Inhalation Injury

Marc G. Jeschke
BACKGROUND
Mortality from major burns has decreased in the past 20 years by improved
intensive care unit practices, improvement in wound management, and better
control of sepsis and hemodynamic disorders. The single most important associated
injury with burns that contributes to mortality is smoke inhalation injury.
New technologies have increased the capability to diagnose clinically significant
inhalation injuries. These studies have demonstrated that 20-30% of all major
burns are associated with a concomitant inhalation injury, with a mortality of
25-50% when patients required ventilatory support for more than one week
postinjury.1
Approximately 80% of fire-related deaths result not from burns but from inhalation
of the toxic products of combustion. The upper airway is able to modify
the temperature of inspired air such that smoke inhalation does not cause a thermal
injury. The exception is the inhalation of high-pressure steam, which has four
times the heat-carrying capacity of dry air and can cause direct thermal injury to
the airways. Therefore the injurious agent in smoke is not temperature, but instead
the toxic chemicals present in smoke. Many of these toxic chemicals may act
together to increase mortality. This is especially true of carbon monoxide (CO)
and hydrogen cyanide (HCN) where a synergism has been found to increase tissue
hypoxia and acidosis and may also decrease cerebral oxygen consumption and
metabolism. Other possible contributing toxic substances are hydrogen chloride
(produced by polyvinyl chloride degradation), nitrogen oxide, or aldehydes which
can result in pulmonary edema, chemical pneumonitis or respiratory irritability.
Lung injury from smoke inhalation is associated with tracheobronchial hyperemic
sloughing of ciliated epithelium, formation of copious tracheal exudates,
and pulmonary capillary permeability changes resulting in a pulmonary edema.
Animal studies showed a progressive increase in lung permeability during the first
6 h following thermal injury.2 The inhalation of toxic smoke causes the release of
thromboxane and other inflammatory mediators which increase pulmonary artery
pressure, cause secondary damage to the respiratory epithelium, and release
chemotactic factors.3 Neutrophils subsequently diapedese from the pulmonary
microvasculature and release enzymes such as elastase and free oxygen radicals
which disrupt endothelial junctions and the epithelial integrity permitting exudate
of protein rich plasma to enter the lung.3 A concomitant reduction in the
pulmonary immune function may lead to bacteria growth and pneumonia.4
CLINICAL PHASES
The clinical course of patients with inhalation injury is divided into three stages:
FIRST STAGE
Acute pulmonary insufficiency—Patients with severe lung injuries show acute
pulmonary insufficiency from 0-36 h after injury with asphyxia, carbon monoxide
poisoning, bronchospasm, upper airway obstruction and parenchymal damage.
SECOND STAGE
Pulmonary edema—This second stage occurs in 5-30% of patients, usually
from 48-96 h after burn.
THIRD STAGE
Bronchopneumonia—Appears in 15-60% of these patients with a reported
mortality of 50-86%. Bronchopneumonia occurs typically 3-10 days after burn
injury, is often associated with the expectoration of large mucus casts formed in
the tracheobronchial tree. Those pneumonias appearing in the first few days are
usually due to penicillin resistant Staphylococcus species, whereas after 3-4 days,
the changing flora of the burn wound is reflected in the appearance in the lung of
gram negative species, especially Pseudomonas species.
DIAGNOSIS
Early detection of bronchopulmonary injury is critical in improving survival
after a suspected inhalation injury.
CLINICAL SIGNS
History of exposure to smoke in closed space (patients who are stuporous or
unconscious)
Physical findings: facial burns/singed nasal vibrissae/bronchorrhea/sooty sputum/
auscultatory findings (wheezing or rales).
Laboratory findings: hypoxemia and/or elevated levels of carbon monoxide.
DIAGNOSTIC METHODS
Chest X-ray was showed to be a insensitive method because admission studies
are very seldom abnormal and may remain normal as long as seven days postburn.
The standard diagnostic method on every burn patient should be bronchoscopy
for upper airway injury. Positive findings are: airway edema/inflammation/
mucosal necrosis/presence of soot and charring in the airway/tissue sloughing/
carbonaceous material in the airway. All patients that have clinical signs of smoke
inhalation injury listed above should undergo bronchoscopy either through an
endotracheal tube or transnasal with sedation to determine the presence of smoke
inhalation injury.
