Aspiration Syndromes: ED Presentation, Evaluation, and Management

Authors: Nancy Huynh, MD (EM Resident Physician, Hospital of the University of Pennsylvania) and Kevin R. Scott, MD, MSEd (EM Attending Physician, Hospital of the University of Pennsylvania) // Reviewed by: Alex Koyfman, MD (@EMHighAK), Brit Long, MD (@long_brit), and Tim Montrief, MD (@EMinMiami) 


An 88-year-old male with a history of dementia is brought to the emergency department from home with cough and shortness of breath that started soon after lunch earlier that day. Vital signs are within normal limits. He is breathing comfortably and has clear breath sounds. Labs demonstrate a mild leukocytosis, but are otherwise unremarkable. Chest X-ray shows an infiltrate in the left lower lobe. Does this patient require antibiotics?



Although this vignette may sound like yet another case of community-acquired pneumonia, the onset of symptoms close to a meal should raise the question, did this patient aspirate? Could this be aspiration pneumonia or aspiration pneumonitis?

These two disease entities are defined by their differences in pathophysiology.

Aspiration pneumonitis

Aspiration pneumonitis is sometimes also called Mendelson’s syndrome, named after the first report in which patients aspirated after undergoing general anesthesia for obstetric procedures.

In aspiration pneumonitis, aspiration of large amounts of gastric acid causes chemical injury to the lung parenchyma, inducing an inflammatory response. From animal studies, both pH and volume appear to be necessary for the development of disease. Aspirated contents must have a pH <2.5 to induce a reaction, and most of these studies used 1-4 mL/kg of inoculum, which would equate to about 70-280 mL based on an average 70kg human weight.1 From one study of rats, initial injury mediated by a physiochemical reaction to the aspirate appears to occur within one hour followed by a subsequent acute inflammatory reaction with neutrophils about four hours after aspiration.2 Of note, aspiration of food particles in particular have been shown to induce lung damage in pneumonitis even with a pH >2.5.3

Initial pneumonitis can develop into pneumonia from bacterial superinfection as several animal studies have shown increased susceptibility to bacterial infection after aspiration and acid injury.4,5 It is still unclear what the timeline for superinfection is and why pneumonia subsequently occurs in some cases but not others.6,7

Aspiration pneumonia

Aspiration pneumonia results from aspiration of secretions that contain pathogenic bacteria. Often, these are colonized oropharyngeal secretions but can also be from colonized gastric contents.6,8

Aspirated contents for both syndromes can include food, gastric contents, saliva, nasopharyngeal secretions, blood, bacteria, and other common substances. Additionally, there have been case reports of aspiration pneumonitis and pneumonia from less common materials, such as hydrocarbons from fire-eating.9,10

Aspiration pneumonia has been estimated to make up about 5-15% of community-acquired pneumonia with the upper end of that range in the elderly.11,12 Patients with aspiration pneumonia had a mortality rate of 19-25% compared to 4-8% in non-aspiration pneumonia.13,14 Relatively fewer studies are available on the prevalence or mortality of aspiration pneumonitis, but two studies have observed a rate of 1.6% in all overdose patients and 11% in patients who overdosed on sedatives or hypnotics specifically.15,16

Clinical presentation

In clinical practice, these two entities are often difficult to distinguish from one another.

Despite aspiration pneumonitis not being caused by a bacterial infection, patients can still present with fever, tachycardia, and hypoxia, sometimes even developing into acute respiratory distress syndrome (ARDS).17 In one study of 50 patients with witnessed aspiration, the most frequent presenting signs were fever (94%) with a cutoff of 99°F, tachypnea (78%), and rales (72%) although these were not further subdivided into frequency in patients with pneumonitis versus pneumonia. All who were ultimately diagnosed with either aspiration syndrome developed symptoms within 2 hours of the event, making time course an unreliable differentiating factor as well.18 Another study that attempted to distinguish between aspiration pneumonitis and pneumonia found no significant differences in rates of cough (44% vs 43%), shortness of breath (40% vs 43%), fever ≥100°F (71% vs 55%), mental status change (22% vs 36%).17

