Carbon monoxide poisoning: A new incidence for an old disease

Center for Hyperbaric Medicine, Section of Pulmonary and Critical Care Medicine, Virginia Mason Medical Center, Seattle, Washington, USA.
Undersea & hyperbaric medicine: journal of the Undersea and Hyperbaric Medical Society, Inc (Impact Factor: 0.77). 05/2007; 34(3):163-8.
Source: PubMed


While carbon monoxide (CO) poisoning is common in the USA, its incidence is uncertain. Fatal poisonings are counted with relative accuracy from death certificate data, but estimates of the more common nonfatal poisonings are either old or limited. This study was performed to estimate the number of emergency department (ED) visits annually in the USA for carbon monoxide poisoning.
ED visit rates in five states (Idaho, Maine, Montana, Utah, and Washington) from three prior studies, each using different methodology, were used to extrapolate independent estimates of national ED visits.
After correcting for regional differences in CO poisoning incidence, estimates of national ED visits per year ranging from 32,413 to 56,037 were obtained. Excluding the estimate derived from the Maine rate because it did not include intentional and fire-related poisonings, the national average is 50,558 +/- 4,843 visits per year.
There are approximately 50,000 ED visits for CO poisoning in the USA annually, 3-5 times the numbers previously estimated. As this disease can result in significant long-term morbidity even when treated, enhanced prevention efforts are warranted.

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    • "These two large series suggest that it is reasonable to use 70–85% as an estimate for the frequency of CO exposures in the US that are nonfatal and accidental, and 60–78% for the frequency of nonfatal, accidental and non-fire related. If 70% is applied to the 50,000 ED visit estimate above (Hampson and Weaver, 2007), a number of 35,000 accidental, non-fire ED visits for CO exposure annually is achieved. This is of similar magnitude as the CDC estimate of 20,626 visits for this category (Centers for Disease Control and Prevention, 2008). "
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    ABSTRACT: Carbon monoxide (CO) poisoning is common in the United States, accounting for hundreds of deaths and thousands of emergency department visits annually. It is believed that most accidental CO poisoning is preventable through public education, warning labels on consumer products, and uniform use of residential CO alarms. However, cost effectiveness of these prevention strategies has not been demonstrated in the United States to date. It was the objective of this study to estimate societal cost of accidental CO poisoning and evaluate the cost-effectiveness of universal installation of residential CO alarms.
    Full-text · Article · Dec 2015
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    • "Carbon monoxide (CO), an odorless, tasteless, and colorless gas, is the second most common environmental pollutant after carbon dioxide. The annual death rate for accidental CO poisoning still ranges from approximately 50 in the United Kingdom to 2700 cases in the United States (Walker and Hay, 1999; Hampson and Weaver, 2007; Gallego et al., 2009). Neurologic sequelae, including the acute brain damage and the delayed encephalopathy, are the most serious complication after CO poisoning. "
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    ABSTRACT: Carbon monoxide (CO) intoxication is one of the most common types of poisoning worldwide, and may result in neuropathologic sequelae, yet its pathogenesis is not clear and there is no optimal management strategy for patients with CO poisoning. In this study, the rat model of CO poisoning was established in a hyperbaric chamber by CO exposure. Rats were administered orally N-Butylphthalide (NBP) at a dose of 1ml/100g. Neuronal apoptosis was assessed by TUNEL stain and flow cytometry. The expressions of neurite outgrowth inhibitor (Nogo), myelin-associated glycoprotein (MAG) and Nogo receptor-1 (NgR1) were observed in rat brain tissue by immunohistochemistry and double immunofluorescence staining. As we expected, CO poisoning could start the mechanism of apoptosis. The number of apoptotic cells and the early neuronal apoptosis percentage (EAR) were significantly increased at 1 day, 3 day after CO exposure. NBP treatment obviously reduce neuronal apoptosis and the EAR (P<0.05). CO poisoning could induce Nogo, MAG and NgR1 expressions. The increased Nogo, MAG and NgR1 proteins were still observed at 4 week after CO poisoning. NBP could significantly reduce the levels of Nogo and NgR1 proteins. Then we suspected that the expressions of Nogo, MAG and NGR1 proteins might be associated with brain injury and demyelination induced by CO poisoning. NBP might inhibit neuronal apoptosis and the EAR, down-regulate the expressions of Nogo and NgR1 proteins (but not MAG), and play a neuro-protective role in brain damage after acute CO poisoning. Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.
    Preview · Article · Feb 2015
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    • "Carbon monoxide (CO) poisoning is one of the most frequent intoxications around the globe, accounting for more than one half of fatal poisonings reported in many countries [1], and more than 50,000 emergency department (ED) visits per year in the US [2]. The transient duration of symptoms in mild intoxication, the ubiquitous and often occult nature of exposure as well as the high frequency of misdiagnosis represent substantial challenges for quantifying the true incidence of CO poisoning. "
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    ABSTRACT: OBJECTIVE: Aim of this study was to assess the role of blood lactate levels at admission in carbon monoxide (CO)-poisoned patients for establishing severity of poisoning and short term prognosis. METHOD: All cases of CO poisoning visited in the emergency department during the years 2012 and 2013 were retrieved from the hospital database. The concentration of COHb and lactate was assessed in arterial blood in all patients with suspected CO poisoning, along with the plasma concentration of troponin I (TnI). The control population for TnI results consisted in 125 blood donors. RESULTS: Twenty three (61%) out of 38 CO-poisoned patients underwent hyperbaric oxygen (HBO) treatment, and 10 (26%) were admitted to a hospital ward. A significant correlation was found between lactate and COHb (r=0.54; p<0.001), and between lactate and TnI (r=0.44; p=0.001). A significant correlation was also found between COHb and TnI (r=0.38; p=0.020). Blood lactate levels were higher in patients treated with HBO and hospital admission. In multivariate analysis, none of the parameters was associated with HBO treatment, whereas increased value of blood lactate (p=0.036) was the only significant predictor of hospital admission. Twenty five (66%) patients had detectable TnI levels compared to 13% controls (p<0.001), whereas 16% CO-poisoned patients had TnI levels >99th percentile compared to 2% controls (p=0.003). The odds ratio for detectable TnI and TnI >99th percentile in CO-poisoned patients were 13.1 (p<0.001) and 7.6 (p=0.006), respectively. CONCLUSION: Initial blood lactate level may be useful for risk stratification of CO-poisoned patients, especially for predicting hospitalization.
    Full-text · Article · Sep 2014 · Clinical Biochemistry
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