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).
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.
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.
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.
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.
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