Aspiration Pneumonitis and Pneumonia

Published on 22/03/2015 by admin

Last modified 22/03/2015

Print this page

This article have been viewed 2661 times

59 Aspiration Pneumonitis and Pneumonia

Aspiration is defined as the misdirection of oropharyngeal or gastric contents into the larynx and lower respiratory tract.¹ The pulmonary syndromes that commonly follow depend on the quantity and nature of the aspirated material, frequency of aspiration, and the nature of the host’s defense mechanisms and response. The most important syndromes include aspiration pneumonitis, or 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 colonized by pathogenic bacteria.¹ There is some overlap between these two syndromes, but they are distinct clinical entities (Table 59-1). Other aspiration syndromes include airway obstruction, lung abscess, exogenous lipoid pneumonia, chronic interstitial fibrosis, and Mycobacterium fortuitum pneumonia.

TABLE 59-1 Contrasting Features of Aspiration Pneumonitis and Aspiration Pneumonia

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 bacterial 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 2 to 5 hours after aspiration	Tachypnea, cough, fever, and signs of pneumonia

Reproduced with permission from Marik PE. Aspiration pneumonitis and pneumonia: a clinical review. N Engl J Med. 2001;344(9):665-672.

Aspiration Pneumonitis

Aspiration pneumonitis is best defined as acute lung injury (ALI) following the aspiration of regurgitated gastric contents.¹ This syndrome occurs in patients with a marked disturbance of consciousness such as drug overdose, seizures, massive cerebrovascular accident, following head trauma, and after or during anesthesia. Drug overdose is the most common cause of aspiration pneumonitis, occurring in approximately 10% of patients hospitalized following a drug overdosage. Adnet and Baut demonstrated that the risk of aspiration increases with the degree of unconscious (as measured by the Glasgow Coma Scale).² Historically, the syndrome most commonly associated with aspiration pneumonitis is Mendelson syndrome, reported in 1946 in obstetric patients who aspirated while receiving general anesthesia.³ Mendelson’s original report consisted of 44,016 non-fasted obstetric patients he studied between 1932 and 1945. Of these, more than half received an “operative intervention” with ether by mask without endotracheal intubation. He described aspiration in 66 patients (1:667). Although several became critically ill from their aspiration, “recovery was usually complete” within 24 to 36 hours, and only 2 patients died (1:22,008).

Epidemiology and Risk Factors

Although aspiration is a widely feared complication of general anesthesia, clinically apparent aspiration in modern anesthesia practice is exceptionally rare, and in healthy patients the overall morbidity and mortality are low. The risk of aspiration with modern anesthesia is about 1 in 3000 anesthetics, with a mortality of approximately 1 : 125,000 and accounting for between 10% and 30% of all anesthetic deaths.^4,⁵ The risk of aspiration is greatly increased in patients intubated emergently in the field, emergency room, or intensive care unit (ICU). The risk factors for aspiration are listed in Table 59-2. In these patients, every effort should be made to reduce the risk of aspiration; this includes removing dentures, clearing the airway, and (in certain circumstances) placing a nasogastric tube to empty the stomach prior to intubation. If there is an immediate risk of airway compromise, endotracheal intubation should be performed prior to placement of a nasogastric tube. However, if the patient is likely to have a full stomach (upper-gastrointestinal bleed, small-bowel obstruction, ileus, etc.), it may be prudent to place a nasogastric tube prior to endotracheal intubation. When intubating emergently, suction equipment must be immediately available and rapid-sequence induction using cricoid pressure should be performed.

TABLE 59-2 Factors That Increase Risk of Aspiration During Endotracheal Intubation

Pathophysiology

Mendelson emphasized the importance of acid when he showed that unneutralized 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.³ However, if the pH of the vomitus was neutralized before aspiration, pulmonary injury was minimal. Experimental studies have demonstrated that the severity of lung injury increases significantly with the volume of aspirate and indirectly with its pH, with a pH of less than 2.5 being required to cause aspiration pneumonitis. However, the stomach contains a variety of other substances in addition to acid. Several experimental studies have revealed that aspiration of small particulate food matter from the stomach may cause severe pulmonary damage, even if the pH of the aspirate is above 2.5.

