Diagnosing Aspiration Pneumonia: Why it’s so hard and what it means for the SLP
By George Barnes MS, CCC-SLP, BCS-S
Edited by Allie Mataras MA, CCC-SLP, CBIS
Aspiration pneumonia (AP) is an elusive beast. It’s difficult to pin point exactly how, when or even why the condition occurs. The diagnosis can be missed when it’s there or thought to be there when it’s not. It is over-diagnosed in some respects and under-diagnosed in others. AP is like that pimple that pops up before the big dance. You don’t know where it came from or how it got there and maybe didn’t even think about it until it became the only thing you thought about. Even though AP can be incredibly difficult to diagnose, that doesn’t make ignoring it a viable option. It is a serious and often preventable condition that can have a terrible impact on a growing number of people as the population ages. Let’s start with some statistics because you KNOW how much I love them…
AP Stats
Pneumonia is the number one cause of infection in hospital admissions. Over a million people are diagnosed with costs of more than $10 billion every year. AP is a piece of this pie, but it’s difficult to tell exactly how big of a piece. Why? Well, because it’s difficult to diagnose of course (more on that later). One of the more frequently cited studies reveals AP as being between 5 and 15% of all pneumonia cases. One study showed an average of 13.6% with some studies going as high as 24%. The discrepancy occurs because the rates will be highly dependent on the populations being studied (i.e. the base rates). For example, in community acquired pneumonia the rates may be lower at only 5%, but in nursing homes it is expected to be much higher at 18%. For those diagnosed in the hospital, the rate of AP may increase to as high as 53%. And in elderly hospitalized patients, this rate goes up to 80%. This should start to give us a picture of the type of patients who are most at risk for the disease. And it’s important to note that these are most likely conservative measures as many cases involve silent aspiration or aspiration that was unwitnessed. Further, AP is a deadlier disease process than other types of pneumonia (2.3x and almost 3x more deadly according to the research). The mortality rate of AP can be up to 70% depending on what and how much is aspirated. This just makes it THAT much important to diagnose quickly and accurately so that we can manage it effectively.
A sticky diagnosis
One of the most difficult issues to grapple with in AP diagnosis is that it’s like a bored dog following you around no matter where you go. If an AP diagnosis is made, even incorrectly, it stays in your chart... Forever. It’s like that bad grade in school they warned would stay on your permanent record. Except this is actually true. When practitioners are trying to make a diagnosis they will most certainly take into account that there is a history of AP. It haunts you. This rule applies to dysphagia as well. That patient who had a little residue and you diagnosed her with mild dysphagia will always have that diagnosis and doctors could use that information to diagnose AP and formulate a treatment plan (even if it’s 6 years from now). This could lead to draconian measures to manage a dysphagia that may not even really exist. Here the patient lives in a dystopian nightmare of feeding tubes, thickened liquids, and mashed up food. Whether they need it or not. As practitioners ourselves we then need to understand how and why the AP diagnosis was made so we can determine the cause of the condition and how dysphagia may (or may not) play an important part.
Nobody agrees
So why is it so hard to diagnose? The issue begins with a lack of consistent and universally agreed up criteria to diagnose AP. For example, look at the smorgasbord of diagnostic descriptions on table 1 in this study. There is no gold standard for diagnosing AP. Pneumonia in general comes in many forms and its diagnosis depends on, well, whoever is doing the diagnosing really. The NIH tells us that pneumonia can be diagnosed with respiratory changes, abnormal chest imaging, and signs of infection in the blood work such as an increased white blood cell count. But the diagnostic process and reasoning will vary from provider to provider both clinically and in the research. Even the type of pneumonia is often disagreed upon. For example, some will diagnose pneumonia by where the patient was when they developed symptoms (e.g. community vs hospital-acquired pneumonia), others if they were using a vent when it occurred (ventilator-associated pneumonia), and others by the type of microbe (e.g. bacterial vs viral). Some may use a combination of these options while others may not use any of them and simply put the location of the lobe that was impacted (e.g. right lower lobe pneumonia). In some ways, having lots of options can be a good thing. It allows us to be super specific with what type of pneumonia is being diagnosed so that we can be better at treating and preventing it. But this doesn’t change the fact that everybody is marching to the beat of their own drum when it comes to pneumonia diagnosis and it seems like nobody is talking to each other to create a common language.
