Aspiration pneumonitis and pneumonia

Aspiration is defined as the misdirection of oropharyngeal or gastric contents into the larynx and lower respiratory tract. The consequent pulmonary syndromes that follow depend on the quantity and nature of the aspirated material, frequency and chronicity of aspiration, and nature of the host’s defense mechanisms. The most important acute syndromes include aspiration pneumonitis, characterized in its most severe form and in a predisposing setting as Mendelson syndrome, a chemical pneumonitis caused by the aspiration of gastric contents, and aspiration pneumonia, an infectious process caused by the aspiration of oropharyngeal secretions that have been colonized by pathogenic bacteria. ^, Although some overlap exists between these two syndromes, they are distinct clinical entities. Consequences of chronic aspiration include bronchiectasis, chronic bronchitis, lipoid pneumonia, interstitial lung disease, organizing pneumonia, bronchiolitis obliterans, diffuse aspiration bronchiolitis, and Mycobacterium fortuitum pneumonia. This chapter focuses on acute aspiration, namely, aspiration pneumonitis and aspiration pneumonia. It is critically important to distinguish between these two syndromes, as their management differs considerably. Aspiration pneumonia is a bacterial pneumonia caused by the aspiration of colonized oropharyngeal secretions. It most commonly develops in elderly patients and those with neurologic disorders. By contrast, aspiration pneumonitis is caused by the inhalation of regurgitated gastric contents, causing a chemical pneumonitis. The administration of antibiotics is central to the management of aspiration pneumonia, whereas the treatment of aspiration pneumonitis is largely supportive. The distinction between these two syndromes is based largely on clinical criteria ( Table 62.1 ). Although gastric biomarkers for aspiration are increasingly available (pepsin, amylase, lipid-laden macrophages), none have been clinically validated. Serum procalcitonin and other inflammatory markers are unable to distinguish aspiration pneumonitis from aspiration pneumonia. This imprecision is not surprising, considering that proinflammatory mediators play a central role in the pathophysiology of both syndromes and are responsible for the transcription of procalcitonin.

TABLE 62.1

Contrasting Features of Aspiration Pneumonitis and Aspiration Pneumonia

Reproduced with permission from New England Journal of Medicine, Copyright Massachusetts Medical Society.

Feature	Aspiration Pneumonitis	Aspiration Pneumonia
Mechanism	Aspiration of sterile gastric contents	Aspiration of colonized oropharyngeal material
Pathophysiologic process	Acute lung injury from acidic and particulate matter	Acute pulmonary inflammatory response to bacteria and bacteria products
Bacteriologic findings	Initially sterile, with subsequent bacterial infection possible	Gram-negative rods, gram-positive cocci, and rarely, anaerobic bacteria
Major predisposing factors	Depressed level of consciousness	Dysphagia and gastric dysmotility
Age group affected	Any age group, but usually young persons	Usually elderly persons
Aspiration event	May be witnessed	Usually not witnessed
Typical presentation	Patient with a history of depressed level of consciousness in whom a pulmonary infiltrate and respiratory symptoms develop	Institutionalized patient who presents with features of a “community-acquired pneumonia” with an infiltrate in a dependent bronchopulmonary segment
Clinical features	No symptoms, or symptoms ranging from a nonproductive cough to tachypnea, bronchospasm, bloody or frothy sputum, and respiratory distress	Tachypnea, cough, fever, and signs of pneumonia

Aspiration pneumonitis

Aspiration pneumonitis is best defined as acute lung injury after the aspiration of regurgitated gastric contents. This problem occurs in patients with marked disturbances of consciousness, such as drug overdose, seizures, coma resulting from acute neurologic insults, massive cerebrovascular accident, head trauma, and general anesthesia. Adnet and Baud demonstrated an association between the degree of altered mental status as measured by Glasgow Coma Scale and aspiration, supporting the pathophysiologic link between these entities. In clinical practice, drug overdose is the most common cause of aspiration pneumonitis, occurring in approximately 10% of patients hospitalized after massive drug ingestion. Aspiration pneumonitis also occurs commonly with acute alcohol intoxication and after a generalized seizure. Historically the syndrome most commonly associated with aspiration pneumonitis is Mendelson syndrome, reported in 1946 in obstetric patients who aspirated while receiving general anesthesia.

