Co-author: Angela Van Sickle, Ph.D., CCC-SLP

Speech-language pathologists (SLPs) often assess patients for the presence of aspiration. If the SLP observes aspiration, diet recommendations, and education concerning the risk of aspiration pneumonia typically follow1. Realizing the profession’s concern for aspiration becoming pneumonia, the authors set out to determine the process by which aspirated material becomes pneumonia. The hope was to find information that explained the sequence of events that occur when food or liquid enters the lungs that are eventually labeled pneumonia. There must be an article or textbook that would simply state something like, “Liquids enter the airway and travel to the gravity-dependent lobe of the lung. There the material enters the alveoli, an infection develops, and there an immune response begins.” Given the level of certainty with which SLPs discuss aspiration pneumonia, we were surprised when search after search yielded little insight. As SLPs, we first searched our own literature. A search of the pulmonology literature followed. Finally, we landed in the microbiology literature. The journey led down a winding and often confusing path that required the addition of a vast, new vocabulary. Along the way, answers were evasive, but many new questions emerged. What follows is a summary of our trek. 

Definition, Prevalence, and Diagnoses  

The Center for Disease Control reported 30,705 inpatient hospital stays for pneumonia in 2014, accounting for 2.1% of all hospitalizations2. A review of billing codes suggests an increasing incidence, making aspiration pneumonia the second most common diagnosis in hospitalized Medicare patients3. One author4 concluded higher reimbursement rates for aspiration pneumonia than for community-acquired pneumonia might falsely increase the frequency.  The statement is disconcerting. Are SLPs responsible for questioning a diagnosis of aspiration pneumonia? It would seem so. 

When a patient receives a diagnosis of aspiration pneumonia, the mind of the SLP may associate the diagnosis with the aspiration of food or liquids. However, “aspiration pneumonia” is a vague diagnosis that may be the result of a pulmonary infection, gastroesophageal reflux, or prandial aspiration. There are 13 or more syndromes labeled as “aspiration pneumonia.” These include community-acquired pneumonia, hospital-associated pneumonia, ventilator-associated pneumonia, and pneumonitis5. A diagnosis of aspiration pneumonia refers to any substance entering the lungs, including a virus or bacteria 4.  Because of the lack of specificity of the terminology, some medical professionals have advocated for the term to be eliminated, as it can be misleading4-7.  


Physicians do not have a standard gold test for the diagnosis of aspiration pneumonia.  About two-fifths of those hospitalized for pneumonia (41.2%) are diagnosed based on a CT scan, about two-thirds involved a chest X-ray (65.1%), and one-third involved a pulmonary function test (33.7%)2. The CDC reported in 2014, 75.3% of inpatient hospitalizations for pneumonia were diagnosed based on bacteriology and microbiology testing. Such testing represents a more reliable diagnosis for pneumonia because it is based on the detection of actual pathogenic agents in the lung parenchyma8. Unfortunately, SLPs, most often have access to, and rely on a chest x-ray alone.  Based on diagnostic sensitivity,  the reliance on x-ray findings should be discouraged. The ability of a chest x-ray, evaluated by a radiologist, to diagnose any type of pneumonia has a sensitivity of 69.0% and a specificity of 77.8% 9.  That means radiologists correctly identify pneumonia on a chest x-ray 69.0% of the time and correctly eliminate those without pneumonia 77.8% of the time. Who knew the accuracy was this poor?  

When reading x-ray reports, SLPs traditionally consider lower lobe infiltrates indicative of aspiration pneumonia10. However, in a group of patients with fluoroscopically documented aspiration, more patients presented with bronchopneumonia (68%) than lower lobe pneumonia (15%)11. Can a chest x-ray accurately provide a diagnosis of “aspiration pneumonia?” There is no simple answer. Does a chest x-ray even allow for the diagnosis of pneumonia, of any type? Not a good portion of the time. Where does aspiration pneumonia show up on a chest x-ray? There is conflicting information.  Have practitioners been searching in all the wrong places? Perhaps. Why does it have to be so complicated? Perhaps, one takeaway is for a more accurate. SLPs need to advocate for tests that would help with differential diagnosis (i.e., microbiology testing). 

