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Are antibiotics indicated for the treatment of aspiration pneumonia?
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Ehab Daoud, MD
Jorge Guzman, MD

Antibiotics are indicated for primary bacterial aspiration pneumonia and secondary bacterial infection of aspiration (chemical) pneumonitis, but not for uncomplicated chemical pneumonitis.

THREE TYPES OF ‘ASPIRATION PNEUMONIA’

Aspiration pneumonia is a broad and vague term mainly used to refer to the pulmonary consequences of abnormal entry of exogenous or endogenous substances into the lower airways. It can be classified as:

  • Aspiration (chemical) pneumonitis
  • Primary bacterial aspiration pneumonia
  • Secondary bacterial infection of chemical pneumonitis.

These three are sometimes difficult to differentiate, as their signs and symptoms can overlap.

CHEMICAL PNEUMONITIS

Aspiration of stomach contents is relatively common, even in healthy people, and usually has no clinical consequences.1 However, it has also been closely related to community-acquired and nosocomial pneumonia in some studies.2,3

Chemical pneumonitis is usually a consequence of the aspiration of a large volume (≥ 4 mL/kg) of sterile acidic (pH < 2.5) gastric contents into the lower airways (Mendelson syndrome).4,5 The clinical picture varies from asymptomatic to signs of severe dyspnea, hypoxia, cough, and low-grade fever; these signs and symptoms may develop rapidly, within minutes to hours after a witnessed or suspected episode of aspiration.2,6,7 However, they represent an inflammatory reaction to the gastric acid rather than a reaction to bacterial infection.8–10

Chemical pneumonitis affects the most dependent regions of the lungs

Chest radiography shows infiltrates in the most dependent regions of the lung. If aspiration occurs while the patient is supine, the posterior segments of the upper lobes and the apical segments of the lower lobes are most affected. The basal segments of the lower lobes are usually affected if aspiration occurs while the patient is standing or upright.1,2,11,12

Clinical course varies

The clinical course varies. In almost 60% of cases, the patient’s condition improves and the lung infiltrates resolve rapidly, within 2 to 4 days. On the other hand, in about 15% of cases, the patient’s condition deteriorates quickly, within 24 to 36 hours, and progresses to hypoxic respiratory failure and acute respiratory distress syndrome.

In the other 25% of cases, the patient’s condition may improve initially but then worsen as a secondary bacterial infection sets in. The death rate in these patients is almost three times higher than the rate in patients with uncomplicated chemical pneumonitis.11,13

Treatment of uncomplicated cases is mainly supportive

The treatment of uncomplicated chemical pneumonitis involves supportive measures such as airway clearance, oxygen supplementation, and positive pressure ventilation if needed. An obstructing foreign body may need to be removed.12,14 Corticosteroids have been tried, without success.11–13,15

Empiric antibiotic treatment is controversial

Chemical pneumonitis can be difficult to differentiate from bacterial aspiration pneumonia, and whether to give antibiotics is controversial. 16 A survey of current practices among intensivists showed that antimicrobial therapy was often given empirically for noninfectious chemical pneumonitis.17 This practice raises concerns of higher treatment costs and antibiotic resistance.16,18,19 Additionally, antibiotics do not seem to alter the clinical outcome, including radiographic resolution, duration of hospitalization, or death rate, nor do they influence the subsequent development of infection.1,11,13,20

In cases of witnessed or strongly suspected aspiration of gastric contents, antibiotics are not warranted since bacterial infection is not likely to be the cause of any signs or symptoms. 2,7,16 However, to detect secondary infection early, the patient’s respiratory status should be monitored carefully and chest radiography should be repeated.

In less clear-cut cases, ie, if it is not clear whether the patient actually has chemical pneumonitis or primary bacterial aspiration pneumonia, it is prudent to start antibiotics empirically after obtaining lower-respiratory-tract secretions for stains and cultures, and then to reassess within 48 to 72 hours. The antibiotics can be discontinued if the patient has rapid clinical and radiographic improvement and negative cultures. Those whose condition does not improve or who have positive cultures should receive a full course of antibiotics.21,22

 

 

PRIMARY BACTERIAL ASPIRATION PNEUMONIA

Primary bacterial aspiration pneumonia—ie, caused by bacteria residing in the upper airways and stomach gaining access to lower airways through aspiration in small or large amounts—is the most common form of aspiration pneumonia, although the actual episode of aspiration is seldom observed.

Signs of bacterial pneumonia

Primary bacterial aspiration pneumonia bears the hallmarks of bacterial pneumonia.12 The clinical picture is more indolent than chemical pneumonitis and includes cough, fever, and putrid sputum, mainly in patients who have clinical conditions predisposing to aspiration (eg, coma, stroke, alcoholism, poor dentition, tube feedings).1,12,20

The characteristic signs on chest radiography are infiltrates involving mainly the lung bases (the right more then the left). If untreated or inadequately treated, complications such as lung abscess, empyema, bronchiectasis, and broncopleural fistula are common.23

Are aerobic organisms replacing anaerobic ones in the community?

The causative organisms in community-acquired aspiration pneumonia are still debated despite abundant research. Older studies1,24,25 found mostly anaerobic organisms (pepto-streptococci, peptococci, Fusobacterium, Prevotela, Bacteroides) as the underlying pathogens, whereas more recent studies16,26,27 found mostly aerobic organisms (Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Enterobacteriaceae) and failed to recover anaerobic organisms. These discrepancies may be the result of different techniques used to isolate organisms: older studies used transtracheal sampling, and transtracheal aspirates may be easily contaminated or colonized by oropharyngeal flora; more recent studies used protected specimen brushes to collect lower-airway specimens.2

In addition, the pathogenic organisms that predominate in community-acquired aspiration pneumonia, as listed above, are different from those most often found in nosocomial cases; gram-negative bacilli (Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli) are most often isolated in patients with aspiration pneumonia acquired in hospitals and nursing homes.16,27,28S aureus also is an important causative organism in nosocomial cases.16,28

Knowing the causative organisms in bacterial aspiration pneumonia is important for guiding antimicrobial therapy.

