Abnormalities of ventilation and oxygenation are common in the immediate postburn period. Several fairly distinct critical disease processes must be recognized and managed aggressively.3 The first three are associated with the inhalation injury complex and are presented below in the approximate order in which symptoms will develop (carbon monoxide toxicity, upper airway obstruction, and chemical burn to the lung). These sections are followed by discussions of lung changes due to the skin burn and, finally, of the effects of impaired chest wall compliance.
Smoke Inhalation Injury Complex
Pulmonary insufficiency caused by the inhalation of heat and smoke is the major cause of mortality among fire victims, accounting for over 50% of fire-related deaths.4,5 The exposure time, concentration of fumes, elements released, and degree of accompanying body burn are critical variables in determining outcome.
Carbon Monoxide and Cyanide Toxicity
Carbon monoxide, a by-product of incomplete combustion, is one of the leading causes of death in fires. Hydrogen cyanide is also a well-recognized cause of morbidity and mortality, especially with burning of synthetics such as polyurethane.
Symptoms of carbon monoxide toxicity usually are not present until the carboxyhemoglobin concentration exceeds 15%. Symptoms are those of decreased tissue oxygenation, with the initial manifestations being neurologic. Cyanide toxicity presents in a very similar fashion, with severe metabolic acidosis and obtundation. Diagnosis, however, is more difficult because measurement of cyanide levels is not always readily available or very reliable. Normal levels are less than 0.1 mg/L (even in smokers). A level near 1 mg/L is lethal. Neurologic dysfunction also can be caused by factors other than carbon monoxide toxicity, such as alcohol or drug intoxication or blunt head trauma. A toxicology screen therefore is warranted. The indications for obtaining a computed tomographic (CT) scan of the head are the same as for other trauma patients.
The persistence of a metabolic acidosis in a patient with adequate volume resuscitation and cardiac output suggests that oxygen transport and use are being impaired by carbon monoxide or cyanide. PaO2 can remain relatively normal because the chemical alteration of hemoglobin by carbon monoxide will not affect the amount of oxygen dissolved in arterial plasma. A high carboxyhemoglobin level also indicates a significant smoke exposure and, therefore, a chemical burn to the airways. Treatment of carbon monoxide toxicity is covered more fully elsewhere in this text; briefly, it consists of the early displacement of carbon monoxide from hemoglobin by administration of 90% to 100% oxygen (see Chap. 102). Treatment of cyanide toxicity involves restoration of hepatic blood flow to clear the cyanide. In addition, [dx id=""]sodium nitrite[/dx] is given, followed by sodium thiosulfate. Hyperbaric oxygen is best used in patients who show severe neurologic compromise with a high carboxyhemoglobin level (>50%) but no major burns and who are not responding to high-flow oxygen. The vast majority of patients can be managed successfully using simply 90% to 100% oxygen.
Upper Airway Obstruction from Airway Edema
Heat produces an immediate injury to the airway mucosa, resulting in edema, erythema, and ulceration. Although these mucosal changes may be present anatomically shortly after the burn, physiologic alterations will not be present until the edema is sufficient to produce clinical evidence of impaired upper airway patency. This may not occur for 12 to 18 hours. The presence of a body burn magnifies the effects of airway injury in direct proportion to the size and depth of the skin burn. The massive amount of fluid administered is in part responsible. A face or neck burn will accentuate these problems by producing marked anatomic distortion and, in the case of a deep neck burn, external compression of the larynx. The airway edema and the external burn edema have a parallel time course so that by the time symptoms of airway edema develop, external and internal anatomic distortion is extensive. The local edema usually resolves in 4 to 5 days.
Inspection of the oropharynx for soot or evidence of a heat injury should be routine in every burn victim. Numerous techniques have been used in further assessing the degree of injury and in determining the need for endotracheal intubation. Fiberoptic bronchoscopy or laryngoscopy will show whether physical evidence of pharyngeal or laryngeal mucosal injury is present. Laryngoscopy will demonstrate the presence of mucosal irritation at and above the cords and provide information about the need for endotracheal intubation.4,5 Unfortunately, unless serial studies are performed, none of these tests can predict the severity of subsequent airway compromise accurately because the edema progresses during the first 18 to 24 hours. Repeated examinations for airway compromise are feasible in patients without facial burns. However, in the presence of a large burn, it is best to proceed with intubation if there is any concern.