Thus, taking a careful history important. From a study of biopsy and resection specimens of aspiration pneumonia, the diagnosis had been clinically suspected in only 4 out of 45 cases (9%).19 Aspiration is usually unwitnessed, so clinical suspicion instead relies on patient risk factors as listed below.7,20 Although many of these factors have been studied in community-acquired pneumonia, likelihood data have been provided only when studies have examined aspiration pneumonia or pneumonitis specifically.

Factors that increase risk of development of pneumonia as opposed to pneumonitis from aspiration include decreased salivary clearance, poor oral hygiene, proton pump inhibitor use (suppresses gastric acid, making it easier for bacteria to grow in less acidic environments), and tube feeds (can promote colonization of gastric contents with pathogens).8,30–32


Diagnosing aspiration syndromes is challenging because no current gold standard exists and therefore remains a clinical diagnosis. Nonetheless, a chest X-ray is the initial recommended test.

With aspiration, contents settle in the most gravity-dependent portions. While lying down, these areas are the posterior segments of the upper lobes. While upright, the basal segments of the lower lobes are most commonly involved as seen in Figure 1, especially the right lower lobe.6,18 However, these findings do not aid in distinguishing between aspiration pneumonia and pneumonitis. Having an infiltrate on chest X-ray is actually part of the definition of aspiration syndromes in research studies. Radiographic findings in aspiration pneumonitis quickly resolve over several days while findings of pneumonia may take weeks, but this difference is not useful in the initial diagnosis and management.33 Chest CT is unlikely to provide any additional useful information. A systematic review found that patients with dysphagia-related aspiration presented with a wide range of findings on CT, including bronchiectasis, ground-glass attenuation, bronchial wall thickening, consolidations, atelectasis, etc.34

Basic laboratory testing, such as a complete blood count, is not helpful in distinguishing between aspiration pneumonia and pneumonitis as both can result in leukocytosis.17 One study also found no significant in white blood cell count quantitatively between these two syndromes with average count ranging from 13-16 x 1000 (per mm3).17 Procalcitonin was originally discovered as a biomarker elevated in patients with severe bacterial infection/sepsis and has also had some similar success as a test for community-acquired pneumonia versus other respiratory tract infections.36,37 Unfortunately, it performs poorly in distinguishing between aspiration pneumonia and pneumonitis in a study using quantitative bronchoalveolar lavage (BAL) culture as the gold standard. No statistically significant difference in procalcitonin levels was found in patients with culture positive vs culture negative bronchoalveolar lavage (BAL) specimens. Attempting to use a cutoff value of 2.0 ng/mL yielded only a sensitivity of 76% and specificity of 38%.38 Other novel biomarkers, such as BAL pepsin, lipid-laden alveolar macrophages, C-reactive protein, various pro-inflammatory cytokines, and exhaled breath condensate leukotrienes, have been explored but have either failed to be specific or sensitive enough for diagnostic purposes or are awaiting further validation in human studies.39

The utility of other laboratory tests has not been studied specifically in aspiration syndromes, so we recommend an approach similar to that with community-acquired pneumonia. The authors of one review of aspiration-related lung injury do not recommend routine bronchoscopy with lavage.7 Although they do not specify exactly what circumstances would merit collection of BAL specimens, because these samples can be difficult to obtain in the ED, our opinion is that they may be useful only in patients requiring admission to the ICU and/or with anticipated long length of stay so that further decisions about antibiotics can be made. Similarly, blood and sputum cultures have been shown to not be useful in non-severe community-acquired pneumonia, but we believe that they can again be considered in severe cases to help guide antibiotic management as an inpatient.40 Ideally, these samples should be obtained prior to starting antibiotics.

