📋 Key Information Summary
- Acute pericarditis is the most common pericardial disease, presenting with pleuritic chest pain that improves on leaning forward, a pericardial friction rub, diffuse ST elevation with PR depression on ECG, and new or worsening pericardial effusion.
- Most cases (80–90%) in Australia are idiopathic or presumed viral; always consider TB in immunocompromised and ATSI populations, and uraemic pericarditis in advanced CKD.
- The diagnosis is clinical — fulfil ≥2 of 4 criteria: characteristic chest pain, pericardial friction rub, ECG changes, or new/worsening pericardial effusion on echocardiography.
- CRP and ESR are essential for confirming inflammation and guiding treatment duration; troponin elevation (myopericarditis) occurs in up to 30% of cases and does not change management in the absence of haemodynamic compromise.
- First-line therapy is aspirin (750–1000 mg PO TDS for 1–2 weeks) or ibuprofen (600 mg PO TDS for 1–2 weeks) PLUS colchicine (500 mcg PO BD for 3 months) — this combination reduces recurrence by approximately 50%.
- Colchicine must be dosed by weight (500 mcg OD if <70 kg) and requires renal dose adjustment; avoid in severe hepatic impairment and pregnancy.
- Corticosteroids are NOT first-line and should be reserved for refractory cases, specific autoimmune aetiologies, or contraindications to NSAIDs; early corticosteroid use increases recurrence risk.
- Cardiac MRI (CMR) with late gadolinium enhancement is recommended when the diagnosis is uncertain, to assess for myocardial involvement, or to guide safe return to activity.
- Recurrent pericarditis occurs in approximately 30% of cases; risk factors include early corticosteroid use, inadequate initial colchicine, and elevated CRP at presentation.
- For refractory recurrent pericarditis, anti-IL-1 agents (anakinra, rilonacept) are effective second-line therapies; intrapericardial corticosteroids and pericardiectomy are reserved for the most resistant cases.
- Patients should be restricted from competitive sport for at least 3 months; return requires normalisation of CRP, no effusion, and normal ECG and CMR findings.
- Uraemic pericarditis requires intensification of dialysis (ideally daily), not anti-inflammatory therapy as first-line; TB pericarditis mandates standard anti-TB therapy with consideration of corticosteroids.
- Aboriginal and Torres Strait Islander Australians have higher rates of TB and rheumatic heart disease, requiring a lower threshold for screening in suspected pericarditis of uncertain aetiology.
Introduction & Australian Epidemiology
Acute pericarditis is inflammation of the pericardial sac, the fibrous double-layered membrane enclosing the heart. It is the most common disease of the pericardium and accounts for approximately 5% of emergency department presentations with non-ischaemic chest pain in Australia. The condition is typically self-limiting but carries risks of recurrence, cardiac tamponade, and constrictive pericarditis if inadequately treated.
In Australia, the annual incidence of acute pericarditis is estimated at 27.7 per 100,000 population, with a peak incidence in males aged 20–50 years. Viral aetiologies predominate, particularly in temperate zones where coxsackievirus B and echovirus circulate seasonally. The post-cardiac injury syndrome (Dressler syndrome) following myocardial infarction or cardiac surgery accounts for a smaller but clinically significant proportion of cases.
Importantly, Australia's burden of rheumatic heart disease and tuberculosis among Aboriginal and Torres Strait Islander communities means that pericardial disease of these aetiologies must be actively considered in relevant populations. TB pericarditis remains a significant differential in immunocompromised patients, including those with HIV, and in migrants from high-prevalence regions.
Key diagnostic pitfall: Acute pericarditis can closely mimic ST-elevation myocardial infarction (STEMI). Failure to distinguish the two may lead to inappropriate thrombolysis or unnecessary coronary intervention. Always consider the clinical context, ST morphology, and absence of reciprocal changes before activating the catheterisation laboratory.
