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Smoke Inhalation Injury clinical trials

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NCT ID: NCT05886998 Recruiting - Acute Lung Injury Clinical Trials

Nebulized Heparin for Prevention of Acute Lung Injury in Smoke Inhalation Injury

Start date: November 1, 2021
Phase: Phase 3
Study type: Interventional

This study aims to examine the value of nebulized heparin for prevention of acute lung injury in adult patients suffering smoke inhalation injury. Patients will be randomized to receive nebulized heparin or an equal volume of normal saline for 14 days and the incidence of acute lung injury will be compared in either group.

NCT ID: NCT03834246 Recruiting - Morality Clinical Trials

Smoke Inhalation Injury in Patients Admitted to Intensive Care

fumeintox
Start date: October 16, 2018
Phase:
Study type: Observational

Many Studies have shown that the smoke-inhalation injury is responsible for a high mortality mainly related to the systemic effects of carbon monoxide and cyanide. Respiratory lesions induced by smoke inhalation, is one of predictive factors of mortality. The aim of the study is to identify the clinical and epidemiological characteristics of smoke-inhalation injury and to identify prognostic factors among these patients .

NCT ID: NCT01386788 Recruiting - Clinical trials for Smoke Inhalation Patients

European Survey: Risk of Cyanide Poisoning in Smoke Inhalation

RISK
Start date: April 2009
Phase: N/A
Study type: Observational

Cyanide poisoning is commonly viewed as a rare but dramatic event, occurring in industrial or laboratory settings as the result of accidental releases of hydrogen cyanide (HCN) gas (e.g. in the case of fire) or salts in the case of suicide attempts. In fact, cyanide poisoning is considerably more common than is generally appreciated. Multiple clinical and post-mortem studies have demonstrated that HCN contributes to the toxicity of fire smoke. Cyanide acts primarily through its strong affinity for the iron-containing heme moiety, binding to numerous critical enzyme systems in the body and rendering them inactive. Of late, increasing attention has been paid to the relationship of cyanide and nitric oxide. The interactions appear to be complex, with cyanide inducing nitric oxide production by binding to N-methyl-D-aspartate (NMDA) receptors, as well as binding to nitric oxide synthase. The latter may be overcome by the presence of nitric oxide synthase inhibitors. Probably, the majority of the cyanide poisoning cases are due to smoke inhalation in closed-space fires. So far, there are no clear data available on the prevalence of cyanide poisoning in smoke inhalation. This information would be of great interest for all emergency physicians since a proven or supposed cyanide poisoning does not only requires an intensive supportive care, including the administration of supplemental oxygen and artificial ventilation, blood pressure support, and anticonvulsants, but also a rapid administration of a cyanide antidote. Therefore, it is the goal of this survey to assess the prevalence of cyanide poisoning in smoke inhalation victims. Only the data of patients with a cyanide measurement before specific antidote treatment will be included