Pericardial Disease

[7]

Meet the patient

A 28-year-old clerk wakes at 3am with sharp chest pain that stabs every time he breathes in, and eases the moment he sits up and leans forward over the bedside table. He had a sore throat a week ago. His ECG shows ST elevation in almost every lead — and the registrar is already reaching for the thrombolysis tray.[2]

Two questions decide his night, and they recur in every pericardial patient you meet on this ward round: is this pericarditis or STEMI? (the pain story and the ECG settle it in a minute) and is a tamponade hiding behind it? (the pulse, the JVP and the echo answer that). Hold those two questions and the whole topic falls into place.[2]

Three syndromes, one sac — name the face before you treat

Pericardial disease is one structure misbehaving in three ways: it inflames, it fills, or it scars. The fibrous pericardium is a tough, non-distensible sac around a serous-lined space that normally holds up to 50 mL of fluid, a plasma ultrafiltrate — anything greater is a pathologic effusion; almost every exam question is a disguised version of "which of the three is this?".[7]

The three faces, with the one-line answer for each:[2]

1. Acute pericarditis — inflammation of the pericardium under 3 months; ESC diagnosis is 2 of 4 (chest pain, rub, ECG changes, effusion). Sub-types are first episode, incessant (over 4 to 6 weeks but under 3 months), recurrent (new episode after a symptom-free interval of at least 4 to 6 weeks), and chronic (over 3 months).
2. Pericardial effusion with tamponade — fluid under pressure; what matters is the rate of accumulation, not the volume. Tamponade is the decompensated end-state where intra-pericardial pressure exceeds ventricular filling pressure.
3. Constrictive pericarditis — chronic thickening, scarring and often calcification that halts diastolic filling and produces a clinical picture of right heart failure with clear lungs.[1][16]

The three clinical skills the examiner is really testing: separate pericarditis from acute MI (both raise the ST segment), spot tamponade before it collapses, and split constriction from restrictive cardiomyopathy (both raise the JVP, only one is cured by surgery).[1][16]

The causes that map to the face — "PERICARD"

Idiopathic or viral is the commonest cause in North America and Western Europe; in TB-endemic regions the same sentence ends with tuberculosis. That regional fact is worth two marks by itself. Acute pericarditis accounts for up to 5 per cent of emergency department visits for non-ischaemic chest pain in North America and Western Europe, and 70 to 85 per cent of appropriately treated patients run a benign course.[2]

Cluster the aetiologies by the face they produce, and they stop being a list:[1]

• Idiopathic / viral — coxsackievirus, echovirus, adenovirus, influenza, EBV, HIV.
• Bacterial (purulent) — Staphylococcus, Streptococcus, Pneumococcus; TB pericarditis is the leading cause in TB-endemic regions such as India and sub-Saharan Africa.
• Uraemic — renal failure; pericarditis in a dialysis patient is an indication for urgent dialysis.
• Post-cardiac injury — acute MI (early fibrinous), Dressler syndrome (later, weeks post-MI), post-cardiac surgery, post-trauma, post-catheter or ablation.
• Autoimmune / connective tissue — SLE, rheumatoid arthritis, scleroderma, vasculitis, sarcoidosis, inflammatory bowel disease.
• Neoplastic — lung, breast, lymphoma, melanoma (metastatic far commoner than primary).
• Radiation — mediastinal radiotherapy, months to years later.
• Drugs — procainamide, hydralazine, isoniazid (drug-induced lupus), phenytoin, doxorubicin.
• Endocrine — hypothyroidism (myxoedema), rarely pregnancy.[1][2]

The risk factors that point at the cause: immunocompromise (HIV, transplant, chemotherapy) for the infective group; chronic dialysis for uraemic; recent open-heart surgery for post-pericardiotomy; mediastinal radiotherapy or known cancer for neoplastic; untreated TB exposure for tuberculous. Constriction follows idiopathic or viral pericarditis, previous cardiac surgery or mediastinal radiation — in a contemporary meta-analysis of pericardiectomy cohorts, aetiology was idiopathic in 50.2 per cent, after cardiac surgery in 26.2 per cent and radiation in 6.9 per cent.[2][17]

