View clinical trials related to Carbon Monoxide Poisoning.
Filter by:Carbon monoxide (CO) poisoning is a condition that occurs as a result of inhaling carbon monoxide gas and can potentially lead to serious health issues. The treatment of CO poisoning requires urgent medical intervention. Methods used in the treatment of CO poisoning include normobaric oxygen (oxygen at normal pressure), high-flow oxygen, non-invasive continuous positive airway pressure (CPAP), and hyperbaric oxygen therapy. Studies on these methods are available in the literature.
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 goal of this pilot, clinical, experimental, biological and prospective study with uso of biological material (venous blood sampling), in patient with acute carbon monoxide (CO) intoxication and in a group of healthy non-intoxicated subject (group of control) is the research of a possible increase of circulating microparticles level in human blood with an acute carbon monoxide intoxication. The main question to answer is: Is there an increase of circulating microparticles levels in subjects with acute carbon monoxide poisoning? Two blood samples will be withdrawn from patients with acute carbon monoxide poisoning, one before and one after hyperbaric oxygen treatment. Researchers will compare a group of healthy volunteers to see if there is a different in circulating microparticles blood level compared to patients with intoxication.
Neurological complications after acute carbon monoxide (CO) poisoning can range from transient headache or dizziness to cognitive dysfunction, seizure, permanent anoxic brain damages or death. A recent study reported that a lack of standard pupillary light reflex (sPLR), assessed using a pen light, was a predictor of 30-day neurological sequelae in patients with CO poisoning. Given that the basic sPLR has a poor inter-rater reliability, more objective and quantitative methods are required in the assessment of PLR. An automated pupillometer has been used in the intensive care unit to quantitatively assess the PLR. Therefore, we hypothesized that quantitative assessment of PLR might be associated with neurocognitive sequelae after acute CO poisoning. The purpose of this study was to assess the value of quantitative pupillary reactivity (NPi and qPLR) in comparison to that of sPLR in predicting neurocognitive outcome at 1 month after acute CO poisoning.
Mitochondrial and oxidative stress participate in the pathogenic mechanisms of carbon monoxide (CO)-induced toxicity. Thus, serum indicators of mitochondrial and oxidative stress could be useful for predicting neurocognitive prognosis of post-CO poisoning. This prospective observational study of consecutive patients requiring hyperbaric oxygen therapy (HBO2) for acute CO poisoning measured serum biomarkers of mitochondrial (growth differentiation factor 15 [GDF15]; fibroblast growth factor 21 [FGF21]) and oxidative (8-Oxo-2'-deoxyguanosine [8-OHdG] and malondialdehyde [MDA]) stresses at arrival at the emergency department (0 h), and at 24 h and 7 days after HBO2 completion. We evaluated neurocognitive outcomes using the Global Deterioration Scale (GDS; favorable [1-3 points] or poor [4-7 points] outcomes).
This randomized trial will investigate important neurocognitive clinical outcomes of patients with acute severe carbon monoxide poisoning (ASCOP) randomized to receive either therapeutic hypothermia or normothermia combined with hyperbaric oxygen therapy (HBO).
The purpose of this study is to access the clinical characteristics and risk factors for neurological sequelae after acute carbon monoxide poisoning.
To observe the effect of different fresh flows (1 L / min and 4 L / min) on the carboxyhemoglobin level non-invasively and continuous measurement and to determine the contribution of smoking to the intraoperative carbon monoxide accumulation.
Hyperbaric oxygen therapy (HBO2) is recommended for symptomatic patients within 24 h of carbon monoxide (CO) poisoning. However, previous major studies found significantly better outcomes with HBO2 in patients treated within 6 h. Currently, there is no consensus on a CO poisoning-to-HBO2 interval that would not be beneficial. Therefore, the investigators aimed to evaluate the difference in therapeutic effect depending on the poisoning-to-HBO2 interval after CO exposure in patients with acute CO poisoning who received HBO2 within 24 h. The investigators compared the neurocognitive outcomes of patients according to HBO2 time intervals based on the outcomes of patients treated within 6 h (control group) with propensity score matching using the CO poisoning registry of our hospital.
This prospective cohort study enrolls subjects who experience carbon monoxide (CO) poisoning. The purpose of the study is to evaluate therapeutic effects of various treatments and short and long-term outcomes in CO poisoned patients. In addition, complications of brain and heart susceptible to CO are investigated through various ways and the association between complications and the patient's prognosis is also investigated. All subjects will be regularly monitored by physicians participating in this study.