive heart failure, and in cases of chronic exposure, neurologic damage is possible. The primary goal of treatment is prevention of neurocognitive sequelae. The presenting symptoms of CO toxicity can easily be misdiagnosed, with deleterious effects. Clinicians must maintain a high index of suspicion for CO toxicity in older adults who present with influenza-like symptoms, myocardial infarction, syncope, and mental status changes, particularly during the winter months. In this article, the authors present the case of an older adult presenting with signs of CO exposure after falling unconscious in his home immediately following his discharge from a prior hospitalization and rehabilitation for syncope.

Key words: Carbon monoxide, toxicity, hyperbaric oxygen, myocardial injury.
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Acute carbon monoxide (CO) toxicity is among the leading causes of poisoning deaths in the United States.1 Toxicity from this colorless, odorless gas can result from accidental or intentional exposure to gas from stoves, faulty furnaces, fires, and from operation of vehicles and gas generators in poorly ventilated areas. The high utilization of indoor generators and stoves in response to power outages from natural disasters has often proven deadly due to increased opportunity for accidental CO exposure.2 Poisoning from CO exposure occurs most commonly in the colder months, often in the home, and tends to affect younger adults, children, and women with greater frequency. However, its true prevalence is not known and is generally considered to be underestimated across all age groups. Particularly in the elderly, for whom many of the principal symptoms of CO poisoning are nonspecific and can mimic those of other chronic geriatric illnesses, maintaining an index of suspicion for CO toxicity is crucial to avoid a potentially dangerous misdiagnosis. This article presents the case of an octogenarian who was hospitalized for CO toxicity, followed by a brief review and a supplementary tip sheet to guide clinicians in diagnosing CO toxicity in the elderly.

Case Report

An 80-year-old man was admitted to the hospital within hours after being found unconscious in his home. He had returned home that morning from inpatient rehabilitation at a long-term care facility following hospital admission for syncope earlier that month. His son found him unconscious on the floor of his bedroom; an odor of natural gas was present in the bedroom. Emergency medical services were called, and a CO reading upon their arrival showed an atmospheric level of 350 parts per million. The patient was placed on high-flow oxygen via a non-rebreather mask, and an improvement in his mental status was noted. On awakening, the patient reported shortness of breath, but denied chest pain or headache.

Upon admission to the hospital, the patient showed no signs of acute distress. His vital signs were within normal ranges except for a labile systolic blood pressure, which ranged from 140 to 190 mm Hg. He was noted to have kept poor records of his medical history. He had clinical signs of congestive heart failure; no focal neurologic deficits were detected. His laboratory test showed a carboxyhemoglobin (COHb) level of 27.7%. The remainder of his diagnostic evaluation is shown in Table 1. Acute CO intoxication was diagnosed, and he was started on hyperbaric oxygen therapy (HBO). In addition, he was resumed on home medications and was given diuretics for his congestive heart failure and cardiomyopathy.

table 1

Less than 1 month prior, the patient had been hospitalized for a syncopal episode. On admission, he had exhibited vomiting, lethargy, and slurred speech, and he had a blood pressure of 190/104 mm Hg. Contrast tomography of the head found no acute intracranial abnormality. His serum troponin was elevated at 0.65 ng/mL, and an echocardiogram (ECG) showed a reduced ejection fraction of 20%; there was no prior ECG for comparison. The patient’s prior medical history was significant for hypertension, atrial fibrillation, congestive heart failure of unknown duration, and prior craniotomy for a subdural hematoma. He had a remote history of cigarette use but did not drink alcohol or use any illicit drugs. He underwent a cardiac catheterization that revealed clean coronary arteries and no renal artery stenosis. He was treated for presumed hypertensive encephalopathy, with a diagnosis of cardiomyopathy of unknown etiology, before being discharged to the rehabilitation facility.

Our patient remained on treatment for his cardiomyopathy. His CO toxicity was determined to be due to a faulty furnace in his bedroom. He likely had experienced prior exposure to CO, leading to his previous admission for syncope, and CO exposure may even have contributed to his non-ischemic cardiomyopathy. For definitive confirmation, however, one would have needed access to an ECG done prior to his two most recent hospitalizations for comparison, something that unfortunately was not available. The patient was discharged to a rehabilitation facility where he would remain while awaiting repair of the faulty furnace in his home.