More Conundrums

Although it has been clear for many years that aspiration alone does not cause pneumonia12-17, studies in the area of dysphagia have consistently counted all types of pneumonia cases (not just aspiration pneumonia) when expressing outcomes5. That is to say, if a patient in a research study concerning dysphagia develops community-acquired pneumonia, the pneumonia is included in the statistics as a negative dysphagia outcome. The practice falsely inflates the number of patients who develop what SLPs think of as aspiration pneumonia.  Considering, in a longitudinal study, 38% of patients known to aspirate developed pneumonia14, and research indicates 5% to 15% of all cases of pneumonia are aspiration pneumonia18, could it be that only 1.9% to 5.7% of people who aspirate ever develop aspiration pneumonia5? The actual incidence remains unknown. 

As new questions emerged, the search widened. 

Additional Culprits

A recent review19 found approximately 25% of patients with an impaired cough reflex and dysphagia developed pneumonia. Additional identified factors were poor oral hygiene, the overuse of sedative medication, impaired immunity, reduced mucociliary transport, and depressed lung function. The review supports studies found in the speech literature that indicated the presence of aspiration alone does not lead to aspiration pneumonia. The development of pneumonia is multifactorial 12-15.  Other studies suggest that repeated episodes of aspiration pneumonia in some elderly individuals is unavoidable 19.  A question to ponder, does this information indicate the need for cough testing and rehabilitation in the presence of dysphagia20-22? All the information is interesting, and it is fun to learn, but the question, “How does aspiration pneumonia develop?” remained unanswered. So, the search continued. 

Oh, The Things We are Learning


Microbiomes are a current area of scientific interest. The term “microbiome” first appeared in 2001 as “the ecological community of commensal symbiotic, and pathogenic microorganisms that literally share our body space” 23. A microbiome is the community of microorganisms (bacteria, archaea, fungi, and viruses, etc.) that inhabit an organism 24.   In more digestible language,  a microbiome is the community of microscopic cells, viruses, and phages that occupy a site (i.e., lungs, gastrointestinal tract, oral cavity, and so on). Microbiomes regularly show a large degree of interpersonal diversity,  depending on factors such as age, geographical location, and diet, even in the absence of disease5,25. Studies provide an understanding that we are not distinct entities from our microbiome, but together we form a “superorganism” with the microbiome playing a significant role in our physiology and health26-28. Some consider the human microbiome to be our “last organ” 29.  When considering pneumonia, it may be essential to understand the microbiomes of the oral cavity, the lungs, and the esophagus. 

Certain oral microorganisms of the mouth are associated with disease30. The mouth provides a suitable habitat for a wide range of bacteria31. Gingival sulci, gums, the tongue, and smooth surfaces, pits, and fissures of the teeth all create microbial ecosystems. The mouth houses the second most diverse microbial community in the body26. Approximately 280 bacterial species from the oral cavity have been isolated and formally named. However, there are likely 500 to 700 common oral species 32. Oral bacteria that travel to other areas of the body have a role in causing diseases,  including cardiovascular disease,  rheumatoid arthritis,  adverse pregnancy outcomes,  stroke,  inflammatory bowel disease, colorectal cancer, respiratory tract infection,  meningitis, brain abscesses, lung,  liver or spleen abscesses,  appendicitis,  pneumonia, and diabetes33-36.  Knowing the influence of the oral microbiome on health, it is not difficult to understand how it would play an essential role in the development of pneumonia. 

Oral health care, consisting of tooth brushing after each meal, cleaning dentures once a day, and professional cleaning, seems the best intervention to reduce the incidence of aspiration pneumonia17,37-39. Could it be the best defense against aspiration pneumonia is a toothbrush? Would patients have less pneumonia if a dentist regularly cleaned their teeth? It seems to be the case. 

Although many textbooks continue to report the environment of the lungs is sterile, this is not the case40. We inhale between 1,500 and 14,000 organisms each hour 41. The lungs are also exposed to diverse communities of microbes from the oropharynx. Typically, this occurs without consequence. The main avenues of microbial immigration into the lungs are aspiration, inhalation of air, and dispersion along the mucosal surfaces42. Healthy adults are constantly supplying their lower respiratory tract with bacteria in the form of microaspiration 43-46. Due to the microaspiration, the nasopharynx, oropharynx, lung, and esophagus share a similar microbiome 47-51, indicating the lungs are accustom to managing material that is entering the esophagus. 