Antibiotics are required for bacterial aspiration pneumonia

A course of antibiotics is required for bacterial aspiration pneumonia. While there are no definitive recommendations for the duration of treatment, 7 to 8 days is probably appropriate in uncomplicated cases (ie, no lung abscess, empyema, bronchopleural fistula).22,29 Patients who have complications may need drainage of abscesses or empyema along with a longer duration of antibiotic therapy until clinical and radiographic signs improve.

For community-acquired cases of aspiration pneumonia, a number of antibiotics have proven effective:

  • Clindamycin (Cleocin) is still the agent most commonly used, although it lacks gram-negative bacterial coverage.
  • Beta-lactam penicillins and newer quinolones have been used successfully.2,29–31 In addition to covering the previously mentioned bacteria, these antibiotics have the added benefit of covering anaerobic bacteria.
  • Metronidazole (Flagyl) should not be used alone because it has a higher clinical failure rate.32,33

For nosocomial aspiration pneumonia, giving a broad-spectrum antibiotic empirically is warranted. Beta-lactam penicillins with extended gram-negative coverage, carbapenems, or monobactams in combination with an anti-staphylococcal drug have been advocated for nosocomial aspiration.2,22 A strategy of broad-spectrum coverage followed by narrowing or de-escalating coverage according to lower respiratory tract cultures is encouraged.21,22,34

SECONDARY BACTERIAL INFECTION OF CHEMICAL PNEUMONITIS

Nearly 25% of patients with chemical pneumonitis improve initially, then show clinical deterioration secondary to superimposed bacterial infection.13 Chest radiographs show worsening of initial infiltrates or the development of new ones. The causative organisms and treatment depend on whether the superimposed infection is community-acquired or nosocomial, as is the case in primary bacterial aspiration pneumonia.

PREVENTING ASPIRATION

Measures should be taken to prevent aspiration pneumonia and chemical pneumonitis, especially in institutionalized patients at high risk.12

Elevation of the head of the bed while feeding, dental prophylaxis, and good oral hygiene are known to reduce the incidence of these problems.35–37

A swallowing evaluation for patients with dysphagia can identify those at higher risk of aspiration. These patients may be candidates for postural adjustments, diet modification, strengthening, and other measures offered by the speech and language pathology teams to improve swallowing physiology, biomechanics, safety, and endurance.2,35

Although percutaneous endoscopic gastrostomy tubes are often placed in patients who have aspirated or who are at high risk of aspiration, they do not protect against aspiration, nor do orogastric or nasogastric tubes.38

To date, we have no evidence that prophylactic antibiotic therapy prevents bacterial aspiration pneumonia. In addition, this practice encourages the development of resistant organisms.19,39,40

