Chronic Pain

Pericarditis is inflammation of the pericardium, the fibrous sac surrounding the heart.

It is most commonly idiopathic or presumed viral in origin, though a wide range of other causes exist, including bacterial infection (rare, but important given the risk of purulent pericarditis), tuberculosis (a significant cause in endemic settings, and an important cause of subsequent constrictive pericarditis), autoimmune disease (systemic lupus erythematosus, rheumatoid arthritis), uremia (in advanced chronic kidney disease), malignancy, radiation, and post cardiac injury syndromes (following myocardial infarction, cardiac surgery, or trauma, sometimes termed Dressler syndrome when delayed after infarction).

Sharp, pleuritic chest pain is the classic presenting symptom, characteristically worse when lying flat and improved by sitting forward, and often worsened by inspiration, coughing, or swallowing.

A pericardial friction rub, a superficial, scratchy sound best heard at the left sternal edge with the patient leaning forward in expiration, is pathognomonic when present, though it is often intermittent and may not be heard at every examination.

Fever and other features of the underlying cause may be present, for example symptoms suggesting a recent viral illness, or features of an autoimmune or malignant process.

Cardiac tamponade is the most feared acute complication, occurring when pericardial fluid accumulates rapidly enough to impair diastolic filling of the heart. It presents with Beck's triad of hypotension, raised jugular venous pressure, and muffled heart sounds, alongside pulsus paradoxus (an exaggerated fall in systolic blood pressure of more than 10 mmHg during inspiration), and represents a medical emergency requiring urgent drainage.

Diagnosis requires at least two of four criteria: characteristic pleuritic, positional chest pain; a pericardial friction rub; characteristic ECG changes; and a new or worsening pericardial effusion on echocardiography.

The ECG classically shows widespread, saddle shaped ST elevation and PR segment depression, distinguishable from an acute coronary syndrome by its diffuse distribution across multiple coronary territories rather than a single vascular pattern, and by the absence of reciprocal ST depression that would be expected with a focal infarction (see Electrocardiogram Interpretation entry).

Echocardiography assesses for a pericardial effusion and, critically, for any evidence of tamponade physiology (right ventricular diastolic collapse, respiratory variation in mitral and tricuspid inflow velocities). Inflammatory markers (CRP, ESR) support the diagnosis and can be used to track resolution. Troponin may be mildly elevated if there is associated myocardial involvement (myopericarditis), which should prompt closer monitoring given the small additional risk of arrhythmia or heart failure in this subgroup.

Further investigation is directed by suspected cause where the presentation is not clearly a typical, uncomplicated idiopathic or viral episode: blood cultures and further infectious workup if bacterial pericarditis is suspected, tuberculosis testing in endemic settings or with a suggestive exposure history, autoimmune serology if a connective tissue disease is suspected, and renal function if uremic pericarditis is a possibility.

Pericardiocentesis, when performed for a large or hemodynamically significant effusion, allows fluid analysis for cytology, culture, and, where relevant, tuberculosis testing.

Differentials include acute coronary syndrome (the most important to exclude given overlapping presentation and very different urgent management), pulmonary embolism, aortic dissection, and pneumonia with pleurisy.

Uncomplicated, presumed viral or idiopathic pericarditis is treated with high dose NSAIDs (for example ibuprofen or aspirin) as first-line therapy, combined with colchicine, which has been shown to reduce both the duration of the initial episode and the risk of recurrence, and is now recommended as standard adjunct therapy from the outset rather than reserved for recurrent cases.

Corticosteroids are generally avoided as first-line treatment given an association with higher recurrence rates, but are used for cases refractory to NSAIDs and colchicine, for specific autoimmune causes, or where NSAIDs are contraindicated.

Exercise restriction is advised until symptoms resolve and inflammatory markers normalize, given a theoretical concern that exertion during active inflammation may worsen outcomes or provoke arrhythmia, particularly where myocardial involvement is present.

Cardiac tamponade requires urgent pericardiocentesis, typically under echocardiographic guidance, which is both diagnostic and immediately life saving. Purulent bacterial pericarditis requires urgent drainage combined with targeted antibiotics. Tuberculous pericarditis is treated with standard antituberculous therapy (see Tuberculosis entry), with corticosteroids sometimes added to reduce the risk of progression to constrictive pericarditis, though evidence for this benefit is mixed.

Recurrent pericarditis, defined as a further episode after a symptom free interval, is managed with a similar approach of NSAIDs and colchicine, with a more prolonged colchicine course than for a first episode. Refractory recurrent cases unresponsive to conventional therapy are increasingly treated with interleukin 1 blocking agents such as anakinra or rilonacept under specialist care.

Constrictive pericarditis, a late complication in which the pericardium becomes rigid and fibrotic, impairing diastolic filling, presents with predominantly right sided heart failure features and is definitively treated with surgical pericardiectomy in symptomatic cases.

Referral: cardiology for diagnostic uncertainty, any evidence of tamponade (urgent), recurrent or refractory pericarditis, or suspicion of an underlying secondary cause requiring specific investigation and treatment.