Acute pericarditis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Acute pericarditis is an inflammatory chest-pain syndrome with ECG, rub or effusion evidence. The opening task is to exclude ACS, PE, dissection and tamponade before accepting a usually benign idiopathic/viral explanation.

Risk stratification separates low-risk outpatient care from admission and cause-directed investigation. Fever, large effusion, haemodynamic effect, myocardial involvement and immunocompromise should change disposition.

Treatment suppresses symptoms and recurrence while the cause is addressed. Aspirin/NSAID plus colchicine is standard for suitable patients; steroids are reserved for defined indications or contraindications after infection is excluded.

Key points

Diagnose acute pericarditis when at least two are present: typical pain, rub, new widespread ST/PR change, or new/worsening effusion.
CRP elevation and CT/CMR inflammation support but do not replace the clinical criteria.
Pain is usually sharp, pleuritic and better sitting forward; no pain description safely excludes ACS or PE.
Admit or investigate intensively when fever above 38°C, subacute onset, large effusion/tamponade, NSAID non-response, myocardial involvement, immunosuppression, trauma or anticoagulation is present.
For uncomplicated idiopathic/viral disease, aspirin or an NSAID plus colchicine is first-line, with gastroprotection and activity restriction.
A UK colchicine oral-solution SmPC licenses adjunct treatment of acute and recurrent pericarditis, but many tablet SmPCs do not list this indication; adjust or avoid treatment for renal-hepatic disease and major CYP3A4/P-gp interactions.
Troponin rise indicates myocardial involvement, not MI by default; assess LV function, coronary probability and arrhythmic risk.
Taper anti-inflammatory therapy according to symptoms and CRP; recurrence often follows inadequate treatment or rapid steroid taper.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Idiopathic or viral inflammation

Many uncomplicated cases have no proven organism and are labelled idiopathic, often after a viral syndrome. The label should follow consideration of dangerous and specific secondary causes rather than assumption from the pain pattern alone.

Autoimmune or autoinflammatory disease

Systemic lupus erythematosus, rheumatoid arthritis and other immune-mediated conditions can inflame the pericardium. Recurrent disease or accompanying systemic features should prompt a directed rather than indiscriminate immune work-up.

Cardiac or thoracic injury

Myocardial infarction, cardiac surgery, catheter procedures, trauma or radiotherapy can expose antigens or directly injure the pericardium, producing an immediate or delayed inflammatory syndrome.

Infection, malignancy or systemic illness

Bacterial or tuberculous infection, cancer and advanced kidney failure with uraemia are less common but clinically important causes. Fever, immunosuppression, a large effusion or subacute onset increases concern.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pericardial inflammation
An infectious, immune or injury signal inflames the visceral and parietal pericardium. Their movement against each other generates pleuritic positional pain and sometimes a transient friction rub.
2
Surface electrical change
When inflammation involves the superficial myocardium and atrial epicardium, it can alter repolarisation across broad territories, producing widespread ST elevation and PR-segment change rather than a single coronary distribution.
3
Effusion formation
Inflammatory capillary leakage adds fluid to the pericardial space. Slowly accumulating fluid may become large before causing pressure, whereas a smaller rapid collection can impair filling.
4
Haemodynamic or myocardial extension
Rising intrapericardial pressure restricts diastolic chamber filling and can cause tamponade. Myocardial involvement ranges from troponin release with preserved ventricular function to dysfunction or arrhythmia, changing risk and follow-up.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Typical pain

Acute sharp retrosternal pain worsened by inspiration or lying flat and relieved by sitting forward; radiation to trapezius ridge is suggestive.

Pericardial rub

A superficial scratchy, often triphasic sound can be transient; repeat auscultation with the patient leaning forward.

ECG evolution

New widespread concave ST elevation and PR depression, reciprocal PR elevation in aVR, then T-wave inversion; focal change or reciprocal ST depression should heighten ACS concern.

Effusion

May be absent, small or large; muffled sounds or enlarging cardiac silhouette are late/non-specific clues.

Tamponade physiologyRed flag

Tachycardia, hypotension, raised JVP, pulsus paradoxus or echo chamber collapse requires emergency drainage assessment.