The pathophysiology in one sentence each — and why constriction is not tamponade

One physical fact drives all three syndromes: the fibrous pericardium cannot stretch acutely. Everything else — the rub, the ST elevation, the chamber collapse, the knock — follows from that.[7]

Acute pericarditis is inflammation of the layers with fibrinous exudate, neutrophil and lymphocyte infiltrate, and often a sympathetic effusion. The two inflamed surfaces rub against each other to make the friction rub; subepicardial injury current produces the diffuse ST elevation, and atrial injury current produces the PR segment depression.[1][2]

Cardiac tamponade is the rate-vs-volume lesson in one disease. The pericardial sac has a curvilinear pressure-volume relationship, so fluid accumulating rapidly (aortic dissection, catheter perforation, trauma) raises intra-pericardial pressure above ventricular filling pressure at a far smaller volume than effusions accumulating slowly, which the sac accommodates. On echo the chambers cave in — right atrial systolic collapse (a sensitive sign), then right ventricular diastolic collapse (more specific). Once pressure exceeds filling, all four chambers share one fixed total volume: filling of one steals from the others — ventricular interdependence, driven to the point of collapse.[3][4][7]

On inspiration, negative intrathoracic pressure augments systemic venous return and right-heart filling; because total cardiac volume is fixed, the septum shifts leftward, left-sided filling and stroke volume fall, and systolic BP drops by more than its normal small inspiratory dip — pulsus paradoxus, which can be sought clinically and as sonographic pulsus paradoxus on echo.[3][4]

Constrictive pericarditis is the healed end-state: an inflamed pericardium becomes fibrotic and non-compliant; fibrosis, scarring and often calcification fuse the layers into a rigid shell. The ventricle fills rapidly in early diastole, then hits the shell and stops abruptly in mid-diastole — producing the pericardial knock and a deep, rapid y descent on the JVP. Because the rigid pericardium insulates the heart from intrathoracic pressure swings, inspiration can no longer lower intrapericardial pressure, so systemic venous pressure does not fall, and may rise — the Kussmaul sign.[16]

Why does constriction usually have NO pulsus paradoxus, while tamponade does?

The pericardium transmits pressure differently. In tamponade, fluid compresses the heart throughout diastole, so there is no rapid early filling and the y descent is blunted — but the heart still feels intrathoracic pressure swings, so inspiration exaggerates the left-sided drop and pulsus paradoxus is marked. In constriction the pericardium is rigid but does not oppose early diastolic filling, so there is a deep y descent and a knock — and because the rigid shell insulates the heart, inspiration cannot lower intrapericardial pressure, venous pressure does not fall (Kussmaul), the pulmonary-venous-to-left-atrial gradient narrows, and pulsus paradoxus is usually absent. Absence of pulsus paradoxus in a patient with a raised JVP and clear lungs is a bedside pointer toward constriction, not tamponade.[16]

Read the ECG like the cath lab does — pericarditis vs STEMI

The ECG is the cardinal test, and the single most reproduced discriminator is: diffuse concave ST elevation, PR depression, and NO reciprocal change. Get those three on the same line in a viva and the pericarditis-versus-STEMI marks are yours.[2]

Stage I (hours to days) — diffuse concave ST elevation in most leads (I, II, aVL, aVF, V3 to V6), with PR depression in the same leads (PR elevation in aVR and V1), and no reciprocal changes. Stage II (days to weeks) — ST returns to baseline, PR depression persists, T waves begin to flatten. Stage III — diffuse T-wave inversion. Stage IV — T waves normalise and the patient recovers. The whole evolution plays out over days to weeks, not hours.[1]

The face-off that decides whether you reach for the lysis tray or the ibuprofen:[1]