References
  1. Bartlett JG, Gorbach SL. The triple threat of aspiration pneumonia. Chest 1975; 68:560–566.
  2. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001; 344:665–671.
  3. Kikuchi R, Watabe N, Konno T, Mishina N, Sekizawa K, Sasaki H. High incidence of silent aspiration in elderly patients with community-acquired pneumonia. Am J Respir Crit Care Med 1994; 150:251–253.
  4. Mendelson CL. The aspiration of stomach contents into lungs during obstetric anesthesia. Am J Obstet Gynecol 1946; 52:191–205.
  5. Cameron JL, Caldini P, Toung JK, Zuidema GD. Aspiration pneumonia: physiologic data following experimental aspiration. Surgery 1972; 72:238–245.
  6. Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 1993; 78:56–62.
  7. DePaso WJ. Aspiration pneumonia. Clin Chest Med 1991; 12:269–284.
  8. Folkesson HG, Matthay MA, Hébert CA, Broaddus VC. Acid aspiration-induced lung injury in rabbits is mediated by interleukin-8-dependent mechanisms. J Clin Invest 1995; 96:107–116.
  9. Goldman G, Welbourn R, Kobzik L, Valeri CR, Shepro D, Hechtman HB. Tumor necrosis factor-alpha mediates acid aspiration-induced systemic organ injury. Ann Surg 1990; 212:513–519.
  10. LeFrock JL, Clark TS, Davies B, Klainer AS. Aspiration pneumonia: a ten-year review. Am Surg 1979; 45:305–313.
  11. Cameron JL, Mitchell WH, Zuidema GD. Aspiration pneumonia. Clinical outcome following documented aspiration. Arch Surg 1973; 106:49–52.
  12. Arms RA, Dines DE, Tinstman TC. Aspiration pneumonia. Chest 1974; 65:136–139.
  13. Bynum LJ, Pierce AK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis 1976; 114:1129–1136.
  14. Merchant SN, Kirtane MV, Shah KL, Karnik PP. Foreign bodies in the bronchi (a 10 year review of 132 cases). J Postgrad Med 1984; 30:219–223.
  15. Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med 1977; 63:719–722.
  16. Kane-Gill SL, Olsen KM, Rebuck JA, et al; Aspiration Evaluation Group of the Clinical Pharmacy and Pharmacology Section. Multicenter treatment and outcome evaluation of aspiration syndromes in critically ill patients. Ann Pharmacother 2007; 41:549–555.
  17. Rebuck JA, Rasmussen JR, Olsen KM. Clinical aspiration-related practice patterns in the intensive care unit: a physician survey. Crit Care Med 2001; 29:2239–2244.
  18. Singh N, Rogers P, Atwood CW, Wagener MM, Yu VL. Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. A proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med 2000; 162:505–511.
  19. Kollef MH, Fraser VJ. Antibiotic resistance in the intensive care unit. Ann Intern Med 2001; 134:298–314.
  20. Lewis RT, Burgess JH, Hampson LG. Cardiorespiratory studies in critical illness. Changes in aspiration pneumonitis. Arch Surg 1971; 103:335–340.
  21. Rello J. Importance of appropriate initial antibiotic therapy and de-escalation in the treatment of nosocomial pneumonia. Eur Respir Rev 2007; 16:33–39.
  22. American Thoracic Society. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005; 171:388–416.
  23. Bartlett JG. Anaerobic bacterial infections of the lung and pleural space. Clin Infect Dis 1993; 16(suppl 4):S248–S255.
  24. Lorber B, Swenson RM. Bacteriology of aspiration pneumonia. A prospective study of community- and hospital-acquired cases. Ann Intern Med 1974; 81:329–331.
  25. Bartlett JG, Gorbach SL, Finegold SM. The bacteriology of aspiration pneumonia. Am J Med 1974; 56:202–207.
  26. Mier L, Dreyfuss D, Darchy B, et al. Is penicillin G an adequate initial treatment for aspiration pneumonia? A prospective evaluation using a protected specimen brush and quantitative cultures. Intensive Care Med 1993; 19:279–284.
  27. Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study. Chest 1999; 115:178–183.
  28. El-Solh AA, Pietrantoni C, Bhat A, et al. Microbiology of severe aspiration pneumonia in institutionalized elderly. Am J Respir Crit Care Med 2003; 167:1650–1654.
  29. Mandell LA, Wunderink RG, Anzueto A, et al; Infectious Diseases Society of America. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007; 44(suppl 2):S27–S72.
  30. Kadowaki M, Demura Y, Mizuno S, et al. Reappraisal of clindamycin IV monotherapy for treatment of mild-to-moderate aspiration pneumonia in elderly patients. Chest 2005; 127:1276–1282.
  31. Ott SR, Allewelt M, Lorenz J, Reimnitz P, Lode H; German Lung Abscess Study Group. Moxifloxacin vs ampicillin/sulbactam in aspiration pneumonia and primary lung abscess. Infection 2008; 36:23–30.
  32. Perlino CA. Metronidazole vs clindamycin treatment of anerobic pulmonary infection. Failure of metronidazole therapy. Arch Intern Med 1981; 141:1424–1427.
  33. Sanders CV, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic infections. Am Rev Respir Dis 1979; 120:337–343.
  34. Alvarez-Lerma F, Alvarez B, Luque P, et al; ADANN Study Group. Empiric broad-spectrum antibiotic therapy of nosocomial pneumonia in the intensive care unit: a prospective observational study. Crit Care 2006; 10:R78.
  35. Johnson JL, Hirsch CS. Aspiration pneumonia. Recognizing and managing a potentially growing disorder. Postgrad Med 2003; 113:99–112.
  36. Scolapio JS. Methods for decreasing risk of aspiration pneumonia in critically ill patients. JPEN J Parenter Enteral Nutr 2002; 26(suppl 6):S58–S61.
  37. Orozco-Levi M, Torres A, Ferrer M, et al. Semirecumbent position protects from pulmonary aspiration but not completely from gastroesophageal reflux in mechanically ventilated patients. Am J Respir Crit Care Med 1995; 152:1387–1390.
  38. Park RH, Allison MC, Lang J, et al. Randomised comparison of percutaneous endoscopic gastrostomy and nasogastric tube feeding in patients with persisting neurological dysphagia. BMJ 1992; 304( 6839):1406–1409.
  39. Donskey CJ, Chowdhry TK, Hecker MT, et al. Effect of antibiotic therapy on the density of vancomycin-resistant enterococci in the stool of colonized patients. N Engl J Med 2000; 343:1925–1932.
  40. Mouw DR, Langlois JP, Turner LF, Neher JO. Clinical inquiries. Are antibiotics effective in preventing pneumonia for nursing home patients? J Fam Pract 2004; 53:994–996.
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Ehab Daoud, MD
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Jorge Guzman, MD
Department of Pulmonary, Allergy, and Critical Care Medicine, Respiratory Institute, Cleveland Clinic

Address: Ehab Daoud, MD, Department of Pulmonary, Allergy, and Critical Care Medicine, G62, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail [email protected]

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Address: Ehab Daoud, MD, Department of Pulmonary, Allergy, and Critical Care Medicine, G62, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail [email protected]

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Antibiotics are indicated for primary bacterial aspiration pneumonia and secondary bacterial infection of aspiration (chemical) pneumonitis, but not for uncomplicated chemical pneumonitis.

THREE TYPES OF ‘ASPIRATION PNEUMONIA’

Aspiration pneumonia is a broad and vague term mainly used to refer to the pulmonary consequences of abnormal entry of exogenous or endogenous substances into the lower airways. It can be classified as:

  • Aspiration (chemical) pneumonitis
  • Primary bacterial aspiration pneumonia
  • Secondary bacterial infection of chemical pneumonitis.

These three are sometimes difficult to differentiate, as their signs and symptoms can overlap.

CHEMICAL PNEUMONITIS

Aspiration of stomach contents is relatively common, even in healthy people, and usually has no clinical consequences.1 However, it has also been closely related to community-acquired and nosocomial pneumonia in some studies.2,3

Chemical pneumonitis is usually a consequence of the aspiration of a large volume (≥ 4 mL/kg) of sterile acidic (pH < 2.5) gastric contents into the lower airways (Mendelson syndrome).4,5 The clinical picture varies from asymptomatic to signs of severe dyspnea, hypoxia, cough, and low-grade fever; these signs and symptoms may develop rapidly, within minutes to hours after a witnessed or suspected episode of aspiration.2,6,7 However, they represent an inflammatory reaction to the gastric acid rather than a reaction to bacterial infection.8–10

Chemical pneumonitis affects the most dependent regions of the lungs

Chest radiography shows infiltrates in the most dependent regions of the lung. If aspiration occurs while the patient is supine, the posterior segments of the upper lobes and the apical segments of the lower lobes are most affected. The basal segments of the lower lobes are usually affected if aspiration occurs while the patient is standing or upright.1,2,11,12

Clinical course varies

The clinical course varies. In almost 60% of cases, the patient’s condition improves and the lung infiltrates resolve rapidly, within 2 to 4 days. On the other hand, in about 15% of cases, the patient’s condition deteriorates quickly, within 24 to 36 hours, and progresses to hypoxic respiratory failure and acute respiratory distress syndrome.