AP of course falls somewhere in this crowded, chaotic, and overlapping group of diagnoses and seems to welcome an even more abstract diagnostic process. So before we get any more lost in the esoteric world of diagnostic practice patterns, let’s get into the nitty gritty of what AP even refers to from a medical and clinical standpoint.
AP unveiled
AP or it’s equally evil stepsister aspiration pneumonitis (inflammation of the airways) occurs from a large volume of aspiration either from anterograde (from above the UES) aspiration from harmful bacteria colonized in the mouth or from retrograde aspiration (from below the UES) after a vomiting or a significant reflux event. It can be difficult to determine if the condition is one or the other as both have similar risk factors (i.e. poor positioning, feeding tube use, medical complexity, poor mentation, etc.) and may result in similar presentations. While textbook aspiration pneumonitis does not involve an infection, this is often not the case in real life examples as undigested food/stomach contents or harmful gut bacteria can cause an infection in a reflux or vomiting event. For the sake of simplicity (take it when you can get it), AP will refer to both aspiration pneumonia and aspiration pneumonitis in this blog. The risk of AP occurring is dependent on a myriad of factors which I will get to in subsequent blogs. Since many of these factors are familiar to us now it becomes a little bit easier to identify those patients who are at an increased risk of developing AP as well as confirming the diagnosis with the presence of those risk factors if it’s suspected. So then why does it still remain so difficult to diagnose?
Differential diagnosis
When a doctor determines what condition a patient has, they are taking as much useful information as possible to make what’s called a “differential diagnosis.” A differential diagnosis is when a doctor says that the condition is either x or y (or z depending on how many possibilities there are). When there are several conditions that share similar characteristics, the best call is often not to make a call at all (cop out, right?). This leaves the possibility of multiple conditions so we can create a plan of care that might effectively manage some, most, or even all of the conditions simultaneously until an effective diagnosis can be made. AP for example could be a different type of pneumonia or a different type of pulmonary condition altogether (i.e. congestive heart failure or COPD exacerbation). So if the diagnosis is unable to be made then the patient may be put on empirical broad-spectrum antibiotic therapy to combat the broad range of potential bacteria as well as general oxygen therapy and respiratory medications to maintain medical stability. This of course won’t be as effective as using antibiotics that are specifically targeted for bacteria after an aspiration pneumonia so it’s best to get an accurate diagnosis as soon as possible in order to ensure the best outcome.
Nailing down AP
AP does have some salient features that can help doctors make a diagnosis. We aren’t completely flying blind here. The diagnosis of AP as reported by the Merck Manual includes abnormal chest imaging involving the gravity dependent areas of the lungs and the inclusion of signs/symptoms of dysphagia. You see, because of the way the mainstem bronchi bifurcate, it creates a sort of slide that encourages foreign contents from the larynx and trachea to end up in the right lobe. And because these contents are heavier than air, they usually end up in the gravity dependent areas of the lung, which is why the right lower lobe is often a suspicious area for AP. BUT, since nothing is easy in life, this of course is not a hard-fast rule. What’s most important to know is actually what position the patient was in during a suspected large-volume aspiration event or what position they are typically in throughout the day if this event was not witnessed. Gravity dependence is the key term here so if a patient is chronically leaning to the left then you may see an abnormality in the lower left lung. OR if the patient is typically lying down then the issue may be seen in the upper and/or posterior lungs.
A fuzzy picture
So if chest imaging is one of the best tools we have for diagnosing AP, then that must be an extremely accurate tool then right? Actually, not quite. Not all chest imaging is created equal. Most radiologists use a chest x-ray (CXR) as it is considered the gold standard for diagnosis and is cheaper, faster, and easier to get results. But a CXR can provide findings that are just as elusive as the condition itself. All a CXR shows us are shadows. Further, it’s 2d vs a CT scan of the chest which is 3d so we are missing an entire dimension. There is also no standardized measure for identifying aspiration pneumonia on a CXR. Radiologists are only about 69% accurate in their judgments and different doctors frequently disagree with each other with the same findings. This all means that the CXR is not super accurate nor is it overly reliable (don’t judge, we have these problems too in dysphagia diagnostics).