Discussion

Cases of unintentional CO poisoning have been noted to occur with greater frequency during the winter (ie, between the months of November and February),3 with the majority occurring in the home.1,3 In the United States, prevalence is higher in the Midwest and Northeast,1 presumably due to the greater utilization of furnaces in colder months. A Centers for Disease Control and Prevention (CDC) study of data from 2000 to 2009 found the incidence of CO poisoning in adults aged 65 years and older to be 6.2 persons per 1 million of US population, compared to children aged 17 years and younger at 25.7, adults aged 18 to 44 years at 19.4, and adults aged 45 to 64 at 11.4.1 However, the data collected represented only a fraction of the total annual recorded hospitalizations from CO exposure. As such, the overall prevalence of acute CO intoxication is thought to be underestimated, potentially more so in the elderly.1 Minimal data exist that specifically examine the presentation and prognosis of CO toxicity in the elderly. The currently available data in young and middle-age adults portray a grim picture of the acute and chronic effects of CO poisoning. One can postulate that CO poisoning may have even more deleterious effects in older adults, who tend to have more comorbidities and lower immunologic reserves than younger adults.

CO toxicity is likely underrecognized or misdiagnosed in older adults in large part because the signs and symptoms of CO toxicity (ie, nausea, dizziness, palpitations, chest pain, syncope, headache, seizures3) are frequently nonspecific and can mimic those of many other types of chronic or acute illnesses seen in the older adult population, including influenza and cognitive syndromes. Refer to Table 2 for a sample of the possible signs and symptoms of CO toxicity. However, chronic exposure to moderate or high levels of CO over time has been linked to an increased risk of heart disease.4-6 Conversely, individuals with chronic heart disease, anemia, or respiratory problems are at greater risk for CO exposure–related toxicity than are healthy individuals.4 Hence, providers must have a high index of suspicion for CO toxicity, particularly in older adults, to avoid the potential life-threatening pitfalls of misdiagnosis. Additionally, prompt identification of CO exposure could also save the lives of individuals who reside with the patient.

table 2

Identification of Acute Carbon Monoxide Poisoning

Acute CO toxicity is marked by tissue ischemia. Physical examination may reveal sinus tachycardia, tachypnea, and focal neurologic deficits. Pulse oximetry is usually normal, as pulse oximeters do not detect COHb levels, the byproduct of CO binding to hemoglobin. A normal COHb level in the blood is 1% to 3% of total hemoglobin; acute CO toxicity is diagnosed when COHb levels are 3% or greater in nonsmokers and 10% or greater in smokers.8 The levels of COHb, however, correlate poorly with the clinical presentation.9 At the same time, higher COHb levels correlate positively with increased risk of acute myocardial injury on presentation.5

CO combines with hemoglobin with an affinity that is more than 300 times greater than with oxygen.6  The binding of CO to hemoglobin results in a leftward shift in the hemoglobin-oxygen dissociation curve and an inability of oxygen to bind to hemoglobin. This leads to tissue hypoxia, particularly in the heart, muscle, and brain, which rely heavily on oxidative phosphorylation. The combination of hypoxia and reduced oxidative phosphorylation may result in lactic acidosis.6 In the heart, CO poisoning can cause an acute myocardial injury leading to chest pain, myocardial infarction (MI), arrhythmias, or congestive heart failure.6 Physicians have missed diagnosing CO toxicity in older adults who present with unstable angina and have treated the patients only for acute MI.10 CO toxicity may also result in transient cardiomyopathy in younger to middle-age adults without any underlying coronary artery disease or spasms.5 The ECG may be normal or may show sinus tachycardia and signs of ischemic changes.6

Acute CO toxicity has also been associated with cognitive impairments in young healthy adults. But adults older than age 50 appear to be more vulnerable to the neurologic effects of acute CO exposure than are younger adults.11 Neuropsychiatric tests in these individuals show impaired memory and inability to retain new information, inattention, and altered visuospatial skills.12

Identification of Chronic Carbon Monoxide Poisoning

Chronic effects of CO poisoning can occur either as sequelae from acute exposure or from repeated unknown exposures. Both short- and long-term mortality outcomes are significantly reduced in individuals with myocardial injury resulting from CO intoxication.13 Blood hyperviscosity from CO poisoning is thought to be one mechanism for the higher incidence of myocardial injury in exposed patients.14 Individuals with CO toxicity and acute myocardial injury may have elevated white blood cell counts, creatine kinase (CK)-MB, pro–brain-type natriuretic peptide levels, and troponin levels.5 The prognostic value of increased troponin levels on mortality has been shown in noncardiac surgical settings.15,16