Clinical Presentation
Chest Pain Characteristics
The hallmark of acute pericarditis is sharp, pleuritic chest pain that is typically retrosternal or left-sided. The pain classically:
- Radiates to the trapezius ridge (pathognomonic) or left shoulder
- Improves when the patient sits up and leans forward
- Worsens with inspiration, coughing, and supine positioning
- May be accompanied by dyspnoea, particularly when a moderate-to-large effusion is present
- Differentiated from ischaemic pain by its pleuritic nature, positional relief, and absence of exertional trigger
ECG Changes
The ECG evolves through four stages in classic pericarditis:
| Stage | Timing | ECG Features |
|---|---|---|
| Stage 1 | Days 1–2 | Diffuse concave ST elevation (except aVR and V1); PR depression (most specific finding); no reciprocal ST depression (except aVR and V1) |
| Stage 2 | Days 2–3 | Normalisation of ST segments; T wave flattening |
| Stage 3 | Weeks | Diffuse T wave inversions |
| Stage 4 | Weeks to months | Normalisation of ECG |
Spodick sign: Downsloping of the TP segment (baseline), particularly noticeable in leads II and V5–V6, is a useful early sign to differentiate pericarditis from STEMI. In STEMI the TP segment is isoelectric.
Pericardial Friction Rub
A pericardial friction rub is the most specific physical finding (specificity ~90%) but sensitivity is only about 35–60%. It is best heard with the diaphragm of the stethoscope with the patient sitting upright and leaning forward, at end-expiration. The rub may be transient, so serial examinations may be required. A three-component rub (atrial systole, ventricular systole, rapid ventricular filling) is classic but a two-component or even monophonic rub may be heard.
Additional Clinical Features
- Low-grade fever (<38°C) is common; high fever (>39°C) should raise suspicion for purulent or tuberculous pericarditis
- Tachycardia may be present as a pain response or compensatory in the setting of significant effusion
- Pulsus paradoxus >10 mmHg suggests haemodynamically significant pericardial effusion or tamponade
- Beck's triad (hypotension, muffled heart sounds, jugular venous distension) indicates cardiac tamponade — a medical emergency
Aetiology
The majority of acute pericarditis cases in Australia are idiopathic (presumed viral). A systematic evaluation is warranted when clinical features suggest a specific underlying cause.
| Category | Aetiology | Key Distinguishing Features |
|---|---|---|
| Idiopathic / Viral | Coxsackievirus B, echovirus, adenovirus, CMV, EBV, parvovirus B19, SARS-CoV-2 | 80–90% of cases; often preceded by URTI; usually self-limiting; diagnosis of exclusion |
| Post-cardiac injury | Post-MI (Dressler syndrome), post-cardiac surgery, post-catheter ablation, post-trauma | Occurs days to weeks after injury; autoimmune mechanism; positive anti-heart antibodies |
| Autoimmune / Inflammatory | SLE, rheumatoid arthritis, systemic sclerosis, sarcoidosis, vasculitis, familial Mediterranean fever | Recurrent episodes; elevated ANA/RF; may be first presentation of underlying connective tissue disease |
| Uraemic | End-stage kidney disease (eGFR <15), dialysis-dependent CKD | Fibrinous pericarditis; responds to intensification of dialysis; WBC within pericardial fluid elevated |
| Malignant | Lung cancer, breast cancer, lymphoma, melanoma, mesothelioma | Large haemorrhagic effusion; cytology positive; progressive; consider in patients with known malignancy and new effusion |
| Tuberculous | Mycobacterium tuberculosis | Insidious onset; high ADA in fluid; predominantly lymphocytic; high prevalence in ATSI communities and immunocompromised patients |
| Purulent / Bacterial | Staphylococcus aureus, Streptococcus pneumoniae, Gram-negatives | High fever, toxic appearance; requires urgent pericardiocentesis and IV antibiotics; mortality up to 40% if untreated |
| Drug-related | Immune checkpoint inhibitors (pembrolizumab, nivolumab), hydralazine, isoniazid, methyldopa, phenytoin | Temporal association with drug initiation; checkpoint inhibitor pericarditis has a high recurrence rate |
| Post-irradiation | Prior mediastinal radiotherapy (lymphoma, breast cancer) | May present years after treatment; risk of constrictive pericarditis |
| Traumatic | Blunt or penetrating chest trauma | Pericardial tear may occur; may present acutely or with delayed post-traumatic syndrome |
Purulent pericarditis: This is a medical emergency with mortality up to 40%. High fever (>39°C), toxic appearance, and rapid tamponade mandate urgent pericardiocentesis (or surgical drainage) combined with broad-spectrum IV antibiotics (e.g., vancomycin 25–30 mg/kg IV loading then 15–20 mg/kg IV BD adjusted to trough, PLUS ceftriaxone 2 g IV OD) pending culture results. Do not delay intervention while awaiting investigations.