In summary, aspiration pneumonia or pneumonitis still remains a clinical diagnosis that can be supported by (1) witnessed or suspected aspiration based on risk factors, (2) signs and symptoms of pneumonia, and (3) chest X-ray findings of infiltrates in posterior aspects of upper lobes or basal segments of lower lobes, depending on patient position. Currently, nothing but time and microbiology data can distinguish between aspiration pneumonitis and pneumonia.


The difficulty in differentiating aspiration pneumonia and pneumonitis has proven to be a limiting factor for research exploring the two entities. As a result, there is limited available evidence providing recommendations in management. Although we have made an effort to provide as many evidence-based recommendations as possible, recommendations based primarily on expert opinion are inevitable, and we will indicate as such when applicable.

Initial management will depend on each individual patient’s clinical status, especially with regards to respiratory symptoms. Managing patients with aspiration pneumonitis or pneumonia involves two primary principles: (1) varying degrees of airway management and (2) administering or withholding antibiotics. Generally, antibiotics should be used in aspiration pneumonia while there is no clear consensus for aspiration pneumonitis.

Airway Management

The first priority in management is assessing and managing the patient’s airway as well as correcting hypoxia if present. Aspiration pneumonitis and aspiration pneumonia can both present in patients within a wide spectrum of respiratory complaints/distress. In a study of 24 symptomatic pre-surgical patients with witnessed aspiration, 13 required mechanical ventilation for more than six hours, and only one was identified as aspiration pneumonia.41 Initial interventions can include simply monitoring (for patients with symptoms but without hypoxia or airway concerns) to provision of supplemental oxygen, repositioning with tracheal suction, non-invasive positive pressure ventilation, or endotracheal intubation with mechanical ventilation for patients in respiratory failure or cases that develop into (acute respiratory distress syndrome) ARDS.1 Other studies have looked at patient positioning in the treatment of aspiration including a small study that found success in improving oxygenation with proning patients in respiratory failure after a witnessed aspiration event albeit in the ICU setting.42 If high concern for potential repeat aspiration episodes, placement of a nasogastric tube or connecting gastrostomy to suction/gravity should be considered.7 No studies yet have examined use of this technique in the ED so although not a technique ready for routine use in the ED, it can be considered in patients with persistent respiratory failure not responding to other interventions.


The biggest difference in the management of aspiration pneumonitis versus pneumonia is the administration of antibiotics. Aspiration pneumonitis, in theory, should not require antibiotics as it is not an infectious process.1 In one study, 8 of 31 patients (26%) who experienced rapid improvement in clinical and radiographic findings after aspiration did not receive any antibiotics, suggesting that these may have been cases of aspiration pneumonitis.18 Additionally, prophylactic antibiotics for patients with aspiration pneumonitis provide no clinical benefit. In one study, those who received antimicrobials versus those who did not had no difference in mortality (OR 0.9) or transfer to critical care (5% vs 6%). Those started on antibiotics stayed on them longer (7.5 vs 10.9 antibiotic-free days) and received more frequent escalation of antibiotic therapy (8% vs 1%).43

In addition to those findings, expert opinion from several opinion/perspective journal articles has recommended holding off on antibiotics in mild to moderate cases of aspiration pneumonitis with monitoring and reassessment in 24-48 hours after a suspected/confirmed aspiration event.6,17,20,33  These recommendations may be supported from the findings of a 1976 study of the clinical course of patients after witnessed aspiration, which found that infection developed in patients from 2 to 10 days after aspiration.18  In another study, patients with <24 hours of symptoms who received either no antibiotics or less than <24 hours of antibiotics all survived as well as improved rapidly after 24-48 hours.17  This practice of withholding antibiotics in select patients also helps avoid unnecessary complications of antibiotic therapy, such as antibiotic resistance and Clostridium difficile infection.44 Some have advocated empiric antibiotics in cases of small bowel obstruction, feeding tubes, or other conditions with increased risk of colonization of gastric contents.6

