Acute Pericarditis

This is acute inflammation of the pericardium, the membranous sac which surrounds the heart. The pericardium is composed of an outer fibrous layer (parietal pericardium) and an inner serous membrane (visceral pericardium), with approximately 50 mL of plasma ultrafiltrate between.¹ The pericardium promotes cardiac efficiency by limiting dilation, maintaining ventricular compliance with preservation of the Starling curve,² and distributing hydrostatic forces. It aids atrial filling by creating a closed chamber, reduces external friction, and acts as a barrier against infection and extension of malignancy. Finally, it anatomically fixes the heart to the sternum, diaphragm, and costal cartilages.

In most cases, the pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes. A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac and a serous or haemorrhagic effusion may develop. In some conditions (TB, sarcoid, fungal infections and rheumatoid arthritis) a granulomatous pericarditis develops.³

Epidemiological data is sparse, but one American study noted a diagnosis of acute pericarditis in 1 in 1000 admissions.⁴ It is commoner in men than women,and is seen more frequently in adults than children.¹

Symptoms^1,3,5

Chest pain is the cardinal symptom. The pain may be dull, sharp, burning or pressing and may range from barely perceptible to severe. It may be felt in the substernal or precordial region and may radiate to the neck, trapezius ridge (especially the left) or shoulders. It may be aggravated by inspiration, swallowing, coughing and lying flat. It is relieved by sitting up and leaning forward.

Other symptoms can include a non-productive cough, tachypnoea, chills, fever and weakness. Dyspnoea and orthopnoea are particularly noticeable when cardiac tamponade develops (haemodynamic changes resulting from restriction to the movement of heart muscle, secondary to pericardial effusion). Abdominal pain occurs occasionally in children.

Signs

A pericardial friction rub is present on auscultation in 60-85% of cases.³
It has been described as a scratchy superficial sound, heard most strongly in the midline and lower left parasternal edge. It varies in strength with respiratory movements and is usually louder in inspiration. More than 50% of friction rubs have presystolic, systolic and diastolic components. 24% of patients with rubs are biphasic. This happens in tachycardia, when an early diastolic rub merges with the atrial component. Rarely, a monophasic rub can occur, particularly in patients with atrial fibrillation. It is sometimes mistaken for a murmur.

Clinically, the presence of a pericardial friction rub is pathognomonic - often a rub can be heard even when a pericardial effusion is present.¹ It is often intermittent and evanescent, so frequent examination should take place if it is absent, but clinical suspicion is high.³

Other signs can include tachypnoea, tachycardia, and fever.¹ Patients with tamponade may exhibit the Beck triad (hypotension, elevated systemic venous pressure often with jugular venous distention, and muffled heart sounds). Slowly developing tamponade may also result in pulsus paradoxus (defined as a 10 mmHg decrease in arterial systolic pressure with inspiration).⁶

Other causes of chest pain need to be excluded, in particular:¹

• Myocardial infarction or ischaemia
• Pleuritic pain
• Pulmonary infarction
• Peptic ulcer disease or oesophagitis.

ECG

Chest X-ray

An enlarged flask-shaped cardiac silhouette may be the first sign of a large pericardial effusion. This may not be evident in patients with small effusions (less than a few hundred millilitres) may present with a normal cardiac silhouette. In one study, pleural effusions were seen in 33% of patients. Approximately 75% of the effusions were left-sided only.¹

Blood Tests

The following may be useful as a minimal set of investigations:¹

• FBC with differential may show leukocytosis.
• Erythrocyte sedimentation rate and C-reactive protein levels are usually raised.
• U + E levels can be measured to evaluate for uraemia.
• Evaluate cardiac enzymes for associated myocarditis or myocardial infarction. In a recent study an elevated troponin I level was found in 32% of patients with viral or idiopathic pericarditis. The troponin I level was related to the extent of myocardial inflammation but was not a negative prognostic marker.⁸

Resolving acute pericarditis (one week or less) may need no further investigations. However, in the event of persisting symptoms, and before labelling the condition 'idiopathic' the following may be clinically indicated:^1,5

