Pathophysiology

Aspiration is best viewed in three stages. Initially, the inhalation of food particles results directly in mechanical obstruction of the airways with distal collapse leading to increased shunt, loss of functional residual capacity, and an increase in the work of breathing. Later, in response to both acid fluid and particulate matter, there is a chemical injury response with bronchorrhea, bronchoconstriction, and mucosal edema. The associated reduction in airway defenses increases the risk of bacterial infection. Histology of airways of animals exposed to gastric contents demonstrates a complete loss of the ciliated epithelial lining during the first 2 days. This leads to vascular leak and increased airway sensitivity to histamine and neuropeptides, all reducing airway patency. Regeneration is rapid unless there is added aspiration of particulate matter, which significantly delays healing. Thus damage is due to both the acidic fluid and the particulate gastric contents. Gastric contents with pH below 2.5 and a volume of 25 to 50 ml have been shown to be far more damaging than an equal volume of a more alkaline fluid. Acid denatures surfactant and activates neutrophils, leading to atelectasis and augmentation of the pro-inflammatory responses. However, even at neutral pH the aspiration of particulate contents is damaging. A comparison of the pulmonary inflammatory potential of small gastric particles to that of acid fluid in rats showed a synergistic increase in alveolar capillary leak from the combination of particles and acid. Use of inert glass particles rather than gastric contents did not have any synergistic effect with acid saline. Lung biopsy of patients with aspiration pneumonia shows parenchymal lung damage with a granulomatous foreign body response and evidence later of fibroproliferation. The final stage of lung injury is due to the inflammatory response with release of tumor necrosis factor, interleukin 1, and other proinflammatory mediators including leukotrienes A4 and B4 and thromboxane A2 which contribute to mucosal edema and bronchoconstriction. This process can develop into acute respiratory distress syndrome.

Sleep Apnea

Sleep Apnea

Have You Been Told Over And Over Again That You Snore A Lot, But You Choose To Ignore It? Have you been experiencing lack of sleep at night and find yourself waking up in the wee hours of the morning to find yourself gasping for air?

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