What now?
So what does this mean? Do we close our eyes and throw our hands up? Of course not. A complex problem requires a complex solution. We need to rely on more than one measure in order to make an effective diagnosis. We need the presence of a combination of factors to align with one another to start painting the picture. The other element of the Merck Manual diagnosis is the presence of dysphagia. Here’s where WE can help. Dr. James Coyle tells us that you can’t have dysphagia without dysphagia. And you can’t have aspiration pneumonia without dysphagia either (but you can have it without oropharyngeal dysphagia- don’t forget about that sneaky retrograde aspiration which can often be silent). A comprehensive workup including an instrumental study will shed much needed light on the problem to determine if, how, when, and with what a patient might be aspirating. This will help us not only make an accurate diagnosis, but also form an effective management strategy too.
Confirming an infection
OK, so far we have an abnormal CXR especially with involvement in the gravity dependent areas of the lungs. Next, we have the presence of dysphagia and/or a high risk for aspiration as confirmed on an instrumental study. What are we missing for an AP diagnosis? You guessed it: The presence of an infection. Pneumonia isn’t pneumonia without a pulmonary infection. So how do we know for sure if we have one? A complete blood count (CBC) will tell us what the white blood cell (WBC) or leukocyte count is. Anything over 10.5-11k WBCs per microliter or cubic centimeter is considered a high WBC or leukocytosis and is indicative of an infection. If you want to dig a little deeper you can also look at the neutrophil count (in the differential blood count), which is indicative of a bacterial infection. These values won’t be a perfect indicator either though as other factors may cause leukocytosis. But don’t give up yet. Simply check in with the infectious disease doctor to make sure an infection is actually present and to determine if it is bacterial and its suspected source.
Which infection?
OK, now that there is concern for aspiration, an abnormal CXR, and a confirmed infection we know for sure what’s going on, right? Of course not. That would STILL be way to easy. We need to make sure there aren’t any other infections going on. To rule this out, the doctor may consider running other tests, such as a urine analysis to rule out a UTI or a blood analysis to rule out bacteremia. A sputum culture is the most effective way to diagnose AP as we can determine what kind of microbes we find in the lungs to see if those came from, say, saliva or gastric contents. But the best way to do this is an invasive bronchoscopy (unless the patient has a tracheostomy) where a sample of the patient’s sputum is taken and evaluated. With this information we can confirm suspicion for anterograde aspiration (from the oropharynx) by confirming the pulmonary presence of microbes that may have originated in the oral cavity (e.g. pneumococcus, Haemophilus influenzae, staphylococcus aureus, and anaerobes). But of course this procedure is often skipped as it is not cheap, easy, nor readily available for many facilities. So, after all of this, we may be left with nothing more than an educated guess (Where’s the good news, am I right?)
The good news
Maybe an educated guess is all we can ask for. It’s a complex world after all and the human body is one of the most complex and poorly understood things in that world despite the obvious fact that it’s the only thing we’ve had available for studying since our creation. Every factor that we can acquire is another piece of the puzzle. Like a puzzle, each piece may not mean very much on its own. It takes time, effort, knowledge, and experience to put those pieces together in order to see the full picture (Or at least part of the picture so we can get a sense of what it looks like). The goal of this essay is not to paint a black and white picture as I’m sure you’ve already learned. I have no clear cut directions that will take you from A to B when managing dysphagia and the risk for aspiration pneumonia. But don’t worry- I won’t leave you completely empty handed. What I’ve constructed with the help of people a lot smarter than me (thank you to Doreen Benson and Dr. James Coyle), is a framework for approaching decision-making for aspiration pneumonia risk management. And what I have for you is an explanation of this approach in a series of blogs over the coming weeks. Excited? Me too. Stay tuned!
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