Aetiology-Specific Testing Strategy
Targeted investigations should be performed based on clinical suspicion:
- Autoimmune screen: ANA, anti-dsDNA, complement (C3/C4), RF, anti-CCP — when recurrent pericarditis or features of connective tissue disease
- TB testing: Interferon-gamma release assay (QuantiFERON-TB Gold), pericardial fluid ADA, fluid AFB stain and culture, PCR for M. tuberculosis — ATSI patients, immunocompromised, migrants from endemic regions
- Uraemic assessment: eGFR, urea, creatinine, phosphate — if eGFR <30 mL/min/1.73 m²
- Malignancy workup: CT chest/abdomen/pelvis, pericardial fluid cytology, tumour markers — when large or recurrent effusion or risk factors present
- Drug history: Review for immune checkpoint inhibitors, hydralazine, isoniazid
Diagnostic Workup
Clinical Diagnostic Criteria
Acute pericarditis is diagnosed when at least 2 of 4 criteria are met:
- Characteristic chest pain (sharp, pleuritic, improved by sitting forward)
- Pericardial friction rub
- ECG changes (new widespread ST elevation or PR depression)
- New or worsening pericardial effusion on imaging
Supportive findings include elevated inflammatory markers (CRP, ESR), elevated troponin (suggesting myopericarditis), and fever.
Investigations
Essential
12-lead ECG
Diffuse concave ST elevation with PR depression (sensitivity 60–80%); serial ECGs to track evolution; differentiate from STEMI
Essential
High-sensitivity troponin (hs-cTnI or hs-cTnT)
Elevated in ~30% of cases (myopericarditis); does not predict prognosis in isolation; MBS item 66504
Essential
C-reactive protein (CRP) and ESR
CRP is the preferred marker for guiding treatment duration and detecting recurrence; levels correlate with disease activity
Essential
FBC, UEC, LFTs
Exclude systemic infection, assess renal function (uraemic pericarditis), baseline hepatic function before drug selection
Available
Transthoracic echocardiography (TTE)
Detects pericardial effusion, assesses size and haemodynamic impact (tamponade physiology); MBS item 55122; perform in all cases
Available
Chest X-ray
"Water-bottle" cardiac silhouette with large effusion; rule out pneumonia, lung mass, pleural effusion; MBS item 58500
Specialist
Cardiac magnetic resonance imaging (CMR)
Gold standard for diagnosis when uncertain; demonstrates pericardial oedema (T2-weighted), pericardial late gadolinium enhancement (LGE); assesses myocardial involvement; guides return to activity; MBS item 63500
Specialist
Pericardiocentesis
Indicated for: suspected purulent pericarditis, cardiac tamponade, large effusion (>20 mm on echo) failing to improve after 7 days of therapy, or suspected malignancy; send fluid for: cell count, protein, glucose, LDH, ADA, culture, cytology, AFB
Specialist
CT chest with contrast
Assess pericardial thickening (>4 mm suggests inflammation or constriction), lymphadenopathy, mediastinal pathology; helpful when CMR unavailable or contraindicated
High-Sensitivity Troponin — Prognostic Implications
Elevated troponin defines myopericarditis (pericarditis with myocardial involvement). In the absence of haemodynamic compromise, heart failure, or sustained arrhythmia, isolated troponin elevation does not change management. Patients with myopericarditis should have prolonged activity restriction (at least 6 months) and be followed with repeat CMR before clearance.
