PULMONARY PROBLEMS (RESUSCITATION PHASE 0 - 48 hours) Continued

Systemic Effects:

A body burn markedly potentiates the inhalation-induced lung dysfunction caused by chemical injury.  Mortality rate for patients with severe inhalation injury alone is 5 to 8%.  Mortality rate of the combination of a major burn and smoke inhalation far exceeds that of either injury alone.⁵

In addition, inhalation injury markedly increased the fluid requirements and oxygen demands required to manage the burn injury.^43-45  There is also evidence of increased systemic vascular permeability and oxidant injury, evidenced by lipid peroxidation, to systemic organs.⁴⁶

Diagnosis:

The diagnosis is first and foremost a high index of suspicion, as the patient’s history may be unavailable or unreliable.  Any clinically important history of exposure to smoke is considered a smoke inhalation injury until proven otherwise.  A long exposure time is not required if the smoke is particularly toxic, e.g. burning mattresses or upholstery, where gases such as cyanide are released in large quantities. 

A particularly important symptom is lack of consciousness at the scene, since the unconscious or disoriented state can readily be caused by smoke.  Also, the victim is likely to consume more smoke once unconscious or confused.  Initial physical findings of carbonaceous sputum, facial burn, singed nasal hairs, or respiratory symptoms of coughing, wheezing, etc. are diagnostic signs, although lung dysfunction is often delayed in onset and may not be present.  Initial blood gases are often normal, with the exception of a decrease in measured arterial oxygen saturation and metabolic acidosis due to carbon monoxides.  Initial chest radiographic findings are also usually relatively normal, since the initial injury is primarily in the airway, not in the parenchyma and often requires several days before radiographic changes of atelectasis, increased water, and focal infiltrate become evident.^47,48

Physical findings on admission that suggest smoke exposure include a facial burn, soot in the sputum, dyspnea, coughing, wheezing and bronchorrhea.^4-8  If present, these findings are helpful indicators.  However, many patients demonstrate minimal symptoms early after injury and symptoms become evident only when airway edema develops.  An increased carboxyhemoglobin level indicates an exposure to the elements in smoke.  Visualization of the upper and lower airways by fiberoptic bronchoscopy can provide information on the anatomical extent of injury, but initial findings have not been found to prognosticate accurately the magnitude of injury to allow anticipation of the subsequent course.^47,50

With the onset of airway inflammation and the mucosal slough (in severe injuries) at 2-3 days, symptoms of progressive lung dysfunction develop with increasing shunt and minute ventilation.

Figure 10:    Smoke Inhalation (12 hrs)

Legend: Fiberoptic bronchoscopic assessment at 12 hours reveals airways erythema and edema with encroachment on the burns.

Treatment:

Initial treatment of a chemical burn consists of an aggressive approach to upper airway maintenance and pulmonary support, which includes maintenance of small airways patency and removal of soot and the mucopurulent secretions. Careful well-monitored fluid resuscitation is necessary to avoid accentuation of the process. Under volume resuscitation will aggravate the pulmonary dysfuntion as much as will over-resuscitation.⁵² The addition of positive end-expiratory pressure (PEEP) is frequently necessary to maintain small airway patency and an adequate functional residual capacity by assisting in holding the edematous airway open until edema resolution. Early endotracheal intubation and PEEP have been reported to decrease pulmonary deaths after severe burns and smoke inhalation. Prevention of airway closure is much more readily accomplished than is the reopening of collapsed airways.⁵³ A large enough tube, i.e. at least a 7mm internal diameter, should be used in adults because very thick secretions develop as a result of the lung injury. If the initial tube is too small, it will be very dangerous to change once massive facial and airway edema develops. Although the nasotracheal route may be more comfortable to the patient, the size of the tube may need to be compromised and lead to later problems for secretion clearance. The continued use of additional humidified oxygen to maintain adequate oxygen delivery as well as to assist in the clearance of secretions is indicated. Elevation of the patient’s head and chest 20 to 30⁰ is also helpful.

Bronchospasm is a frequent component of the chemical injury. However, diagnosis can be complicated by rhonchi and upper airways noises, caused by increased secretions. A helpful clue to determining the magnitude of increased airways resistance is the difference between dynamic and static compliance. The difference between the two reflects increased resistance to airflow, as seen with bronchospasm and bronchial edema. Bronchospasm can be treated with bronchodilators, either parenteral or via aerosol.⁵⁴  Beginning about 18 to 24 hrs after a burn, increasing airway resistance is often due to bronchiolar edema and airway plugging rather than to bronchospasm.  The impaired gas exchange often responds to further increases in PEEP in addition to bronchodilators.  Prophylactic antibiotics are not indicated.

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