A 32 yo patient presents with a one week history of chest pain. The pain was not sudden in origin and was initially over a small area lateral to the sternum. It quickly spread to the whole chest. There is also pain on the left side of the back at the level of the scapula. The pain does not radiate, is worst on inspiration and when the patient lies down and improves when the patient is sitting up. There is no dyspnoea.
The patient has no past medical history, is on no medications and has not had any illness prior to this episode. The GP prescribed anti-inflammatories on initial consultation a week previously. These have not improved the pain.
Vitals are normal. The patient is afebrile with a HR of 82, BP of 130/68 and sats of 100% on room air.
Examination demonstrates dual heart sounds and no extra sounds, a clear chest and soft abdomen. There is no reproducibility in the chest pain on palpation of the chest wall. There is no spinal pain or reproducible back pain.
The ECG and chest x-ray are normal.
Bloods are also normal, specifically, a normal troponin, D-dimer and CRP.
The patient is initially treated with 300mg Aspirin. Fentanyl is used to control the pain, however it continues to recur.
What is your working diagnosis?
My suspicion for a Pulmonary Embolism is low, so I can rule that out with a normal D-Dimer or even the PERC rule. There is no epigastric pain and no symptoms for reflux and the pain is not consistent with oesophageal spasm. My working diagnosis is pericarditis. What do I do with this patient? Is this pericarditis? Why are there no ECG changes?
Things I needed to remind myself of:
- The pericardium itself is electrically silent, so that inflammation of only the pericardium produces no ECG changes. The ECG changes occur when the epicardium is involved.
- Most cases are classified as idiopathic.
- A small number are infectious in origin ie., viral, bacterial or tuberculous in origin.
- Other causes include myocardial infarction and uraemia and neoplasms.
How do we make the diagnosis of Pericarditis?
There must be at least two of the following four criteria present(1):
This is usually sharp, but may not be and it is worst on inspiration or coughing. It usually improves when sitting up and forward. Radiation occurs to the trapezius ridge (2). There is some uncertainty about where the trapezius ridge actually is. Most references place it at the top of the trapezius ie., adjacent to the neck. Although some references locate it at the level of the lower end of the scapula.
This is a squeaking sound, usually heard at the left sternal border at the end of expiration, with the patient leaning forward. It represents the rubbing of the inflamed layers of the pericardium. It is not always present and it can be mistaken for a murmur. Listen to the sound below.
The ECG changes in pericarditis can progress, through four stages as shown in the diagram below(7). This does not happen with all patients.
Stage I: Diffuse ST elevation and PR depression
Stage II: Normalization of the ST and PR segments
Stage III: Widespread T-wave inversions
Stage IV: Normalization of the T waves
A pericardial effusion
The pericardial effusion can vary in size:
- Small is < 10mm
- Moderate is 10-20mm
- Large is 21-25 mm
- Very large is > 25mm
How do we distinguish these changes from myocardial infarction?
- ST-segment elevations in pericarditis are diffuse ie., across multiple vascular territories. They are concave in shape. MI ST elevation is usually convex and restricted to an arterial territory rather than being widespread
- Q-wave formation and loss of R-wave voltage often occur in MI
- T-wave inversions appear before the ST segments return to baseline in MI
- PR-segment depression is uncommon in MI.
- Reciprocal changes or ST depression should not be present in pericarditis, although ST depression is acceptable in V1 and aVR.
- If the ratio of ST- segment elevation to T-wave amplitude in V6is greater than 0.24 it is almost always pericarditis (3).
Echocardiography may be normal in about 40% of cases of pericarditis. It may role is to look for a pericardial effusion, however it is also able to identify wall motion abnormalities, which may indicate ischaemia. It is also used to determine ventricular function ie., ejection fraction, which may be altered in myocarditis and is often used as a marker in the progressive assessment of the patient.
Cardiac MRI(CMRI) can be used when the echo images are not definitive. It gives a good indication of the degree of pericardial inflammation. It can identify via Late Gadolinium Enhancement, patients with a high risk of complications(4).
Laboratory Tests such as Troponin are useful in determining if there is cardiac involvement. One third of patients will have a troponin leak. This will indicate a subepicardial myocardial involvement.
CRP and white cell count are elevated in a large proportion of patients, but are not specific. They do however indicate a group of patients that may have abetter response to anti-inflammatory drugs.
Non-Steroidal anti-inflammatory drugs(NSAID) are usually the first course of treatment. Ibuprofen 600-800mg orally every 8 hours is the main agent used. Indomethacin at 50mg every 8 hours can also be used. Patients with known coronary artery disease can have 750-1000 mg of Aspirin three times per day
Colchicine has been proven for both acute and recurrent pericarditis. It can be used with NSAIDs. It reduces the recurrence rate and hospitalisation rate (5,6). Dosage is 0.6 mg po twice daily for 3 months. Its use in myopericarditis, has not been as well studied.
Corticosteroids(prednisolone), when used at lower doses ie., 0.2-0.5mg/kg are associated with lower recurrence rates and hospitalisations when compared with high doses.
Other treatments will depend on causative factors.
Triggers for admission
- Patients with myocardial involvement. These patients have up to 30% chance of mortality and morbidity
- Pain that cannot be controlled
- Prolonged course of pain.
Patients with pericarditis are encouraged to restrict physical activity and exertion (maintain heart rate below 100 bpm) for at least 3 months. This decreases the shear forces on the pericardium and thus the chance of increased inflammation. In those patients with myocardial involvement, strenuous activity should be restricted for at least 6 months.
- Adler Y, et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC). Eur Heart J 2015;36:2921–64.
- Lange RA, et al. Clinical practice. Acute pericarditis. N Engl J Med 2004;351:2195–2202.
- Ginzton LE, et al. The differential diagnosis of acute pericarditis from the nor- malvariant: new electrocardiographic criteria. Circulation 1982;65:1004-9.
- Kumar A, Sato K, Yzeiraj E, et al. Quantitative Pericardial Delayed Hyperenhancement Informs Clinical Course in Recurrent Pericarditis. J Am Coll Cardiol Img 2017;10:1337–46.
- Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute peri- carditis. N Engl J Med 2013;369:1522–8.
- Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation 2005;112: 2012–6.
- Chiabrando JG et al. Management of Acute and recurrent Pericarditis. JACC 2020;75:76-9