Myocardial involvementRed flag

Troponin rise, ventricular dysfunction, heart-failure signs or ventricular arrhythmia requires admission and myocarditis-level evaluation.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECG with serial comparisonFirst step
Why
Support pericarditis and screen ACS/arrhythmia.
Interpretation and limitations
Typical widespread changes support diagnosis but occur in a minority; territorial change demands ACS assessment.
02
High-sensitivity troponin
Why
Detect myocardial involvement and assess ACS differential.
Interpretation and limitations
Elevation indicates myocardial injury; interpret with symptoms, ECG, LV function and coronary probability rather than relabelling automatically.
03
CRP/ESR, FBC, U&E/eGFR and LFT
Why
Support inflammation, identify infection and establish treatment safety.
Interpretation and limitations
Trend CRP to remission/taper; normal CRP does not completely exclude early disease.
04
TTE
Why
Assess effusion size/distribution, tamponade physiology and LV/RV function.
Interpretation and limitations
A normal echo does not exclude pericarditis; haemodynamic signs matter more than effusion volume alone.
05
CXR
Why
Look for pulmonary/mediastinal alternative and a very large effusion.
Interpretation and limitations
Often normal; cardiomegaly requires imaging rather than assumptions about chronicity.
06
CMR or CT in selected cases
Why
Confirm inflammation, assess myocardium and find thickening/mass or alternative thoracic disease.
Interpretation and limitations
CMR oedema/LGE can document active pericardial or myocardial inflammation when criteria are incomplete or disease persists.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute coronary syndrome

Pressure-like pain, territorial ST change, reciprocal ST depression beyond aVR or V1, or a coronary-pattern wall-motion abnormality favours myocardial infarction. Troponin elevation alone cannot distinguish ACS from myopericardial injury.

Pulmonary embolism

Sudden dyspnoea, hypoxaemia, venous thromboembolism risk or right-heart strain suggests PE. Pleuritic pain may be identical, so probability-based pulmonary vascular assessment remains necessary.

Acute aortic syndrome

Abrupt maximal chest or back pain, pulse or blood-pressure asymmetry, aortic regurgitation or neurological deficit points towards dissection and requires time-critical aortic imaging.

Predominant myocarditis

Heart failure, ventricular arrhythmia, significant LV dysfunction or myocardial oedema and non-ischaemic scar suggest myocardial involvement dominates; overlap with pericarditis is common rather than binary.

Pleural or chest-wall pain

Pneumonia, pleurisy and costochondritis may give respiratory or reproducible pain, but do not explain a pericardial rub, characteristic widespread ECG change or a new effusion. Absence of any one of those findings does not exclude pericarditis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Front doorAcute pleuritic chest painFirst stepPossible pericarditis.

1Assess ABCDE, ECG, troponin, CRP/FBC/U&E and urgent TTE; pursue ACS, PE or aortic imaging immediately when the phenotype warrants.
2Confirm at least two diagnostic criteria and document supportive inflammation; do not diagnose from positional pain alone.
3Check fever, subacute course, effusion size/tamponade, NSAID response, troponin/LV function, immunosuppression, trauma and anticoagulants.
4Admit any major/minor risk feature or uncertain dangerous differential; otherwise arrange treatment and review within about one week.

02Low riskUncomplicated idiopathic/viral pericarditisStable, no high-risk feature and no specific cause identified.

1Start ibuprofen or aspirin at anti-inflammatory dose plus colchicine and gastroprotection after renal, GI, bleeding, pregnancy and interaction checks.
2Restrict strenuous activity until symptoms, CRP, ECG and cardiac function have normalised; athletes need specialist return-to-sport review.
3EscalationReview at about one week for pain, temperature, CRP, adherence and effusion; escalate admission/imaging if non-responsive.
4Once symptom-free and CRP normal, taper NSAID/aspirin; complete colchicine for 3 months unless toxicity or contraindication intervenes.

03High riskCause-directed admissionFever, large effusion, tamponade, subacute course, non-response, myocardial injury, immunosuppression, trauma or anticoagulation.

1Admit with telemetry when myocardial/haemodynamic risk exists and obtain blood cultures before antibiotics if bacterial disease is plausible.
2Investigate targeted causes—TB exposure, malignancy, autoimmune/systemic disease, uraemia, post-injury or drug-related—rather than indiscriminate serology.
3Drain urgently for tamponade and consider diagnostic drainage for suspected bacterial/neoplastic disease or a large persistent symptomatic effusion.
4Treat the cause; purulent disease needs drainage plus IV antibiotics, and suspected TB needs infection-specialist therapy.