The ability of the lungs to withstand the damaging effects of microbial and immune activities is complex, precisely regulated, and seminal in health. Both immune resistance and tissue resilience are dynamic and change throughout the lifetime of the individual. Science is only beginning to understand the lung’s defenses against severe pneumonia52. But, the good news is the lungs and airways possess natural and adaptive immune defenses that selectively recognize, kill, and clear unwanted microorganisms 40. The balance of three factors determines the total microbial burden of the lungs: microbial immigration, microbial elimination, microbial reproduction 40. In health, the microbiome is mostly a product of the balance of immigration and elimination, with little contribution from the reproduction rates42.  The elimination of microbes from the lungs is a continuous process. Airways of healthy individuals employ a mucociliary escalator to eliminate microbes 53. To accomplish this task, healthy individuals cough roughly once every other hour54. Coughing propels microbes from the lungs into the larynx and pharynx, where they are either swallowed or expectorated. Together, the mucociliary escalation and cough protect the lungs against disease (Are you thinking about how often you cough?).

When discussing lung health, it is also necessary to consider the microbiome of the gut as the gut microbiota affects the lungs through micro and macro aspiration.55  In addition, there is a complex connection between the gut and the lungs56. Disruption of intestinal–pulmonary connection is linked to increased susceptibility to airway diseases and infections57. Studies show that gut microbiota plays a protective role against bacterial and viral pulmonary infections by regulating innate and adaptive immune responses58,59. A disrupted or altered biome provides the opportunity for  illness56. In other words, when a bacteria travels to a location in the body where it should not be, it can lead to opportunistic infection in people who are already sick or weak. Knowing the microbiome of the gut is impacted by diet5, aging60, and being instutionalized61, SLPs need to consider that we have no idea how altering diets and liquids may impact this delicate balance. Is altering diets causing inflammation in the gut that impacts the lungs? We do not know. This is a legitimate question that begs investigation. 

Another Question

Research exists concerning the possible benefits of free water protocols, even in the presence of known aspiration of thin liquids 62-65. The unanswered question is, could the same benefits be true for other liquids with a pH similar to water? The underlying assumption is that the defense mechanisms of the lungs easily manage water66. What if this is the case for other liquids as well? What if this is a matter of the microbiome of the lungs and not a matter of the liquid aspirated? These questions deserve investigation. In addition, could the same be true for foods? Does the food alone cause inflammation? It seems that it would, but we have not been able to find the answer to that question in an exhaustive search on the topic, which included many disciplines (e.g., speech-language pathology, respiratory, medicine, microbiology, and others). 

Considering the Host in Light of Aspiration 

Typically, pneumonia is thought to be linear: Changes in few key factors (the presence of aspiration, size of the bacterial inoculum, virulence of the pathogen, and strength of the host defense) would cause a proportionate and predictable inflammatory response in the lungs. However, pneumonia occurs abruptly and unpredictably from the complex adaptive system of the respiratory microbiome. Unlike linear systems, complex and adaptive systems cannot be reduced to such a simple model 53. The discovery of the lung microbiome and the recognition that the lungs are a dynamic ecosystem has changed the understanding of pneumonia40. The existing literature points to an issue with the balance of oral, pharyngeal, and gut bacteria (microbiome) and the reaction of the host. It may be the presence of certain bacteria in the oral cavity and gut cause inflammation and infection in the lungs. It may be the host’s ability to respond to the bacteria in the lungs. Many questions remain unanswered. Some people develop pneumonia in the presence of prandial aspiration, and others do not13-15.  The development of pneumonia depends on multiple factors that often defy explanation. Consequently, rather than considering pneumonia to be the invasion of the lungs by a specific pathogen or material, perhaps a better model is to think of it as an emergent phenomenon of low microbial diversity, a high concentration of undesirable microorganisms, and host inflammation that arises from a preexisting issue of biodiversity53. It is not as simple as, I observed aspiration on a swallow study, it must be stopped, or aspiration pneumonia will develop, and the patient may die. Perhaps, instead of the focus being aspiration, the thought process should focus on the host. Such an approach requires the SLP to investigate numerous factors and not make decisions based on the presence or absence of aspiration. Consider the following flowchart.