[1] [2]

The classic trap: a STEMI patient on day 2 develops diffuse concave ST elevation with PR depression and pleuritic pain — that is early post-MI fibrinous pericarditis, and the ECG pattern (diffuse, concave, PR down, no reciprocal) is what stops you re-activating the cath lab. PR depression is the most specific single sign of pericarditis.[1]

A mild troponin rise does not exclude pericarditis — it means myopericarditis; only a markedly raised troponin with a focal wall-motion abnormality pushes you toward infarction. Always read the troponin with the ECG and the pain story, never alone.[2]

The 2-of-4 rule — the ESC diagnosis you can recite in one breath

Acute pericarditis needs at least 2 of these 4 — chest pain, pericardial rub, new widespread ST elevation or PR depression on ECG, and a new or worsening pericardial effusion. Two of four, plus raised inflammatory markers, and you have made the diagnosis the way the ESC 2015 guideline asks for it — and a 2024 JAMA review confirms the same criteria.[1][2]

1. Pericarditic chest pain (present in about 90 per cent) — sharp, pleuritic, positional (worse on inspiration and lying flat, relieved by sitting forward); often radiates to the left trapezial ridge because the pericardium shares phrenic-nerve-referred innervation with the shoulder.
2. Pericardial friction rub (found in under 30 per cent) — best heard at the left sternal border with the patient leaning forward in full expiration; a high-pitched, scratching, leather-like, superficial sound with up to three components (atrial systole, ventricular systole, rapid ventricular filling).
3. ECG (about 25 to 50 per cent) — new widespread ST elevation or PR depression.
4. Effusion (about 60 per cent, most often small) — new or worsening on imaging.[2]

Etymology for viva gold: pericardium from the Greek peri ("around") and kardia ("heart") — literally "around the heart". Kussmaul sign carries Adolf Kussmaul's name; Beck triad carries Claude Beck's, the thoracic surgeon who first described the tamponade pattern he was trying to relieve. Dressler syndrome is William Dressler's post-MI auto-immune pericarditis. Names outlive their namers because the signs do.[1]

Meet the tamponade patient — Beck plus the bedside that decides

Tamponade is the resuscitation emergency of this topic, and the bedside — not the blood pressure — makes the call. The decompensated picture is Beck triad: hypotension, raised JVP, distant (muffled) heart sounds — though beware, the full triad appears uncommonly. Add pulsus paradoxus and you have the clinical diagnosis before the echo loads; dyspnoea is the most frequently reported symptom.[3][4]

• Beck triad (acute) — hypotension, raised JVP, muffled heart sounds.
• Pulsus paradoxus — an exaggerated fall in systolic BP on normal inspiration, detected clinically and sonographically.
• Dyspnoea progressing to orthopnoea with clear lungs (no rales), weakness, fatigue, tachycardia and oliguria.
• Shock with clear lungs and a raised JVP is the key discriminator from pulmonary oedema.
• In tamponade on top of acute pericarditis, expect fever and chest pain that increases on inspiration and radiates to the trapezius ridge.[3]

Measure pulsus paradoxus yourself: inflate the sphygmomanometer and deflate slowly, comparing the Korotkoff sounds heard only in expiration with the point where they are heard throughout the respiratory cycle — a wide difference is abnormal. Bedside echo shows the same physiology as respiratory septal shift and inflow variation.[4]

Atypical presentations are the ones that bite. The classic triad is often incomplete — the diagnosis should be clinical and confirmed by echocardiography, not dismissed because the textbook picture is absent. TB pericarditis runs an insidious course with constitutional features. In pregnancy and in the elderly, rely on the echo when the picture is muted.[3][15]

Echo is the test that decides the next hour

Echocardiography is the key imaging for pericardial disease — tamponade is a clinical diagnosis that echo confirms, it sizes the effusion, and pericardiocentesis is preferably echo-guided. In a crashing patient, a bedside echo showing a large effusion with tamponade physiology is the green light for pericardiocentesis without waiting for anything else.[3]

The echo signs of tamponade (high-yield list):[4]

• Pericardial effusion — the larger the effusion, the more likely tamponade.
• Right ventricular diastolic collapse — the more specific sign.
• Right atrial systolic collapse — sensitive.
• Plethoric, non-collapsible inferior vena cava — sensitive.
• Sonographic pulsus paradoxus — respiratory septal shift and variation in ventricular inflow.
• Swinging heart (electrical alternans on ECG) in large effusions.

