Differentiating pulmonary diseases with inflammatory markers

In this video, we look at which markers to order when you’re not sure whether your patient’s pulmonary condition is inflammatory in nature, why radiographic changes for CHF and pneumonia are not enough to diagnose either, and why routine blood work will miss important diagnostic clues (and what to use instead).

Pete Yunyongying, MD FACP
Pete Yunyongying, MD FACP
9th Nov 2021 • 4m read

Systemic inflammatory markers can help us distinguish between inflammatory and non-inflammatory pulmonary conditions, such as pneumonia and congestive heart failure. In this video, we look at which markers to order when you’re not sure whether your patient’s pulmonary condition is inflammatory in nature, why radiographic changes for CHF and pneumonia are not enough to diagnose either, and why routine blood work will miss important diagnostic clues (and what to use instead). Inflammation got you all flustered? With this course, you'll master the use of inflammatory markers to get to the right diagnosis.

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Video transcript

Systemic inflammatory markers in the history can help distinguish between inflammatory and non inflammatory conditions, such as pneumonia and congestive heart failure. The presence of fevers, chills, rigors would suggested inflammatory processes. However, consider a patient that presents with acute onset of shortness of breath, and is found to have low blood pressure. She has a history of CHF, but also risk factors for pneumonia like underlying COPD. Her low blood pressure could be due to poor cardiac output from CHF, but also sepsis from pneumonia.

The clinical dilemma is the following, does she had pneumonia that would require antibiotics? Or does she need diuresis for management of volume overload? Inflammatory markers can help distinguish the two. But unfortunately, the patient doesn't always present with this specific history, or they may not initially present with a fever. Thus, this makes a diagnosis more difficult. Adding basic lab work may show leukocytosis and other inflammatory markers of infection that is useful, but lack of these doesn't rule out infection.

This is crucial when we know that early antibiotic therapy is important for lowering mortality in the setting of pneumonia with sepsis. Traditional workup for this would also include plane chest X ray. This is far from definitive most of the time. Radiographic changes for CHF and pneumonia are often very similar, which is not reassuring when management decisions are so divergent. Of course, one option is to treat for all consideration simultaneously. But this poses other problems.

This strategy could lead to an overuse of antibiotics, and the development of antibiotic resistance. Moreover, the management of volume status is truly completely opposite and mutually exclusive. Diuresis for volume overload versus early aggressive fluid resuscitation for pneumonia and sepsis. To help aid with our diagnosis, I suggest the use of procalcitonin. It's a protein produced at very low levels by the thyroid for the regulation of calcium. In response to severe systemic inflammation procalcitonin levels rise dramatically. There is also additional production of procalcitonin in other tissues like the liver.

Procalcitonin levels therefore, are a wonderful inflammatory marker to help distinguish between these two divergent clinical considerations. Elevated levels are more suggestive of sepsis, pneumonia, and COPD exacerbations. It is proven to be a useful marker of infections in several other settings as well. It is important to note procalcitonin is still elevated in infected patients with neutropenia, where most other inflammatory markers like fever chills, leukocytosis are often lacking.

Procalcitonin is also helpful in post operative fevers. Fevers are a common occurrence post operatively with a wide range of ideologies, such as deep vein thrombosis, atelectasis, and wound infection. Procalcitonin tends to be elevated infections and not DVT or atelectasis. Time is of the essence in the presentation of a critically ill patient with shortness of breath. One of the diagnostic considerations is diffuse alveolar hemorrhage. Distinguishing this condition from sepsis or other causes of acute respiratory distress syndrome is crucial as the management is quite different. The use of inflammatory markers in history and physical exam certainly can help.

But routine bloodwork, like CBC, ESR and CRP are usually not enough to distinguish between all the inflammatory conditions leading to critical illness. Radiology likewise is sometimes helpful, but often not specific enough to distinguish between different autoimmune syndromes. Advanced serology is sometimes needed to further identify the ideology. For example, when diffuse alveolar hemorrhage is a consideration. Aside from bronchoscopy, inflammatory markers and serology become the most useful test. Elevation of the nonspecific inflammatory markers like ESR and CRP is not particularly helpful in this situation.

A critically ill patient with sepsis will have equally elevated levels compared to patients with autoimmune diffuse alveolar hemorrhage. Thus, we must rely on more specific auto antibodies in common combination with complement levels. The most common diagnostic considerations include systemic lupus erythematosus, Goodpasture syndrome, immunoglobulin A vasculitis or IGA vasculitis, also known as Henoch-Schonlein purpura, and antineutrophil cytoplasmic antibodies associated or ANCA associated vascular deities.

The ANCA positive diseases are Granulomatosis with polyangiitis and eosinophilic Granulomatosis with polyangiitis, you may have learned these as Wegener's and Churg Strauss syndromes. Of note, there is a movement away from those nomenclatures. Each is associated with a slightly different pattern of antibodies, and each vary slightly in their presentation. However, because there is so much overlap in their presentation, most clinicians will order all of their associated markers as a panel. It is beyond the scope of this lesson to cover the specific patterns for each of the causes for diffuse alveolar hemorrhage. Suffice it to say, though, that any elevation or abnormality in these panels should be enough to trigger several things. One consideration for empiric therapy with high dose corticosteroids or other immunosuppressants, two, early consultation with specialists and three, early transfer of care to intensive care units as these patients are at high risk for rapidly becoming unstable.

Clinicians encounter inflammation daily and there are lots of inflammatory markers to consider. Which should you order for your patient? Here, you’ll learn the strengths and limitations of each marker, when they’re useful, and when they’re not. We’ll look at laboratory markers of inflammation as well as radiologic and clinical signs so you can take your diagnostic skills to the next level.