III_C. TRACHEOBRONCHITIS from INHALATION INJURY
Pathophysiology:
The chemical burn to the airways results in a
spectrum of clinical manifestations during
this period. At the very least, a mucosal
irritation will persist for several days
causing a bronchorrhea, increased cough, and
mucus production.32
As airways inflammation and bronchial blood
flow increases over the next several days.
Even modest volume overload can markedly
potentiate airways edema. The magnitude of the
pulmonary infection is in large part dependent
on the status of host defenses and the
aggressiveness of pulmonary support.42
The combination of the chemical lung burn and
a body burn markedly potentiate the morbidity
and mortality of either process. If infection
can be controlled and secretions cleared, the
acute process will resolve over the next 7 to
10 days. However, the risk of pulmonary
infection persists for several weeks,
extending well into the inflammation period.5,44
The damaged ciliary function of the airways
lining leads to a high risk for infection
manifested first by a bacterial
tracheobronchitis followed by a
bronchopneumonia.32,62-64 Bacterial
colonization is inevitable. Characteristically
with a severe injury, the damaged mucosa
becomes necrotic at 3 to 4 days post-injury
and begins to slough.55,62-64 The
increasingly viscous and copius secretions can
lead to increasing airway resistance, distal
airway obstruction, atelectasis, and a high
risk of a rapidly developing bronchopneumonia.
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Figure 1:
Airway lining at 5 days |
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 |
|
Note
absence of airways epithelium and
celia severely impairing immune
defenses. |
If infection can be controlled and secretions
cleared, the acute process will resolve over
the next 7 to 10 days. However, the risk of
infection persists for several weeks,
extending well into the inflammation period.
Symptoms:
In the first several days after injury,
remaining soot continues to be present in the
airways secretions. Diffuse rhonchi are
usually present, once inflammation develops.
Wheezing also frequently persists as a result
of continued bronchospasm and bronchial edema,
the latter being the more prominent cause.
Continued coughing and pulmonary toilet as
well as the residual airways edema and some
bronchospasm increase the work of breathing,
which can lead to fatigue and hypoventilation.54,65-66
Secretions then become tenacious and more
difficult to clear. Rales compatible with an
edema process will noted in the most severe
airways injuries, especially with concomitant
volume overload. Evidence of bacterial
tracheobronchitis is common, followed by
bronchopneumonia in a substantial number of
patients.
Lung function may be deceptively
good on day 2 only to deteriorate
rapidly on day 3 to 4.
Diagnosis of severity of injury is based on
the course of the disease process rather than
on initial findings from fiberoptic bronchoscopy, which basically only indicate
that an injury is present. Chest radiographs
during this period, in general, underestimate
the severity of lung damage because the injury
is usually initially confined to the airways.47,49
Alveolar injury is seen in severe cases.
Clinical evidence of continued respiratory
compromise; namely, dyspnea, tachypnea,
diffuse wheezing, and rhonchi precede
radiographic changes. The first evidence on
radiography of lung damage is usually that of
either diffuse atelectasis, pulmonary edema,
or bronchopneumonia. Altered gas exchange
reflected in blood gas analysis and assessment
of changes in sputum characteristics are
useful parameters to monitor.42,65-68
Chest radiographic findings invariable
underestimate the magnitude of the chemical
inhalation-induced airways injury. Parenchymal
changes are late findings.
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Figure 2: Reactive
Airways
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 |
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Legend:
airways remain hyper-reactive in the
post inhalation injury period.
Peribronchial edema and inflammation
is evident. |
Treatment:
The clearance of soot, mucopurulent exudate,
and sloughing mucosa is essential to avoid
progression of the lung injury. An
endotracheal tube may be necessary if
clearance of secretions is inadequate.
Ventilator assist may also be necessary if the
patient is fatiguing and if gas exchange is
worsening. Continued readjustments in tidal
volume, rate, and positive end-expiratory
pressure (PEEP) are necessary to maintain gas
exchange while minimizing barotrauma. Sedation
(narcotic infusion) or paralysis may be
necessary if the patient’s spontaneous
ventilatory attempts further impair lung
function while on ventilator support.
Bronchodilators, provided by aerosols, are
also very helpful, along with frequent changes
in position for postural drainage. High
frequency pressure ventilation has also been
shown to be effective at clearing secretions.67-68
Continuous rotating beds have advantages for
the patient with an inhalation injury and a
large body burn where side to side patient
movement is difficult because of pain and
stiffness from tissue edema. The constant
postural drainage assists in removing airway
plugs. If the respiratory dysfunction is
prolonged, tracheostomy may be of benefit.79
Infection surveillance is crucial during this
early period in order to detect a bacterial
bronchitis prior to development of a
pneumonia. Sputum smears and monitoring of the
character of the sputum are useful early
guides. Systemic antibiotics are not given
prophylactically but initiated when a
bacterial process becomes evident.71
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