In the other 25% of cases, the patient’s condition may improve initially but then worsen as a secondary bacterial infection sets in. The death rate in these patients is almost three times higher than the rate in patients with uncomplicated chemical pneumonitis.11,13

Treatment of uncomplicated cases is mainly supportive

The treatment of uncomplicated chemical pneumonitis involves supportive measures such as airway clearance, oxygen supplementation, and positive pressure ventilation if needed. An obstructing foreign body may need to be removed.12,14 Corticosteroids have been tried, without success.11–13,15

Empiric antibiotic treatment is controversial

Chemical pneumonitis can be difficult to differentiate from bacterial aspiration pneumonia, and whether to give antibiotics is controversial. 16 A survey of current practices among intensivists showed that antimicrobial therapy was often given empirically for noninfectious chemical pneumonitis.17 This practice raises concerns of higher treatment costs and antibiotic resistance.16,18,19 Additionally, antibiotics do not seem to alter the clinical outcome, including radiographic resolution, duration of hospitalization, or death rate, nor do they influence the subsequent development of infection.1,11,13,20

In cases of witnessed or strongly suspected aspiration of gastric contents, antibiotics are not warranted since bacterial infection is not likely to be the cause of any signs or symptoms. 2,7,16 However, to detect secondary infection early, the patient’s respiratory status should be monitored carefully and chest radiography should be repeated.

In less clear-cut cases, ie, if it is not clear whether the patient actually has chemical pneumonitis or primary bacterial aspiration pneumonia, it is prudent to start antibiotics empirically after obtaining lower-respiratory-tract secretions for stains and cultures, and then to reassess within 48 to 72 hours. The antibiotics can be discontinued if the patient has rapid clinical and radiographic improvement and negative cultures. Those whose condition does not improve or who have positive cultures should receive a full course of antibiotics.21,22

 

 

PRIMARY BACTERIAL ASPIRATION PNEUMONIA

Primary bacterial aspiration pneumonia—ie, caused by bacteria residing in the upper airways and stomach gaining access to lower airways through aspiration in small or large amounts—is the most common form of aspiration pneumonia, although the actual episode of aspiration is seldom observed.

Signs of bacterial pneumonia

Primary bacterial aspiration pneumonia bears the hallmarks of bacterial pneumonia.12 The clinical picture is more indolent than chemical pneumonitis and includes cough, fever, and putrid sputum, mainly in patients who have clinical conditions predisposing to aspiration (eg, coma, stroke, alcoholism, poor dentition, tube feedings).1,12,20

The characteristic signs on chest radiography are infiltrates involving mainly the lung bases (the right more then the left). If untreated or inadequately treated, complications such as lung abscess, empyema, bronchiectasis, and broncopleural fistula are common.23

Are aerobic organisms replacing anaerobic ones in the community?

The causative organisms in community-acquired aspiration pneumonia are still debated despite abundant research. Older studies1,24,25 found mostly anaerobic organisms (pepto-streptococci, peptococci, Fusobacterium, Prevotela, Bacteroides) as the underlying pathogens, whereas more recent studies16,26,27 found mostly aerobic organisms (Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Enterobacteriaceae) and failed to recover anaerobic organisms. These discrepancies may be the result of different techniques used to isolate organisms: older studies used transtracheal sampling, and transtracheal aspirates may be easily contaminated or colonized by oropharyngeal flora; more recent studies used protected specimen brushes to collect lower-airway specimens.2

In addition, the pathogenic organisms that predominate in community-acquired aspiration pneumonia, as listed above, are different from those most often found in nosocomial cases; gram-negative bacilli (Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli) are most often isolated in patients with aspiration pneumonia acquired in hospitals and nursing homes.16,27,28S aureus also is an important causative organism in nosocomial cases.16,28

Knowing the causative organisms in bacterial aspiration pneumonia is important for guiding antimicrobial therapy.

Antibiotics are required for bacterial aspiration pneumonia

A course of antibiotics is required for bacterial aspiration pneumonia. While there are no definitive recommendations for the duration of treatment, 7 to 8 days is probably appropriate in uncomplicated cases (ie, no lung abscess, empyema, bronchopleural fistula).22,29 Patients who have complications may need drainage of abscesses or empyema along with a longer duration of antibiotic therapy until clinical and radiographic signs improve.

For community-acquired cases of aspiration pneumonia, a number of antibiotics have proven effective:

  • Clindamycin (Cleocin) is still the agent most commonly used, although it lacks gram-negative bacterial coverage.
  • Beta-lactam penicillins and newer quinolones have been used successfully.2,29–31 In addition to covering the previously mentioned bacteria, these antibiotics have the added benefit of covering anaerobic bacteria.
  • Metronidazole (Flagyl) should not be used alone because it has a higher clinical failure rate.32,33

For nosocomial aspiration pneumonia, giving a broad-spectrum antibiotic empirically is warranted. Beta-lactam penicillins with extended gram-negative coverage, carbapenems, or monobactams in combination with an anti-staphylococcal drug have been advocated for nosocomial aspiration.2,22 A strategy of broad-spectrum coverage followed by narrowing or de-escalating coverage according to lower respiratory tract cultures is encouraged.21,22,34

SECONDARY BACTERIAL INFECTION OF CHEMICAL PNEUMONITIS

Nearly 25% of patients with chemical pneumonitis improve initially, then show clinical deterioration secondary to superimposed bacterial infection.13 Chest radiographs show worsening of initial infiltrates or the development of new ones. The causative organisms and treatment depend on whether the superimposed infection is community-acquired or nosocomial, as is the case in primary bacterial aspiration pneumonia.