In such cases as well as those of longer duration of symptoms (>24-48 hours as above) more concerning for aspiration pneumonia, antibiotics can be considered. A systematic review of eight studies on the microbiology of aspiration pneumonia showed predominantly Gram negative and positive bacteria. Of these eight studies, only two recovered any anaerobic bacteria with a third study finding anaerobes only if lung abscess was also present. Both of these studies isolated anaerobes from about 20% of their samples.45,46  The most common Gram negative bacteria isolated were Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa while the most Gram positive were Staphylococcus aureus and Streptococcus pneumoniae.47

Guidance as to antibiotic choice is limited by the lack of randomized control trials and other high quality evidence. Recommendations from the Infectious Diseases Society of America jointly with the American Thoracic Society (IDSA/ATS) still lean towards anaerobic coverage with a β-lactam/β-lactamase inhibitor or clindamycin as first line.47,48  Although no doses are mentioned in the guidelines, dosing for clindamycin in studies of aspiration pneumonia are 600mg IV q8h or BID. The most common β-lactam/β-lactamase inhibitor used in studies is ampicillin-sulbactam (with doses varying from 1.5g q8h IV to 1.5g BID to 3g).49,50  Another similarly effective alternative from a recent study is azithromycin (500 mg IV q24h x 5 days followed by PO for 3 days), which was found to have similar efficacy to ampicillin-sulbactam for aspiration pneumonia as single antibiotic therapy, perhaps because one of the more common causative anaerobes is Prevotella spp, which is sensitive to azithromycin.47,50  Prevalence data of methicillin-resistant Staphylococcus aureus (MRSA) from culture varies widely from 0% to 30%, and no studies have explicitly addressed the need for MRSA coverage in aspiration pneumonia, but MRSA is not covered by ampicillin-sulbactam, which currently appears to be one of the antibiotics of choice for aspiration pneumonia. A more recent 2008 study compared ampicillin-sulbactam versus moxifloxacin for aspiration pneumonia and lung abscess with similar success rate of 67%, suggesting that an antibiotic regimen similar to what is used for community-acquired pneumonia may be sufficient for aspiration pneumonia as well.51

Based on current evidence, we recommend the following treatment regimens when giving antibiotics for suspected aspiration pneumonitis:

  • First-line: β-lactam/β-lactamase inhibitor (e.g. ampicillin-sulbactam 1.5g IV q8h or BID) or clindamycin (600mg IV q8h or BID)
  • Alternate agent: azithromycin (500 mg IV q24h x 5 days followed by PO for 3 days)

Based on expert opinion and newer microbiological data suggesting less need for anaerobic coverage, we believe it would also be reasonable to consider the following regimens:

  • Standard regimens for community-acquired or hospital-acquired pneumonia (refer to the pneumonia section of this emDocs post on antimicrobial regimens)
  • Addition of anaerobic coverage only in cases of severe dental disease, necrotizing pneumonia, or lung abscess for which we would recommend switching to clindamycin or a β-lactam/β-lactamase inhibitor as above.6,52

Of note, although metronidazole also has anaerobic activity, it clinically performs poorly in aspiration pneumonia.53,54


The administration of corticosteroids has not demonstrated a benefit in managing aspiration pneumonitis or pneumonia with one study even showing that pneumonia may be more common after aspiration with corticosteroid treatment.55–58


No explicit guidelines or data exists regarding disposition management for aspiration pneumonia or pneumonitis. Disposition will be largely clinically based on patient’s acuity and risk factors and/or comorbidities. Recognizing variations in practice amongst various health care settings, in the authors’ opinion, we recommend the following:

  • If strong suspicion for aspiration pneumonia, disposition decisions can be made similar to those of patients with community or hospital-acquired pneumonia.

