This week in Morning Report, we discussed the case of a patient who had recurrent stabbing and positional chest pains for a week, with a symptom history and initial investigations very consistent with pericarditis. Let’s recap our high-yield approach to pericarditis!

1. What is the pericardium, and what does it do?

Recall that the heart is protected with a tough outer fibrous pericardium and an inner serous pericardium (see figure below). The serous pericardium itself is made up of a parietal layer and an inner visceral layer, between which exists a ‘potential space’, which, in a normal physiological state, can be filled with anywhere from 15-50cc of pericardial fluid.

The function of the pericardium is to protect and tether the heart in the mediastinum, and to act as a limit against which ventricular filling can occur. It also serves as a protective barrier against infection.

2. What is pericarditis and how is it diagnosed?

Pericarditis refer to an inflammation of the pericardial sac, and can occur due to a number of etiologies that we’ll discuss in detail. The diagnosis of pericarditis requires 2 of 4 cardinal features, which I havmmarized in the table below:

It is important to remember that the above diagnostic criteria apply only to acute pericarditis (< 6 weeks), which presents differently from chronic pericarditis (> 6 weeks). Chronic pericarditis often manifests without the above typical symptoms, and patients may experience more constitutional symptoms of fevers, malaise, weight loss, etc.

Finally, remember that pericarditis can occur due to a whole host of medical conditions. There is an excellent recent review of pericarditis with helpful summary tables that can guide your history-taking. I especially like the one below, which summarizes some high-yield associated symptoms that can guide your differential diagnosis:

3. What are some causes of pericarditis?

Most estimates place the incidence of acute pericarditis in the emergency room setting at up to 5% of chest pain presentations. A vast majority of acute pericarditis (50-90%, depending on the source) is idiopathic and presumed secondary to viral infection.

When thinking of causes of pericarditis, I like to break down causes into ‘infectious’ and ‘non-infectious’. We generated a very comprehensive differential in Morning Report, which I have summarized in a flowchart below:

4. What are some complications of pericarditis?

Most idiopathic viral pericarditis seen in the ambulatory setting resolves with treatment, but a small percentage of presentations are susceptible to complications. We discussed the following complications of pericarditis:

• Tamponade: We discussed what happens if a large pericardial effusion is present, and how tamponade physiology can occur. This is the video I was referring to that illustrates these concepts well and demonstrates how a pulsus paradoxus works.
• Myopericarditis: This is technically not a classic complication of pericarditis itself, but rather an inflammation of the myocardium that can coexist with pericarditis. The characteristic feature of myopericarditis is a positive troponin biomarker and/or myocardial inflammation on imaging such as cardiac MRI. Myocardial involvement can lead to systolic dysfunction, arrhythmias, and even fulminant heart failure, so these patients require close monitoring and inpatient surveillance.
• Constrictive pericarditis: Untreated chronic pericarditis can lead to scarring and loss of normal elasticity of the pericardium, though it only occurs <0.5% of the time after idiopathic acute pericarditis. This can lead to impaired ventricular filling and diminished cardiac output. These patients can experience symptoms of right heart failure (peripheral edema, anasarca) and forward failure (fatigue, exertional dyspnea). This is most often seen in more chronic etiologies of pericarditis (e.g. TB).

5. What workup should be initiated?

All patients with symptoms concerning for pericarditis should have the following workup:

• Routine bloodwork (CBC, lytes, Cr)
• Troponin (if positive, concerning for myopericarditis or perimyocarditis – or ischemia)
• ECG
• CXR
• ESR/CRP (these should be trended over time to ensure resolution with treatment)
• TTE to rule out pericardial effusion
• Considering advanced cardiac imaging (e.g. Cardiac MRI) if concern regarding myopericarditis, to establish degree of myocardial inflammation or scar

Consider history-directed investigations if there is a clinical suspicion of other contributing systemic diseases, e.g. ANA, viral serologies, TSH, blood cultures, etc.

6. What are the principles of treatment in pericarditis?

Always ask yourself two questions: Where should this pericarditis be treated (inpatient or outpatient)? and How should this pericarditis be treated?

• Remember that most pericarditis can be treated in the outpatient setting with close follow-up, but the following risk factors should prompt consideration of inpatient admission and monitoring: Fever, immunocompromised state, positive troponin biomarkers, arrhythmias, hemodynamic instability, history of trauma, being on oral anticoagulation (due to risk of rapid intrapericardial bleeding).
• The principles of pericarditis treatment are to a) treat the pain and b) treat the inflammation. For this reasons, high-dose NSAIDs and colchicine are the backbone of treatment for pericarditis. I strongly recommend you review the ACC and ESC treatment guidelines for acute and recurrent pericarditis.
  • For first instance of pericarditis: a typical treatment regimen is high-dose ASA/NSAID x 2 weeks, plus Colchicine x 3 months
  • For recurrence of pericarditis: high-dose ASA/NSAID x 2 weeks, plus Colchicine x 6 months
• A few special situations:
  • Post-MI pericarditis (Dressler’s): Use ASA instead of other NSAIDs + Colchicine
  • Steroids are used for autoimmune etiologies of pericarditis (e.g. SLE/RA) and very selectively in recurrent pericarditis, as steroid treatment in itself can lead to recurrence
  • Pregnancy: There is a paucity of evidence in this scenario, with some principles of treatment provided by the European Society for Cardiology. Colchicine is not used in pregnancy; ASA and NSAIDs can be used before 20 weeks GA and should be avoided if possible after 20 weeks GA due to risk of premature closure of the fetal ductus arteriosus.

Further Reading

I hope you found this Morning Report useful – this is certainly a high-yield topic relevant to many fields of medicine! The following resources are good reads and contain lots of high-yield information on pericarditis diagnosis, treatment, and management:

• Ismail TF. Acute pericarditis: Update on diagnosis and management. Clin Med (Lond). 2020;20(1):48-51. doi:10.7861/clinmed.cme.20.1.4
• Phelan D, Collier P, Grimm RA. Pericardial Disease. Cleveland Clinic Center for Continuing Education.
• Journal of the American College of Cardiology. Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review.

Thanks for participating in Morning Report!