- The injury results directly from chemical irritation of the pulmonary tisues at the
alveolar level
- Inhalation injuries below glottis cause loss of ciliary action, hypersecretion, severe
mucosal edema and bronchospasm
- The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alveoli)
- Expectoration of carbon particles in the sputum is the cardinal sign of this injury
- The pathophysiology effects are due to tissue hypoxia a result of carbon monoxide
combining with hemoglobin to form carboxyhemoglobin which competes with oxygen
for available hemoglobin sites
- The effinity of hemoglobin for carbon monoxide is 200 times greater than that for
oxygen
- Treatment usually consists of ealy intubation and mechnical ventilation with 100%
oxygen - Administering 100% O2 is essential to accelerate the removal of carbon monoxide
from the hemoglobin molecule
- restrictive defects arise when edema develops under full-thickness burns encircling
the neck and thorax
- Chest expansion may be greatly restricted resulting in decreased tidal volume
- In such situation escharotomy is necessary
- More than half of all burn victims with pulmonary involvement do not initially
demonstrate pulmonary signs and symptoms - Any pat with possible inhalation injury must be observed for at least 24 h for
respiratory complications
Pulmonary response
- Airway obstruction may occur very rapidly in hours
- Decreased lung compliance, decreased arterial oxygen levels and respiratory acidosis
may occur gradually over the first 5 days after a burn
Indication of possible pulmonary damages include
- History indicating that the burn occured in an enclosed area
- Burns of the face and neck
- Hoarseness , voice change, dry cough, stridor.
- Bloody sputum