For aspiration pneumonitis:

  • For healthy patients:
    • If presenting within <24-48 hours after symptom onset, discharge home with follow-up with a primary care physician for antibiotics if symptoms persist >48 hours.
    • If presenting >48 hours after symptom onset, discharge home with outpatient antibiotics.
  • For elderly, immunocompromised, or other at-risk patients, disposition will depend on clinical status but broadly:
    • If presenting <24-48 hours after symptom onset, consider placing in an observation unit until 48 hours of symptom onset. If symptoms resolve, patient likely had pneumonitis. If symptoms persist, treat for possible pneumonia.
    • If presenting >24-48 hours after symptom onset, admit.

Case Conclusion:

Given a highly suspected aspiration event and <24-48 hours of symptoms, and our patient generally appearing well with stable vital signs, the decision is made to hold antibiotics and place in observation to be closely monitored for the development of any respiratory distress or signs of infection.  Over the observation period, the patient remains stable, his symptoms resolve, and he is ultimately discharged home.

Take Home Points 

  • Distinguishing between aspiration pneumonitis and aspiration pneumonia remains a clinical diagnosis.
  • Chest X-ray findings of infiltrates in dependent parts of the lung can suggest aspiration but do not help distinguish between aspiration pneumonia and pneumonitis.
  • Mild to moderate cases of aspiration pneumonitis do NOT benefit from antibiotics. Consider holding antibiotics and monitoring for 24-48 hours after symptom onset.
  • Current guidelines for antibiotic choice for aspiration pneumonia recommend beta-lactam/beta-lactamase inhibitor or clindamycin as first-line with flagyl being ineffective for anaerobic coverage. However, more recent data strongly suggests that anaerobic coverage may not be needed and may be considered in certain at-risk groups, but otherwise standard pneumonia regimens can be used.
  • Corticosteroids are NOT recommended in management of aspiration pneumonia or pneumonitis.

Further Reading

  1. ED Evaluation of Community-Acquired Pneumonia
  2. Pediatric Pneumonia
  3. Corticosteroids for Pneumonia: Ready for Primetime?
  4. Choosing Wisely: Non-invasive ventilation in patients with acute respiratory failure from pneumonia
  5. Pneumonia Mimics: Pearls and Pitfalls
  6. Ultrasound for Pneumonia in the ED


