Lucan · Conditions

Acute pericarditis

Australian guidance: eTG Cardiovascular — Pericarditis

1. Definition and epidemiology

Acute pericarditis is an inflammatory syndrome of the pericardium lasting less than four to six weeks, most commonly caused by viral infection or remaining idiopathic after standard workup. It accounts for approximately five percent of emergency presentations for non-ischaemic chest pain. Males aged 16 to 65 years are disproportionately affected, and recurrence occurs in 15 to 30 percent of cases following a first episode.

2. Pathophysiology

The pericardium consists of an outer fibrous layer and an inner serous bilayer enclosing a potential space containing roughly 15 to 50 mL of fluid. In acute pericarditis, the dominant mechanism is inflammatory cell infiltration of the pericardial layers, typically triggered by viral infection, which causes direct cytopathic injury and immune-mediated tissue damage. This produces fibrinous exudate, friction rub, and vascular dilatation. When fluid accumulates rapidly in the pericardial space it raises intrapericardial pressure, compresses cardiac chambers, and reduces diastolic filling, potentially progressing to cardiac tamponade. Non-infective causes include autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis, uraemia, malignancy, post-myocardial infarction (Dressler syndrome), trauma, and iatrogenic injury from immune checkpoint inhibitor therapy or COVID-19 vaccination. The underlying aetiology shapes the inflammatory milieu: viral causes produce predominantly lymphocytic infiltration, while bacterial purulent pericarditis yields neutrophilic exudate with a far higher risk of constrictive sequelae. Per Robbins Ch 12, fibrinous pericarditis is the hallmark morphological pattern, with a characteristic "bread-and-butter" appearance on gross pathology when adjacent pericardial surfaces are pulled apart.

3. Clinical presentation and diagnostic criteria

The cardinal symptom is sharp, pleuritic chest pain that is worst in the supine position and relieved by sitting forward. A pericardial friction rub heard on auscultation is pathognomonic but transient and often missed. Fever, malaise, and a preceding viral prodrome are common. Dyspnoea may indicate pericardial effusion. The diagnosis of acute pericarditis requires at least two of the following four criteria: pericarditic chest pain, pericardial friction rub, new widespread ST elevation or PR depression on ECG, and new or worsening pericardial effusion on imaging. Supporting findings include elevated inflammatory markers and pericardial inflammation on cardiac MRI or CT. Life-threatening differentials that must be actively excluded include acute coronary syndrome, myocarditis, pulmonary embolism, and aortic dissection.

4. Investigations and AU-specific cutoffs

All patients with suspected acute pericarditis should undergo the following investigations. An ECG is essential and typically shows diffuse saddle-shaped ST elevation in most leads with reciprocal depression only in aVR and V1, plus PR depression. A chest X-ray is indicated to assess cardiac silhouette enlargement (greater than 250 mL effusion required to see cardiomegaly). Inflammatory markers including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white cell count are sent to confirm inflammation and guide treatment duration. Cardiac troponin concentration is required to detect concurrent myocardial injury (myopericarditis), which influences management and return-to-sport timing. A transthoracic echocardiogram evaluates effusion size and haemodynamic significance. If tamponade is clinically suspected, assess for Beck's triad: soft heart sounds, elevated jugular venous pressure, and hypotension. No AU-specific laboratory cutoffs differ materially from international standards; CRP normalisation is used to guide duration of anti-inflammatory therapy.

5. Management

Inpatient admission is required when a treatable underlying cause is identified or when any of the following high-risk features are present: fever above 38 degrees Celsius, subacute onset over several days without a clear acute presentation, large pericardial effusion, cardiac tamponade, or failure to respond within seven days of drug therapy. Additional risk factors warranting inpatient management include myopericarditis, immunosuppression, trauma, and concurrent oral anticoagulant therapy.

Exercise restriction is a cornerstone of management for all patients, with return to competitive sport typically deferred until symptoms resolve and inflammatory markers normalise, and for at least three months in those with myopericarditis.

For most patients with idiopathic or viral acute pericarditis, the mainstay of therapy is colchicine combined with an NSAID. This combination improves remission rates at one week and substantially reduces recurrence compared with anti-inflammatory monotherapy. The treating clinician should select the NSAID based on the patient's history of prior efficacy or adverse effects, presence of contraindications, and comorbidities. Aspirin may be preferred when the patient is already taking it for antiplatelet indication.

Specific aetiologies require targeted therapies: dialysis for uraemic pericarditis, antibiotics for purulent bacterial pericarditis, and immunosuppression for connective tissue disease-related pericarditis.

Corticosteroids should be reserved for cases where NSAIDs are contraindicated or ineffective, or for defined immune-mediated causes. They carry a risk of rebound pericarditis on tapering and are associated with long-term corticosteroid complications, so their routine use is discouraged. For recurrent or refractory pericarditis, specialist cardiology referral is indicated.

6. Pharmacology and AU PBS notes

Colchicine is dosed weight-dependently. For patients weighing 70 kg or more: 500 micrograms orally twice daily for three months. For patients weighing less than 70 kg: 500 micrograms orally once daily for three months. The dose of colchicine must be reduced in renal impairment. Tapering colchicine on completion is not required. Colchicine is available generically in Australia (e.g. Colgout, Lengout) and is listed on the PBS for acute gout; its use in pericarditis is off-label and not PBS-subsidised in that indication.

Aspirin (first-choice NSAID when already on antiplatelet therapy): 750 to 1000 mg orally every eight hours for one to two weeks, then tapered by 250 to 500 mg every one to two weeks until stopped. Available over the counter as Aspirin, Disprin.

Ibuprofen (alternative NSAID): 600 mg orally every eight hours for one to two weeks, then tapered by 200 to 400 mg every one to two weeks until stopped. Available generically (e.g. Nurofen) and on the PBS for general anti-inflammatory indications. The NSAID course is continued until symptom resolution and CRP normalisation guide cessation.

Interleukin-1 inhibitors (e.g. anakinra) have shown promising results in resistant or recurrent pericarditis in trial data but are not approved by the Therapeutic Goods Administration (TGA) for this indication at the time of writing.

7. Complications and monitoring

The principal complications of acute pericarditis are pericardial effusion, cardiac tamponade, constrictive pericarditis, and recurrence. Cardiac tamponade is a medical emergency requiring pericardiocentesis. Constrictive pericarditis is a rare late complication more common with bacterial or tuberculous aetiology than viral or idiopathic pericarditis.

Monitoring during an acute episode includes serial CRP to guide duration of NSAID therapy and confirm resolution of inflammation before stopping treatment. Troponin elevation at presentation identifies myopericarditis, which requires more prolonged exercise restriction and cardiology follow-up. Echocardiography is repeated if effusion was present at diagnosis to confirm resolution. For patients with recurrent disease, specialist review is required and repeat imaging with cardiac MRI may be indicated to assess for pericardial thickening or late gadolinium enhancement consistent with evolving constrictive change.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.