View clinical trials related to Carbon Monoxide Poisoning.
Filter by:Carbon monoxide (CO) is reported to cause around 30 deaths, 200 admissions and 4000 presentations to Emergency Departments each year in the UK. In the longer term, CO poisoning is recognised to cause persistent neurological problems (including impairments of thinking and behavioural changes), which can develop days to weeks after the initial exposure. However, the incidence of these long-term sequelae is unknown. In addition, there is evidence of long-lasting inflammatory changes in the brain and on-going brain cell injury, although how long this persists is also unknown. Initial assessments of CO exposure can be unreliable if blood tests are not carried out within a relatively short period after the exposure and other biomarkers (such as imaging) are insensitive to detecting previous CO exposure. Certain proteins that are found in brain cells can be detected in the blood of individuals following brain injury and brain cell death. These proteins have been found to be raised in the acute period after minor head injury, persistently raised in patients with a traumatic brain injury and evidence of on going neurodegeneration (i.e. on going brain cell death) and in patients with various types of dementia. The investigators will assess the presence of these proteins in the blood of 50 participants with proven CO exposure in the sub-acute to chronic timescale (2 weeks to 2 years). This has not been done before and will allow assessment of the presence of on going brain injury in these participants. The investigators will also assess cognitive (e.g. memory, attention and speed of thinking) and behavioural impairments in these participants to help characterise the common impairments suffered following CO exposure and relate these to evidence of persistent brain injury and severity of CO exposure.
Previous report showed that 37% of patients with moderate to severe carbon monoxide (CO) poisoning experienced a myocardial injury, defined as elevated cardiac enzyme [creatine kinase, CK-MB, and cardiac troponin I (TnI)] or ischemic electrocardiogram (ECG) change. In other study, 24% of the patients with the myocardial injury after CO poisoning died during a median follow-up of 7.6 years. The myocardial injury was the major predictor of mortality. In addition, in the Taiwanese nationwide population-based cohort study, CO poisoning itself reported as a higher risk of a major adverse cardiovascular event. According to the previous study of investigators, among CO poisoned patients with myocardial injury, 74.4% of patients experienced CO-induced cardiomyopathy. All CO-induced cardiomyopathy recovered to normal status. In this situation, there is no definite approved reason why more cardiovascular events are occurred in CO poisoned patients with myocardial injury during long term follow-up period despite normalization of CO-induced elevated TnI and cardiac dysfunction. Two image cases related to cardiac magnetic resonance imaging (CMR) in acute CO poisoning previously reported. One image case reported that patient had mildly depressed left ventricular (LV) systolic function with hypokinesis of the anterior wall and regional akinesis of the inferior wall on the transthoracic echocardiography performed during hospitalization and late gadolinium-enhancement (LGE) images of CMR demonstrated multiple focal areas of high signal consistent with myocardial necrosis or fibrosis. Another image case reported an image case that in CMR, inferolateral mid-wall myocardial fibrosis, which was defined as LGE, was present despite the setting of a completely normal echocardiogram at 4-month follow-up in CO poisoned patients. Therefore, the investigators evaluate prevalence (frequency of LGE positive) and patterns (involved LV wall and range of LGE positive) of myocardial fibrosis (LGE positive) in acute CO-poisoned patients during acute (within seven days after CO exposure) and chronic phase (at 4-5 months after CO exposure) and whether LGE positive developed in acute phase have been changed through cardiac MRI performed at chronic phase. The investigators also evaluate LV ejection fraction and global longitudinal strain in transthoracic echocardiography performed at the ED (baseline) and within seven days (follow-up). The investigators also assessed the association between neurocognitive outcomes using the global deterioration scale (at 1, 6, and 12 months after CO exposure) and the presence of LGE positive.
In some patients, a few days or weeks after recovery from carbon monoxide poisoning, new symptoms develop. These can affect mood, ability to think or remember clearly, and movements. Some people develop movement problems that are similar to Parkinson's disease. This damage to brain tissue is called "encephalopathy," and this study will look at the effect of pressurized oxygen therapy on long term, or chronic, encephalopathy.
The primary objective of the study is to determine prognostic factors for hospital-mortality following carbon monoxide (CO)-induced coma. The secondary objective is to determine prognostic factors of CO related cognitive sequelae, at the time of hospital discharge.
The aim of the study is to test whether oxygen therapy delivered through high-flow nasal cannula devices in patients admitted to the emergency department for acute carbon monoxide poisoning is superior to the non-rebreathing oxygen face mask therapy with a 15 L/minute oxygen flow (currently the first-line therapy), in terms of reduction of carboxyhemoglobin (COHb) concentration and delayed neurological sequelae incidence.
Suspicions of carbon monoxide poisoning that lead to the treatment of victims are numerous. Measurement of transcutaneous carbon monoxide saturation (SpCO) is a useful diagnostic and triage tool for victims and the toxic threshold is clearly defined for both non-smokers (SpCO> 5%) and smokers ( SpCO> 10%). Currently, the use of e-cigarettes is democratizing. Unfortunately, the threshold for toxic SpCO is not defined for this patient profile. The risk is treating in excess or worse than underestimating carbon monoxide poisoning in e-cigarette users who would be exposed to carbon monoxide exposure.
determination of the half-life of COHb in CO-poisoned patients with high flow nasal oxygen therapy in the ED.
The purpose of the study is to assess device performance in the presence of carbon monoxide.
The purpose of this study is to determine the clinical utility of triage screening for anemia and carbon monoxide poisoning (COP) in the ED setting.This is a prospective, nonrandomized, multi-center study of the performance of simultaneous non-invasive testing for two common disorders (COP and anemia). We will determine the limits of agreement and performance characteristics of non-invasive carboxyhemoglobin (SpCO) and hemoglobin (SpHb) values compared to standard blood tests for measurement of carboxyhemoglobin and hemoglobin, in the emergency department setting.
The purpose of this study is to collect non-invasive observational data in suspected or known carbon monoxide poisoning.