Aspiration of gastric contents results in a chemical burn of the tracheobronchial tree and pulmonary parenchyma, with an intense parenchymal inflammatory reaction. Proinflammatory cytokines, including tumor necrosis factor α (TNF-α) and CXC chemokines such as interleukin 8 (IL-8), are crucial to the development of aspiration pneumonitis by mediating neutrophil recruitment. Once localized to the lung, neutrophils play a key role in the development of lung injury through release of oxygen radicals and proteases. Gastric acid prevents the growth of bacteria, so stomach contents are normally sterile. Bacterial infection, therefore, does not play a significant role in the early stages of acute lung injury following aspiration of gastric contents. However, acid aspiration pneumonitis reduces host defenses against infection, increasing the risk of superinfection.⁶ The incidence of this complication has not been well studied, but experimental models suggest that acid-aspiration pneumonitis “primes the lung,” making secondary infection more severe.^6,⁷ Colonization of gastric contents by potentially pathogenic organisms may occur when the gastric pH is increased by the use of antacids, H₂ blockers, or proton pump inhibitors. In addition, gastric colonization by gram-negative bacteria occurs in patients receiving gastric enteral feedings, as well as in patients with gastroparesis and small-bowel obstruction. In these circumstances, the pulmonary inflammatory response is likely to result from both bacterial infection and the inflammatory response of the gastric particulate matter. It is also important to note that atrophic gastritis and gastric colonization is common in elderly patients; aspiration of vomitus by these patients is likely to result in an inflammatory response due to bacteria and particulate matter.

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. Many patients may not develop signs or symptoms associated with aspiration, whereas others may develop a 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.⁴ Forty-two (64%) of these patients were totally asymptomatic, 13 required mechanical ventilatory support for more than 6 hours, and 4 died.

Management

The upper airway should be suctioned following a witnessed aspiration. Endotracheal intubation should be considered in patients who are unable to protect their airway. While common practice, the prophylactic use of antibiotics in patients with suspected or witnessed aspiration is not recommended. Similarly, the use of antibiotics shortly after an aspiration episode in a patient who develops fever, leukocytosis, and a pulmonary infiltrate is discouraged, because it may select for more resistant organisms in a patient with an uncomplicated chemical pneumonitis. However, empirical 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 the stomach. Antimicrobial therapy should be considered in patients with an aspiration pneumonitis that fails to resolve within 48 hours. Empirical therapy with broad-spectrum agents is recommended. Antimicrobials with anaerobic activity are not routinely required. Lower respiratory tract sampling (protected specimen brush/bronchoalveolar lavage) and quantitative culture in intubated patients may allow targeted antimicrobial therapy and discontinuation of antibiotics in culture-negative patients.⁸

Immunomodulating Agents

Corticosteroids have been used in the management of aspiration pneumonitis since 1955.⁹ However, limited data exist for evaluating the role of these agents, with only a single prospective placebo-controlled study having been performed. In that study, Sukumaran et al. randomized 60 patients with “aspiration pneumonitis” to methylprednisolone (15 mg/kg/day for 3 days) or placebo.¹⁰ The patients were subdivided into two groups: a younger group with drug overdose as the predominant diagnosis and an older group with neurologic disorders. In the overdose group, 87% had an initial gastric pH below 2.5, compared to 12.8% in the neurologic group; 77.6 patients in the overdose group were admitted from the community, compared to 12.8% of patients in the neurologic group. Radiographic changes improved more rapidly in the steroid group, as did oxygenation. The number of ventilator and ICU days was significantly shorter in the overdose patients who received corticosteroids; however, these variables were longer in the neurologic group. There was no significant difference in the incidence of complications or outcome. The results of this study are somewhat difficult to interpret, as it is likely that the patients in the overdose group had true aspiration pneumonitis, whereas many patients in the neurologic group probably developed aspiration pneumonia. In addition, patients received a short course of high-dose corticosteroids. Current evidence suggests that patients with ARDS may benefit from a prolonged course of low-dose corticosteroids, but a short course of high-dose corticosteroids may be harmful.^11,¹² Wolfe and colleagues performed a case-controlled study of 43 patients with aspiration pneumonitis, of whom 25 received high-dose corticosteroids (approximately 600 mg prednisolone/day for 4 days).¹³ There was no difference in mortality, but secondary gram-negative pneumonia was reported to be more frequent in the steroid group (7/20 versus 0/13); however, ventilator days tended to be fewer in this group (4.3 versus 9.8 days). Based on these limited data, it is not possible to make evidence-based recommendations on the use of corticosteroids in patients with acid-aspiration pneumonia. However, more recent literature suggests that patients with ARDS may benefit from a prolonged course of low dose corticosteroids, so this approach should be considered.^11,¹²

In animal models, a number of pharmacologic interventions (e.g., inhaled β₂-agonists, pentoxifylline, antiplatelet drugs, omega-3 fatty acids) have been shown to attenuate acute lung injury following acid aspiration,¹⁴^–¹⁹ but the role of these interventions in humans remains to be tested. Because of their inherent safety, these agents should at least be considered in patients with severe acid-aspiration pneumonitis.