PULMONARY PROBLEMS (RESUSCITATION PHASE 0 - 48 hours) Continued

II_b. UPPER AIRWAY INJURY FROM SMOKE EXPOSURE MONOXIDE

(Obstruction from tissue edema)

Pathophysiology:

Direct heat injury caused by the inhalation of air heated to a temperature (150° C or higher) ordinarily results in burns to the face, oropharynx, and upper airway (above the vocal cords).  Even superheated air is rapidly cooled before reaching the lower respiratory tract because of the tremendous heat-exchanging efficiency of the oropharynx and nasopharynx.^15-21

Heat and chemicals in smoke produces an immediate injury to the airway mucosa, resulting in edema, erythema, and ulceration. Although these mucosal changes may be anatomically present 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 injury to airways in direct proportion to the size and depth of the skin burn. The massive fluid requirements necessary to treat the skin burn is in part responsible, as are mediators released from the burned skin.  Oxidants in smoke and from inflammatory cells are an important cause of injury.

Another compounding injury is any face or neck burn that will produce marked anatomic distortion and, in the case of the deep neck burn, external compression on the larynx. A particularly dangerous injury is the third degree facial burn in which minimal external edema is present. The lack of external edema is due to the non-elastic third degree burn, which does not allow expansion. Intraoral edema in this case is usually massive but unrecognized unless looked for. A more superficial burn causes massive external edema but may produce much less mucosal edema and airway compromise. The effect of deep face burns on airway maintenance are presented.  The local edema usually resolves in 4 to 5 days.

Symptoms:

Symptoms of obstruction, namely, stridor, dyspnea, increased work of breathing, and eventually cyanosis, do not develop until a critical narrowing of the airway is present. Upper airway noise indicative of increased turbulent airflow often precedes obstruction. It is difficult to distinguish noise from a narrowed airway from that caused by increased oral and nasal secretions due to smoke irritation. The airway edema and the external burn edema process have a parallel time course so that by the time symptoms of airway edema develop, external and internal anatomic distortion will be extensive.

Diagnosis:

A history must be obtained regarding the nature of the burn, the presence of smoke and the patients initial neurologic status. Inspection of the oropharynx looking for soot or evidence of a heat or chemical injury should be done with every burn victim. A number of techniques have been used to assess further the degree of injury and to determine the need for early endotracheal intubation.  Direct laryngoscopy is a valuable method to determine whether an injury is present.  Typically erythema and edema will be found.  Repeat exams will be needed if an injury is present and intubation is not performed , as this process often progresses over the next 24 hours.  Fiberoptic bronchoscopy is also very useful and can be done very safely.^22-23

Treatment:

A very important judgement decision must be made in the initial assessment as to whether the injured airway can be maintained safely without an endotracheal tube.  When in doubt or if progressive edema is likely, it is safer to intubate.  Three major categories of patients at risk for airway compromise.^20-24 

Heat and smoke injury plus extensive face, neck burns:

This group invariably requires early intubation.

Deep facial burns but no smoke injury:

These patients have difficulty controlling secretions as edema evolves and external edema can compress the airway.  Early intubation is a safe approach as anatomical distortion of the face makes intubation at a later period very difficult.

Heat and smoke injury; no facial burn:

If there is no evidence of severe edema, this group can be carefully observed.  The lack of a facial and mouth distortion makes it feasible to intubate later.

Aerosolized adrenaline has also been found to be beneficial in decreasing the edema process, improving airway patency.²⁴  It is also beneficial, in both the non-intubated and intubated patient, to maintain a semi-erect position if hemodynamically stable, to minimize the airway and facial edema process.  Edema forms much faster than it resolves, so early preventative measures are important.²⁶ 

If intubation is performed, the oral route is preferred as a larger tube can be placed which will be needed for proper pulmonary toilet.  The tube must be well-secured since it may be extremely difficult to replace if it becomes dislodged, as the process of edema evolves.

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