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materials that enter the bronchial tree, usually oral or gastric contents (including food, saliva, or
nasal secretions). Depending on the acidity of the aspirate, a chemical pneumonitis can develop,
and bacterial pathogens (particularly anaerobic bacteria) may add to the inflammation.
Pathophysiology Concepts
Aspiration is the introduction of a foreign substance into the lungs, but the mere instillation of
foreign substance into the subglottic airway is not sufficient to produce disease. Damage to the
pulmonary tree, which ranges from mild to fatal, depends on the nature, volume and pH of the
aspirated contents, and the pathogenicity of the organisms. Physiologic changes resulting from
aspiration of acidic fluid or gastric contents include a decline in arterial blood oxygen tension,
increased alveolar capillary membrane permeability, and a decrease in intravascular volume. The
lungs can become edematous and gas exchange abnormalities are the result. Histologic
examination shows tracheal mucosal desquamation, damage to the cells of the alveolar lining and
capillary inflammation 24 to 36 hours after aspiration.
Gastric acid aspirant results in chemical burns that destroy alveoli, which results in acute onset of
respiratory distress secondary to widespread bronchospasm, hypoxemia, and parenchymal
infection. The lower the pH (less than or equal to 2.5) the more severe the injury. There is a 30%
incidence of subsequent development of adult respiratory distress syndrome (ARDS) after acidic
aspiration.
Normally, micro-aspirates are cleared by several mechanisms or lines of defense. The materials
are entrapped and removed by filtration, coughing, or by action of the cilia. At the cellular level,
the immune system clears by using inactivation, IgA antibodies, or opsonization, and subsequent
phagocytosis. Loss of these defense mechanisms results in infection and colonization by
pathogenic organisms.