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Smoke inhalation injury results in serious respiratory failure. When smoke inhalation injury is combined with burn injury or pneumonia, the physiological responses are different and more severe than those of smoke inhalation injury alone. Treatment strategies should be planned based on these pathophysiological aspects.
Smoke inhalation injury is one of the primary determinants of survival following major burn injury. The primary site of injury in smoke inhalation appears to be the small airway rather than the alveoli, and thus small airway occlusion caused by edema and pseudomembrane formation are the primary mechanisms of progressive hypoxia. Ventilation-perfusion (VA/Q) alterations after smoke inhalation are characterized by increased blood flow to low VA/Q compartments, although an increase in true shunt (VA/Q = 0) was not a consistent finding. This differs considerably from most adult respiratory distress syndrome (ARDS) patients or oleic acid-induced lung edema models, in which an increase in true shunt is the major mechanism of hypoxia. Such differences lead to different responses to nitric oxide (NO) inhalation therapy, and NO does not improve oxygenation and outcome in patients with smoke inhalation injury. In the treatment of inhalation injury, meticulous removal of pseudomembrane by fiberoptic bronchoscopy is essential, the use of high concentrations of oxygen should be avoided since it can cause absorption atelectasis. High-frequency percussive ventilation is a suitable treatment for inhalation injury, as it improves oxygenation and facilitates removal of pseudomembrane.
Smoke inhalation injury in children still represents a significant cause of pulmonary disease and mortality. Carbon monoxide and other toxic products of combustion are major determinants of severity. Early hypoxemia is a contributor to over 50% of deaths. There are several clinical entities: upper airway obstruction, bronchospasm, consolidation, pulmonary edema, ARDS, and late pneumonia. Intensive care has improved outcome from burns, but pulmonary injury is still an important cause of mortality. New therapies such as high frequency ventilation may improve the outcome. Primary prevention is the most important way to reduce the poor outcome from significant exposure.
Smoke inhalation injury now represents the most frequent cause of death in burn patients, and accounts for 20-80 per cent of overall mortality. We have studied the use of extracorporeal membrane oxygenation (ECMO) to support sheep which have received lethal pulmonary smoke damage. The animals (n = 19) received inhalation injury induced by insufflation with smoke derived from burning cotton delivered with a bee smoker. The treatment group, those placed on ECMO at the time of injury (n=6), were systemically heparinized and placed on a venovenous perfusion circuit consisting of a roller pump, membrane oxygenator and heat exchanger. Blood flow rate in the circuit approximated 20-25 per cent of cardiac output. The animals remained on partial venovenous bypass until the termination of the experiment 96 h after injury. All animals in the treatment group survived. The control sheep (n = 7) received inhalation injury alone and had a 100 per cent mortality (P = 0.0015 ECMO vs. control). Ventilatory management of treatment and control groups followed an identical protocol. We have also studied a third group (n = 6) composed of animals receiving inhalation injury with systemic heparinization but not ECMO. This group had a 66 per cent mortality at 96 h. These studies suggest that partial venovenous ECMO may be a valuable form of adjunctive treatment in severe inhalation injury.
Smoke inhalation injury is a complex of disease processes best understood and treated when defined in terms of the time period after injury. The early phase (0 to 36 hrs) is characterized by diagnosis and treatment of carbon monoxide and cyanide toxicity and by management of early airways edema, bronchorrhea, and bronchoconstriction with aggressive pulmonary toilet. Between 1 and 5 days, the major characteristic is airways mucosal slough, tracheobronchitis, and increasing lung water and impaired gas exchange. Pulmonary toilet and infection control, as well as close management of fluid shifts, is the major treatment. With onset of the inflammation-infection phase, the risk of nosocomial pneumonia increases markedly, as does the impairment in lung function as a result of marked increase in oxygen consumption and CO2 production. Nutrition, stress modification, avoidance of muscle fatigue, and control of infection are the key treatment modalities.
