Carbon Monoxide Poisoning
1999; Elsevier BV; Volume: 115; Issue: 2 Linguagem: Inglês
10.1378/chest.115.2.322
ISSN1931-3543
Autores Tópico(s)Neonatal Health and Biochemistry
ResumoCarbon monoxide (CO) is an odorless, colorless, and tasteless product of incomplete fuel combustion, whose ubiquitous but silent presence accounts for it being the leading cause of poisoning death in the United States. CO poisoning may account for as many as 5,000 deaths each year in the United States, with an additional 10,000 patients seeking medical attention for toxic exposure.1Hardy KR Thom DR Pathophysiology and treatment of carbon monoxide poisoning.Clin Toxicol. 1994; 32: 613-629Crossref Scopus (163) Google Scholar CO poisoning may be deliberate (as reported in this issue of CHEST [see page 580]) or accidental; in the latter case, it may be acute,2Meigs JW Hughes JPW Acute carbon monoxide poisoning: an analysis of 105 cases.Arch Ind Hyg Occup Med. 1952; 6: 344-356Google Scholar subacute,3Grace TW Platt FW Subacute carbon monoxide poisoning: another great imitator.JAMA. 1981; 246: 1698-1700Crossref PubMed Scopus (68) Google Scholar or chronic.4Stewart RD The effect of carbon monoxide on humans.Ann Rev Pharmacol. 1975; 15: 409-423Crossref PubMed Scopus (121) Google Scholar Accidental CO poisoning at home typically occurs during severe winter months from the use of defective or improperly installed household appliances that operate on combustible fuel (gas, oil, coal, wood, and kerosene).5Howell J Keiffer MP Berger LR Carbon monoxide hazards in rural Alaskan homes.Alaska Med. 1997; 39: 8-11PubMed Google Scholar A second ingredient is poor ventilation due to blocked chimneys, improper venting of appliances, and overzealous home insulation (a vestige of the fuel crisis and harsh winters of the 1970s). CO poisoning from idling automobiles has occurred even with open garage doors or windows, suggesting that passive ventilation may not be adequate to reduce the risk of CO toxicity in semi-enclosed spaces. Poisoning has also occurred in working or living quarters adjacent to garages.6From the Centers for Disease Control and Prevention Deaths from motor vehicle-related unintentional carbon monoxide poisoning: Colorado, 1996, New Mexico, 1980–1995, and United States, 1979–1992.JAMA. 1996; 276: 1942-1943Crossref PubMed Scopus (6) Google Scholar Snow-obstructed motor vehicle exhaust systems may result in outdoor CO poisoning.7Rao R Touger M Gennis P et al.Epidemic of accidental carbon monoxide poisonings caused by snow-obstructed exhaust systems.Ann Emerg Med. 1997; 29: 290-292Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar Accidental CO poisoning can also occur in some unexpected venues: in the tragic case of tennis star Vitas Gerulaitis, in a summer cottage with improper venting of a pool heater into the air conditioning duct8Stout D Man indicted in the death of Gerulaitis.The New York Times. May 23, 1995; : B1Google Scholar; in indoor ice-skating rinks9Carbon monoxide poisoning at an indoor ice arena and bingo hall—Seattle, 1996.JAMA. 1996; 275: 1468-1469Crossref PubMed Google Scholar; outdoors on tractors10Outdoor carbon monoxide poisoning attributed to tractor exhaust—Kentucky, 1997.MMWR. 1997; 46: 1224-1227PubMed Google Scholar and motor boats.11Silvers SM Hampson NB Carbon monoxide poisoning among recreational boaters.JAMA. 1995; 274: 1614-1616Crossref PubMed Google Scholar The symptoms and signs of CO poisoning are varied. Nonspecific symptoms include headache, nausea, vomiting, fatigue, and malaise. Because of the fixed oxygen needs of the circulatory and nervous systems, cardiovascular and neurologic symptoms are common and include symptoms and signs of myocardial ischemia, hypotension, congestive heart failure, arrhythmias, mental confusion, clumsiness, emotional lability, impaired judgment, diminished visual acuity, stupor, and coma. Patients with loss of consciousness are at risk of developing delayed neuropsychiatric symptoms, which vary from mild intellectual impairment or personality changes to specific neurologic deficits such as deafness, blindness, and parkinsonism.12Choic IS Delayed neurologic sequelae in carbon monoxide intoxication.Arch Neurol. 