Chart adapted from Komyia, 2013

The journey to learn the connection between aspiration and pneumonia has been enlightening and frustrating. It seems our significant accomplishments are creating a stack of articles to clutter our desks, an extensive new vocabulary, and a slight headache. Based on extensive reading, a direct cause and effect relationship between prandial aspiration does not exist. Thus, the search for a greater understanding continues. What is clear is that it is the responsibility of SLPs to take a gestalt view of the patient and not just consider what is happening in the pharynx and larynx. Is observing aspiration and making predictions concerning the outcome within the ability of any healthcare provider? Is aspiration of primary concern?  In light of the current information, should stopping aspiration at all costs be the goal of swallowing therapy?  The answers are elusive. When it comes to aspiration pneumonia, it seems the more we learn, the less we know.


1. McCurtin A, Healy C. Why do clinicians choose the therapies and techniques they do? Exploring clinical decision-making via treatment selections in dysphagia practice. Int J Speech Lang Pathol. 2017;19(1):69-76.

2. Williams S, Gousen S, DeFrances C. National hospital care survey demonstration projects: Pneumonia inpatient hospitalizations and emergency department visits. Hyattsville, MD August 24, 2018 2018.

3. Baine W, Yu W, Summe J. Epidemiologic trends in the hospitalization of elderly Medicare patients for pneumonia, 1991-1998. American Journal of Public Health. 2001;91(7):1121-1123.

4. DiBardino DM, Wunderink RG. Aspiration pneumonia: a review of modern trends. J Crit Care. 2015;30(1):40-48.

5. Ferguson J, Ravert, B., Gailey, M. Aspiration: /asp ə’ rā  SH(ə)n/: Noun: An ambiguous term used for a diagnosis of uncertainty. Topics in Pulmonary Medicine. 2018;25(5):177-183.

6. Raghavendran K, Nemzek J, Napolitano LM, Knight PR. Aspiration-induced lung injury. Critical Care Medicine. 2011;39(4):818-826.

7. Mandell LA, Niederman MS. Aspiration Pneumonia. N Engl J Med. 2019;380(7):651-663.

8. Garin N, Marti C, Scheffler M, Stirnemann J, Prendki V. Computed tomography scan contribution to the diagnosis of community-acquired pneumonia. Current Opinion in Pulmonary Medicine. 2019;25(3):242-248.

9. Laursen CB, Sloth E, Lambrechtsen J, et al. Diagnostic performance of chest X-ray for the diagnosis of community acquired pneumonia in acute admitted patients with respiratory symptoms. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2013;21(S2):A21.

10. Bartlett JG, Gorbach SL. The Triple Threat of Aspiration Pneumonia. Chest. 1975;68(4):560-566.

11. Komiya K, Ishii H, Umeki K, et al. Computed tomography findings of aspiration pneumonia in 53 patients. Geriatr Gerontol Int. 2013;13(3):580-585.

12. Feinberg M, Knebl, J., Tully, J., Segall, L., . Aspiration and the Elderly. Dysphagia. 1990;5:61-71.

13. Feinberg MJ, Knebl J, Tully J. Prandial aspiration and pneumonia in an elderly population followed over 3 years. Dysphagia. 1996;11(2):104-109.

14. Langmore SE, Terpenning MS, Schork A, et al. Predictors of aspiration pneumonia: how important is dysphagia? Dysphagia. 1998;13(2):69-81.

15. Langmore SE, Skarupski KA, Park PS, Fries BE. Predictors of Aspiration Pneumonia in Nursing Home Residents. Dysphagia. 2002;17(4):298-307.

16. DePippo KL, Holas MA, Reding MJ, Mandel FS, Lesser ML. Dysphagia therapy following stroke: a controlled trial. Neurology. 1994;44(9):1655-1660.

17. Ashford J. NPO and dysphagia: What the SLP needs to know. Paper presented at: ASHA Convention2016; Philadelphia, PA.

18. Marik PE. Aspiration syndromes: aspiration pneumonia and pneumonitis. Hosp Pract (1995). 2010;38(1):35-42.

19. Komiya K, Ishii H, Kadota J-I. Healthcare-associated Pneumonia and Aspiration Pneumonia. Aging and Disease. 2015;6(1):27.

