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PULMONARY PROBLEMS (RESUSCITATION PHASE 0 - 48
hours) Continued
Degree of
Smoke Exposure:
The degree of smoke exposure is dependent on the
smoke mass inhaled, the depth of the breaths,
and the time of exposure. Unfortunately, the
only marker we have at present to define this
exposure is the time in the smoke environment,
neurologic status, and carbon monoxide
toxicity. A high carboxyhemoglobin level
(i.e., >40%) produces an obtunded state and
provides evidence of prolonged exposure time.
This assessment assumes that other factors that
cause obtundation, such as head injury, drugs,
and alcoholism, are not present. There is a
clear proportional increase in the degree of
initial lung injury with increasing smoke
exposure.
Pathophysiology of Airway Injury:
The initial response to smoke is usually that
caused by intense airways irritation, and
airways edema producing increased airways
resistance. The late response, typically seen 2
to 5 days after the insult is the result of the
initial mucosal injury leading to mucosal
slough, increased secretions, intense airways
inflammation and impaired immune function.8-12
The Lung Injury:
The degree of initial and late injury will, in
large part, be related to the status of the
pre-injured lung. A lung with any element of
reactive airway disease or chronic changes from
smoke, for example, will likely react more
severely to a smoke exposure than a healthy
lung. In addition, the inflammatory response
caused by the injury will lead to much of the
subsequent damage. Oxidants in smoke and those
released by inflammatory cells play a critical
role in the airways injury. A decrease in lung
anti-oxidants is also seen further increasing
the degree of injury.31-35
The mechanism of the airway and parenchymal
injury is complex. The cell toxic agents,
present on the particulates lead to a number of
pathologic events.
First, there is direct mucosal
injury, loss of ciliary activity with subsequent
impairment of particulate, and mucous clearance
and later bacterial clearance.
Second,
there is a marked, early increase in bronchial
blood flow, as well as increased bronchial
vessel permeability, leading to submucosal edema
and vascular-engorgement narrowing of the airway
lumen.36
Third, there is tissue
destruction due to the above response, as well
as a secondary inflammatory response. The
result is a slough of mucosa in both large and
small airways, and a marked increase in mucous
production.
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Figure 6:
Small Airway Damage |
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Small airways injury from smoke. (Broncho
constriction caused by the mucosal injury)
Alveolar edema is not present |
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Figure
7:
Mucosal Damage |
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| Fatal
Smoke Inhalation Injury (Note: Airway and
alveolar collapse with massive atelectasis. Note
also the mucosal cast in the opened airway |
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