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Smoke inhalation

About: Smoke inhalation is a research topic. Over the lifetime, 913 publications have been published within this topic receiving 19909 citations. The topic is also known as: smoke inhalation.


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Journal ArticleDOI
TL;DR: In this paper, the specific effects of inhalation injury and pneumonia on mortality in burn patients were assessed and a multiple logistic equation was developed to estimate expected mortality at any age and burn size for patients without either inhaling injury or pneumonia.
Abstract: In order to assess the specific effects of inhalation injury and pneumonia on mortality in burn patients, the records of 1058 patients treated at a single institution over a five-year period, 1980-1984, were reviewed. Of these patients, 373 (35%) had inhalation injury diagnosed by bronchoscopy and/or ventilation perfusion lung scan. Of the 373 patients, 141 (38%) had subsequent pneumonia. Among the patients without inhalation injury, pneumonia occurred in 60 of 685 (8.8%). A multiple logistic equation was developed to estimate expected mortality at any age and burn size for patients without either inhalation injury or pneumonia, with either alone, or with both. Subtraction of the expected mortality without either inhalation injury or pneumonia from the expected mortality in the presence of either or both permitted the estimation of additional mortality attributable to these complications. Inhalation injury alone increased mortality by a maximum of 20% and pneumonia by a maximum of 40%, with a maximum increase of approximately 60% when both were present. The influence on mortality was maximal in the midrange of expected mortality without these complications for any age group. These data indicate that inhalation injury and pneumonia have significant, independent, additive effects on burn mortality and that these effects vary with age and burn size in a predictable manner.

534 citations

Journal ArticleDOI
TL;DR: In this paper, the authors measured cyanide concentrations in blood samples obtained at the scene of residential fires from 109 fire victims before they received any treatment, and compared the results with those in 114 persons with drug intoxication (40 subjects), carbon monoxide intoxication (29 subjects), or trauma (45 subjects).
Abstract: Background The nature of the toxic gases that cause death from smoke inhalation is not known. In addition to carbon monoxide, hydrogen cyanide may be responsible, but its role is uncertain, because blood cyanide concentrations are often measured only long after exposure. Methods We measured cyanide concentrations in blood samples obtained at the scene of residential fires from 109 fire victims before they received any treatment. We compared the results with those in 114 persons with drug intoxication (40 subjects), carbon monoxide intoxication (29 subjects), or trauma (45 subjects). The metabolic effect of smoke inhalation was assessed by measuring plasma lactate at the time of admission to the hospital in 39 patients who did not have severe burns. Results. The mean (±SD) blood cyanide concentrations in the 66 surviving fire victims (21.6±36.4 μmol per liter, P<0.001) and the 43 victims who died (116.4±89.6 μmol per liter, P<0.001) were significantly higher than those in the 114 control subjects (5.0±5.5 ...

395 citations

Journal Article
TL;DR: As the desirable change to clean fuels is unlikely, efforts have been made to use efficient, vented wood or coal stoves, with varied success due to inconsistent acceptance by the community.
Abstract: Domestic pollution is relevant to health because people spend most of their time indoors. One half of the world's population is exposed to high concentrations of solid fuel smoke (biomass and coal) that are produced by inefficient open fires, mainly in the rural areas of developing countries. Concentrations of particulate matter in kitchens increase to the range of milligrams per cubic meter during cooking. Solid fuel smoke possesses the majority of the toxins found in tobacco smoke and has also been associated with a variety of diseases, such as chronic obstructive pulmonary disease in women, acute respiratory infection in children and lung cancer in women (if exposed to coal smoke). Other tobacco smoke-associated diseases, such as tuberculosis, asthma, respiratory tract cancer and interstitial lung diseases, may also be associated with solid fuel smoke inhalation, but evidence is limited. As the desirable change to clean fuels is unlikely, efforts have been made to use efficient, vented wood or coal stoves, with varied success due to inconsistent acceptance by the community.

