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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