Effusion size is graded semiquantitatively by echo — and remember the anchor number: the normal pericardial sac contains up to 50 mL of plasma ultrafiltrate; anything greater is a pathologic effusion.[1][7]

[1]

Other first-line tests: 12-lead ECG (cardinal); bloods — FBC, CRP, troponin, urea and electrolytes, LFTs, TSH as clinically directed; blood cultures if septic; autoimmune screen (ANA, dsDNA, RF) only if suspicion; HIV testing where the clinical picture prompts it. Chest X-ray may be normal; a large effusion enlarges the cardiac silhouette, and pericardial calcification points to constriction. If TB is suspected in an endemic region, send pericardial fluid for adenosine deaminase, AFB smear and culture, and Xpert MTB/RIF — a positive Xpert is close to confirmatory (pooled specificity 0.994) but a negative result does not exclude TB pericarditis (pooled sensitivity 0.676).[1][15][18]

The classic trap — constriction vs restriction

Both raise the JVP and swell the legs; only one is cured by surgery. Splitting constriction from restrictive cardiomyopathy is the discriminator the examiner lives for, and the table is the answer.[16]

[16] [17]

The discriminator line: calcification plus a knock plus septal bounce plus a normal BNP equals constriction; myocardial LGE plus a high BNP equals restriction. Say it that way and you will not confuse the two.[16]

Echo in constriction adds the signs beyond tamponade: septal bounce (abrupt early-diastolic septal motion as the RV hits the constraint), pericardial thickening, exaggerated respiratory variation in mitral inflow, a plethoric IVC, and annulus paradoxus — preserved medial annular e-prime despite restrictive transmitral filling, because the myocardium itself is normal in constriction and diseased in restriction.[16]

Cardiac CT and MRI settle the case when echo cannot. CT is the modality of choice for pericardial calcification and pericardial thickness; MRI adds pericardial late gadolinium enhancement (active inflammation, may predict response to medical therapy in transient constriction), real-time cine confirming the septal bounce, and tagged sequences showing pericardial-myocardial adherence — failure of normal sliding, a specific sign of constriction.[16]

Other causes of a raised JVP with clear lungs to exclude: decompensated cirrhosis (low JVP), cor pulmonale, tricuspid regurgitation, and RV infarction (which itself can show a Kussmaul sign). History, the JVP waveform, and echo separate them.[1]

Treat acute pericarditis the ESC way — NSAID plus colchicine, steroids last

The first-line regimen has not changed since ESC 2015: a high-dose NSAID plus colchicine for three months. This is the prescription the examiner wants.[1][2]

• High-dose aspirin or ibuprofen at full anti-inflammatory dose — continue until chest pain has resolved and CRP has normalised (typically over several weeks), then taper.[2]
• Plus colchicine 0.5 mg once daily if 70 kg or under, or 0.5 mg twice daily if over 70 kg — for 3 months. In ICAP this reduced incessant or recurrent pericarditis from 37.5 to 16.7 per cent (absolute risk reduction 20.8 per cent, number needed to treat 4).[8][2]
• PPI gastroprotection for the duration of high-dose NSAID therapy.
• Restricted physical activity until symptoms settle and CRP normalises.[1]
• Treat the underlying cause — haemodialysis for uraemic, antibiotics for purulent, anti-TB therapy for tuberculosis, immunosuppression for autoimmune.[1][15]

What did the colchicine trials actually show?