  1. Bartlett JG, Gorbach SL. The triple threat of aspiration pneumonia. Chest. 1975;68(4):560-566. doi:10.1378/chest.68.4.560
  2. Kennedy TP, Johnson KJ, Kunkel RG, Ward PA, Knight PR, Finch JS. Acute Acid Aspiration Lung Injury in the Rat. Anesth Analg. 1989;69(1):87???92. doi:10.1213/00000539-198907000-00017
  3. Schwartz DJ, Wynne JW, Gibbs CP, Hood CI, Kuck EJ. The pulmonary consequences of aspiration of gastric contents at pH values greater than 2.5. Am Rev Respir Dis. 1980;121(1):119-126. doi:10.1164/arrd.1980.121.1.119
  4. Mitsushima H, Oishi K, Nagao T, et al. Acid aspiration induces bacterial pneumonia by enhanced bacterial adherence in mice. Microb Pathog. 2002;33(5):203-210. doi:10.1006/mpat.2002.0529
  5. Van Westerloo DJ, Knapp S, Van’t Veer C, et al. Aspiration pneumonitis primes the host for an exaggerated inflammatory response during pneumonia. Crit Care Med. 2005;33(8):1770-1778. doi:10.1097/01.CCM.0000172277.41033.F0
  6. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med. 2001;344(9):665-671. doi:10.1056/NEJM200103013440908
  7. Raghavendran K, Nemzek J, Napolitano LM, Knight PR. Aspiration-induced lung injury. Crit Care Med. 2011. doi:10.1097/CCM.0b013e31820a856b
  8. Son YG, Shin J, Ryu HG. Pneumonitis and pneumonia after aspiration. J Dent Anesth Pain Med. 2017. doi:10.17245/jdapm.2017.17.1.1
  9. Yigit O, Bektas F, Sayrac AV, Senay E. Fire-eater’s pneumonia: two case reports of accidentally aspirated paraffin oil. J Emerg Med. 2012;42(4):417-419. doi:10.1016/j.jemermed.2010.11.025
  10. Franzen D, Kohler M. Severe pneumonitis after fire eating. BMJ Case Rep. 2012;2012. doi:10.1136/bcr-2012-006528
  11. Fernández-Sabé N, Carratalà J, Rosón B, et al. Community-acquired pneumonia in very elderly patients: causative organisms, clinical characteristics, and outcomes. Medicine (Baltimore). 2003;82(3):159-169. doi:10.1097/
  12. Jeon I, Jung GP, Seo HG, Ryu JS, Han TR, Oh BM. Proportion of aspiration pneumonia cases among patients with community-acquired pneumonia: A single-center study in Korea. Ann Rehabil Med. 2019. doi:10.5535/arm.2019.43.2.121
  13. Hayashi M, Iwasaki T, Yamazaki Y, et al. Clinical features and outcomes of aspiration pneumonia compared with non-aspiration pneumonia: A retrospective cohort study. J Infect Chemother. 2014. doi:10.1016/j.jiac.2014.04.002
  14. Lanspa MJ, Jones BE, Brown SM, Dean NC. Mortality, morbidity, and disease severity of patients with aspiration pneumonia. J Hosp Med. 2013;8(2):83-90. doi:10.1002/jhm.1996
  15. Aldrich T, Morrison J, Cesario T. Aspiration after Overdosage of Sedative or Hypnotic Drugs. South Med J. 1980. doi:10.1097/00007611-198004000-00017
  16. Isbister GK, Downes F, Sibbritt D, Dawson AH, Whyte IM. Aspiration pneumonitis in an overdose population: Frequency, predictors, and outcomes. Crit Care Med. 2004. doi:10.1097/01.CCM.0000104207.42729.E4
  17. Mylotte JM, Goodnough S, Gould M. Pneumonia versus aspiration pneumonitis in nursing home residents: Prospective application of a clinical algorithm. J Am Geriatr Soc. 2005. doi:10.1111/j.1532-5415.2005.53258.x
  18. Bynum LJ, Pierce AK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis. 1976;114(6):1129-1136. doi:10.1164/arrd.1976.114.6.1129
  19. Mukhopadhyay S, Katzenstein ALA. Pulmonary disease due to aspiration of food and other particulate matter: A clinicopathologic study of 59 cases diagnosed on biopsy or resection specimens. Am J Surg Pathol. 2007. doi:10.1097/01.pas.0000213418.08009.f9
  20. Mandell LA, Niederman MS. Aspiration Pneumonia. Longo DL, ed. N Engl J Med. 2019;380(7):651-663. doi:10.1056/NEJMra1714562