STEMI vs pericarditis: If there is any clinical uncertainty between STEMI and pericarditis, treat as STEMI and activate the catheterisation pathway. Do not withhold reperfusion therapy on the basis of suspected pericarditis alone. Diffuse ST elevation without reciprocal changes, PR depression, and absence of Q waves favour pericarditis — but these features are not 100% specific.
Treatment
Risk Stratification — Inpatient vs Outpatient Management
Low Risk
Outpatient Management Appropriate
No fever (<38°C), no large effusion (<10 mm), no tamponade, no immunosuppression, normal troponin, responsive to NSAIDs within 7 days, no oral anticoagulant use
Setting: Discharge with outpatient follow-up within 1 week
Moderate Risk
Inpatient Observation
Any one or more: fever ≥38°C, large effusion (10–20 mm), elevated troponin, oral anticoagulant use, failure to respond to NSAIDs at 7 days, immunosuppression
Setting: Cardiology ward admission, telemetry monitoring
High Risk
Urgent Intervention Required
Cardiac tamponade, suspected purulent or TB pericarditis, haemodynamic instability, suspected malignant effusion, ventricular arrhythmias
Setting: ICU/CCU; urgent pericardiocentesis or surgical drainage; cardiology/cardiothoracic surgical consult
First-Line Pharmacotherapy
The cornerstone of treatment is a combination of an anti-inflammatory agent plus colchicine. Aspirin or ibuprofen is preferred over other NSAIDs due to the best available evidence.
Aspirin
Cardiprin® · Cartia® · NSAID (preferred in post-MI pericarditis)
Adult dose
750–1000 mg PO every 8 hours for 1–2 weeks, then taper over 2–3 weeks (reduce by 250–500 mg every 1–2 weeks)
Paediatric dose
Not routinely used in children <16 years (Reye syndrome risk); use ibuprofen instead
Renal adjustment
Avoid if eGFR <30 mL/min/1.73 m²; use with caution if eGFR 30–60
Hepatic adjustment
Avoid in severe hepatic impairment (Child-Pugh C)
PBS status
✔ PBS General Benefit
Ibuprofen
Nurofen® · Brufen® · NSAID
Adult dose
600 mg PO every 8 hours for 1–2 weeks, then taper over 2–3 weeks
Paediatric dose
5–10 mg/kg PO every 8 hours (max 40 mg/kg/day); use weight-based dosing
Renal adjustment
Avoid if eGFR <30 mL/min/1.73 m²
Hepatic adjustment
Avoid in severe hepatic impairment
PBS status
✔ PBS General Benefit
Colchicine
Colgout® · Colchicine tablets · Anti-inflammatory / Anti-mitotic
Adult dose
≥70 kg: 500 mcg PO BD; <70 kg: 500 mcg PO OD — for 3 months
Paediatric dose
Limited data; consult paediatric cardiology; 20 mcg/kg OD to BD for 3 months in specialised settings
Renal adjustment
eGFR 10–30: 500 mcg OD then 500 mcg after 3 days (repeat course); avoid in eGFR <10 unless on dialysis
Hepatic adjustment
Avoid in severe hepatic impairment; dose reduction with moderate impairment
PBS status
✔ PBS General Benefit
COPILOT / CORP trial evidence: Colchicine added to aspirin or ibuprofen reduced the recurrence rate of pericarditis from ~50% to ~25% (relative risk reduction ~50%). The combination of NSAID + colchicine for at least 3 months is now the standard of care for a first episode of acute pericarditis.
Gastroprotection
All patients receiving high-dose NSAIDs should receive concurrent gastroprotection with a proton pump inhibitor (PPI), e.g., pantoprazole 40 mg PO daily, particularly if aged >65 years, history of peptic ulcer disease, or on concomitant anticoagulation or corticosteroids.