Smoke inhalation injury is responsible for more deaths after fire than actual body burns. Many of the effects of heat and chemical burns to the airways are delayed and may not be clinically evident at first. Chest films are often not helpful, and direct laryngoscopic or bronchofibroscopic examination or a ventilation-perfusion scan may be necessary to verify the diagnosis. Treatment depends on the components involved, with chemically induced airway injury being the most complex to manage. Death rates remain high when inhalation injury is combined with severe body burns.
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Smoke inhalation is a leading cause of death in burns patients. Conventional ventilation cannot always maintain adequate tissue oxygenation. Extracorporeal membrane oxygenation (ECMO) has rarely been used in the treatment of smoke inhalation injuries. ECMO is a proven therapy in severe neonatal respiratory failure and has also been used to good effect in the treatment of children and adults. We report the cases of two children who developed severe respiratory failure refractory to maximal ventilation, one case followed smoke inhalation alone, the other followed smoke inhalation and burns. Pre-ECMO PaO2/FIO2 ratios were 6.5 and 8 kPa, respectively. The patients were treated with veno venous ECMO for 72 and 144 h, respectively. The use of ECMO for respiratory failure due to smoke inhalation and thermal injury is discussed.
A smoke inhalation model was created in 22 adult male sheep with pine smoke inhalation through an endotracheal tube for 6 min. Arterial blood gases, HbCO, HbO2 and pulmonary compliance (Cdyn) were monitored, and the morphology of the tracheobronchial tree and pulmonary parenchyma were studied by light and electron microscopy. Severe carbon monoxide poisoning with fatal levels of HbCO (greater than 50 percent) was found at the end of smoke inhalation. Acute respiratory distress, progressive hypoxemia, decreased pulmonary compliance and increased P(A-a)O2 and Qs/QT occurred after injury. Tracheobronchial blockade by pseudomembrane cast, pulmonary edema, atelectasis and necrosis of pulmonary epithelia were demonstrated pathologically. The mechanisms of CO poisoning and ARF are discussed.
OBJECTIVE: To investigate the influence of N-acetyl-L-cysteine (NAC) on pulmonary injury and oxygen stress caused by smoke inhalation injury. METHODS: Rats inflicted with smoke inhalation injury were employed as the model. WBC in BALF (bronchoalveolar lavage fluid), MPO (myeloperoxidase) activity, hydrogen peroxide (H(2)O(2)) content, GSH (glutathione) content and total antioxidant (TAO) capacity in pulmonary tissue were determined. RESULTS: Postinjury WBC in BALF, MPO activity in pulmonary tissue and H(2)O(2) content decreased obviously after NAC treatment. But the pulmonary tissue contents of GSH and ATO increased evidently after the treatment with NAC. CONCLUSION: NAC treatment could ameliorate pulmonary oxygen stress after smoke inhalation injury. AS a result, the pulmonary antioxidant capacity was improved.
Smoke-inhalation injury may range from lethal effects of entrapment in a burning closed structure to a minor exacerbation of preexisting asthma or bronchitis following a transient whiff of smoke. This article reviews the pathophysiology of smoke-inhalation injury and the clinical pattern of respiratory tract injury. Various diagnostic tools are used to determine the presence and severity of respiratory injury in order to guide management decisions. Despite improved understanding of the pathogenesis of smoke-inhalation injury, there is no proven, specific treatment which offers superior outcomes, and management focuses on the nonspecific effects of smoke inhalation on respiratory function, general support of the patient, and avoidance of iatrogenic problems.