To define parenchymal injury the most specific method is the 133 Xe lung scanning,
which involves intravenous injection of radioactive xenon gas followed by
serial chest scintiphotograms. This technique identifies areas of air trapping from
small airway partial or total obstruction by demonstrating areas of decreased alveolar
gas washout.
Additionally pulmonary function tests can be performed and could show an
increased resistance and decreased flow in those with abnormal 133 Xe scans.
TREATMENT
GENERAL TREATMENT
The treatment of the inhalation injury should start immediately with the administration
of 100% oxygen via face mask or nasal cannula. This helps reverse
the effects of CO poisoning and aids in its clearance, as 100% oxygen lowers its
half-life time from 250 to less than 50 minutes. Maintenance of the airway is critical.
If early evidence of upper airway edema is present, early intubation is required
because the upper airway edema normally increases over 8-12 h. Prophylactic
intubation without good indication however should not be performed. The
method of intubation should be that with which the intubator is most familiar;
both the nasal and oral routes are appropriate. Occasionally, the injury around
the face and neck may be such that the airway is at risk from edema, and the
standard intubation techniques with paralysis may not be safe. In those situations,
an awake nasotracheal intubation or fiberoptic intubation by the most experienced
personnel is preferred.
Table 9.1. Intubation criteria
Criteria Value
PaO2 (mm Hg) < 60
PaCO2 (mm Hg) > 50 (acutely)
P/F ratio < 200
Respiratory/ventilatory failure Impending
Upper airway edema Severe
Several clinical studies have shown that pulmonary edema was not prevented
by fluid restriction. Indeed, fluid resuscitation appropriate for the patient’s other
needs results in no increase in lung water, has no adverse effect on pulmonary
histology, and improves survival. Although overhydration could induce pulmonary
edema, inadequate hydration increases the severity of pulmonary injury by
sequestration of polymorphonuclear cells and leads to increased mortality.1 In
both animal and clinical studies, it was shown that fluid resuscitation is adequate
if normal cardiac index or urine output were maintained. This might require
2cc/kg/% TBSA burn more fluid volume than required for an equal size burn
without inhalation injury.
Prophylactic antibiotics for inhalation injury are not indicated, but are clearly
indicated for documented lung infections. Empiric choices for treatment of pneumonia
prior to culture results should include coverage of methicillin-resistant
Staphylococcus aureus in the first few days postburn (these develop within the first
week after burn) and of gram-negative organisms (especially Pseudomonas or
Klebsiella) which mostly occur after one week postburn. Systemic antibiotics regimes
are based on serially monitored sputum cultures, bronchial washings, or
transtracheal aspirates.
PHARMACOLOGICAL MANAGEMENT
The theoretical benefits of corticosteroid therapy include a reduction in mucosal
edema, reduced bronchospasm and the maintenance of surfactant function.
Table 9.2. Pharmacological management
Treatment Time/Dosage
Bronchodilators (Albuterol) Q 2 h
Nebulized heparin 5.000 to 10.000 units with 3 cc normal saline
Q 4 h which alternates with
Nebulized acetylcysteine 20%, 3 cc Q 4 h
Hypertonic saline Induce effective coughing
Racemic epinephrine Reduce mucosal edema
Table 9.3. Airway clearance techniques
Criteria Time/Dosage
Chest physiotherapy Q 2 h
Cough deep breathing exercise Q 2 h
Turn patient side to side Q 2 h
Flow humidification High
NTS/OTS As needed
Sputum cultures Q M-W-F
Bronchoscopy evaluation and lavage Q OP visit and therapeutically if needed
Ambulation Early
However, in several animal and clinical studies mortality increased with the administration
of corticosteroids and bronchopneumonia showed a more extensive
abscess formation. Thus the use of corticosteroids is contraindicated.
In recent studies, the importance of localized heparin treatment of the airway
in combination with acetylcysteine and albuterol was shown. In these studies,
mortality and ventilator days improved because of these results. These treatments
are used routinely on all our patients with inhalation injury (Table 4.2).
Ventilator management (guideline from the American College of Chest physicians):
Target ventilator settings should be those designed to elicit an acceptable
oxygen saturation at a plateau pressure of less than 35 cm H2O (clinical conditions
that are associated with a decreased chest wall compliance, plateau pressures
greater than 35 cm H2O may be acceptable). To accomplish the goal of limiting
plateau pressures, pCO2s should be permitted to rise (permissive hypercapnia)
unless other contraindications exist that demand a more normal PCO2 or pH.
