Updated: Aug 7, 2009
Aspiration, ie, the act of taking foreign material into the lungs, can cause a number of syndromes determined by the quantity and nature of the aspirated material, the frequency of aspiration, and the host factors that predispose the patient to aspiration and modify the response. Three types of material cause 3 different pneumonic syndromes. Aspiration of gastric acid causes chemical pneumonia (CP). Aspiration of bacteria from oral and pharyngeal areas causes bacterial pneumonia (BP). Aspiration of oil, eg, mineral oil or vegetable oil, causes exogenous lipoid pneumonia, a rare form of pneumonia. In addition, aspiration of a foreign body may cause an acute respiratory emergency and, in some cases, may predispose the patient to bacterial pneumonia.
Aspiration pneumonia, according to common usage, includes both CP and BP, although the pathophysiology, clinical presentation, treatment, and complications of CP and BP are different.
Aspiration, particularly during sleep, is a common event in healthy individuals. No disease ensues because the aspirated material is cleared by mucociliary action and alveolar macrophages. The nature of the aspirated material, volume of the aspirated material, and state of the host defenses are 3 important determinants of aspiration pneumonia.
CP, also known as Mendelson syndrome, is due to the parenchymal inflammatory reaction caused by a large volume of gastric contents independent of infection. If the pH of the aspirated fluid is less than 2.5 and the volume of aspirate is greater than 0.3 mL/kg of body weight (20-25 mL in adults), it has a greater potential for causing CP. The initial chemical burn is followed by an inflammatory cellular reaction fueled by the release of potent cytokines, particularly tumor necrosis factor–alpha and interleukin-8.
BP caused by aspiration can occur in the community or in the hospital (ie, nosocomial). In both situations anaerobic organisms alone or in combination with aerobic and/or microaerophilic organisms play an important role. Nosocomial BP caused by aspiration is common, and the major pathogens involved are hospital-acquired flora through oropharyngeal colonization (eg, enteric gram-negative bacteria, staphylococci).
In anaerobic pneumonia, the pathogenesis is related to the large volume of aspirated anaerobes (eg, as in persons with periodontal disease) and to host factors (eg, as in alcoholism) that suppress cough, mucociliary clearance, and phagocytic efficiency. Selection and colonization of gram-negative organisms in the oropharynx, sedation, and intubation of the patient's airways are important pathogenetic factors in nosocomial pneumonia.
A reliable estimate of incidence of CP is not available. BP caused by aspiration is reported to cause 5-15% of community-acquired pneumonia (CAP) cases. Nosocomial BP is the second most likely cause of nosocomial infections, second only to urinary tract infection, and is the leading cause of death from hospital-acquired infections.
In Mendelson's original series in 1946, Mendelson described 61 obstetric patients who aspirated gastric acid during anesthesia, all of whom had a complete clinical recovery within 24-36 hours.1 In subsequent studies, which have included older sicker patients, CP has a reported mortality rate of 30-62% because CP often leads to acute respiratory distress syndrome (ARDS).
Nosocomial BP caused by aspiration is much more frequent in adults than in children. Predisposing factors (see Causes) are more common among elderly people; therefore, this population is more prone to develop aspiration pneumonia.
Acute Respiratory Distress Syndrome
Lung Abscess
Tuberculosis
Necrotizing pneumonia
Bronchopleural fistula
Lung carcinoma
Mycoses
No role for surgical care exists, except in cases with complications.
In patients with stroke or other risk factors for aspiration, a comprehensive swallowing evaluation is recommended. A speech and language therapist can perform this bedside evaluation and, if abnormalities are found, can teach the patient compensatory strategies with soft or pureed foods.
Antibiotics are usually not necessary unless an infection develops.
Chemical pneumonia
Antibiotics are not routinely indicated for patients with CP. If pneumonia occurs days after the aspiration event, antibiotics are indicated. As noted earlier, various organisms are causative. Therefore, choosing antibiotics based on organisms cultured from sputum, tracheal aspirates, or aspirate obtained through a protected catheter by bronchoscopy rather than empirically is more appropriate. The choice of antibiotics is also dictated by the severity of the pneumonia, patient-related risk factors (eg, malnutrition, comorbid illnesses) and intervention-related factors (eg, prior use of antibiotics, corticosteroids, cytotoxic agents, endotracheal tube), and the duration of hospitalization.
As examples, dual treatment involving a carefully chosen second-generation cephalosporin or nonpseudomonal third-generation cephalosporin and clindamycin, aztreonam, or fluoroquinolones is appropriate in many cases. However, in severe pneumonia occurring many days after initiation of mechanical ventilation, the probability of resistant organisms, including Pseudomonas aeruginosa, Acinetobacter species, and methicillin-resistant S aureus is increased, and, therefore, antibiotic treatment should be broader and aggressive; the choices include ciprofloxacin, quinolones, aminoglycoside with antipseudomonal penicillin, ceftazidime, imipenem, and vancomycin.
Bacterial pneumonia
In BP, clindamycin is the antibiotic of choice. Alternatives to clindamycin include amoxicillin with clavulanate (Augmentin) and metronidazole (Flagyl). Metronidazole used alone is not recommended because of a high failure rate. Similarly, macrolides, cephalosporins, and fluoroquinolones are additional alternatives that are not recommended as first-line agents because they are not well studied.
Antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Available in parenteral form (ie, clindamycin phosphate) and oral form (ie, clindamycin hydrochloride). Oral clindamycin is absorbed rapidly and almost completely and is not appreciably altered by the presence of food in the stomach. Appropriate serum levels are reached and sustained for at least 6 h following an oral dose. No significant levels are attained in the cerebrospinal fluid. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
600 mg IV q8h; continue treatment with 300 mg PO q6h; doses as high as 4800 mg qd have been used in life-threatening severe infections
8-20 mg/kg/d PO as hydrochloride and 8-25 mg/kg/d as palmitate divided tid/qid
20-40 mg/kg/d IV/IM equally divided tid/qid
Use the higher dose for more severe infections
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity; regional enteritis, ulcerative colitis, pseudomembranous colitis; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment is necessary in renal insufficiency; associated with severe and possibly fatal colitis; if diarrhea develops during the course of treatment, clindamycin should be stopped
Combines a semisynthetic antibiotic (ie, amoxicillin) and a beta-lactamase inhibitor (ie, clavulanate potassium) and provides for an extended spectrum of coverage to include bacteria resistant to amoxicillin and other beta-lactam antibiotics. It is well absorbed from the gastrointestinal tract and can be administered without regard to the time of a meal. The half-life of oral Augmentin is 1-1.3 h. Augmentin has good tissue penetration but does not enter the cerebrospinal fluid. Drug combination treats bacteria resistant to beta-lactam antibiotics.
500 mg q12h PO or 875 mg PO q12h in severe infections
<3 months: Not established
>3 months: Base dosing protocol on amoxicillin content
<40 kilograms: 20-40 mg/kg/d PO divided bid; do not use 250-mg tab until child weighs >40 kg
>40 kilograms: Administer as in adults
Probenecid decreases renal tubular secretion and may result in prolonged and high level of amoxicillin; concurrent use of allopurinol substantially increases incidence of skin rashes; coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause antibiotic-associated diarrhea and because this is associated with pseudomembranous colitis, stop administration of the drug if diarrhea occurs; hepatic dysfunction manifested by rise in liver enzymes may occur; increased incidence of erythematous skin rash in patients with infectious mononucleosis who are administered ampicillin
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[Guideline] Coffin SE, Klompas M, Classen D, Arias KM, Podgorny K, Anderson DJ, et al. Strategies to prevent ventilator-associated pneumonia in acute care hospitals. Infect Control Hosp Epidemiol. Oct 2008;29 Suppl 1:S31-40. [Medline].
[Guideline] Tablan OC, Anderson LJ, Besser R, Bridges C, Hajjeh R. Guidelines for preventing health-care--associated pneumonia, 2003: recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR Recomm Rep. Mar 26 2004;53:1-36. [Medline].
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aspiration pneumonia, Mendelson syndrome, chemical pneumonitis, anaerobic bacterial pneumonia, chemical pneumonia, CP, aspiration of gastric acid, bacterial pneumonia, BP, aspiration of bacteria from oral and pharyngeal areas, exogenous lipoid pneumonia, aspiration of oil, aspiration of a foreign body, acute respiratory emergency, parenchymal inflammatory reaction, community-acquired pneumonia, CAP, nosocomial pneumonia, acute respiratory distress syndrome, ARDS
Anita B Varkey, MD, Assistant Professor, Department of Medicine, Loyola University Medical Center; Associate Program Director, Internal Medicine Residency; Medical Director, General Internal Medicine Clinic, Loyola Outpatient Center
Anita B Varkey, MD is a member of the following medical societies: American College of Physicians and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Basil Varkey, MD, FCCP, Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Medical College of Wisconsin; Consulting Pulmonologist, Froedtert Memorial Lutheran Hospital
Basil Varkey, MD, FCCP is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Chest Physicians, American Federation for Clinical Research, American Thoracic Society, and Royal College of Physicians
Disclosure: Nothing to disclose.
Laurie Robin Grier, MD, Medical Director of MICU, Associate Professor of Medicine, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Science Center at Shreveport
Laurie Robin Grier, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Society for Parenteral and Enteral Nutrition, and Society of Critical Care Medicine
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Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
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Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.
Clinical guidelines
Coffin SE, Klompas M, Classen D, Arias KM, Podgorny K, Anderson DJ, Burstin H, Calfee DP, Dubberke ER, Fraser V, Gerding DN, Griffin FA, Gross P, Kaye KS, Lo E, Marschall J, Mermel LA, Nicolle L, Pegues DA, Perl TM, Saint S, Salgado CD, Weinstein RA, Wise R, Yokoe DS. Strategies to prevent ventilator-associated pneumonia in acute care hospitals. Infect Control Hosp Epidemiol 2008 Oct;29 Suppl 1:S31-40. 2
Tablan OC, Anderson LJ, Besser R, Bridges C, Hajjeh R. Guidelines for preventing health-care--associated pneumonia, 2003: recommendations of CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR Recomm Rep 2004 Mar 26;53(RR-3):1-36. 3
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