PREVENTING ASPIRATION

Measures should be taken to prevent aspiration pneumonia and chemical pneumonitis, especially in institutionalized patients at high risk.12

Elevation of the head of the bed while feeding, dental prophylaxis, and good oral hygiene are known to reduce the incidence of these problems.35–37

A swallowing evaluation for patients with dysphagia can identify those at higher risk of aspiration. These patients may be candidates for postural adjustments, diet modification, strengthening, and other measures offered by the speech and language pathology teams to improve swallowing physiology, biomechanics, safety, and endurance.2,35

Although percutaneous endoscopic gastrostomy tubes are often placed in patients who have aspirated or who are at high risk of aspiration, they do not protect against aspiration, nor do orogastric or nasogastric tubes.38

To date, we have no evidence that prophylactic antibiotic therapy prevents bacterial aspiration pneumonia. In addition, this practice encourages the development of resistant organisms.19,39,40

Antibiotics are indicated for primary bacterial aspiration pneumonia and secondary bacterial infection of aspiration (chemical) pneumonitis, but not for uncomplicated chemical pneumonitis.

THREE TYPES OF ‘ASPIRATION PNEUMONIA’

Aspiration pneumonia is a broad and vague term mainly used to refer to the pulmonary consequences of abnormal entry of exogenous or endogenous substances into the lower airways. It can be classified as:

  • Aspiration (chemical) pneumonitis
  • Primary bacterial aspiration pneumonia
  • Secondary bacterial infection of chemical pneumonitis.

These three are sometimes difficult to differentiate, as their signs and symptoms can overlap.

CHEMICAL PNEUMONITIS

Aspiration of stomach contents is relatively common, even in healthy people, and usually has no clinical consequences.1 However, it has also been closely related to community-acquired and nosocomial pneumonia in some studies.2,3

Chemical pneumonitis is usually a consequence of the aspiration of a large volume (≥ 4 mL/kg) of sterile acidic (pH < 2.5) gastric contents into the lower airways (Mendelson syndrome).4,5 The clinical picture varies from asymptomatic to signs of severe dyspnea, hypoxia, cough, and low-grade fever; these signs and symptoms may develop rapidly, within minutes to hours after a witnessed or suspected episode of aspiration.2,6,7 However, they represent an inflammatory reaction to the gastric acid rather than a reaction to bacterial infection.8–10

Chemical pneumonitis affects the most dependent regions of the lungs

Chest radiography shows infiltrates in the most dependent regions of the lung. If aspiration occurs while the patient is supine, the posterior segments of the upper lobes and the apical segments of the lower lobes are most affected. The basal segments of the lower lobes are usually affected if aspiration occurs while the patient is standing or upright.1,2,11,12

Clinical course varies

The clinical course varies. In almost 60% of cases, the patient’s condition improves and the lung infiltrates resolve rapidly, within 2 to 4 days. On the other hand, in about 15% of cases, the patient’s condition deteriorates quickly, within 24 to 36 hours, and progresses to hypoxic respiratory failure and acute respiratory distress syndrome.

In the other 25% of cases, the patient’s condition may improve initially but then worsen as a secondary bacterial infection sets in. The death rate in these patients is almost three times higher than the rate in patients with uncomplicated chemical pneumonitis.11,13

Treatment of uncomplicated cases is mainly supportive

The treatment of uncomplicated chemical pneumonitis involves supportive measures such as airway clearance, oxygen supplementation, and positive pressure ventilation if needed. An obstructing foreign body may need to be removed.12,14 Corticosteroids have been tried, without success.11–13,15

Empiric antibiotic treatment is controversial

Chemical pneumonitis can be difficult to differentiate from bacterial aspiration pneumonia, and whether to give antibiotics is controversial. 16 A survey of current practices among intensivists showed that antimicrobial therapy was often given empirically for noninfectious chemical pneumonitis.17 This practice raises concerns of higher treatment costs and antibiotic resistance.16,18,19 Additionally, antibiotics do not seem to alter the clinical outcome, including radiographic resolution, duration of hospitalization, or death rate, nor do they influence the subsequent development of infection.1,11,13,20

In cases of witnessed or strongly suspected aspiration of gastric contents, antibiotics are not warranted since bacterial infection is not likely to be the cause of any signs or symptoms. 2,7,16 However, to detect secondary infection early, the patient’s respiratory status should be monitored carefully and chest radiography should be repeated.

In less clear-cut cases, ie, if it is not clear whether the patient actually has chemical pneumonitis or primary bacterial aspiration pneumonia, it is prudent to start antibiotics empirically after obtaining lower-respiratory-tract secretions for stains and cultures, and then to reassess within 48 to 72 hours. The antibiotics can be discontinued if the patient has rapid clinical and radiographic improvement and negative cultures. Those whose condition does not improve or who have positive cultures should receive a full course of antibiotics.21,22

 

 

PRIMARY BACTERIAL ASPIRATION PNEUMONIA

Primary bacterial aspiration pneumonia—ie, caused by bacteria residing in the upper airways and stomach gaining access to lower airways through aspiration in small or large amounts—is the most common form of aspiration pneumonia, although the actual episode of aspiration is seldom observed.

Signs of bacterial pneumonia

Primary bacterial aspiration pneumonia bears the hallmarks of bacterial pneumonia.12 The clinical picture is more indolent than chemical pneumonitis and includes cough, fever, and putrid sputum, mainly in patients who have clinical conditions predisposing to aspiration (eg, coma, stroke, alcoholism, poor dentition, tube feedings).1,12,20

The characteristic signs on chest radiography are infiltrates involving mainly the lung bases (the right more then the left). If untreated or inadequately treated, complications such as lung abscess, empyema, bronchiectasis, and broncopleural fistula are common.23

Are aerobic organisms replacing anaerobic ones in the community?