In addition to the increased long-term mortality and cardiac injury, another common chronic effect of CO toxicity is neurologic damage. Symptoms usually present within 6 weeks after exposure and are marked by parkinsonism and evidence of frontal lobe dysfunction.11 Individuals with chronic CO exposure who develop neurologic sequelae are more likely than those without neurologic sequelae to be admitted to the hospital with altered mental status, to have radiologic findings of hypoxic brain injury, and to have elevated CK, metabolic acidosis, and lactate dehydrogenase levels on laboratory testing.17 Sensorineural hearing loss is another rare, chronic neurologic effect that may result from CO toxicity.18 For a list of the signs and symptoms that should alert clinicians to CO toxicity, refer to Table 2. Refer to the supplementary tip sheet for additional information on identifying and diagnosing CO toxicity in newly admitted long-term care residents.

Management of Carbon Monoxide Toxicity

In patients who present with acute CO poisoning, clinicians must also consider toxicity from other substances such as cyanide and ethanol. Polysubstance toxicity can affect the clinical picture and management of CO poisoning.4 Hyperbaric oxygen is typically used to treat toxicity from CO exposure, however, normobaric oxygen can be used when HBO is not available. No clinical guidelines exist to guide patient selection for HBO. In most treatment centers, HBO is administered when COHb levels exceed 10% in asymptomatic patients with suspected exposure. HBO is also given to patients who have been exposed to CO but whose COHb levels are less than 10% and who present with suggestive symptoms, or who have an abnormal ECG or evidence of focal neurologic deficits.19

When HBO is used, three series of treatments are usually administered within a 24-hour period. The oxygen in the HBO displaces CO from the hemoglobin binding site, allowing the displaced CO to be exhaled. The estimated average half-life of COHb in individuals treated with HBO is 74 minutes, which is independent of age, underlying pulmonary disease, smoking status, or degree of mental status change on admission.20 The primary goal of treatment with HBO is prevention of neurocognitive sequelae,21 however, a Cochrane database review failed to show a superiority of HBO over normobaric oxygen for this treatment goal.22

Conclusion

Clinicians can easily set upon a path of incorrect diagnostic work-up in an older patient whose presenting symptoms are from CO poisoning. Clinicians must maintain a high index of suspicion for CO toxicity in older adults who present with influenza-like symptoms, MI, syncope, and mental status changes, particularly during the winter months. Patients who are misdiagnosed and treated for the wrong condition are at risk of continued re-exposure and/or death if the presence of CO toxicity has been missed. Importantly, an accurate diagnosis of CO toxicity may not only save the life of the patient, but also the lives of those with whom the patient resides.

References

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15.   van Waes JA, Nathoe HM, de Graaff JC, et al. Myocardial injury after noncardiac surgery and its association with short-term mortality. Circulation. 2013;127(23):
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16.   Devereaux PJ, Chan MT, Alonso-Coello P, et al; Vascular Events In Noncardiac Surgery Patients Cohort Evaluation (VISION) Study Investigators. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery [published correction appears in JAMA. 2012;307(24):2590]. JAMA. 2012;307(21):2295-2304.

17.   Kudo K, Otsuka K, Yagi J, et al. Predictors for delayed encephalopathy following acute carbon monoxide poisoning. BMC Emerg Med. 2014;14:3.

18.   Mehrparvar AH, Davari MH, Mollasadeghi A, et al. Hearing loss due to carbon monoxide poisoning. Case Rep Otolaryngol. 2013;2013:940187.

19.   Hampson NB, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med. 1995;13(2):227-231.

20.   Weaver LK, Howe S, Hopkins R, Chan KJ. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest. 2000;117(3):801-808.

21.   Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347(14):1057-1067.

22.   Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011;(4):CD002041.


Disclosures: The authors report no relevant financial relationships.

Address correspondence to: Steven R. Gambert, MD, University of Maryland Medical Center, N3E09, 22 S. Greene Street, Baltimore, MD 21201; sgambert@medicine.umaryland.edu

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