293 citations

Journal ArticleDOI
TL;DR: It is reported that a combination of aerosolized heparin and a mucolytic agent, N-acetylcystine, can ameliorate cast formation and reduce pulmonary failure secondary to smoke inhalation and a significant decrease in incidence of reintubation for progressive pulmonary failure and a reduction in mortality.
Abstract: Smoke-inhalation injury causes a destruction of the ciliated epithelium that lines the tracheobronchial tree. Casts produced from these cells, polymorphonuclear leukocytes and mucus, can cause upper-airway obstruction, contributing to pulmonary failure. We have reported that a combination of aerosolized heparin and a mucolytic agent, N-acetylcystine [corrected], can ameliorate cast formation and reduce pulmonary failure secondary to smoke inhalation. In this study, 90 consecutive pediatric patients between 1985 and 1995 who had bronchoscopically diagnosed inhalation injury requiring ventilatory support were studied. Forty-three children admitted between 1985 and 1989 acted as controls. Forty-seven children admitted between 1990 and 1994 received 5000 units of heparin and 3 ml of a 20% solution of N-acetylcystine [corrected] aerosolized every 4 hours the first 7 days after the injury. All patients were extubated when they were able to maintain spontaneously a PaO2/FIO2 ratio of more than 400. The number of patients requiring reintubation for successive pulmonary failure was recorded, as was mortality. The results indicate a significant decrease in reintubation rates, in incidence of atelectasis, and in mortality for patients treated with the regimen of heparin and N-acetylcystine [corrected] when compared with controls. Heparin/N-acetylcystine [corrected] nebulization in children with massive burn injury and smoke-inhalation injury results in a significant decrease in incidence of reintubation for progressive pulmonary failure and a reduction in mortality.

204 citations

Journal ArticleDOI
TL;DR: Progress in mortality from inhalation injury are mostly due to widespread improvements in critical care rather than focused interventions for smoke inhalation, particularly as related to carbon monoxide and cyanide.
Abstract: Lung injury resulting from inhalation of smoke or chemical products of combustion continues to be associated with significant morbidity and mortality. Combined with cutaneous burns, inhalation injury increases fluid resuscitation requirements, incidence of pulmonary complications and overall mortality of thermal injury. While many products and techniques have been developed to manage cutaneous thermal trauma, relatively few diagnosis-specific therapeutic options have been identified for patients with inhalation injury. Several factors explain slower progress for improvement in management of patients with inhalation injury. Inhalation injury is a more complex clinical problem. Burned cutaneous tissue may be excised and replaced with skin grafts. Injured pulmonary tissue must be protected from secondary injury due to resuscitation, mechanical ventilation and infection while host repair mechanisms receive appropriate support. Many of the consequences of smoke inhalation result from an inflammatory response involving mediators whose number and role remain incompletely understood despite improved tools for processing of clinical material. Improvements in mortality from inhalation injury are mostly due to widespread improvements in critical care rather than focused interventions for smoke inhalation. Morbidity associated with inhalation injury is produced by heat exposure and inhaled toxins. Management of toxin exposure in smoke inhalation remains controversial, particularly as related to carbon monoxide and cyanide. Hyperbaric oxygen treatment has been evaluated in multiple trials to manage neurologic sequelae of carbon monoxide exposure. Unfortunately, data to date do not support application of hyperbaric oxygen in this population outside the context of clinical trials. Cyanide is another toxin produced by combustion of natural or synthetic materials. A number of antidote strategies have been evaluated to address tissue hypoxia associated with cyanide exposure. Data from European centers supports application of specific antidotes for cyanide toxicity. Consistent international support for this therapy is lacking. Even diagnostic criteria are not consistently applied though bronchoscopy is one diagnostic and therapeutic tool. Medical strategies under investigation for specific treatment of smoke inhalation include beta-agonists, pulmonary blood flow modifiers, anticoagulants and antiinflammatory strategies. Until the value of these and other approaches is confirmed, however, the clinical approach to inhalation injury is supportive.

203 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20241
202313
202223
202120
202029
201919