Acute lung injury with smoke inhalation results in significant morbidity and mortality. Previously we have shown that synthetic smoke composed of carbon and acrolein, a common component of smoke, causes delayed-onset noncardiogenic pulmonary edema. To study the possible role of the vasoactive and edemagenic sulfidopeptide leukotrienes (SPLT) in smoke inhalation injury, we measured pulmonary hemodynamics, lung lymph flow, and SPLT and leukotriene (LT) B4 in lung lymph before and after 10 min of synthetic acrolein smoke exposure. After smoke exposure there was a significant rise in pulmonary vascular resistance caused by a rise in pulmonary arterial pressure, a fall in cardiac output, and no change in pulmonary capillary wedge pressure. This was accompanied by an increase in total systemic vascular resistance (P less than 0.05), lung lymph flow (P less than 0.05), and extravascular lung water-to-lung dry weight ratio (P less than 0.05). Both SPLT and LTB4 clearance rose significantly (P less than 0.05), but there was a 10-fold increase in SPLT over LTB4 clearance. In sheep pretreated with FPL55712, a SPLT antagonist, the early rise in pulmonary vascular resistance was attenuated, and the rise in systemic vascular resistance was blocked. This was associated with an attenuated and delayed fall in cardiac output. FPL55712 had no effect on lung lymph flow or extravascular lung water-to-dry weight ratio. SPLT, and especially LTD4, may have a role in increased pulmonary and systemic vascular resistance after smoke inhalation injury but does not appear to affect vascular permeability.
OBJECTIVE: To investigate the changes in the pulmonary surface tension and the tissue content of surfactant substance protein B (SP-B) in rabbits during early post-injury stage after smoke inhalation injury. METHODS: Thirty-two healthy rabbits inflicted with smoke inhalation injury were employed in the study as injury group, and they were sacrificed at 0.5, 2.0, 6.0, 12.0 post injury hours (PIH), with 8 rabbits at each time point. Another 8 rabbits were assigned to normal control group. The pulmonary tissue samples of the rabbits in each group were harvested for the collection of bronchial-alveolar lavage fluid (BALF). The changes in maximal tension (Tmax), minimal tension (Tmin) and hysteresis square (HS) of BALF were measured after the addition of 0.5, 1.0 and 3.0 ml of SP-B antibody into the BALF of the rabbits in each group. The changes in SP-B and SP-B mRNA contents in rabbit pulmonary tissue of each group were assessed with immunohistochemistry and in situ hybridization techniques, respectively. RESULTS: There was no obvious difference in Tmax in BALF of each group or at each time point before and after the action of different concentrations of SP-B antibody in BALF (P > 0.05). But the Tmin in injury group at 2, 6 and 12 PIH was much higher than that before the addition of the antibody (P < 0.05). And the change in HS was similar to that in Tmin. The SP-B content in alveolar type II epithelial cells (AT-II) was decreased significantly at 2, 6 and 12 PIH, whereas the expression in SP-B mRNA exhibited no change. CONCLUSION: There was no obvious change in SP-B synthesis by AT-II in the lung tissue of the rabbits inflicted with smoke inhalation injury during early post injury stage. The increase of SP-B secretion from AT-II cells might be beneficial to the early protection of pulmonary tissue of the rabbits with smoke inhalation injury.
OBJECTIVE: To observe the rule of the change of apoptosis and proliferation of pulmonary tissue cells in rats with inhalation injury, so as to explore the significance of apoptosis in the repairing process of pulmonary tissue injury. METHODS: Smoke inhalation injury model was established in rats. The rats were randomly divided into normal control (NC) and smoke inhalation injury (SI) groups. TUNEL and immunohistochemistry methods were employed to determine the changes in cellular apoptotic and proliferating cell nuclear antigen (PCNA) indices of the pulmonary tissue at different postburn time points. RESULTS: (1) The apoptotic index increased at 2 postburn hours (PBHs) and remained at high levels thereafter. (2) The PCNA index increased at 12 PBHs, reaching top level at 3 postburn days (PBDs), remaining kept at relativly high level later. CONCLUSION: Apoptosis not only played roles in the early pulmonary injury after smoke inhalation injury, but also participated in the repair and modification of the proliferated tissue during later reconstruction.
