Respiratory complications in burned patients are often serious, and with infections, are now the leading cause of death in these patients. A third of the burned requiring hospitalization have inhalation injury. This increases to 20% mortality in burned, being a predictor of as much or more weight as age or extent of the burn. Inhalation injury is also associated with significant morbidity, constituting the main reason for mechanical ventilation of burned patients. (Judkins, 1996)
It is important to consider inhalation injury on any victim rescued from a fire, particularly if there is altered level of consciousness or has facial burns. The data should make us suspect inhalation injury are:
1 - Medical history with evidence of exposure enclosed, entrapment, loss of awareness, knowledge of fuels or toxic chemical,
2 - Signs-respiratory symptoms in the initial care, such as dyspnea, hoarseness, cough, stridor, wheezing, cyanosis, hemoptysis, expectoration of bronchial cylinders, shortness of breath (most of these signs are late and may take hours to appear),
3 - Cervico-facial burns (absent in more than 20 % of patients with inhalation injury) or oropharyngeal, singed whiskers, conjunctival irritation, skin burns very extensive, and
4 - Sputum carbonaceous, which are present in more than one third of patients with inhalation injury and may persist for up to 2 weeks. Respiratory complications of burning may occur at different levels with different timing and pathophysiological mechanisms. Thus, we find, thermal injury of the airway, lung injury by toxic chemicals inhaled pulmonary restriction reduced chest wall compliance secondary to burn, systemic toxicity by inhalation of toxic substances released during combustion, or even death immediate secondary to asphyxia. In a subsequent clinical phase can appear other complications such as cardiogenic pulmonary edema from volume overload, pulmonary thromboembolism, pulmonary or bronchial infections, etc. (Rogde, 1996)
Most immediate deaths occur by inhalation during a fire are due to asphyxia produced a profound hypoxemia motivated by breathing ambient air with low oxygen concentration (it can reach 5-10%), which is well used in combustion, or displaced by other gases such as carbon dioxide, nitrogen, methane. Generated hypoxemia becomes a stimulus for respiration, increasing the inhalation of toxic products.
Moreover, in patients who are associated with a decreased level of consciousness, you lose the defense mechanisms of the airway, increasing exposure to toxic-irritant, so the effects of inhalation are usually much more severe.( Anderson, 1981)
Discussion
Direct heat injury of the airway is usually limited to upper respiratory tract, as the dry air has a low specific heat and is cooled very effectively in the upper airway. In addition, intense heat causes apnea reflects, protecting the airway. Inhaling steam with a specific heat 4000 times greater than dry air, it can damage the lower airway.
Thermal injury of airway inflammation and edema of the face, oropharynx and larynx (especially vocal), inducing laryngospasm and increased mucus production. These inflammatory lesions progress through the first 24-48 hours, and can be asymptomatic to generate a critical narrowing of ...