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Pulmonary aspiration is defined as the passage of foreign material or fluid into the lungs during inspiration. Although food or gastric contents are considered the main culprits, anything from saliva to plastic toys can be aspirated. Aspiration of saliva and gastric contents can occur in normal individuals silently, especially at night. The degree of pathology seen in aspiration syndromes relates to the volume, the type and causticity, and the chronicity of material aspirated. Pathologic aspiration events can be divided into 2 main categories: acute and chronic. The acute events include large-volume aspiration of gastric contents or other fluid, hydrocarbon aspiration, near drowning, and foreign body aspiration. The chronic events include recurrent, small-volume aspiration of saliva, food, upper airway secretions, or gastroesophageal reflux disease (GERD). Large-volume aspiration events (with the exception of many cases of foreign body aspiration, discussed in more detail in Chapter 118) are usually witnessed and can be addressed directly. Recurrent small-volume aspirations often are silent and more difficult to diagnose and manage. It is important to recognize the risk factors to properly diagnose aspiration (Table 504-1).
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PATHOGENESIS AND EPIDEMIOLOGY
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The true hazards of aspiration were not reported in the medical literature until 1946, when Mendelson described the clinical and pathologic findings in obstetric patients who aspirated large-volume gastric contents. He described the “asthma-like” symptoms of these patients and then showed in animal models that acidic material, with pH less than 2.5, caused inflammation, damage, and desquamation of the mucosa in the lungs. Small amounts of aspirated material are usually cleared without consequence. Large-volume aspiration of gastric contents causes a pneumonitis that is the same as that seen with near drowning and consists of desquamation of the epithelium of the bronchi, bronchioles, and alveoli; edema; and hemorrhage. There is a secondary infiltrate of neutrophils and fibrin around the alveoli with resulting atelectasis. Within 48 to 72 hours, hyaline membranes begin to form, and fibroblasts start to ...