  21. Miyata E, Tanaka A, Emori H, Taruya A, Miyai S, Sakagoshi N. Incidence and risk factors for aspiration pneumonia after cardiovascular surgery in elderly patients. Gen Thorac Cardiovasc Surg. 2017;65(2):96-101. doi:10.1007/s11748-016-0710-8
  22. Kawanishi K, Kato J, Toda N, et al. Risk Factors for Aspiration Pneumonia After Endoscopic Hemostasis. Dig Dis Sci. 2016;61(3):835-840. doi:10.1007/s10620-015-3941-0
  23. Kawai S, Yokota T, Onozawa Y, et al. Risk factors for aspiration pneumonia after definitive chemoradiotherapy or bio-radiotherapy for locally advanced head and neck cancer: A monocentric case control study. BMC Cancer. 2017;17(1). doi:10.1186/s12885-017-3052-8
  24. Feng M-C, Lin Y-C, Chang Y-H, et al. The Mortality and the Risk of Aspiration Pneumonia Related with Dysphagia in Stroke Patients. J Stroke Cerebrovasc Dis. 2019;28(5):1381-1387. doi:10.1016/j.jstrokecerebrovasdis.2019.02.011
  25. Van Der Maarel-Wierink CD, Vanobbergen JNO, Bronkhorst EM, Schols JMGA, De Baat C. Meta-analysis of dysphagia and aspiration pneumonia in frail elders. J Dent Res. 2011. doi:10.1177/0022034511422909
  26. Manabe T, Teramoto S, Tamiya N, Okochi J, Hizawa N. Risk Factors for Aspiration Pneumonia in Older Adults. PLoS One. 2015;10(10):e0140060. doi:10.1371/journal.pone.0140060
  27. Terpenning MS, Taylor GW, Lopatin DE, Kerr CK, Liza Dominguez B, Loesche WJ. Aspiration pneumonia: Dental and oral risk factors in an older veteran population. J Am Geriatr Soc. 2001;49(5):557-563. doi:10.1046/j.1532-5415.2001.49113.x
  28. Wada H, Nakajoh K, Satoh-Nakagawa T, et al. Risk factors of aspiration pneumonia in Alzheimer’s disease patients. Gerontology. 2001;47(5):271-276. doi:10.1159/000052811
  29. Herzig SJ, LaSalvia MT, Naidus E, et al. Antipsychotics and the Risk of Aspiration Pneumonia in Individuals Hospitalized for Nonpsychiatric Conditions: A Cohort Study. J Am Geriatr Soc. 2017;65(12):2580-2586. doi:10.1111/jgs.15066
  30. Hu X, Lee JS, Pianosi PT, Ryu JH. Aspiration-related pulmonary syndromes. Chest. 2015;147(3):815-823. doi:10.1378/chest.14-1049
  31. Bonten MJ, Gaillard CA, van der Hulst R, et al. Intermittent enteral feeding: the influence on respiratory and digestive tract colonization in mechanically ventilated intensive-care-unit patients. Am J Respir Crit Care Med. 1996;154(2 Pt 1):394-399. doi:10.1164/ajrccm.154.2.8756812
  32. Bonten MJM, Gaillard CA, Van der Geest S, et al. The role of intragastric acidity and stress ulcus prophylaxis on colonization and infection in mechanically ventilated ICU patients: A stratified, randomized, double-blind study of sucralfate versus antacids. Am J Respir Crit Care Med. 1995;152(6 I):1825-1834. doi:10.1164/ajrccm.152.6.8520743
  33. Paintal HS, Kuschner WG. Aspiration syndromes: 10 Clinical pearls every physician should know. Int J Clin Pract. 2007;61(5):846-852. doi:10.1111/j.1742-1241.2007.01300.x
  34. Scheeren B, Gomes E, Alves G, Marchiori E, Hochhegger B. Achados de TC de tórax em pacientes com disfagia e aspiração pulmonar: Uma revisão sistemática. J Bras Pneumol. 2017;43(4):313-318. doi:10.1590/s1806-37562016000000273
  35. Glick Y. Acute Aspiration Pneumonitis [Image]. Published 2017.
  36. Müller B, Harbarth S, Stolz D, et al. Diagnostic and prognostic accuracy of clinical and laboratory parameters in community-acquired pneumonia. BMC Infect Dis. 2007. doi:10.1186/1471-2334-7-10
  37. Assicot M, Bohuon C, Gendrel D, Raymond J, Carsin H, Guilbaud J. High serum procalcitonin concentrations in patients with sepsis and infection. Lancet. 1993. doi:10.1016/0140-6736(93)90277-N