20. Pitts T, Bolser D, Rosenbek J, Troche M, Sapienza C. Voluntary cough production and swallow dysfunction in Parkinson’s disease. Dysphagia. 2008;23(3):297-301.

21. Troche MS, Rosenbek JC, Okun MS, Sapienza CM. Detraining outcomes with expiratory muscle strength training in Parkinson disease. J Rehabil Res Dev. 2014;51(2):305-310.

22. Kim J, Davenport P, Sapienza C. Effect of expiratory muscle strength training on elderly cough function. Arch Gerontol Geriatr. 2009;48(3):361-366.

23. Lederberg J, McCray AT. `Ome Sweet `Omics–A Genealogical Treasury of Words. In. The Scientist. Vol 152001:8.

24. Lloyd-Price J, Abu-Ali G, Huttenhower C. The healthy human microbiome. Genome Medicine. 2016;8(1).

25. Turnbaugh PJ, Ley RE, Hamady M, Fraser-Liggett CM, Knight R, Gordon JI. The Human Microbiome Project. Nature. 2007;449(7164):804-810.

26. Kilian M, Chapple ILC, Hannig M, et al. The oral microbiome – an update for oral healthcare professionals. British Dental Journal. 2016;221(10):657-666.

27. Grice EA, Segre JA. The Human Microbiome: Our Second Genome. Annual Review of Genomics and Human Genetics. 2012;13(1):151-170.

28. Foster KR, Schluter J, Coyte KZ, Rakoff-Nahoum S. The evolution of the host microbiome as an ecosystem on a leash. Nature. 2017;548(7665):43-51.

29. Baquero F, Nombela C. The microbiome as a human organ. Clinical Microbiology and Infection. 2012;18:2-4.

30. Wade W. Characterisation of the human oral microbiome. Journal of Oral Biosciences. 2013;55(3):143-148.

31. Hardie JM, Bowden GH. The normal microbial flora of the mouth. Soc Appl Bacteriol Symp Ser. 1974;3(0):47-83.

32. Paster BJ, Boches SK, Galvin JL, et al. Bacterial Diversity in Human Subgingival Plaque. Journal of Bacteriology. 2001;183(12):3770-3783.

33. Dewhirst FE, Chen T, Izard J, et al. The Human Oral Microbiome. Journal of Bacteriology. 2010;192(19):5002-5017.

34. Han YW, Wang X. Mobile Microbiome: Oral Bacteria in Extra-oral Infections and Inflammation. Journal of Dental Research. 2013;92(6):485-491.

35. Chapple ILC, Genco R, workshop* obowgotjEA. Diabetes and periodontal diseases: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. Journal of Periodontology. 2013;84(4S):S106-S112.

36. de Pablo P, Chapple IL, Buckley CD, Dietrich T. Periodontitis in systemic rheumatic diseases. Nat Rev Rheumatol. 2009;5(4):218-224.

37. Mori H, Hirasawa H, Oda S, Shiga H, Matsuda K, Nakamura M. Oral Care Reduces Incidence of Ventilator-Associated Pneumonia in ICU Populations. Intensive Care Medicine. 2006;32(2):230-236.

38. Yoneyama T, Yoshida M, Matsui T, Sasaki H. Oral care and pneumonia. The Lancet. 1999;354(9177):515.

39. van der Maarel-Wierink CD, Vanobbergen JNO, Bronkhorst EM, Schols JMGA, de Baat C. Oral health care and aspiration pneumonia in frail older people: a systematic literature review. Gerodontology. 2013;30(1):3-9.

40. Dickson RP, Erb-Downward JR, Huffnagle GB. Towards an ecology of the lung: new conceptual models of pulmonary microbiology and pneumonia pathogenesis. The Lancet Respiratory Medicine. 2014;2(3):238-246.

41. Thomson SC, Hewlett RT. THE FATE OF MICRO-ORGANISMS IN INSPIRED AIR. The Lancet. 1896;147(3776):86-87.

42. Venkataraman A, Bassis CM, Beck JM, et al. Application of a Neutral Community Model To Assess Structuring of the Human Lung Microbiome. mBio. 2015;6(1):e02284-02214.