Corticosteroids — When Indicated
Do NOT use corticosteroids as first-line therapy. Early corticosteroid use (before adequate trial of NSAIDs + colchicine) is associated with a significantly increased risk of recurrence. Reserve corticosteroids for: (1) refractory pericarditis failing ≥2 weeks of optimal NSAID + colchicine, (2) specific autoimmune aetiologies (e.g., SLE), (3) contraindications to NSAIDs (severe renal impairment, GI bleeding), and (4) TB pericarditis (as adjunctive therapy).
Prednisolone
Prednisolone® · Solone® · Corticosteroid (refractory / autoimmune)
Adult dose
0.25–0.5 mg/kg/day PO (typically 15–25 mg/day) for 2–4 weeks, then very slow taper (reduce by 2.5 mg every 2–4 weeks) over 3–6 months; taper guided by CRP
Renal adjustment
No adjustment required; preferred anti-inflammatory when eGFR <30 (NSAIDs contraindicated)
Hepatic adjustment
No adjustment required; prednisolone is active form (no hepatic conversion needed)
PBS status
✔ PBS General Benefit
Treatment Summary — Quick Reference
First episode, low risk
Aspirin 750–1000 mg TDS or Ibuprofen 600 mg TDS + Colchicine
NSAID 1–2 wks then taper; Colchicine 3 months
Gastroprotection with PPI; reassess CRP at 1 week
First episode, post-MI
Aspirin 750–1000 mg TDS + Colchicine 500 mcg BD
Aspirin taper over 2–3 wks; Colchicine 3 months
Avoid ibuprofen/naproxen — may interfere with aspirin's antiplatelet effect
Uraemic pericarditis
Intensify dialysis (daily HD if possible)
Until pericarditis resolves
NSAIDs are relatively contraindicated; colchicine adjusted for renal function; tamponade requires urgent drainage
Purulent pericarditis
Pericardiocentesis/drainage + Vancomycin + Ceftriaxone
4–6 weeks IV antibiotics; guided by cultures
Surgical drainage often required; ~40% mortality without intervention
TB pericarditis
Standard RIPE therapy + Prednisolone 40 mg OD × 2 wks then taper
6–9 months anti-TB; steroid taper over 4–6 weeks
Consult infectious disease; referral to pericardiocentesis if large effusion; monitor for constriction
Activity Restriction
All patients with acute pericarditis should abstain from competitive and strenuous physical activity. The 2015 European Society of Cardiology guidelines recommend a minimum of 3 months restriction from competitive sport following an acute episode. In myopericarditis, restriction extends to 6 months. Return to competitive activity requires:
- Normalisation of CRP and ESR
- Resolution of pericardial effusion on echocardiography
- Normal 12-lead ECG and Holter monitoring
- CMR demonstrating no residual oedema or LGE (especially in myopericarditis)
- Normal LV systolic function
Recurrent Pericarditis
Definition & Incidence
Recurrent pericarditis is defined as a symptomatic recurrence of pericarditis after a documented first episode with a symptom-free interval of at least 4–6 weeks. It occurs in approximately 30% of patients after an initial episode, with the highest risk in the first 18 months.
Risk Factors for Recurrence
- Inadequate initial treatment (NSAID dose too low, insufficient duration, no colchicine)
- Early use of corticosteroids in the first episode (approximately doubles recurrence risk)
- Incompletely treated or missed underlying aetiology (autoimmune, TB, malignancy)
- Large pericardial effusion at presentation
- Elevated CRP at diagnosis that was not monitored to confirm normalisation
- Younger age and female sex
- Immune checkpoint inhibitor-related pericarditis
Prevention Strategies
- Colchicine 500 mcg BD (or OD if <70 kg) for 3 months at first episode — the single most important intervention to prevent recurrence
- Adequate NSAID dose and duration; do not stop NSAIDs prematurely
- Monitor CRP and do not taper anti-inflammatories until CRP is normal
- Avoid corticosteroids at first episode unless specifically indicated
- If corticosteroids are required, use the lowest effective dose (0.25 mg/kg/day) and taper very slowly guided by CRP
Management of Recurrent Pericarditis — Step-Up Approach
1
Re-initiate NSAIDs + Colchicine
Aspirin or ibuprofen at full dose + colchicine 500 mcg BD for ≥6 months; add PPI; taper very slowly guided by CRP. Success rate: ~60–70%.
