Inhalational Injury

Inhalation Injury: Pathogenesis and complications
Authors: Marshall Thibedeau, W Fraser Hill, Paloma Arteaga Juarez Reviewers: Spencer Yakaback, Tony Gu, Dami Omotajo, Ben Campbell, Yan Yu*, Michael Liss*, Duncan Nickerson*, Donald McPhalen* * MD at time of publication
Smoke Inhalation
Suspect if patient found unconscious, history of fire in a confined space and presence of facial burns
Convective heat transfer
Exposure to chemical irritants
Tracheobronchial injury
Injury stimulates vasomotor and sensory nerves of the trachea and bronchi
Neuropeptides from neurons are released into local circulation and activate nitric oxide
Inhalation of toxins
Lack of O2 in an enclosed space
Asphyxiation
(O2 deprivation in lungs)
Acute hypoxemia
Loss of consciousness
Death
Upper airway injury (above vocal cords)
Cell lysis & necrosis
Local release of inflammatory substances
↑ Vascular permeability à edema of tissues in upper airway
Damage to lower respiratory tract cilia
↓ Mucus clearance from alveoli
Parenchymal injury
(delayed reaction dependent on severity of burn)
Alveolar epithelial and endothelial barrier irritation/damage
Inflammatory response
Carbon monoxide poisoning
Cyanide poisoning
Cyanide binds to mitochondrial cytochrome oxidase a3
CO binds more strongly to hemoglobin than O2
↑ Carboxyhemoglobin in blood, ↓ free hemoglobin available to bind O2 in the lungs
↑ Affinity for O2 on remaining binding sites in hemoglobin (i.e. hemoglobin binds O2 more strongly and is slow to release it)
↓ O2 delivered to tissues
Inhibition of cytochrome c oxidase
Mucous obstructs airways
Air retained
distal to the obstruction is resorbed from nonventilated alveoli
Regions without gas collapse i.e atelectasis
↑ Risk of infection
↓ Mitochondrial respiratory chain function
Impaired oxidative phosphorylation & cellular energy production
Cellular dysfunction in high metabolic tissues
Nitric oxide acts as a vasodilator in alveolar arterioles
Loss of hypoxic vasoconstriction (constriction of arterioles in alveoli due to ↓ O2)
Reactive inflammation & bronchoconstriction
Stridor
Complete airway obstruction
↑ Vascular permeability leading to fluid leakage into interstitium and alveoli
Blood flow to poorly ventilated alveoli is maintained
Ventilation/perfusion (V/Q) mismatch (regions of lung not effectively ventilated despite being well perfused by blood)
Acute Respiratory Distress Syndrome See ARDS Pathogenesis slide
Hypoxemia
Lower airway edema
Wheezing Coughing
Impaired brain function
Muscle weakness
Impaired heart function
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
First published November 10, 2019; Updated on February 12, 2023 on www.thecalgaryguide.com