الفهرس 
• Pathophysiology of smoke inhalation injuryOnly 14 pages are availabe for public view
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Abstract
Inhalation injury can result from direct local thermal & chemical exposures, immune responses to these factors, systemic effects of inhaled toxins, accrual of endobronchial debris, and secondary infection. Structural fires generate smoke that contains a large variety of chemicals, products of incomplete combustion, and aerosolized debris of widely varying particle sizes.
There is no ideal respiratory support strategy for the patient with inhalation injury. Consensus recommendations for mechanical ventilation continue to serve as general guidelines.
Bronchodilators act to decrease airflow resistance and improve dynamic compliance. β2-adrenergic agents lead to decreased airway pressure via smooth muscle relaxation and increased PaO2/FiO2 by limiting the degree of broncho-constriction. Muscarinic receptor antagonists, such as tiotropium or ipratropium, prevent smooth muscle constriction within the airways (Boyer et al., 2016).
NAC (N-acetylcysteine ) is a powerful mucolytic agent commonly used in the treatment of smoke inhalation injury, and it is indicated for patients with abnormal inspissated mucus secretions (Enkhbaatar et al., 2016).
Inhaled anticoagulants decrease the formation of fibrin casts following inhalation injury but do not alter systemic markers of clotting and anticoagulation (Mlcak, 2017).
AT (antithrombin) therapy for patients with major burn and inhalation injuries may be a very valuable adjunct to standard treatment (Kowal-Vern et al., 2016).