CORE (2005) added colchicine (1.0 to 2.0 mg on day 1, then 0.5 to 1.0 mg daily for 6 months) to conventional therapy for a first recurrence: actuarial recurrence at 18 months 24.0 vs 50.6 per cent (NNT 4), and previous corticosteroid use was an independent risk factor for further recurrences (odds ratio 2.89). ICAP (2013, NEJM) treated the first episode with colchicine 0.5 mg daily for 3 months (weight-adjusted): incessant or recurrent pericarditis 16.7 vs 37.5 per cent, symptom persistence at 72 hours 19.2 vs 40.0 per cent, recurrences per patient 0.21 vs 0.52, hospitalisation 5.0 vs 14.2 per cent. COPPS (2010) gave 1 month of postoperative colchicine after cardiac surgery: post-pericardiotomy syndrome at 12 months 8.9 vs 21.1 per cent (NNT 8). The practical rule that follows: colchicine is first-line for the index episode, not just for recurrence.[10][8][9]

Corticosteroids are NOT first-line — they raise recurrence. In CORE, previous corticosteroid use independently predicted further recurrences (odds ratio 2.89), and contemporary reviews place steroids after NSAID and colchicine failure. The ESC reserves them for specific situations: autoimmune aetiology, uraemic pericarditis after dialysis, pregnancy (NSAIDs contraindicated), true NSAID or colchicine contraindication, and refractory disease — at the lowest effective dose, tapered slowly once symptoms and CRP normalise.[10][2][1]

Dressler and the post-MI trap — aspirin only, never steroids early

After a myocardial infarction the rule is aspirin, and aspirin alone, for any pericarditis — because NSAIDs and steroids impair healing and raise the risk of free-wall rupture in the first weeks. This is the single most testable safety point in the topic.[1][4]

• Early fibrinous pericarditis (first days post-STEMI) — usually benign; high-dose aspirin is preferred.
• Dressler syndrome (weeks post-MI) — autoimmune; fever, pleuritic pain, raised inflammatory markers; high-dose aspirin first-line, corticosteroids reserved for refractory cases only after the infarct has healed. Rare in the modern primary-PCI era.[1]

TB pericarditis — the Indian reality

In a TB-endemic country, any large or recurrent effusion warrants evaluation for tuberculosis — untreated tuberculous pericarditis progresses to constriction. The Indian context changes both the differential and the default.[15]

• Standard antitubercular therapy — the standard 4-drug antituberculosis regimen for 6 months.[15]
• Adjunctive corticosteroids — the IMPI trial (1400 adults, two-thirds with HIV co-infection) randomly assigned prednisolone for 6 weeks: no significant effect on the composite of death, tamponade requiring pericardiocentesis or constrictive pericarditis (23.8 vs 24.5 per cent), but significantly less constrictive pericarditis (4.4 vs 7.8 per cent) and less hospitalisation (20.7 vs 25.2 per cent), at the price of more cancers (1.8 vs 0.6 per cent, mainly HIV-associated). Never give steroids without concomitant anti-TB therapy.[14]
• Pericardiocentesis for tamponade; pericardiectomy for established constriction — many experts recommend a trial of medical therapy first in non-calcific constriction, reserving surgery for non-responders after 4 to 8 weeks of antituberculosis chemotherapy.[15][3]

Diagnosis is challenging — a definite diagnosis requires tubercle bacilli in pericardial fluid or on pericardial histology; a probable diagnosis rests on proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated adenosine deaminase, and/or an appropriate response to a trial of antituberculosis chemotherapy.[15] On molecular testing, Xpert MTB/RIF on pericardial fluid has robust specificity (pooled 0.994) but unsatisfactory sensitivity (0.676) — a positive result swiftly confirms TB pericarditis; a negative result cannot rule it out.[18] Constrictive pericarditis developed in 7.8 per cent of placebo-treated IMPI patients, and HIV co-infection is common in endemic cohorts.[14]