2
Low-Dose Corticosteroids + Colchicine
If NSAID + colchicine fails after ≥4 weeks: add prednisolone 0.2–0.3 mg/kg/day with very slow taper over ≥3 months. Maintain colchicine. Success rate: ~70–80%.
3
Anti-IL-1 Therapy
For steroid-dependent or frequently recurring pericarditis: anakinra 100 mg SC OD or rilonacept 320 mg SC loading then 160 mg SC weekly. Taper corticosteroids concurrently. Evidence from AIRTRIP and RHAPSODY trials.
4
Intrapericardial Corticosteroids
Methylprednisolone 50–200 mg instilled via pericardial drain — delivers high local concentration with minimal systemic side effects. Performed by interventional cardiology.
5
Pericardiectomy
Last resort for refractory recurrent pericarditis; subtotal pericardiectomy is preferred; associated with 2–4% surgical mortality; reserved for patients failing all medical therapy.
Anti-IL-1 Agents — Detail
Anakinra
Kineret® · IL-1 receptor antagonist
Adult dose
100 mg SC once daily; duration typically ≥6 months; taper guided by CRP and symptoms
Key evidence
AIRTRIP trial: anakinra after colchicine failure reduced recurrence from 90% to 10%; NNT ≈ 1.4
Renal adjustment
eGFR 30–60: 100 mg SC every other day; eGFR <30: 100 mg SC every 2–3 days
Key adverse effects
Injection site reactions (very common); hepatotoxicity (monitor LFTs); increased infection risk; reactivation of latent TB (screen before initiation)
PBS status
✘ Not PBS listed for pericarditis — may require Special Access Scheme (SAS) or private prescription
Rilonacept
Arcalyst® · IL-1α and IL-1β trap (Fc fusion protein)
Adult dose
Loading: 320 mg SC (2 × 160 mg on same day); maintenance: 160 mg SC once weekly
Key evidence
RHAPSODY trial: rilonacept reduced recurrence by 96% vs placebo in recurrent pericarditis; FDA approved for recurrent pericarditis (2021)
Renal adjustment
No specific dose adjustment; use with caution in severe renal impairment
Key adverse effects
Upper respiratory infections, injection site reactions; immunosuppression — screen for latent TB
PBS status
✘ Not PBS listed in Australia — Special Access Scheme required
Colchicine for recurrence prevention: In Australia, colchicine (Colgout®) is PBS-listed as a general benefit. Ensure patients are counselled on common side effects including diarrhoea, nausea, and abdominal cramps. Serious toxicity (myelosuppression, rhabdomyolysis) is rare at anti-inflammatory doses but risk increases with CYP3A4 inhibitors (clarithromycin, ketoconazole) and statins.
Corticosteroid Tapering Protocol (Recurrent Pericarditis)
When corticosteroids are required in recurrent pericarditis, a slow taper is critical to prevent rebound flares:
- Start prednisolone 0.25–0.5 mg/kg/day (max ~25 mg/day)
- Maintain initial dose for 2–4 weeks until CRP normalises
- Reduce by 2.5 mg every 2–4 weeks
- Below 10 mg/day: reduce by 1.25 mg every 2–4 weeks
- If CRP rises during taper: pause taper, increase dose to last effective dose, and consider adding anti-IL-1 agent
- Complete taper over 3–6 months minimum; concurrent colchicine mandatory throughout
Special Populations
Pregnancy
Preferred NSAID
Aspirin is relatively safe in the 2nd trimester at low doses (≤100 mg OD for preeclampsia prophylaxis), but high-dose aspirin (750–1000 mg TDS) is generally avoided. Ibuprofen may be used in the 2nd trimester but is contraindicated in the 3rd trimester (premature ductus arteriosus closure, oligohydramnios). Paracetamol for pain relief with colchicine if benefit outweighs risk.