PEEP is useful in supporting oxygenation. The level of PEEP required should
be established by empiric trials and reevaluated on a regular basis. PEEP levels
should start at 5 cm H2O and be increased in 2.5 cm H2O increments. PEEP trials
should be performed to optimize oxygenation and cardiac output. The effectiveness
of PEEP is related to surface tension abnormalities and the marked tendency
for atelectasis in these patients. Large tidal volumes (12-15 ml/kg) with PEEP may
be needed if pressure limited strategies fail to maintain oxygenation. Peak flow
rates should be adjusted as needed to satisfy patient inspiratory demands, usually
set between 40-100 l/min, depending on expired volume and inspiratory demand.
Typical ventilatory settings would begin with volume controlled ventilation
with a volume of 12-15 ml/kg and a rate of 10 breaths/minute and 40% O2 with
5 cm H2O positive end expiratory pressure. The rate and tidal volume are then
adjusted to maintain a normal arterial pCO2. If the plateau pressures on these
settings are above 35 mm Hg, the tidal volume can be decreased and the rate
increased to maintain the same minute ventilation. Rates greater than 20 breaths
per minute may not be well tolerated. If this is unsuccessful, a change to pressure
controlled ventilation to control the peak pressures may be required. Care must
be taken when performing this maneuver to ensure that minute ventilation is
maintained the same as the settings with volume control. As the patients’ pulmonary
compliance changes with progression of the disease, the delivered tidal volumes
for the set pressure may change, thus altering minute ventilation and CO2
removal. Only clinical assessment by arterial blood gases or end tidal CO2 monitoring
and appropriate changes in the ventilator settings will maintain targeted
blood CO2 concentrations. Volume control settings are safer in this respect, but
this safety may be sacrificed to control inspiratory pressures.
Oxygenation may also be difficult at this point because the process that is decreasing
pulmonary compliance requiring the high pressures to gain the necessary
tidal volumes is also increasing the intrapulmonary shunt. As the opening
pressure for alveoli increases with decreased compliance, more alveoli are closed,
allowing blood to run through their associated capillaries without contact with
air to exchange gases. This unoxygenated blood mixes with oxygenated blood from
open alveoli, decreasing the oxygen content in the whole. Strategies to increase
oxygenation include increasing the fractional inspired content of O2 (FiO2) above
40%. Percent O2 concentrations above 60% might be toxic because of the increase
in reactive oxygen metabolites. Therefore, efforts should be made to keep the FiO2
below this level. The next strategy employed should be to increase the PEEP, which
should not be set above 15 cm H2O to avoid barotrauma. If this is not successful,
increasing inspiratory times to increase the inspiratory-expiratory ratio of the respiratory
cycle might also improve oxygenation. Ratios as high as 3:1 may be required
(normal 1:4). In general, alert patients do not tolerate increasing the inspiratory-
expiratory ratio, and higher levels of sedation and even paralysis may be
necessary. Further measures to improve oxygenation such as inhaled nitric oxide
and partial liquid ventilation are experimental, but might be attempted in the
presence of a controlled clinical trial.
When an acceptable combination of ventilator settings are reached to provide
for adequate ventilation and oxygenation, the process of weaning from the ventilator
begins. In general, ventilator weaning should be done by one physician with
a defined plan. In terms of oxygenation, FiO2 should be decreased first to 40%,
then decreasing the inspiratory-expiratory ratio to 1:2, followed by decreasing
PEEP to 5 cm H2O. Ventilation should be addressed by decreasing the set ventilator
rate on an SIMV volume control mode with the addition of pressure support
for spontaneous breaths, until a machine rate of 4 is reached. At that point, if the
spontaneous respiratory mechanics are adequate, the patient may be extubated.
The reader is referred to other ICU handbooks for a more in depth discussion of
this and alternative weaning techniques.
SUMMARY
Inhalation injury is commonly associated with burns. Mortality from this condition
has markedly improved with better ICU techniques and prevention of complications.
Recognition of the possibility of inhalation injury and directed treatment
will improve outcomes.
Table 9.4. Extubation criteria
Criteria Value
PaO2/FiO2 (P/F) ratio > 250
Maximum inspiratory pressure (MIP) (cm H2O) > 60
Spontaneous tidal volume (ml/kg) > 5-7
Spontaneous vital capacity (ml/kg) > 15-20
Maximum voluntary ventilation > present twice the minute
Audible leak around the ET tube with cuff deflated volume
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