Smoke inhalation is a significant comorbid factor in thermal trauma. The effect of inhaled nitric oxide (NO) on smoke inhalation injury was evaluated in an ovine model. Following smoke exposure, group 1 animals (n = 9) spontaneously breathed room air, and group 2 animals (n = 8) breathed 20 parts per million of NO in air for 48 hours. Cardiopulmonary variables and blood gases were serially measured; bronchoalveolar lavage (BAL) was performed and wet-to-dry lung weight ratios (W/D) determined at 48 hours. Pulmonary vasoconstriction following smoke inhalation was significantly attenuated by inhaled NO (p < 0.05), which exerted no apparent effect on the systemic circulation. In group 2, the serial decline in pulmonary oxygenation was less than in group 1, consistent with a smaller physiologic shunt (p < 0.05). There were no significant differences in W/D, lung compliance, BAL fluid analysis results, or histologic evaluation findings between the two groups. These results suggest that inhaled NO exerted beneficial effects on pulmonary arterial hypertension and oxygenation following smoke inhalation without apparent amelioration of airway inflammation.
In this study we examined the role of inducible nitric oxide synthase (iNOS) in acute respiratory distress syndrome (ARDS) in sheep with severe combined burn and smoke inhalation injury. BBS-2, a potent and highly selective iNOS dimerization inhibitor, was used to exclude effects on the endothelial and neuronal NOS isoforms. Seven days after surgical recovery, sheep were given a burn (40% of total body surface, 3rd degree) and insufflated with cotton smoke (48 breaths, < 40 degrees C) under anesthesia. BBS-2 was provided by constant infusion at 100 microg/kg/hour, beginning 1 hour after injury. During 48 hours, control sheep developed multiple signs of ARDS. These included decreased pulmonary gas exchange, increased pulmonary edema, abnormal lung compliance, and extensive airway obstruction. These pathologies were associated with a large increase in tracheal blood flow and elevated plasma NO2-/NO3- (NOx) levels. These variables were all stable in sham animals. Treatment of injured sheep with BBS-2 attenuated the increases in tracheal blood flow and plasma NOx levels, and significantly attenuated all the pulmonary pathologies that were noted. The results provide definitive evidence that iNOS is a key mediator of pulmonary pathology in sheep with ARDS resulting from combined burn and smoke inhalation injury.
Inhalation of chemical and particulate products of smoke is one of the principal determinant of mortality following burn injury. Inflammatory responses have been implicated in the pathogenesis of lung injury after smoke inhalation. In the current study, we tested the inhibitory effect of Fucoidin on the neutrophil rolling stage of inflammatory response and determined the degree of pulmonary injury. Fifteen rats were divided into three groups: sham group (N: 5) of rats inhaled room air; control group (N: 5) inhaled smoke, and experimental group inhaled smoke and received Fucoidin. All the rats were sacrificed 24h after smoke inhalation. The trachea and lungs were removed totally; samples for histopathological and biochemical (myeloperoxidase (MPO)) analysis were taken from each lung and trachea. Morphologic studies using light and electron microscopes showed a decrease in lung parenchymal and tracheoepithelial injury in the experiment group of rats. Also, biochemical analysis of tissue MPO was significantly lower in test group than in control group. These results suggest that the inhibition of neutrophil rolling leads to a reduction of neutrophil invasion to pulmonary parenchyma and trachea, which may be beneficial for attenuating neutrophil mediated inhalation injury.
Following the use of a rabbit smoke inhalation injury model established in this institute, there were marked reductions in elastase activities in neutrophils and alveolar macrophages; rapid increases in elastase activity in broncho-alveolar lavage fluid (BALF); reductions of serum trypsin inhibitory capacity; a decrease of Pao2 and an increase of PaCO2, and marked increases of lung water volume. Significant correlations were found between the increased extravascular lung water content and the rising elastase activity in BALF. It seems probable that the imbalance between elastase and antiprotease played an important role in the development of acute lung injury after smoke inhalation.