The causative organisms in community-acquired aspiration pneumonia are still debated despite abundant research. Older studies1,24,25 found mostly anaerobic organisms (pepto-streptococci, peptococci, Fusobacterium, Prevotela, Bacteroides) as the underlying pathogens, whereas more recent studies16,26,27 found mostly aerobic organisms (Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Enterobacteriaceae) and failed to recover anaerobic organisms. These discrepancies may be the result of different techniques used to isolate organisms: older studies used transtracheal sampling, and transtracheal aspirates may be easily contaminated or colonized by oropharyngeal flora; more recent studies used protected specimen brushes to collect lower-airway specimens.2

In addition, the pathogenic organisms that predominate in community-acquired aspiration pneumonia, as listed above, are different from those most often found in nosocomial cases; gram-negative bacilli (Pseudomonas aeruginosa, Klebsiella pneumoniae, Escherichia coli) are most often isolated in patients with aspiration pneumonia acquired in hospitals and nursing homes.16,27,28S aureus also is an important causative organism in nosocomial cases.16,28

Knowing the causative organisms in bacterial aspiration pneumonia is important for guiding antimicrobial therapy.

Antibiotics are required for bacterial aspiration pneumonia

A course of antibiotics is required for bacterial aspiration pneumonia. While there are no definitive recommendations for the duration of treatment, 7 to 8 days is probably appropriate in uncomplicated cases (ie, no lung abscess, empyema, bronchopleural fistula).22,29 Patients who have complications may need drainage of abscesses or empyema along with a longer duration of antibiotic therapy until clinical and radiographic signs improve.

For community-acquired cases of aspiration pneumonia, a number of antibiotics have proven effective:

  • Clindamycin (Cleocin) is still the agent most commonly used, although it lacks gram-negative bacterial coverage.
  • Beta-lactam penicillins and newer quinolones have been used successfully.2,29–31 In addition to covering the previously mentioned bacteria, these antibiotics have the added benefit of covering anaerobic bacteria.
  • Metronidazole (Flagyl) should not be used alone because it has a higher clinical failure rate.32,33

For nosocomial aspiration pneumonia, giving a broad-spectrum antibiotic empirically is warranted. Beta-lactam penicillins with extended gram-negative coverage, carbapenems, or monobactams in combination with an anti-staphylococcal drug have been advocated for nosocomial aspiration.2,22 A strategy of broad-spectrum coverage followed by narrowing or de-escalating coverage according to lower respiratory tract cultures is encouraged.21,22,34

SECONDARY BACTERIAL INFECTION OF CHEMICAL PNEUMONITIS

Nearly 25% of patients with chemical pneumonitis improve initially, then show clinical deterioration secondary to superimposed bacterial infection.13 Chest radiographs show worsening of initial infiltrates or the development of new ones. The causative organisms and treatment depend on whether the superimposed infection is community-acquired or nosocomial, as is the case in primary bacterial aspiration pneumonia.

PREVENTING ASPIRATION

Measures should be taken to prevent aspiration pneumonia and chemical pneumonitis, especially in institutionalized patients at high risk.12

Elevation of the head of the bed while feeding, dental prophylaxis, and good oral hygiene are known to reduce the incidence of these problems.35–37

A swallowing evaluation for patients with dysphagia can identify those at higher risk of aspiration. These patients may be candidates for postural adjustments, diet modification, strengthening, and other measures offered by the speech and language pathology teams to improve swallowing physiology, biomechanics, safety, and endurance.2,35

Although percutaneous endoscopic gastrostomy tubes are often placed in patients who have aspirated or who are at high risk of aspiration, they do not protect against aspiration, nor do orogastric or nasogastric tubes.38

To date, we have no evidence that prophylactic antibiotic therapy prevents bacterial aspiration pneumonia. In addition, this practice encourages the development of resistant organisms.19,39,40

