Pericardial effusion
Overview
•Inflammatory/autoimmune - pericarditis (viral, bacterial, TB), Dressler's syndrome, SLE, rheumatoid arthritis
•Malignancy - metastatic (lung, breast, melanoma most common); often haemorrhagic and haemodynamically significant
•Iatrogenic - post-cardiac surgery, post-coronary angiogram/PCI, pacemaker lead perforation
•Trauma - haemopericardium can develop rapidly even with modest volumes
•Metabolic - hypothyroidism, uraemia, hypoalbuminaemia
Dressler's syndrome vs early post-MI pericarditis
| Feature | Early post-MI pericarditis | Dressler's syndrome |
|---|---|---|
| Onset | Within 48 hours of MI | 2-6 weeks post-MI |
| Mechanism | Direct pericardial inflammation | Autoimmune - antibodies against myocardial proteins released during infarct healing |
| Shared features | Pleuritic chest pain, fever, raised ESR/CRP/WBC, pericardial friction rub | Pleuritic chest pain, fever, raised ESR/CRP/WBC, pericardial friction rub |
Presentation
•Dyspnoea - most common symptom; reduced cardiac output
•Pleuritic chest pain - sharp, worse on inspiration and lying flat; relieved by sitting forward (when pericarditis is the cause)
•Muffled heart sounds - fluid attenuates sound transmission
•Raised JVP - impaired right heart filling
•Pulsus paradoxus - fall in systolic BP >10 mmHg on inspiration; right ventricular expansion bows septum left, reducing LV filling
•Tachycardia - compensatory response to falling stroke volume
•Hypotension - late sign indicating haemodynamic decompensation
Cardiac tamponade vs constrictive pericarditis - key differentiators
| Feature | Cardiac tamponade | Constrictive pericarditis |
|---|---|---|
| Beck's triad | Present (hypotension, raised JVP, muffled heart sounds) | Not a classic feature |
| Kussmaul's sign | Absent - JVP does not change with inspiration | Positive - JVP rises/fails to fall with inspiration |
| Pulsus paradoxus | Present | Usually absent |
| Pericardial knock | Absent | Present |
| Lung fields | Usually clear | Usually clear |
Investigations
•Gold standard/First-line: Transthoracic echocardiogram (TTE) - quantifies effusion size; right atrial systolic collapse and right ventricular diastolic collapse indicate tamponade; required in all suspected acute pericarditis (ESC guideline)
•ECG - saddle-shaped ST elevation in all leads (pericarditis); low QRS voltage (large effusion); PR depression; electrical alternans (beat-to-beat QRS variation - heart swings in fluid; highly specific for large effusion/tamponade)
•Chest X-ray - large effusions give globular 'flask-shaped' cardiac silhouette; may be normal with smaller effusions
•Bloods - FBC, CRP, ESR (inflammation); U&E (uraemia); TFTs (hypothyroidism); troponin; blood cultures if infective
•CT chest - loculated effusions, pericardial thickening, underlying malignancy
•Pericardial fluid analysis (from pericardiocentesis) - protein, LDH, cell count, culture, AFB smear, cytology
Management
•Small asymptomatic effusion - treat underlying cause; monitor with serial echocardiography every 3-6 months
•Inflammatory cause (Dressler's/viral pericarditis) - NSAIDs + colchicine for 3 months; restrict strenuous activity
•Cardiac tamponade - urgent echo-guided pericardiocentesis; IV fluid bolus to maintain preload while arranging drainage
•Malignant effusion - percutaneous balloon pericardiotomy preferred due to high recurrence rate; ongoing oncological management
•Post-pericardiocentesis - repeat echo at 24-48 hours; drain left in situ until <25 mL/day output
Complications
•Cardiac tamponade - rising intrapericardial pressure → equalisation of diastolic pressures across all chambers → impaired filling → falling cardiac output → cardiogenic shock
•Constrictive pericarditis - fibrotic pericardial thickening restricts diastolic filling; presents with raised JVP, Kussmaul's sign, pericardial knock, ascites; causes include prior cardiac surgery/catheterisation, TB, viral pericarditis
•Recurrence - particularly idiopathic, viral, or malignant effusions; up to one-third of large idiopathic effusions may develop tamponade unexpectedly