Recurrent pericarditis — colchicine is the cornerstone, IL-1 the rescue

Recurrence is defined as a new episode after a symptom-free interval, and it is the rule, not the exception — 15 to 30 per cent of patients recur after the first episode, and multiple recurrences can run for years. Colchicine halves that risk and is the cornerstone of every recurrence.[2][8]

Treat each recurrence with the standard NSAID-plus-colchicine regimen; with a first recurrence, colchicine should be continued for at least 6 months (CORE used 6 months), with doses tapered once chest pain has resolved and CRP has normalised.[2][10]

Refractory recurrent pericarditis (multiple recurrences, colchicine resistance or corticosteroid dependence) is transformed by IL-1 blockade: in AIRTRIP, anakinra 2 mg/kg/day subcutaneously (up to 100 mg) for 2 months induced remission, and withdrawal to placebo caused recurrence in 90 vs 18.2 per cent over a median 14 months; in RHAPSODY, once-weekly subcutaneous rilonacept was followed by recurrence in 7 vs 74 per cent of randomized patients (hazard ratio 0.04). Corticosteroids remain an option but carry the highest recurrence on withdrawal; IL-1 blockers may be preferred as steroid-sparing therapy.[12][13][2]

Pericardiocentesis — the procedure the examiner expects you to describe

Tamponade with haemodynamic compromise is the indication; echo-guided percutaneous drainage is the technique. Describe it the way a consultant would and you will pass the viva.[6][3]

Indications: cardiac tamponade with haemodynamic instability, impending deterioration or cardiac arrest; a large symptomatic effusion; diagnostic fluid sampling (suspected TB, bacterial, neoplastic); and effusive-constrictive physiology.[4][3]

Approach: echocardiographic guidance is the standard of care — the entry site is chosen over the largest, shallowest fluid pocket with no intervening vital structures, classically the subxiphoid (subcostal) route aimed toward the left shoulder, with an apical window when that is where the fluid sits. Blind pericardiocentesis is reserved for imminent arrest. Drain slowly to avoid pericardial decompression syndrome.[4][6]

Technique: aseptic prep with generous local anaesthesia; needle, then guidewire (Seldinger), dilate, and a multi-side-hole pericardial catheter. Extended catheter drainage has become standard practice — in the Mayo series its adoption (23 to 75 per cent of cases) coincided with significantly fewer recurrences and less surgical reintervention.[4][6]

Send the fluid for cell count and differential, protein, LDH, glucose, Gram stain and culture, AFB smear and culture plus Xpert MTB/RIF, adenosine deaminase (elevated in the lymphocytic exudate of TB pericarditis), and cytology. Transudate versus exudate narrows the differential.[15][18]

Complications: in the Mayo series of 1127 echo-guided pericardiocenteses, the procedural success rate was 97 per cent with a total complication rate of 4.7 per cent (major 1.2, minor 3.5 per cent) — never attempt blind pericardiocentesis when echo and a trained operator are available.[6]

Constriction — pericardiectomy is the only cure

Definitive treatment of constrictive pericarditis is pericardiectomy. In a meta-analysis of 27 studies (2114 patients), operative mortality was 6.9 per cent and 5-year mortality 32.7 per cent (roughly two-thirds survive 5 years); radiation-induced and post-surgical constriction carried 3-fold and 2-fold higher long-term mortality respectively than idiopathic disease.[17]

One caution before you book theatre: transient constrictive physiology (post-viral, post-surgery) may resolve with medical therapy — many experts recommend a trial of medical therapy for non-calcific constriction, with pericardiectomy reserved for non-responders after 4 to 8 weeks of therapy.[15][16]

Surgical drainage (subxiphoid pericardiotomy or pericardial window) is preferred over needle drainage for bleeding or purulent infection that cannot be controlled percutaneously, for aortic dissection and severe chest trauma, for loculated effusions, and when tissue for histology (TB, malignancy) is required.[3]