Although aspiration is a widely feared complication of general anesthesia, clinically apparent aspiration in nonemergent situations is exceptionally rare in modern anesthesia practice, and in healthy patients the overall morbidity and mortality are low. Nevertheless, aspiration pneumonitis is an important perioperative complication and remains the most common cause of anesthesia-associated fatality, accounting for between 10% and 30% of all anesthetic deaths. The risk of aspiration with modern anesthesia is reported to be between 2.9 and 4.7 per 10,000 general anesthetics (about 1 in 3000 anesthetics), with a mortality incidence of approximately 1:125,000. ^, Emergency surgery (particularly trauma and abdominal surgery with delayed gastric emptying), procedures performed at night, inadequate anesthesia, obesity, obstetric patients, elderly immobilized patients, and patients with obstructive sleep apnea are considered to be at a higher risk of such aspiration. ^,

Pathophysiology

Mendelson emphasized the importance of acid when he showed that un-neutralized gastric contents introduced into the lungs of rabbits caused severe pneumonitis indistinguishable from that caused by an equal amount of 0.1 N hydrochloric acid. ^, ^, However, if the pH of the vomitus was neutralized before aspiration, the pulmonary injury was minimal. Experimental studies have demonstrated that the severity of lung injury increases significantly with the volume of the aspirate and less directly with its pH; a pH of less than 2.5 is typically required to cause severe aspiration pneumonitis. In experimental models, a two-phase injury results when acid is instilled into the lungs. The initial injury phase (within 1 hour of acid exposure) is primarily because of the acid’s direct caustic effects on pulmonary tissue, whereas the second injury phase (beginning at 3–4 hours and peaking at 4–6 hours postexposure) results from the products released by recruited neutrophils. ^, The intensity of the alveolar neutrophil infiltration correlates with the severity of the acute lung injury. Once localized to the lung, neutrophils play a key role in the development of lung injury through the release of reactive oxygen species (ROS) and proteases that are injurious to the lung. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the major source of ROS in activated polymorhpho nuclear leukocytes, (PMNs;). Other sources of ROS after gastric aspiration include superoxide anions generated by xanthine oxidase. ROS exacerbate acute lung injury through several mechanisms, including direct cellular injury, nuclear factor-κB (NF-κB) activation, and activation of other proinflammatory mediators such as tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8). The activation of NADPH oxidase in neutrophils is linked to the generation of neutrophil extracellular traps (NETs). NETs are extracellular strands of decondensed (unwound) DNA in complex with histones and neutrophil granule proteins. NETs contain serine proteases and other antimicrobial products that damage the lung.

The stomach contains a variety of substances in addition to acid. Several experimental studies have demonstrated that aspiration of small, particulate food matter from the stomach may cause severe pulmonary damage, even if the pH of the aspirate exceeds 2.5. ^, These studies suggest that cell recruitment and expression of inflammatory mediators are most pronounced after injury with combined acid and small food particles. These data are supported by findings in patients in whom the most severe lung injury was observed after aspiration of gastric fluids with particulate food matter. ^, In healthy subjects, gastric acid prevents the growth of bacteria, and the contents of the stomach are normally sterile. Bacterial infection therefore does not play a significant role in the early stages of acute lung injury after aspiration of gastric contents.

