Publication: Perfil clínico de pacientes con sospecha de síndrome de inhalación ingresados en una unidad de grandes quemados
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2016-07-07
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Universidad Complutense de Madrid
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Abstract
El síndrome de daño de la vía aérea por inhalación de humo consiste en la inspiración de gases calientes o vapor, así como de tóxicos que son a menudo productos incompletos que se producen en la combustión. Se produce por varios mecanismos: daño térmico de la vía aérea superior, afectación de las vías respiratorias inferiores y el parénquima pulmonar y toxicidad sistémica por intoxicación por monóxido de carbono o cianuros. La gravedad del daño por inhalación depende de si el fuego se produce en un ambiente cerrado, de la fuente de ignición, de la temperatura, la concentración y la solubilidad de los gases tóxicos generados. La incidencia de inhalación varía del 0.3-43% (13-18% de los ancianos con quemaduras graves). La diferencia de incidencia radica en una clara definición del síndrome de inhalación, y en considerar a paciente sólo con sospecha o a aquellos con confirmación diagnóstica. Es frecuente la aparición de síndrome de inhalación cuando la quemadura se produce por llama (en el 17% de los casos según la American Burn Association, ABA). El tratamiento del síndrome de inhalación es fundamentalmente de soporte, con control de la vía aérea, no existiendo un tratamiento específico. El síndrome de inhalación se asocia con mayor mortalidad y con peor pronóstico...
Inhalation injury may describe pulmonary trauma caused by inhalation of thermal or chemical irritants. Anatomically, injuries are divided into three classes: 1) Heat injury which is restricted to upper airway structures except in the case of steam jet exposure. Injury to these airway structures may cause massive swelling of the tongue, epiglottis, and aryeepiglottic folds with obstruction. Severity of obstruction may occur from time after inhalation. 2) Local chemical irritation throughout the respiratory tract. Most substances when are burned, generate material toxic to the respiratory tract. Smoke-related toxins damage epithelial and capillary endothelial cells of the airway. Histologic changes resemble tracheobronchitis. Mucociliary transport is destroyed and bacterial clearance reduced. Alveolar collapse and atelectasis occur due to surfactant loss. Alveolar macrophages are stressed leading to inflammatory response with chemotaxins. Early inflammatory changes occurring in the airway are followed by a period of diffuse exudate formation. Bronchiolar edema may become severe. A combination of necrotizing bronchitis, bronchial swelling, and bronchospasm causes obstruction of large and small airways. Wheezing occurs with bronchial swelling and irritant receptor stimulation. Increased capillary permeability magnifies airway and pulmonary edema. Respiratory failure may occur from 12 to 48 hours after smoke exposure. Characteristics are decreased lung compliance, increased ventilation perfusion mismatch, and increase in dead space ventilation. Injury may progress to mucosal sloughing and intrapulmonary hemorrhage with mechanical obstruction of lower airways and flooding of alveoli. Because of necrosis of respiratory epithelium, patients are predisposed to secondary bacterial invasion and superimposed bacterial pneumonia...
Inhalation injury may describe pulmonary trauma caused by inhalation of thermal or chemical irritants. Anatomically, injuries are divided into three classes: 1) Heat injury which is restricted to upper airway structures except in the case of steam jet exposure. Injury to these airway structures may cause massive swelling of the tongue, epiglottis, and aryeepiglottic folds with obstruction. Severity of obstruction may occur from time after inhalation. 2) Local chemical irritation throughout the respiratory tract. Most substances when are burned, generate material toxic to the respiratory tract. Smoke-related toxins damage epithelial and capillary endothelial cells of the airway. Histologic changes resemble tracheobronchitis. Mucociliary transport is destroyed and bacterial clearance reduced. Alveolar collapse and atelectasis occur due to surfactant loss. Alveolar macrophages are stressed leading to inflammatory response with chemotaxins. Early inflammatory changes occurring in the airway are followed by a period of diffuse exudate formation. Bronchiolar edema may become severe. A combination of necrotizing bronchitis, bronchial swelling, and bronchospasm causes obstruction of large and small airways. Wheezing occurs with bronchial swelling and irritant receptor stimulation. Increased capillary permeability magnifies airway and pulmonary edema. Respiratory failure may occur from 12 to 48 hours after smoke exposure. Characteristics are decreased lung compliance, increased ventilation perfusion mismatch, and increase in dead space ventilation. Injury may progress to mucosal sloughing and intrapulmonary hemorrhage with mechanical obstruction of lower airways and flooding of alveoli. Because of necrosis of respiratory epithelium, patients are predisposed to secondary bacterial invasion and superimposed bacterial pneumonia...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Medicina, leída el 03/11/2015