Effusive-constrictive pericarditis is the trap within the trap: tamponade physiology persists after pericardiocentesis, and it is one of the settings in which fluoroscopic guidance can increase the feasibility and safety of drainage. Suspect it when the JVP fails to fall after drainage; definitive treatment is surgical.[3]

[2] [3] [4]

Purulent (bacterial) pericarditis is a medical emergency: systemic antibiotics plus urgent percutaneous or surgical drainage — surgical management is indicated when infection cannot be controlled percutaneously. Neoplastic effusion gets pericardiocentesis with extended catheter drainage (which reduces recurrence and the need for surgery) alongside treatment of the underlying tumour; NSAIDs and colchicine after drainage can be considered to prevent recurrence and effusive-constrictive evolution.[3][4][6]

The preventable-harm list — what kills these patients

Most pericardial deaths are preventable. Carry this list on the ward round and tick it before you write the drug chart.[1]

• Giving steroids for first-episode idiopathic pericarditis — predicts further recurrences (odds ratio 2.89 in CORE).[10]
• NSAIDs or steroids in early post-MI pericarditis — aspirin only; the risk is free-wall rupture.
• Misdiagnosing STEMI as pericarditis (or vice versa) — check reciprocal changes, PR depression, and diffuse concave ST elevation; urgent coronary angiography if in doubt.
• Missing tamponade because the blood pressure looks normal — measure pulsus paradoxus and the JVP; rely on echo for any large effusion.
• Anticoagulating a haemopericardium (e.g. post-catheter) — worsens tamponade.
• Forgetting TB in the Indian patient with an effusion — a missed TB pericarditis will progress to constriction.
• Mislabelling constrictive pericarditis as cirrhosis — ascites with a raised JVP is constriction; cirrhosis has a low JVP.[1]

Special populations — the dose changes, the diagnosis does not

• Pregnancy — NSAIDs are avoided in pregnancy; corticosteroids are preferred when anti-inflammatory therapy is needed for symptomatic pericarditis.[1]
• Renal failure or dialysis — uraemic pericarditis is an indication for intensified dialysis; NSAIDs and colchicine are renal-excreted and need dose adjustment or avoidance.[1]
• Elderly or immunocompromised — atypical, often muted presentations; lower threshold for echo and admission.[4]
• Children and small adults — colchicine dosing is weight-adjusted (halved below 70 kg); the main trials used 0.5 mg twice daily above 70 kg and 0.5 mg once daily below.[11]
• Anticoagulated patient — high risk of haemopericardium and tamponade; remember that in any patient with an effusion, dehydration, vasodilators and IV diuretics can precipitate tamponade.[3]

Who goes home, who is admitted: outpatient with a safety net if the effusion is small or absent with no fever and no high-risk feature. Admit if any ESC high-risk marker is present — fever, large effusion, tamponade, immunocompromise, trauma, oral anticoagulation, failure of outpatient therapy, or myopericarditis.[1]

The mantra

NSAID plus colchicine for three months; steroids last; aspirin-only after MI; drain a tamponade, strip a constriction.[1][2]

[7] [8] [15] [17] [1]

Ward-round test — answer without another resource

1. The clerk from the top of the topic — diffuse ST elevation at 3am. Is this pericarditis or STEMI, and what is your first drug?

Pericarditis, not STEMI. The pain is sharp, pleuritic, and eased by sitting forward; the ECG is diffuse, concave ST elevation with PR depression and no reciprocal change, evolving over days — the discriminator from a territorial, convex, reciprocal STEMI. First drug: a high-dose NSAID (aspirin or ibuprofen) plus colchicine 0.5 mg once daily if 70 kg or under, or 0.5 mg twice daily if over 70 kg, for 3 months, with a PPI. Check the troponin and get an echo to size any effusion, but do not thrombolyse.[2][8]

2. A woman with known lung cancer, dyspnoeic, SBP 92, JVP to the ear, clear lungs, muffled heart sounds. What is the syndrome, the bedside sign to measure, and the definitive move?