Clinical presentation

Aspiration of gastric contents can present dramatically, with a full-blown picture that includes gastric contents in the oropharynx, wheezing, coughing, shortness of breath, cyanosis, pulmonary edema, hypotension, and hypoxemia, which may progress rapidly to severe acute respiratory distress syndrome (ARDS) and death ( Fig. 62.1 ). However, many patients may not express impressive signs or symptoms associated with aspiration, whereas others may simply develop a new cough or wheeze. In some patients, aspiration may be clinically silent, manifesting only as arterial desaturation with radiologic evidence of aspiration. Warner and colleagues studied 67 patients who aspirated while undergoing anesthesia. Forty-two (63%) of these patients were totally asymptomatic, 13 required mechanical ventilatory support for more than 6 hours, and 4 died.

Fig. 62.1, Chest radiograph demonstrating severe bilateral air space disease (ARDS) in a patient who aspirated after anesthesia.

Management of aspiration pneumonitis

The upper airway should be suctioned after a witnessed aspiration. Endotracheal intubation should be strongly considered in patients who are unable to protect the airway. Although common practice, the prophylactic use of antibiotics in patients with strongly suspected or witnessed aspiration is not recommended. ^, Similarly, the use of antibiotics shortly after an aspiration episode is discouraged in most patients who develop a fever, leukocytosis, and a pulmonary infiltrate, as their use may simply encourage overgrowth of resistant organisms in an otherwise uncomplicated chemical pneumonitis. However, empiric antimicrobial therapy is appropriate in patients who aspirate gastric contents in the setting of small bowel obstruction or in other circumstances associated with colonization of gastric contents. Antimicrobial therapy should be considered in patients with an aspiration pneumonitis that fails to resolve within 48 hours. Empiric therapy with broad-spectrum agents is recommended. Antimicrobials with anaerobic activity are not routinely required.

Corticosteroids are potent antiinflammatory agents that act largely by repression of the transcriptional activity of NF-κB. Glucocorticoids have been used in the management of aspiration pneumonitis since 1955 ; however, their role as monotherapy appears restricted, possibly because of their limited effects on neutrophils and ROS. Vitamin C, acting synergistically with low-dose corticosteroids and thiamine, has emerged as an important strategy in treating various conditions characterized by widespread and profound inflammation. Vitamin C is a potent antioxidant and inhibitor of NAPDH oxidase and would likely reduce the severity of acute lung injury after acid aspiration. In addition, vitamin C inhibits NETosis. We have previously described two patients with “anesthesia-related” aspiration pneumonitis and severe ARDS who were treated with hydrocortisone, ascorbic acid, and thiamine (HAT therapy) who appeared to respond dramatically to this intervention. Mixed results have been reported from prospective randomized controlled trials that explored the potential benefits of this treatment strategy in the management of sepsis and ARDS. We suggest, however, that this simple, safe, readily available, and cheap intervention be strongly considered in patients with acid aspiration–induced acute lung injury.

Prevention of aspiration during anesthesia

In recent years, more liberal preoperative fasting guidelines have been promoted. In heathy adults without an increased risk of regurgitation or aspiration, solids should be avoided after midnight; however, a light meal such as dry toast may be considered up to 6 hours before anesthesia, and clear liquids such as water, coffee without milk, or fruit juice can be ingested up to 2 hours before induction. ^, Meta-analyses of randomized controlled trials comparing fasting times of 2–4 hours with more than 4 hours report smaller gastric volumes and higher gastric pH values in adult patients given clear liquids 2–4 hours before a procedure, and this approach is currently endorsed by the American Society of Anesthesiology (ASA).

Preoperative antacids, histamine-2 (H2) receptor blockers, proton pump inhibitors (PPIs), and prokinetic agents have been used to reduce the volume and/or acidity of the gastric contents and hence the risk of aspiration and its consequences. There is, however, a lack of data indicating that any of these drugs reduce the risk of aspiration pneumonia. The routine use of these drugs is not recommended by the ASA guidelines. Standard teaching suggests that rapid-sequence induction with cricoid pressure should be performed when intubating patients at increased risk of aspiration. Although not proven to reduce the risk of aspiration during emergent intubations, cricoid pressure is currently considered the standard of care in this situation.

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