1983; 40: 433-435Crossref PubMed Scopus (466) Google Scholar However, every organ system may be affected either primarily or secondarily to coma (pulmonary aspiration, crush injury with renal insufficiency and peripheral neuropathy). Pathognomic physical findings of flame-shaped retinal hemorrhages or cherry-red skin are specific but not sensitive signs of CO poisoning.3Grace TW Platt FW Subacute carbon monoxide poisoning: another great imitator.JAMA. 1981; 246: 1698-1700Crossref PubMed Scopus (68) Google Scholar Hence, because of the insidious, protean, and often nonspecific manifestations of CO toxicity, a high level of suspicion is needed, particularly when individuals or groups living or working together present with an afebrile influenza-like illness or are found with unconsciousness of uncertain etiology.13Fisher J Rubin KP Occult carbon monoxide poisoning.Arch Intern Med. 1982; 142: 1270-1271Crossref PubMed Scopus (26) Google Scholar,14Kasanof D Could it be carbon monoxide poisoning?.Patient Care. November 15, 1983; : 154-177Google Scholar,15Heckerling PS Leikin JB Maturen A et al.Predictors of occult carbon monoxide poisoning in patients with headache and dizziness.Ann intern Med. 1987; 107: 174-176Crossref PubMed Scopus (59) Google Scholar CO diffuses rapidly across the alveolar membrane and binds reversibly to hemoglobin with a 200-fold greater affinity than oxygen. Hence, exposure to even low concentrations of CO can result in a clinically significant diminution in the oxygen-carrying capacity of the blood. Moreover, the presence of carboxyhemoglobin shifts the oxyhemoglobin dissociation curve to the left; tissue oxygen tension must fall to lower levels before oxygen can be released by oxyhemoglobin. This combined effect of reduced blood oxygen-carrying capacity and impaired release of oxygen at the tissue level results in oxygen starvation more severe than an equivalent reduction in Po2 or hemoglobin. Tissue hypoxia is exacerbated by CO binding to the cytochrome system, myoglobin, guanylate cyclase, nitric oxide synthetase, and endothelial and platelet dysfunction.1Hardy KR Thom DR Pathophysiology and treatment of carbon monoxide poisoning.Clin Toxicol. 1994; 32: 613-629Crossref Scopus (163) Google Scholar The resultant severe tissue hypoxia causes anaerobic metabolism and lactic acidosis. In addition, CNS manifestations may be exacerbated by the release of leukocyte proteases, free radicals, and alterations in excitatory amino acids.1Hardy KR Thom DR Pathophysiology and treatment of carbon monoxide poisoning.Clin Toxicol. 1994; 32: 613-629Crossref Scopus (163) Google Scholar Clinical manifestations of CO poisoning are related to the blood carboxyhemoglobin level, time course of exposure, respiratory rate, age and health of the victim, and concomitant medications (affecting hepatic enzymes) or toxins (drugs, alcohol, etc).1Hardy KR Thom DR Pathophysiology and treatment of carbon monoxide poisoning.Clin Toxicol. 1994; 32: 613-629Crossref Scopus (163) Google Scholar The carboxyhemoglobin level is dependent upon the ambient CO level, which is determined by the source of CO production, meteorologic and climatic factors, size of space, and adequacy of ventilation.4Stewart RD The effect of carbon monoxide on humans.Ann Rev Pharmacol. 1975; 15: 409-423Crossref PubMed Scopus (121) Google Scholar Arterial blood gas measurement reveals metabolic acidosis, a normal Po2, variable Pco2, and decreased oxygen saturation when measured by co-oximetry. Calculated oxygen saturation or that measured via pulse oximetry may be in the normal range. In this issue of CHEST, Vossberg and Skolnick report the changing face of intentional CO poisoning via automobile exhaust due to the presence of a catalytic converter. With the institution of the use of catalytic converters, smog, “freeway” angina due to CO poisoning,16Aronow WS Harris CN Isbell MW et al.Effect of freeway travel on angina pectoris.Ann Intern Med. 1972; 77: 669-676Crossref PubMed Scopus (97) Google Scholar and successful suicides have decreased.17Clarke RV Lester D Toxicity of car exhaust and opportunity for suicide: comparison between Britain and the United States.J Epidemiol Community Health. 1987; 41: 114-120Crossref PubMed Scopus (46) Google Scholar,18Landers D Unsuccessful suicide by carbon monoxide: a secondary benefit of emissions control.West J Med. 1981; 135: 360-363PubMed Google Scholar,19Hays P Bornstein RA Failed suicide attempt by emission gas poisoning.Am J Psychiatry. 1984; 141: 592-593Crossref PubMed Scopus (17) Google Scholar Suicidologists have documented a dramatic decrease in suicide attempts using domestic gas in the United Kingdom between 1963 and 1971, concomitant with the conversion to natural gas with reduced CO content, and a decline in the rate of car exhaust suicides in the United States following the introduction of catalytic converters in the 1960s17Clarke RV Lester D Toxicity of car exhaust and opportunity for suicide: comparison between Britain and the United States.J Epidemiol Community Health. 1987; 41: 114-120Crossref PubMed Scopus (46) Google Scholar; these unfortunate souls want to terminate, not exacerbate, their suffering. However, the syndrome of CO poisoning via automobile exhaust may change further in the future: catalytic converters have been implicated as a significant contributor to global warming.20Wald ML Autos' converters cut smog but add to global warming.The New York Times. May 29, 1998; : A1, A18Google Scholar If the automobile catalytic converter is further modified, so again may be the face of CO poisoning.
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