References
  1. Bartlett JG, Gorbach SL. The triple threat of aspiration pneumonia. Chest 1975; 68:560–566.
  2. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001; 344:665–671.
  3. Kikuchi R, Watabe N, Konno T, Mishina N, Sekizawa K, Sasaki H. High incidence of silent aspiration in elderly patients with community-acquired pneumonia. Am J Respir Crit Care Med 1994; 150:251–253.
  4. Mendelson CL. The aspiration of stomach contents into lungs during obstetric anesthesia. Am J Obstet Gynecol 1946; 52:191–205.
  5. Cameron JL, Caldini P, Toung JK, Zuidema GD. Aspiration pneumonia: physiologic data following experimental aspiration. Surgery 1972; 72:238–245.
  6. Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 1993; 78:56–62.
  7. DePaso WJ. Aspiration pneumonia. Clin Chest Med 1991; 12:269–284.
  8. Folkesson HG, Matthay MA, Hébert CA, Broaddus VC. Acid aspiration-induced lung injury in rabbits is mediated by interleukin-8-dependent mechanisms. J Clin Invest 1995; 96:107–116.
  9. Goldman G, Welbourn R, Kobzik L, Valeri CR, Shepro D, Hechtman HB. Tumor necrosis factor-alpha mediates acid aspiration-induced systemic organ injury. Ann Surg 1990; 212:513–519.
  10. LeFrock JL, Clark TS, Davies B, Klainer AS. Aspiration pneumonia: a ten-year review. Am Surg 1979; 45:305–313.
  11. Cameron JL, Mitchell WH, Zuidema GD. Aspiration pneumonia. Clinical outcome following documented aspiration. Arch Surg 1973; 106:49–52.
  12. Arms RA, Dines DE, Tinstman TC. Aspiration pneumonia. Chest 1974; 65:136–139.
  13. Bynum LJ, Pierce AK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis 1976; 114:1129–1136.
  14. Merchant SN, Kirtane MV, Shah KL, Karnik PP. Foreign bodies in the bronchi (a 10 year review of 132 cases). J Postgrad Med 1984; 30:219–223.
  15. Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med 1977; 63:719–722.
  16. Kane-Gill SL, Olsen KM, Rebuck JA, et al; Aspiration Evaluation Group of the Clinical Pharmacy and Pharmacology Section. Multicenter treatment and outcome evaluation of aspiration syndromes in critically ill patients. Ann Pharmacother 2007; 41:549–555.
  17. Rebuck JA, Rasmussen JR, Olsen KM. Clinical aspiration-related practice patterns in the intensive care unit: a physician survey. Crit Care Med 2001; 29:2239–2244.
  18. Singh N, Rogers P, Atwood CW, Wagener MM, Yu VL. Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. A proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med 2000; 162:505–511.
  19. Kollef MH, Fraser VJ. Antibiotic resistance in the intensive care unit. Ann Intern Med 2001; 134:298–314.
  20. Lewis RT, Burgess JH, Hampson LG. Cardiorespiratory studies in critical illness. Changes in aspiration pneumonitis. Arch Surg 1971; 103:335–340.
  21. Rello J. Importance of appropriate initial antibiotic therapy and de-escalation in the treatment of nosocomial pneumonia. Eur Respir Rev 2007; 16:33–39.
  22. American Thoracic Society. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005; 171:388–416.
  23. Bartlett JG. Anaerobic bacterial infections of the lung and pleural space. Clin Infect Dis 1993; 16(suppl 4):S248–S255.
  24. Lorber B, Swenson RM. Bacteriology of aspiration pneumonia. A prospective study of community- and hospital-acquired cases. Ann Intern Med 1974; 81:329–331.
  25. Bartlett JG, Gorbach SL, Finegold SM. The bacteriology of aspiration pneumonia. Am J Med 1974; 56:202–207.
  26. Mier L, Dreyfuss D, Darchy B, et al. Is penicillin G an adequate initial treatment for aspiration pneumonia? A prospective evaluation using a protected specimen brush and quantitative cultures. Intensive Care Med 1993; 19:279–284.
  27. Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study. Chest 1999; 115:178–183.
  28. El-Solh AA, Pietrantoni C, Bhat A, et al. Microbiology of severe aspiration pneumonia in institutionalized elderly. Am J Respir Crit Care Med 2003; 167:1650–1654.
  29. Mandell LA, Wunderink RG, Anzueto A, et al; Infectious Diseases Society of America. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007; 44(suppl 2):S27–S72.
  30. Kadowaki M, Demura Y, Mizuno S, et al. Reappraisal of clindamycin IV monotherapy for treatment of mild-to-moderate aspiration pneumonia in elderly patients. Chest 2005; 127:1276–1282.
  31. Ott SR, Allewelt M, Lorenz J, Reimnitz P, Lode H; German Lung Abscess Study Group. Moxifloxacin vs ampicillin/sulbactam in aspiration pneumonia and primary lung abscess. Infection 2008; 36:23–30.
  32. Perlino CA. Metronidazole vs clindamycin treatment of anerobic pulmonary infection. Failure of metronidazole therapy. Arch Intern Med 1981; 141:1424–1427.
  33. Sanders CV, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic infections. Am Rev Respir Dis 1979; 120:337–343.
  34. Alvarez-Lerma F, Alvarez B, Luque P, et al; ADANN Study Group. Empiric broad-spectrum antibiotic therapy of nosocomial pneumonia in the intensive care unit: a prospective observational study. Crit Care 2006; 10:R78.
  35. Johnson JL, Hirsch CS. Aspiration pneumonia. Recognizing and managing a potentially growing disorder. Postgrad Med 2003; 113:99–112.
  36. Scolapio JS. Methods for decreasing risk of aspiration pneumonia in critically ill patients. JPEN J Parenter Enteral Nutr 2002; 26(suppl 6):S58–S61.
  37. Orozco-Levi M, Torres A, Ferrer M, et al. Semirecumbent position protects from pulmonary aspiration but not completely from gastroesophageal reflux in mechanically ventilated patients. Am J Respir Crit Care Med 1995; 152:1387–1390.
  38. Park RH, Allison MC, Lang J, et al. Randomised comparison of percutaneous endoscopic gastrostomy and nasogastric tube feeding in patients with persisting neurological dysphagia. BMJ 1992; 304( 6839):1406–1409.
  39. Donskey CJ, Chowdhry TK, Hecker MT, et al. Effect of antibiotic therapy on the density of vancomycin-resistant enterococci in the stool of colonized patients. N Engl J Med 2000; 343:1925–1932.
  40. Mouw DR, Langlois JP, Turner LF, Neher JO. Clinical inquiries. Are antibiotics effective in preventing pneumonia for nursing home patients? J Fam Pract 2004; 53:994–996.
References
  1. Bartlett JG, Gorbach SL. The triple threat of aspiration pneumonia. Chest 1975; 68:560–566.
  2. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001; 344:665–671.
  3. Kikuchi R, Watabe N, Konno T, Mishina N, Sekizawa K, Sasaki H. High incidence of silent aspiration in elderly patients with community-acquired pneumonia. Am J Respir Crit Care Med 1994; 150:251–253.