An early decision regarding the need for airway intubation is crucial. When there is doubt, it is safer to intubate. A patient with a significant inhalation injury and deep facial burns usually should be managed by early endotracheal intubation. There are many other indications for intubation in burn patients besides airway edema, such as hemodynamic instability and impaired consciousness. A large orotracheal tube (at least 7 mm in internal diameter) should be used in adults because very thick secretions develop. If the initial tube is too small, it will be dangerous to change once massive facial and airway edema develops. An algorithm for this approach is presented in Fig. 98-1.
Initial assessment of airway (for the decision of whether or not to intubate).
Chemical Burns of the Upper and Lower Airways
Toxic gases contained in smoke, as well as carbon particles coated with irritating aldehydes and organic acids, can injure both upper and lower airways (Table 98-1). The location of injury will depend on the duration of exposure, the size of the particles, and the solubility of the gases.
Table 98–1. Toxic Elements in Housefire Smoke
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Table 98–1. Toxic Elements in Housefire Smoke
|Carbon monoxide||Any organic matter||Tissue hypoxia|
|Nitrogen dioxide||Wallpaper, wood||Bronchial irritation, dizziness, pulmonary edema|
|Hydrogen chloride (from phosgene)||Plastics (polyvinyl chloride)||Severe mucosal irritation|
|Hydrogen cyanide||Wool, silk, nylons (polyurethane)||Headache, respiratory failure, coma|
|Benzene||Petroleum plastics||Mucosal irritation, coma|
|Aldehydes||Wood, cotton, paper||Severe mucosal damage, extensive lung damage|
Breath holding and laryngospasm are protective mechanisms against excessive exposure in the conscious patient. The unconscious patient, however, loses this protection and sustains more severe injury to the lower airways. Information regarding loss of consciousness at the scene should be sought in the history.
Symptoms may well be absent on admission, with the true magnitude of injury becoming evident only after 24 to 48 hours. Early symptoms usually consist of wheezing and bronchorrhea. This intense initial bronchorrhea caused by irritation of the airway mucosa in combination with increased oral and nasal secretions can give the false appearance of fulminant pulmonary edema. Soot in the lung secretions is certain evidence of smoke exposure but is not always present.
Early bronchospasm and bronchiolar edema initiated by the irritant gases cause a marked decrease in dynamic lung compliance with increased work of breathing. Impaired clearance of secretions will accentuate this problem.
Impairment of gas exchange is due to ventilation/perfusion (V̇/Q̇) mismatching related to airway injury rather than to alveolar edema.6–8 A body burn markedly potentiates the inhalation-induced lung dysfunction caused by chemical injury. The combination of a major burn and smoke inhalation is more lethal than either injury alone.
Initial treatment of this component consists of an aggressive approach to upper airway maintenance and pulmonary support that includes maintenance of small-airways patency and removal of soot and mucopurulent secretions. Careful, well-monitored fluid resuscitation is necessary to avoid accentuation of the process. The addition of positive end-expiratory pressure (PEEP) frequently is necessary to maintain small-airways patency and an adequate functional residual capacity (FRC), assisting in holding the edematous airway open until edema resolves. Endotracheal intubation and PEEP have been reported to decrease the rate of early pulmonary death after severe burns and smoke inhalation.9
Beginning about 18 to 24 hours after a burn, increasing airway resistance is often due to bronchiolar edema and airway plugging rather than to bronchospasm. The associated impairment of gas exchange often responds to further increases in PEEP in addition to bronchodilator administration. The injured airway mucosa frequently becomes colonized with bacteria. Prophylactic antibiotic administration only selects for resistant organisms and therefore is not indicated. Corticosteroids increase morbidity and mortality in the presence of a body burn and are, therefore, contraindicated.10
Impaired Chest Wall Compliance
Respiratory excursion can be impaired markedly by a burn to the chest wall, especially a circumferential third-degree burn.11,12 The loss of chest wall compliance increases the work of breathing. Symptoms may not be evident until edema formation peaks. The first clinical evidence of chest wall restriction is often labored breathing, followed by rapid respiratory deterioration, particularly in the patient who is not receiving ventilatory support. Clearance of secretions can be impaired owing to the inability to generate enough hyperinflation to cough well.
Treatment involves surgical decompression or escharotomy of the chest wall. Longitudinal incisions placed in the midaxillary lines should be connected across the lower chest wall. Bleeding usually is controlled easily if the incisions stay within the margins of the third-degree burn because the dermal vessels are thrombosed. The incision must extend into the subeschar area to allow adequate chest wall expansion. Escharotomies usually are not required in a second-degree burn unless the edema is so massive that the burned skin is tight. (This approach is diagrammed in Fig. 98-2.)
Treatment of chest wall burn.