Pericardial Disease: Difference between revisions

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|bgcolor="F0F8FF"|'''''Pericardial Disease'''''

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The pericardium comprises two layers; the visceral layer that adheres to epicardial surface of the heart, and the parietal layer that surrounds most of the heart. Pericardial disease is common, and diagnosis is usually straightforward as the pericardium reacts to disruption by a wide variety of agents and processes in a relatively uniform manner. Typical presentation is with chest pain and fever, production of pericardial fluid with possible cardiac tamponade, or a constrictive pattern by thickening, retraction and calcification.  

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==Pericardial Disease - Acute==

===Cardiac Tamponade===

Acute inflammation of the pericardium may result from a wide variety of etiologies (Table 1), and typically presents with chest pain, a pericardial friction rub on auscultation, and repolarization changes on the electrocardiogram.   

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!Table 1. Causes of acute pericarditis

In 8 to 80% of patients, pericarditis recurs after a first episode of acute pericarditis. A continuous type, in which symptoms recur shortly after cessation of anti-inflammatory therapy, and an intermittent type, in which symptom-free periods of more than 6 weeks separate recurrences, can be distinguished. Frequently resulting from inadequate therapy or corticosteroid-use during the initial episode, subsequent recurrences are usually less severe. A recurrence should be treated according to the same procedures as for the first event. Pericardiectomy may be considered the last resort in severely refractory recurrent pericarditis, but its results are unpredictable. Prognosis of the disease is excellent, as severe complications are rare.  

Fluid accumulation in the pericardium, pericardial effusion, is a common finding on routine echocardiography, and is asymptomatic in the absence of inflammation or cardiac tamponade. It may result from any disease of the pericardium, or be iatrogenic. Most frequently it results from idiopathic pericarditis, malignancy, or iatrogenic defects (Table 2).  

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!Table 2. Causes of pericardial effusion

Treatment of pericardial effusion depends on the extent of symptoms, and the etiology underlying the effusion. Asymptomatic mild pericardial effusion (<10mm sum of echo-free spaces in anterior and posterior sacs) may be left untreated. Control echocardiography is indicated at 3-6 months. In moderate (10-20mm sum of echo-free space) to large effusions, a complete history, routine physical examination, ECG, chest radiography and routine blood analysis is indicated. Treatment is then based upon its expected etiology, standard treatment with aspirin or NSAIDs to relief pain, with invasive procedures indicated in case of tamponade with hemodynamic compromise or recurrent pericarditis as discussed previously. Specific etiologies of pericardial effusion must be managed accordingly.

====Chronic pericardial effusion====

Pericardial effusion is considered chronic when moderate to large effusions persist for at least 3 months. Resulting most frequently from idiopathic cause, intrapericardial pressure is frequently elevated in these patients, which may lead to unexpected tamponade in up to 30% of patients. Hence, pericardiocentesis is indicated to alleviate the fluid accumulation, and pericardiectomy should be considered when large effusions recur. Long term outcome is excellent with this approach.

The pericardial layers may become rigid, thickened, and may fuse, resulting in restriction of cardiac filling; constrictive pericarditis. In contrast to cardiac tamponade, where cardiac is hampered throughout diastole, cardiac filling is prohibited in the last two-thirds of diastole in constrictive pericarditis, with preserved abrupt filling in early diastole.

Any form of pericarditis may end in constrictive pericarditis, presenting with chronic fatigue, dyspnoea, jugular distension, proto-diastolic pericardial knock, hepatomegaly, ascites, peripheral oedema, and pleural effusion. Atrial fibrillation is a common finding, and diffuse flattened or negative T-waves are usually present. These suggestive clinical findings, in addition to a physiology of restriction or constriction on echocardiography, and the presence of a thickened pericardium provide the diagnosis. However, a thickened pericardium may be absent, which does not rule out constrictive pericarditis. Pericardiectomy is the only effective treatment, which should be instituted shortly after diagnosis, as surgical mortality increases with increasing age and functional impairment.

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!colspan="2"|Table 3.  Differential diagnosis between chronic constrictive pericarditis and restrictive cardiomyopathy

Clinical and hemodynamic features of constrictive pericarditis may dissipate spontaneously, which is seen commonly (20%) in idiopathic acute pericarditis with effusion, but may also be seen in tuberculous and purulent pericarditis. Hence, a primarily conservative approach may alleviate the need for epicardiectomy.

===Infectious pericarditis===

Weeks to months after myocardial infarction, pleuropericarditis of autoimmune nature may prevail, termed Dressler’s syndrome. However, this syndrome is rare, and treatment with corticosteroids yields a good prognosis.

Lung cancer is the most frequent cause of neoplastic pericarditis. Cardiac tamponade in patients with a history of malignancy, in the absence of inflammatory signs indicates a possible malignant etiology, as is lack of response to NSAIDs in this patient group. When the effusion is indeed of malignant origin (approximately 40% of cases), treatment aims at alleviation of symptoms and the prevention of recurrences. A balance should be sought between pericardiocentisis in which recurrence is frequent, and pericardiectomy, which may be overly aggressive in this critically ill subset of patients.