Colchicine
Category A in the Australian TGA pregnancy classification system is NOT applicable here — colchicine is generally avoided in pregnancy due to teratogenicity data in animal studies, although human data is conflicting. Use only if benefit clearly outweighs risk, and at the lowest effective dose. Consult maternal-fetal medicine.
Corticosteroids
Prednisolone is considered relatively safe in pregnancy (minimal placental transfer); first-line if anti-inflammatory therapy is required. Use minimum effective dose.
Anakinra
Limited human pregnancy data. Use only if clearly needed. Discuss with rheumatology/cardiology and maternal-fetal medicine.
Paediatrics
NSAIDs
Ibuprofen 5–10 mg/kg PO TDS is preferred. Avoid aspirin in children <16 years due to Reye syndrome risk. Diclofenac 1 mg/kg/day BD–TDS is an alternative.
Colchicine
Limited paediatric data; 0.03–0.05 mg/kg BD (max 500 mcg BD) for 3 months in specialist settings; monitor FBC.
Echocardiography
Perform in all paediatric cases; children are more susceptible to tamponade due to smaller pericardial volume. Consider CMR if myocarditis suspected (viral aetiology common in children).
Return to sport
Minimum 3 months restriction; in myopericarditis, 6 months; echocardiography and ECG required before clearance. Paediatric cardiology follow-up recommended.
Elderly (>65 years)
NSAIDs
Use with extreme caution — increased risk of GI bleeding, renal impairment, and cardiovascular events. Consider aspirin at lower dose if tolerated. Gastroprotection with PPI is mandatory. If NSAIDs contraindicated, use corticosteroids at low dose with colchicine.
Colchicine
Start at 500 mcg OD regardless of weight due to age-related decline in renal clearance. Adjust further if eGFR <30.
Consider malignancy
A higher threshold for malignancy workup is warranted in patients >65 presenting with first pericarditis, especially with large effusion.
Renal Impairment
eGFR 30–60
NSAIDs at reduced dose and shorter duration; colchicine 500 mcg OD. Monitor renal function closely.
eGFR <30 / Dialysis
NSAIDs are generally contraindicated. Use prednisolone 0.2–0.3 mg/kg/day + colchicine (dose-adjusted; avoid if eGFR <10 unless on dialysis). If uraemic: intensify dialysis as first-line. Anakinra dose: 100 mg SC every 2–3 days if eGFR <30.
Hepatic Impairment
NSAIDs
Avoid in Child-Pugh C (severe impairment); use with caution in Child-Pugh B. Monitor LFTs. Elevated risk of GI bleeding with concomitant coagulopathy.
Colchicine
Dose reduction in moderate hepatic impairment; avoid in severe hepatic impairment. Hepatotoxicity is a rare but recognised adverse effect.
Preferred alternative
Prednisolone (active form, no hepatic conversion needed) + colchicine at reduced dose.
Immunocompromised
HIV-positive patients
High index of suspicion for TB pericarditis; CD4 count guides differential — CD4 <200: include Mycobacterium avium complex and fungal causes. Perform pericardiocentesis early for definitive diagnosis.
Transplant recipients
CMV pericarditis, post-transplant lymphoproliferative disorder, and drug-induced pericarditis (mTOR inhibitors) should be considered. Coordinate with transplant team for immunosuppression adjustments.
Checkpoint inhibitor patients
Immune checkpoint inhibitor (ICI) pericarditis is increasingly recognised. High recurrence rate. May require ICI discontinuation, high-dose corticosteroids, and anti-IL-1 therapy. Oncology and cardiology co-management essential.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
📚 References
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