PULMONARY PROBLEMS (RESUSCITATION PHASE 0 - 48 hours) Continued

II_c. chemical burn to upper & lower airways

Pathophysiology:

This aspect of inhalation injury is often an extension of the upper airways injury just described but is generally much more serious than that produced by heat alone. Toxic gases contained in smoke as well as carbon particles coated with irritating aldehydes and organic acids can result in injury to both upper and lower airways. The location of injury will depend on the duration of exposure, the size of the particles, and the solubility of the gases. 

Components in Smoke:

The components in smoke causing injury are defined as follows: 

a)     Heat injury from the hot gas is usually confined to the area above the cords, as heat is rapidly neutralized in the oro and nasopharynx.

b)     The gas phase contains a host of toxins, including carbon monoxide, cyanide gas, acids, and aldehydes.^8-13,25-28  Oxidants are also clearly present in the gas phase.  These agents produce both a systemic response and local airway injury.  The vapors, in large part, are mucous membrane irritants leading to intense bronchorrhea, bronchoconstriction, and airway edema.  The process often peaks hours after injury, although patients with pre-existing airway reactivity disease can develop very early intense bronchoconstriction.^4,8,27-28

c)     The particulate phase injury of smoke produces a severe injury.  The degree of exposure to the lung is dependent on particle size and breathing pattern.^29-31  The particle deposition willl depend on particle size.  Particles range from 0.1 to 15 ųm in size, depending on the heat of the smoke and what is burning.  Particles of 3 to 5 ųm appear to predominate in many of the smoke inhalation studies.  In general, particles >5 ųm are cleared by the nasopharynx if the patient is a nasal breather.  With mouth breathing, most of the larger particles will deposit in the larynx, trachea, and large airways.  Particles <5 ųm will deposit in both large and small airways, and alveoli.  The degree of deposition in distal lung is accentuated by deeper breaths, as would be evident in an attenuated hypox patient or in a patient attempting to actively escape the insult.  As opposed to the gas phase, which is short lived, the particulates can adhere to the mucosa and perpetuate the local tissue injury.  Particulate clearance, in turn, will be impeded byu the impaired mucociliary action perpetuating the injury.³² 

Of major importance is the fact that smoke from different environments varies dramatically in toxicity.  Examples of extremely toxic smoke includes smoke from burning automobile interiors, upholstery, and chemical plants in which hydrocarbons are a major component.^11,12   

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