View clinical trials related to Carbon Monoxide Poisoning.
Filter by:Carbon monoxide (CO) poisoning results in high morbidity and mortality worldwide. CO is described as a "silent killer" because CO is colorless, odorless, and tasteless but highly toxic. The diagnosis of acute CO poisoning depends on the history of exposure to a source of fire in a closed space along with the clinical and laboratory findings. The pathophysiology of CO poisoning is not fully understood; however, it is proved that CO induces hypoxia by forming carboxyhemoglobin (COHb) and shifting the oxygen dissociation curve to the left. The molecular mechanisms of CO poisoning include oxidative injury through the generation of free radicals. In addition, oxygen therapy might enhance the reactive oxygen species (ROS) production and result in reperfusion injury. Free radicals could induce a serious impact on vital organs, including the heart, and brain. L-Carnitine is an endogenous mitochondrial constituent that contributes to normal mitochondrial activities. L-Carnitine is an antioxidant with potent ROS scavenging ability. ROS-mediated pathology of CO suggests that antioxidants are potentially useful agents in the alleviation of CO toxicity. Thus, the current study will investigate the therapeutic efficacy of L-Carnitine in improving the prognosis of acute CO poisoning. The current clinical trial will include patients with moderate and severe acute carbon monoxide poisoning according to Poisoning Severity Score.
The purpose of this study is to access the clinical characteristics and risk factors for neurological sequelae after acute carbon monoxide poisoning.
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.