04MyocardiumMyopericardial involvementTroponin rise, LV dysfunction or ventricular arrhythmia.

1Admit and monitor; obtain CMR and exclude ACS according to coronary probability and presentation.
2If LV function is preserved and symptoms remain pericarditic, manage inflammation cautiously; if LV dysfunction exists, follow myocarditis/HF restrictions and treatment.
3EscalationAvoid exercise until specialist-confirmed remission with normal function and rhythm assessment; escalate fulminant HF or malignant arrhythmia to an advanced centre.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

First-line anti-inflammatory for suitable uncomplicated pericarditis, given with gastroprotection.

Ibuprofen

600 mg orally three times daily for 1-2 weeks, then taper by about 200 mg per dose each week when pain has resolved and CRP normalised; maximum 2400 mg/day.

Avoid/modify with active ulcer or bleeding, severe renal disease, decompensated HF, NSAID hypersensitivity and late pregnancy; review anticoagulants and cardiovascular risk.

Adjunct to aspirin/NSAID that improves response and reduces recurrence; this regimen is licensed for a UK oral solution, while many tablet products do not list pericarditis.

Colchicine

0.5 mg orally once daily if body weight is 70 kg or less, or 0.5 mg twice daily if over 70 kg, usually for 3 months in a first episode; no loading dose.

In mild or moderate renal or hepatic impairment use 0.5 mg once daily; severe impairment is contraindicated. Do not combine with strong CYP3A4/P-gp inhibitors when renal or hepatic function is impaired, and reduce or interrupt treatment even with normal function according to the interacting medicine. Stop and assess diarrhoea, vomiting, cytopenia or myopathy.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Pericardial effusion and tamponade

Rapid or large fluid accumulation raises intrapericardial pressure, reduces venous return and cardiac output, and can progress to obstructive shock requiring urgent drainage assessment.

Myocardial involvement

Troponin elevation with preserved ventricular function is often termed myopericarditis; new ventricular dysfunction suggests predominant myocardial involvement or perimyocarditis. Either pattern can change monitoring and activity advice after ACS has been considered.

Recurrent pericarditis

Persistent immune activation can produce repeated painful episodes and cumulative disability. Inadequate initial treatment or withdrawal before clinical and inflammatory remission may contribute to recurrence and the need for more complex anti-inflammatory strategies.

Constrictive pericarditis

Chronic scarring and loss of pericardial compliance can restrict diastolic filling, causing raised venous pressure and right-sided heart failure; risk is higher with bacterial or tuberculous disease.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review pain, fever and functional status within about one week; lack of response is a risk feature.
Trend CRP to guide remission and NSAID/aspirin taper rather than tapering on a fixed date despite inflammation.
Check renal function, BP, GI bleeding and fluid status during high-dose NSAID therapy.
Check colchicine interactions at every medicine change; monitor FBC/CK/LFT when toxicity risk or symptoms arise.
Repeat echo for moderate/large effusion or any haemodynamic/symptom deterioration.
For myocardial involvement, document normal LV function, biomarkers and rhythm before return to strenuous exercise.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Two of four

Pain alone is insufficient, and an effusion is not required when another criterion is present.

Diffuse does not mean harmless

Classic ECG changes can coexist with effusion or myocardial injury; disposition depends on risk, not pattern beauty.

CRP guides the taper

Clinical remission and normal inflammation reduce rebound risk better than an arbitrary rapid stop.

Troponin changes the pathway

It signals myocardial involvement and need for ventricular/rhythm assessment, but does not by itself distinguish myocarditis from ACS.

Steroids can buy recurrence

When needed, use a defined indication, exclude infection and taper very slowly after remission rather than giving an early high-dose burst.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing pericarditis from positional pain without two criteria or dangerous-differential assessment.
02
Discharging fever, a large effusion, anticoagulation or troponin-positive disease as low risk.
03
Prescribing colchicine without renal/hepatic and CYP3A4/P-gp interaction review.
04
Stopping anti-inflammatory treatment while symptoms or CRP remain active.
05
Allowing early intense exercise after myopericardial involvement.