  38. El-Solh AA, Vora H, Knight PR, Porhomayon J. Diagnostic use of serum procalcitonin levels in pulmonary aspiration syndromes. Crit Care Med. 2011. doi:10.1097/CCM.0b013e31820a942c
  39. Jaoude PA, Knight PR, Ohtake P, El-Solh AA. Biomarkers in the diagnosis of aspiration syndromes. Expert Rev Mol Diagn. 2010. doi:10.1586/erm.10.7
  40. Theerthakarai R, El-Halees W, Ismail M, Solis RA, Khan MA. Nonvalue of the initial microbiological studies in the management of nonsevere community-acquired pneumonia. Chest. 2001;119(1):181-184. doi:10.1378/chest.119.1.181
  41. Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology. 1993. doi:10.1097/00000542-199301000-00010
  42. Easby J, Abraham BK, Bonner SM, Graham S. Prone ventilation following witnessed pulmonary aspiration: The effect on oxygenation. Intensive Care Med. 2003. doi:10.1007/s00134-003-1983-9
  43. Dragan V, Wei Y, Elligsen M, Kiss A, Walker SAN, Leis JA. Prophylactic antimicrobial therapy for acute aspiration pneumonitis. Clin Infect Dis. 2018;67(4):513-518. doi:10.1093/cid/ciy120
  44. Joundi RA, Wong BM, Leis JA. Antibiotics “Just-In-Case” in a Patient With Aspiration Pneumonitis. JAMA Intern Med. 2015. doi:10.1001/jamainternmed.2014.8030
  45. Allewelt M, Schüler P, Bölcskei PL, et al. Ampicillin + sulbactam vs. clindamycin ± cephalosporin for the treatment of aspiration pneumonia and primary lung abscess. Clin Microbiol Infect. 2004. doi:10.1111/j.1469-0691.2004.00774.x
  46. Tokuyasu H, Harada T, Watanabe E, et al. Effectiveness of Meropenem for the Treatment of Aspiration Pneumonia in Elderly Patients. doi:10.2169/internalmedicine.48.1308
  47. Bowerman TJ, Zhang J, Waite LM. Antibacterial treatment of aspiration pneumonia in older people: a systematic review. Clin Interv Aging. 2018. doi:10.2147/CIA.S183344
  48. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on the Management of Community-Acquired Pneumonia in Adults. Clin Infect Dis. 2007. doi:10.1086/511159
  49. 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. doi:10.1378/chest.127.4.1276
  50. Marumo S, Teranishi T, Higami Y, Koshimo Y, Kiyokawa H, Kato M. Effectiveness of azithromycin in aspiration pneumonia: A prospective observational study. BMC Infect Dis. 2014. doi:10.1186/s12879-014-0685-y
  51. Ott SR, Allewelt M, Lorenz J, et al. Moxifloxacin vs ampicillin/sulbactam in aspiration pneumonia and primary lung abscess. Infection. 2008;36(1):23-30. doi:10.1007/s15010-007-7043-6
  52. Marik PE, Carcan P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: A prospective study. Chest. 1999;115(1):178-183. doi:10.1378/chest.115.1.178
  53. Perlino CA. Metronidazole vs clindamycin treatment of anerobic pulmonary infection. Failure of metronidazole therapy. Arch Intern Med. 1981;141(11):1424-1427. Accessed July 5, 2019.
  54. Sanders C V, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic infections. Am Rev Respir Dis. 1979. doi:10.1164/arrd.1979.120.2.337
  55. Bone RC, Fisher CJ, Clemmer TP, Slotman GJ, Metz CA. Early methylprednisolone treatment for septic syndrome and the adult respiratory distress syndrome. Chest. 1987;92(6):1032-1036. doi:10.1378/chest.92.6.1032
  56. Bernard GR, Luce JM, Sprung CL, et al. High-Dose Corticosteroids in Patients with the Adult Respiratory Distress Syndrome. N Engl J Med. 1987;317(25):1565-1570. doi:10.1056/NEJM198712173172504
  57. Lowrey LD, Anderson M, Calhoun J, Edmonds H, Flint LM. Failure of corticosteroid therapy for experimental acid aspiration. J Surg Res. 1982;32(2):168-172. Accessed July 4, 2019.
  58. Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med. 1977. doi:10.1016/0002-9343(77)90157-7


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