43. QUINN LH, MEYER OO. THE RELATIONSHIP OF SINUSITIS AND BRONCHIECTASIS. Archives of Otolaryngology. 1929;10(2):152-165.

44. Gleeson K, Maxwell SL, Eggli DF. Quantitative Aspiration During Sleep in Normal Subjects. Chest. 1997;111(5):1266-1272.

45. Huxley EJ, Viroslav J, Gray WR, Pierce AK. Pharyngeal aspiration in normal adults and patients with depressed consciousness. Am J Med. 1978;64(4):564-568.

46. Amberson JB. A clinical consideration of abscesses and cavities of the lung. Bull Johns Hopkins Hosp. 1954;94(5):227-237.

47. Jandhyala SM. Role of the normal gut microbiota. World Journal of Gastroenterology. 2015;21(29):8787.

48. Le Chatelier E, Nielsen T, Qin J, et al. Richness of human gut microbiome correlates with metabolic markers. Nature. 2013;500(7464):541-546.

49. Hollister EB, Gao C, Versalovic J. Compositional and Functional Features of the Gastrointestinal Microbiome and Their Effects on Human Health. Gastroenterology. 2014;146(6):1449-1458.

50. Tuddenham S, Sears CL. The intestinal microbiome and health. Curr Opin Infect Dis. 2015;28(5):464-470.

51. Arumugam M, Raes J, Pelletier E, et al. Enterotypes of the human gut microbiome. Nature. 2011;473(7346):174-180.

52. Quinton LJ, Mizgerd JP. Dynamics of Lung Defense in Pneumonia: Resistance, Resilience, and Remodeling. Annual Review of Physiology. 2015;77(1):407-430.

53. Dickson RP, Erb-Downward JR, Martinez FJ, Huffnagle GB. The Microbiome and the Respiratory Tract. Annual Review of Physiology. 2016;78(1):481-504.

54. Munyard P, Bush A. How much coughing is normal? Archives of Disease in Childhood. 1996;74(6):531-534.

55. Marsland BJ, Trompette A, Gollwitzer ES. The Gut-Lung Axis in Respiratory Disease. Ann Am Thorac Soc. 2015;12 Suppl 2:S150-156.

56. Dang AT, Marsland BJ. Microbes, metabolites, and the gut–lung axis. Mucosal Immunology. 2019;12(4):843-850.

57. Keely S, Talley NJ, Hansbro PM. Pulmonary-intestinal cross-talk in mucosal inflammatory disease. Mucosal Immunology. 2012;5(1):7-18.

58. Ichinohe T, Pang IK, Kumamoto Y, et al. Microbiota regulates immune defense against respiratory tract influenza A virus infection. Proceedings of the National Academy of Sciences. 2011;108(13):5354-5359.

59. Chen L-W, Chen P-H, Hsu C-M. Commensal Microflora Contribute to Host Defense Against Escherichia Coli Pneumonia Through Toll-Like Receptors. Shock. 2011;36(1):67-75.

60. Salazar N, Valdés-Varela L, González S, Gueimonde M, De Los Reyes-Gavilán CG. Nutrition and the gut microbiome in the elderly. Gut Microbes. 2017;8(2):82-97.

61. Kinross J, Nicholson JK. Gut microbiota: Dietary and social modulation of gut microbiota in the elderly. Nat Rev Gastroenterol Hepatol. 2012;9(10):563-564.

62. Carlaw C, Finlayson H, Beggs K, et al. Outcomes of a pilot water protocol project in a rehabilitation setting. Dysphagia. 2012;27(3):297-306.

63. Gillman A. Implementing the Free Water Protocol does not Result in Aspiration Pneumonia in Carefully Selected Patients with Dysphagia: A Systematic Review 2017:345–361, Dysphagia.

64. Murray J, Doeltgen S, Miller M, Scholten I. Does a Water Protocol Improve the Hydration and Health Status of Individuals with Thin Liquid Aspiration Following Stroke? A Randomized Controlled Trial. Dysphagia. 2016;31(3):424-433.

65. Karagiannis M, Karagiannis TC. Oropharyngeal dysphagia, free water protocol and quality of life: an update from a prospective clinical trial. Hell J Nucl Med. 2014;17 Suppl 1:26-29.

