Page 109 - JSOM Summer 2022

the cold until it was time to return to base. Finally, all of this Inhalation injury is damage to the respiratory tract or lung
was compounded by an already weakened respiratory system tissue due to exposure to heat, smoke, or toxic chemicals
due to his preexisting chest cold. Alone, none of these could during inhalation. Inhalation injuries can encompass the en-
have led to a patient with acute pulmonary edema to be at risk tire respiratory track or be isolated to either the upper airway,
2
of progressing into ARDS. However, with the right combina- tracheobronchial tree, or the lung itself. Injuries to the upper
tion of minor insults it does not take a catastrophic event for a airway are primarily caused by exposure to high heat and can
SOF medic to suddenly find themselves practicing critical care lead to significant edema and production of thick secretions
medicine in an austere environment. requiring early and aggressive airway management. Injuries to
the tracheobronchial tree and lungs are primarily caused by
the inhalation of toxic chemicals, the most common of which
Pathophysiology
being smoke. This exposure can cause bronchial swelling,
Positive pressure pulmonary edema is a primary blast injury bronchospasm and necrotizing bronchitis, causing obstruc-
that results from the blast wave of an explosion damaging the tion of large and small airways. In addition, inhalation injury
9
alveoli and pulmonary vessels of the lungs. During an explo- causes a breakdown of surfactant in the alveoli, leading to de-
sion, the blast wave accelerates away from the source of the creased surface tension and atelectasis. An associated increase
explosion in a sphere at an extremely high velocity. It consists of in capillary permeability also magnifies airway and pulmonary
an initial wave of high pressure, followed by a drop to negative edema. 2
8
pressure. This massive shift from positive to negative pressure
causes compression of gas bubbles in liquid, quickly followed The severity of an inhalation injury varies based on several
by explosive re-expansion. As the pressure wave strikes the factors including the ignition source, the size and diameter of
lungs, the velocity also changes as it passes through tissues with the particles in the smoke, the duration of the exposure, and
abrupt density changes, thereby causing the most damage where the solubility and heat of the gases involved. The onset time
9
air-fluid interface occurs. This can result in the rupture of alve- also varies depending on the severity of the exposure and the
oli and hemorrhage of the pulmonary vessels, leading to pul- anatomical structure most effected. An inhalation injury to the
monary edema, atelectasis, or pneumothorax in severe cases. 11 upper airway can present in a matter of minutes, while an in-
halation injury to the lungs and lower airway may take hours
The onset of positive pressure pulmonary edema is highly de- to develop significant signs and symptoms.
pendent on the severity of the patient’s exposure and can pres-
ent immediately or be delayed up to 48 hours. There are several A final consideration for inhalation injuries is the possibility
contributing factors to primary blast injury that a SOF medic of systemic cyanide or carbon monoxide (CO) toxicity. While
should be aware of in order to raise or lower his index of sus- not the focus of this article, cyanide and CO toxicity should
picion for a BLI. The first factor is the size of the explosion. be considered in all inhalation injury patients, especially those
The larger the blast, the larger the blast wave, the higher the with suspected smoke inhalation. 9
chance for the patient to develop a BLI. A blast pressure of 40
psi is enough to cause pulmonary contusion and pneumotho- ARDS is a severe lung inflammatory disorder that is charac-
rax while pressures of 100 psi and above are considered po- terized by acute respiratory failure presenting with progressive
11
tentially lethal. The second contributing factor is the distance hypoxemia, dyspnea, and a marked increase in the work of
of your patient from the epicenter of the blast. The intensity breathing. ARDS is a secondary development and represents
of the blast wave decreases exponentially the further away you the failure of the lung to repair itself after an initial insult.
move from the epicenter, with a person 10 ft away from a blast Pneumonia and sepsis are the two leading causes of ARDS,
experiencing nine times the pressure of a person standing 20 ft however other causes include major trauma, aspiration of gas-
8
away. A third factor to be aware of is the environment in which tric contents, inhalation injury and BLI. The onset of ARDS is
1
the blast occurs. In an enclosed environment the blast wave is typically delayed by several days up to one week, but can have
amplified and reflected off the surrounding structures. Blasts a rapid onset of around 24 hours in certain cases. Important
in enclosed spaces such as buildings, tunnels, buses, etc., have for the SOF medic is that this early-onset ARDS is mainly as-
a much higher mortality rate as well as an abnormal pressure sociated with hemorrhagic shock and pulmonary contusion,
wave from reflections. This difference is illustrated below with with later-onset ARDS associated with pneumonia, and com-
graph A representing a normal blast pressure wave and graph B plications of resuscitation efforts. 10
representing one occurring in an enclosed structure (Figure 1). 11
In the acute phase of ARDS (between 1 and 7 days), there
FIGURE 1 (A) Normal blast pressure wave. (B) Blast pressure wave is diffuse pulmonary edema as a result of increased capillary
in enclosed structure. permeability, inflammation, and cellular damage. The pulmo-
nary edema disrupts the diffusion of gases within the alveoli
and can lead to atelectasis causing hypoxia and hypercapnia.
As the disease progresses (days 7–14 and beyond) some of the
edema will be reabsorbed and the development of fibrosis or
1
a “scarification” of the lungs may begin to occur. This may
cause a decrease in the pulmonary edema and lung sounds
normally associated with ARDS but may not indicate an in-
crease in oxygenation. This “scarring” leads to a stiffening
of the lungs, maintaining collapsed alveoli, inhibiting gas ex-
change, and causing long term damage to the patient’s respi-
ratory system.

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