Aspiration Pneumonia

Burden of Disease

Microaspiration of oropharyngeal secretions is the main pathogenic mechanism of most cases of community- and hospital-acquired pneumonias. Macroaspiration (large volume) of oropharyngeal or upper gastrointestinal contents is the cause of AP.

AP is an important part of the pneumonia continuum that includes both community- and hospital-acquired infections. Unfortunately, unlike community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP), diagnostic criteria for AP are unavailable. It is thought that up to 15% of CAP cases are AP and they are associated with a higher mortality rate than other forms of CAP (29.4% vs. 11.6%).

Patients with AP usually have risk factors for macroaspiration and the resultant syndromes may involve the airways or pulmonary parenchyma. Macroaspiration can lead to either AP, an infection, or to CP which represents an inflammatory reaction secondary to aspiration of gastric contents.

Microbiology and Pathogenesis

Until recently it was thought that in healthy individuals the lower respiratory tract was sterile. Genomic methods, however, have demonstrated numerous bacterial phylotypes. A complex taxonomic bacterial landscape that includes diverse microbial communities exists in the lung and studies are helping to define the role of the lung microbiome in health and disease and in the pathogenesis of pneumonia. In healthy individuals it is believed that the lung microbiome helps calibrate the immune tone of the airways and alveoli.

To explain the role of the microbiome in the pathogenesis of pneumonia various models have been proposed. An interplay between movement of bacteria into and out of the lungs and local feedback loops may be central to the development of pneumonia. Bacteria may gain access to the lungs by microaspiration and are eliminated by coughing and ciliary clearance. Positive and negative feedback loops can promote or suppress inflammation. An inflammatory event resulting in epithelial or endothelial injury may create a positive loop which can further increase inflammation and local susceptibility to infection.

The complex adaptive system model may help explain the interplay between the lung microbiome and AP. A change in the lung microbiome (dysbiosis) may occur as the result of illness and may then impair local defenses. A significant macroaspiration event could then possibly overwhelm the host’s ability to clear the bacteria further disrupting bacterial homeostasis thereby triggering an increase in a positive feedback loop.

Substances such as cytokines, neurotransmitters, and hormones (e.g., glucocorticoids) can promote growth of bacteria such as S. pneumoniae , and certain gram-negative rods and may result in a shift from a diverse microbiome to one with a dominant species (e.g., pneumococcus or P. aeruginosa ).

With illness or aging, cell surface fibronectin may be lost from the surface of airway epithelial cells exposing receptors on these cells to gram-negative rods which may adhere to them, thereby shifting the oral microbial flora to more virulent bacteria. Colonization of the oropharynx by these new potential pathogens may be followed by their micro- or macroaspiration to the lung.

Historically anaerobes with or without aerobes were typically associated with AP. CP on the other hand is an inflammatory response to acidic gastric contents or bile acids and is not the result of infection. A shift has been noted away from anaerobes to bacteria typically seen with CAP and HAP. In one study, pathogens in community-acquired cases were S. pneumoniae , Staphylococcus aureus , Haemophilus influenzae , and Enterobacteriaceae while in hospital-acquired cases gram-negative rods including P. aeruginosa predominated. Anaerobes are more likely to occur in patients with lung abscess but are far less common in those with AP but no abscess or empyema.

Less importance of anaerobes has also been noted in AP among the elderly. It is postulated that this may be the result of a shift in patient demographic characteristics and to earlier sampling for cultures in the course of infection rather than after development of empyema or abscess.

Risk Factors

Risk factors for AP are those resulting in either increased access of oral or gastric contents to the lower airways or reduced clearance or both ( Fig. 29.1 ). Swallowing dysfunction and impaired cough reflex can occur in a number of settings including neoplasms involving the head, neck, or esophagus, esophageal strictures and motility disorders, chronic obstructive pulmonary disease (COPD), and seizures. Other swallowing difficulties may arise with central nervous system dysfunction, for example multiple sclerosis, parkinsonism, dementia, and impaired consciousness. Reduced consciousness may be secondary to a variety of drugs including narcotics, anesthetic agents, antidepressants, and alcohol. Stroke and cardiac arrest may also be significant. Many of the above may impair the cough reflex which is the primary clearance mechanism.

In some patients, multiple risk factors may exist significantly increasing the risk of AP. Interestingly, if one compares patients with traditional CAP to those with AP there are no significant increases in risk of aspiration in the former group.

Clinical Manifestations

The initial macroaspiration event is often unwitnessed so the magnitude of exposure is often unknown. Even in situations such as aspiration during anesthesia neither clinical nor chest radiographic features develop in 64% of patients.

The clinical presentation may range from mild to severe and occasionally respiratory failure may occur. The findings are dependent to some extent on the nature of the aspirate; for example, bacteria versus noninfectious material such as gastric acid, blood, tube feeding, or a foreign body.

Cases of CP usually require macroaspiration of large-volume, low-pH (<2.5) gastric content. Initially described in the setting of obstetrical anesthesia, it is now uncommon in such circumstances. Lung damage in CP is due to the inflammatory response to the acidic material and involves various chemokines, pro-inflammatory cytokines, and neutrophils.

Following the acute inciting event symptoms may appear within hours to days. These can include cough, wheezing, shortness of breath, tachycardia, and fever. In cases of a solid foreign body aspiration distal airway obstruction may result which could lead to postobstructive pneumonia.

Findings on physical examination may include cyanosis, use of accessory muscles of respiration, wheezing, and rales. Chest radiographic findings may initially be normal but early on or subsequently are more likely to demonstrate bronchopneumonia rather than lobar pneumonia (68% vs. 15%) and posterior infiltrates are common. As a result of airway anatomy right-sided clinical and radiographic findings are more frequent. In cases of aspiration of blood or tube feedings neither CP nor AP usually develops because of the relatively high pH and lack of bacteria.