Cardiac tamponade from a malignant effusion. The picture is Beck triad (hypotension, raised JVP, muffled sounds) with shock and clear lungs — the key discriminator from pulmonary oedema. Measure pulsus paradoxus. Confirm with bedside echo — RA and RV collapse, plethoric IVC — then urgent echo-guided pericardiocentesis, leaving the catheter in for extended drainage because malignant effusions re-accumulate. Avoid positive-pressure ventilation and IV sedation where possible and avoid IV diuretics; a gentle crystalloid bolus helps about half of patients — those with a baseline systolic BP under 100 mmHg respond best.[3][4][5][6]

3. A 60-year-old with a JVP that rises on inspiration, a pericardial knock, ascites, and clear lungs. BNP is normal. What is the diagnosis, the mimic to exclude, and the definitive treatment?

Constrictive pericarditis. The triad is Kussmaul sign, pericardial knock, and pericardial calcification on CXR or CT; the normal BNP and the septal bounce on echo (annulus paradoxus on tissue Doppler) split it from restrictive cardiomyopathy, which has a high BNP and myocardial LGE. The other mimics — decompensated cirrhosis (low JVP), cor pulmonale, tricuspid regurgitation, RV infarct — separate on history, JVP waveform, and echo. Before surgery, exclude transient constriction (a trial of medical therapy, with pericardiectomy reserved for non-responders after 4 to 8 weeks); definitive treatment is pericardiectomy — operative mortality 6.9 per cent with roughly two-thirds 5-year survival in contemporary series.[16][15][17]

4. Day 2 after an anterior STEMI, the patient develops pleuritic chest pain, a transient rub, and diffuse concave ST elevation. The registrar suggests ibuprofen. Correct the plan.

Aspirin only — not ibuprofen, not steroids. This is early post-MI fibrinous pericarditis (first days post-STEMI); the diffuse concave ST elevation and PR depression distinguish it from re-infarction, so the cath lab is not the answer either. NSAIDs and corticosteroids are avoided because of the risk of free-wall rupture of the necrotic wall. The same logic — steroids without cover — applies to suspected TB pericarditis.[1][4]

References

1. [1]Adler Y, Charron P, Imazio M, 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)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS) Eur Heart J, 2015.PMID 26320112
2. [2]Cremer PC, Klein AL, Imazio M Diagnosis, Risk Stratification, and Treatment of Pericarditis: A Review JAMA, 2024.PMID 39235771
3. [3]Adler Y, Ristić AD, Imazio M, et al. Cardiac tamponade Nat Rev Dis Primers, 2023.PMID 37474539
4. [4]Alerhand S, Adrian RJ, Long B, Avila J Pericardial tamponade: A comprehensive emergency medicine and echocardiography review Am J Emerg Med, 2022.PMID 35696801
5. [5]Sagristà-Sauleda J, Angel J, Sambola A, Permanyer-Miralda G Hemodynamic effects of volume expansion in patients with cardiac tamponade Circulation, 2008.PMID 18332261
6. [6]Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years Mayo Clin Proc, 2002.PMID 12004992
7. [7]Azarbal A, LeWinter MM Pericardial Effusion Cardiol Clin, 2017.PMID 29025543
8. [8]Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis N Engl J Med, 2013.PMID 23992557
9. [9]Imazio M, Trinchero R, Brucato A, et al. COlchicine for the Prevention of the Post-pericardiotomy Syndrome (COPPS): a multicentre, randomized, double-blind, placebo-controlled trial Eur Heart J, 2010.PMID 20805112
10. [10]Imazio M, Bobbio M, Cecchi E, et al. Colchicine as first-choice therapy for recurrent pericarditis: results of the CORE (COlchicine for REcurrent pericarditis) trial Arch Intern Med, 2005.PMID 16186468
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