• Blood cultures
• Tuberculin testing with sputum for acid-fast bacilli
• Antistreptolysin titre
• Rheumatoid factor, antinuclear antibody, and anti-DNA values
• Thyroid function (if significant pericardial effusion is present)
• Antibodies for HIV, coxsackie virus, influenza virus and echovirus
• Examination of pericardial fluid or pericardial biopsy specimens for fungi and malignant cells
• Pericardial biopsy for culture and microscopic examination in cases of recurrent or persistent effusion

Echocardiography

This is appropriate if pericardial effusion or tamponade is suspected.¹ M-mode demonstrates persistence of the echo-free space between the parietal pericardium and the epicardium during the cardiac cycle. Fluid adjacent to the right atrium is an early indicator of an effusion. Other causes of echo-free space that must be considered include pericardial masses, pleural effusion and epicardial fat.

CT or MRI

This is helpful in cases of diagnostic doubt.¹ A pericardial thickening >5mm may be seen. When pericardial thickening or fluid cannot be demonstrated, the diagnosis of restrictive cardiomyopathy should be considered.

Pulse oximetry waveform

This is a non-invasive method of diagnosing pulsus paradoxicus which is particularly useful in paediatric patients.^9,10

Surgical procedures

Pericardiocentesis under echocardiographic monitoring is occasionally used in cases of diagnostic difficulty, especially in cases of impending tamponade.¹ The majority of cardiologists would recommend this if there was echocardiographic evidence of right atrial or ventricular diastolic collapse, irrespective of whether clinical signs of tamponade were present.¹¹ If tamponade recurs, a pericardial biopsy should be performed with histologic and bacteriologic examination. Endomyocardial biopsy and cardiac catheterisation may also be indicated in cases of diagnostic difficulty.

Patients with suspected pericarditis should be admitted to hospital to exclude other life-threatening causes of chest pain, and assess the patient for evidence of haemodynamic instability, the onset of complications (e.g. tamponade) and the development of adverse prognostic signs. The latter include fever of more than 38°C, trauma, anticoagulation therapy, myopericarditis, subacute onset, immunosuppression, severe pericardial effusion and cardiac tamponade. In their absence, patients can be followed up on an outpatient basis.^1,12

Treatment should be provided for the underlying cause. For viral or idiopathic cases, the following have been shown to effective:

• NSAIDs - e.g.indometacin 50 mg 8 hourly.¹³
• Colchicine - there is evidence that this reduces the incidence of recurrence, and may be ultimately considered first line in patients with idiopathic pericarditis.¹⁴
• Cessation of possible causative drugs (e.g. phenytoin).⁵
• Anticoagulants should be avoided unless the pericarditis is secondary to acute MI, as they can cause intrapericardial bleeding and possibly fatal tamponade.⁵
• Bacterial or mycotic infections should be treated with appropriate antimicrobials.
• Uraemic pericarditis may respond to increased frequency of dialysis, systemic or local steroid therapy, and aspiration. therapy. Intrapericardial triamcinolone may be useful.⁵
• Immediate pericardiocentesis may be required when cardiac tamponade develops rapidly with falling BP and shock develops. This may be done without echocardiographic guidance in an emergency, but open thoracotomy is safer.⁵
• Symptomatic constrictive chronic pericarditis usually requires pericardial resection. Recurrent or persistent symptomatic effusive pericarditis may be treated with balloon pericardiotomy, a surgical pericardial window, or sclerosis with tetracycline. Asymptomatic effusions of unknown cause may simply require observation.
• Recurrent pericarditis - idiopathic pericarditis or pericarditis due to cardiac surgery, MI, or trauma, may recur. Colchicine, 1 mg a day, may be helpful,¹³ in addition to NSAIDs.⁵ The role of steroids is controversial.^5,14 Uncommonly, pericardial resection is required.

This will depend on the aetiology. Most viral and idiopathic cases follow a self-limiting course within one to three weeks. Not unexpectedly, pericarditis associated with neoplasm, purulent effusion or tuberculosis has a complicated course and worse outcome.⁵