66. Panther K. The Frazier Free Water Protocol. Perspectives on Swallowing and Swallowing Disorders (Dysphagia). 2005;14:4-9.


Previous articleRaising Dysphagia Awareness Requires Recognition of Multiphase Dysphagia
Next articleImpact of a Tracheostomy on Swallowing
Ed Bice, M.Ed., CCC-SLP
Angela Van Sickle, Ph.D., CCC-SLP is an assistant professor at Texas Tech University Health Sciences Center. She is the instructor for Dysphagia, Voice/Voice Disorders, and Special Topics in Speech-Language Pathology. She also supervises students in the university clinic. Her research interests include swallowing and swallowing disorders, pedagogy related to swallowing and swallowing disorders, acquired apraxia of speech, and transgender voice. Ed Bice, M.Ed., CCC-SLP is a Speech-Language Pathologist currently in the role of Clinical Consultant for IOPI Medical, LLC. Ed has worked in the health care industry with extensive training in dysphagia. His experience includes a variety of settings; acute care, outpatient, home health and skilled nursing. In addition to his clinical experience, Ed has held various leadership positions. He has worked as a Regional Manager, Vice President of Clinical Services, and Chief Operating Officer. He has been an invited speaker for universities, as well as national and state conventions.


  1. Thanks Ed for writing on this topic!
    I wanted to clarify, in the first paragraph, you mentioned “the authors” and “our,” which was not clear with only your name as author here. Was the other author Dr Van Sickle noted in the bio section?
    Great article!
    Great to review what we know and don’t know.
    I have always loved the term mucocilliary clearance, but i love the escalator or elevator concept for patients to understand that too. Helps when discussing purpose of flutter valves/Acapella devices and EMST.

    GREAT to stress HOST factors rather than just the aspiration.
    Good chart to show that.
    I like to put Langmore’s aspiration pneumonia predictors and other research into a complex “recipe” on how to brew up a pneumonia. Definitely not linear (ie., not at all aspiration = pneumonia). Recipe starts with all the things that alter the oral microbiome (ie., institutionalization, meds, dry mouth, dependence, etc), plus all the ways of adding a dash/pinch of aspiration, reflux, saliva, viruses and other microbes (dependence on feeding, bedridden, reflux, etc). Then lay that all on top of ways to create a decreased host resistance. That was certainly the short version.

    And yes, as SLPs, we should find that the more we know, research and learn, the more we KNOW that we DON’T know. If you are feeling like you got all the answers, and you are super quick with your evals and documentation, then start to worry and do more self education. Include that critical thinking and rationale in your documentation.

  2. Angela, and Ed, thank you for this excellent overview highlighting that aspiration pneumonia is a multi-factorial disease process that requires a multidisciplinary approach and familiarity with literature outside of our own discipline. Over a decade ago, the Institute for Healthcare Improvement implemented the Ventilator Bundle, which included strategies to reduce the occurrence of ventilator associated pneumonia. Some steps have now been incorporated into the care SLP provide patients with dysphagia, and include oral and pulmonary hygiene. As you point out in your review, aspiration pneumonia is an opportunistic infection, and even with the best protocols and approaches, the patient remains a variable, and various co-morbidities and host conditions can always influence the expected outcome of care. I have often thought of aspiration pneumonia like hurricanes. Not all tropical storms brewing in the Atlantic turn into a hurricane, but when the conditions are right, and the structures vulnerable, a costly disaster can be the result. As we gain in our understanding of causes and treatments which might mitigate the occurrence of aspiration pneumonia, the patient and their preferences must remain at the center of our decision making, in particular when recommending feeding tubes or altered consistency diets which may in some instances prolong, but not improve quality of life.

  3. Oh God, excelent review and coments.
    Now im thinking if dysphagia therapy should be done just for people who develops Aspiration pneumonia?
    Well, maybe we should convern not just about pneumonia but intesticial lesions despite pneumonia presence or not. Some of my Patients who aspirantes but doens’t develop pneumonia and stay eating for choice starts to have small points of lesion on their CT like a fibrosis. Probably for their regcuperation lungs process. Maybe this open one more concern to free water protocolol at least for me.
    I dont know. Thinking a lot now!

    What an article!


Please enter your comment!
Please enter your name here