  4. Mendelson CL. The aspiration of stomach contents into lungs during obstetric anesthesia. Am J Obstet Gynecol 1946; 52:191–205.
  5. Cameron JL, Caldini P, Toung JK, Zuidema GD. Aspiration pneumonia: physiologic data following experimental aspiration. Surgery 1972; 72:238–245.
  6. Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 1993; 78:56–62.
  7. DePaso WJ. Aspiration pneumonia. Clin Chest Med 1991; 12:269–284.
  8. Folkesson HG, Matthay MA, Hébert CA, Broaddus VC. Acid aspiration-induced lung injury in rabbits is mediated by interleukin-8-dependent mechanisms. J Clin Invest 1995; 96:107–116.
  9. Goldman G, Welbourn R, Kobzik L, Valeri CR, Shepro D, Hechtman HB. Tumor necrosis factor-alpha mediates acid aspiration-induced systemic organ injury. Ann Surg 1990; 212:513–519.
  10. LeFrock JL, Clark TS, Davies B, Klainer AS. Aspiration pneumonia: a ten-year review. Am Surg 1979; 45:305–313.
  11. Cameron JL, Mitchell WH, Zuidema GD. Aspiration pneumonia. Clinical outcome following documented aspiration. Arch Surg 1973; 106:49–52.
  12. Arms RA, Dines DE, Tinstman TC. Aspiration pneumonia. Chest 1974; 65:136–139.
  13. Bynum LJ, Pierce AK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis 1976; 114:1129–1136.
  14. Merchant SN, Kirtane MV, Shah KL, Karnik PP. Foreign bodies in the bronchi (a 10 year review of 132 cases). J Postgrad Med 1984; 30:219–223.
  15. Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med 1977; 63:719–722.
  16. Kane-Gill SL, Olsen KM, Rebuck JA, et al; Aspiration Evaluation Group of the Clinical Pharmacy and Pharmacology Section. Multicenter treatment and outcome evaluation of aspiration syndromes in critically ill patients. Ann Pharmacother 2007; 41:549–555.
  17. Rebuck JA, Rasmussen JR, Olsen KM. Clinical aspiration-related practice patterns in the intensive care unit: a physician survey. Crit Care Med 2001; 29:2239–2244.
  18. Singh N, Rogers P, Atwood CW, Wagener MM, Yu VL. Short-course empiric antibiotic therapy for patients with pulmonary infiltrates in the intensive care unit. A proposed solution for indiscriminate antibiotic prescription. Am J Respir Crit Care Med 2000; 162:505–511.
  19. Kollef MH, Fraser VJ. Antibiotic resistance in the intensive care unit. Ann Intern Med 2001; 134:298–314.
  20. Lewis RT, Burgess JH, Hampson LG. Cardiorespiratory studies in critical illness. Changes in aspiration pneumonitis. Arch Surg 1971; 103:335–340.
  21. Rello J. Importance of appropriate initial antibiotic therapy and de-escalation in the treatment of nosocomial pneumonia. Eur Respir Rev 2007; 16:33–39.
  22. American Thoracic Society. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005; 171:388–416.
  23. Bartlett JG. Anaerobic bacterial infections of the lung and pleural space. Clin Infect Dis 1993; 16(suppl 4):S248–S255.
  24. Lorber B, Swenson RM. Bacteriology of aspiration pneumonia. A prospective study of community- and hospital-acquired cases. Ann Intern Med 1974; 81:329–331.
  25. Bartlett JG, Gorbach SL, Finegold SM. The bacteriology of aspiration pneumonia. Am J Med 1974; 56:202–207.
  26. Mier L, Dreyfuss D, Darchy B, et al. Is penicillin G an adequate initial treatment for aspiration pneumonia? A prospective evaluation using a protected specimen brush and quantitative cultures. Intensive Care Med 1993; 19:279–284.
  27. Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a prospective study. Chest 1999; 115:178–183.
  28. El-Solh AA, Pietrantoni C, Bhat A, et al. Microbiology of severe aspiration pneumonia in institutionalized elderly. Am J Respir Crit Care Med 2003; 167:1650–1654.
  29. Mandell LA, Wunderink RG, Anzueto A, et al; Infectious Diseases Society of America. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007; 44(suppl 2):S27–S72.
  30. Kadowaki M, Demura Y, Mizuno S, et al. Reappraisal of clindamycin IV monotherapy for treatment of mild-to-moderate aspiration pneumonia in elderly patients. Chest 2005; 127:1276–1282.
  31. Ott SR, Allewelt M, Lorenz J, Reimnitz P, Lode H; German Lung Abscess Study Group. Moxifloxacin vs ampicillin/sulbactam in aspiration pneumonia and primary lung abscess. Infection 2008; 36:23–30.
  32. Perlino CA. Metronidazole vs clindamycin treatment of anerobic pulmonary infection. Failure of metronidazole therapy. Arch Intern Med 1981; 141:1424–1427.
  33. Sanders CV, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic infections. Am Rev Respir Dis 1979; 120:337–343.
  34. Alvarez-Lerma F, Alvarez B, Luque P, et al; ADANN Study Group. Empiric broad-spectrum antibiotic therapy of nosocomial pneumonia in the intensive care unit: a prospective observational study. Crit Care 2006; 10:R78.
  35. Johnson JL, Hirsch CS. Aspiration pneumonia. Recognizing and managing a potentially growing disorder. Postgrad Med 2003; 113:99–112.
  36. Scolapio JS. Methods for decreasing risk of aspiration pneumonia in critically ill patients. JPEN J Parenter Enteral Nutr 2002; 26(suppl 6):S58–S61.
  37. Orozco-Levi M, Torres A, Ferrer M, et al. Semirecumbent position protects from pulmonary aspiration but not completely from gastroesophageal reflux in mechanically ventilated patients. Am J Respir Crit Care Med 1995; 152:1387–1390.
  38. Park RH, Allison MC, Lang J, et al. Randomised comparison of percutaneous endoscopic gastrostomy and nasogastric tube feeding in patients with persisting neurological dysphagia. BMJ 1992; 304( 6839):1406–1409.
  39. Donskey CJ, Chowdhry TK, Hecker MT, et al. Effect of antibiotic therapy on the density of vancomycin-resistant enterococci in the stool of colonized patients. N Engl J Med 2000; 343:1925–1932.
  40. Mouw DR, Langlois JP, Turner LF, Neher JO. Clinical inquiries. Are antibiotics effective in preventing pneumonia for nursing home patients? J Fam Pract 2004; 53:994–996.
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Cleveland Clinic Journal of Medicine - 77(9)
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Cleveland Clinic Journal of Medicine - 77(9)
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573-576
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Cleveland Clinic Journal of Medicine
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Are antibiotics indicated for the treatment of aspiration pneumonia?
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Are antibiotics indicated for the treatment of aspiration pneumonia?
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