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      Inhalation injury: epidemiology, pathology, treatment strategies

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          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.

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          Hyperbaric oxygen for acute carbon monoxide poisoning.

          Patients with acute carbon monoxide poisoning commonly have cognitive sequelae. We conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. We randomly assigned patients with symptomatic acute carbon monoxide poisoning in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after carbon monoxide poisoning. The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in each group. Cognitive sequelae at six weeks were less frequent in the hyperbaric-oxygen group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.007), even after adjustment for cerebellar dysfunction and for stratification variables (adjusted odds ratio, 0.45 [95 percent confidence interval, 0.22 to 0.92]; P=0.03). The presence of cerebellar dysfunction before treatment was associated with the occurrence of cognitive sequelae (odds ratio, 5.71 [95 percent confidence interval, 1.69 to 19.31]; P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.03). Cognitive sequelae were less frequent in the hyperbaric-oxygen group at 12 months, according to the intention-to-treat analysis (P=0.04). Three hyperbaric-oxygen treatments within a 24-hour period appeared to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning. Copyright 2002 Massachusetts Medical Society
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            Clinical practice. Carbon monoxide poisoning.

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              Delayed neurologic sequelae in carbon monoxide intoxication.

              Of 2,360 victims of acute carbon monoxide intoxication examined between 1976 and 1981, delayed neurologic sequelae were diagnosed in 65 (2.75% of the total group, 11.8% of those admitted). There were 25 men and 40 women. Ages ranged from 34 to 80 years (mean, 56.1 years), with the peak incidence in the sixth and seventh decades. The lucid interval before appearance of neurologic sequelae varied from two to 40 days (mean, 22.4 days). The most frequent symptoms were mental deterioration, urinary or fecal incontinence, gait disturbance, and mutism; the most frequent signs were masked face, glabella sign, grasp reflex, increased muscle tone, short-step gait, and retropulsion. There were no important contributory factors except age and the severity of anoxia. Previous associated disease did not hasten the development of sequelae. Of 36 patients followed up for two years, 27 (75%) recovered within one year.
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                Author and article information

                Contributors
                Journal
                Scand J Trauma Resusc Emerg Med
                Scand J Trauma Resusc Emerg Med
                Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
                BioMed Central
                1757-7241
                2013
                19 April 2013
                : 21
                : 31
                Affiliations
                [1 ]Department of Surgery, Regions Hospital, 640 Jackson Street, St. Paul, MN, 55101, USA
                [2 ]The Burn Center, Regions Hospital, 640 Jackson Street, St. Paul, MN, 55101, USA
                Article
                1757-7241-21-31
                10.1186/1757-7241-21-31
                3653783
                23597126
                a7a4c76b-0417-476d-935e-824d1e8150db
                Copyright ©2013 Dries and Endorf; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 November 2012
                : 11 April 2013
                Categories
                Review

                Emergency medicine & Trauma
                smoke inhalation,burns,carbon monoxide,cyanide,bronchoscopy
                Emergency medicine & Trauma
                smoke inhalation, burns, carbon monoxide, cyanide, bronchoscopy

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