Pericarditis
Fabio R. Tavora, M.D., Ph.D.
Allen P. Burke, M.D.
Incidence and Clinical Findings
Pericardial inflammation can be the result of infections, autoimmune disease, renal failure, radiation, malignancy, or trauma (Tables 167.1 and 167.2). In most cases, no specific etiology is found. Pericarditis is frequently associated with pleuritis, as the pericardium and pleura are contiguous.
Acute pericarditis accounts for ˜1 in 1,000 hospital admissions and causes chest pain and ST-segment elevation in 1% of patients admitted to the emergency room.37 The clinical presentation is characterized by chest pain, dyspnea, and fever. In children, abdominal pain may be the presenting symptom. In addition, a pericardial friction rub tachypnea is present, and if the fluid accumulation causes cardiac tamponade, hypotension and jugular venous distention can occur. The diagnosis of pericardial effusion can be easily detected by echocardiogram, which is capable of detecting an excess of 50 mL of fluid, beyond the physiologic amount in the pericardial sac.38
Acute idiopathic pericarditis (with or without associated myocarditis) is usually treated with anti-inflammatory drugs unless there is significant fluid accumulation necessitating pericardiocentesis or progressive fibrosis requiring pericardial resection. Recurrent pericarditis may be caused by recurrent viral infection or may represent an isolated autoimmune condition. In cases of recurrence, exclusion of bacterial and viral infection by PCR of pericardial fluid has been recommended before initiating aggressive anti-inflammatory treatment, which includes steroids, colchicine, and other anti-inflammatory agents.39
TABLE 167.1 Organisms Implicated in Infectious Pericarditis | ||||||||||
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Etiology
Idiopathic or nonspecific pericarditis is by far the most common cause of acute pericarditis, accounting for 199 of 213 patients admitted for acute pericarditis in one series.40 Many idiopathic cases are believed to be viral/postviral analogous to myocarditis.41 The most common suspected and proven viral agent is cytomegalovirus, especially in immunocompromised patients; in immunocompetent individuals, coxsackievirus A and B, echovirus, and adenovirus have been implicated (Table 167.1). Viral detection may be difficult and may depend on PCR of pericardiocentesis fluid.
The clinical differential diagnoses of pericarditis are pericardial neoplasms, myocardial infarction, radiation therapy, tuberculosis and other mycobacterial infection, bacterial and fungal pericarditis, viral infections, and connective tissue diseases.
Inflammatory noninfectious pericarditis can occur by involvement of systemic collagen diseases, most commonly lupus erythematous and rheumatoid arthritis. Pericarditis can present in the acute phases of the diseases or be subclinically detected as small effusions.
Bacterial pericarditis including the purulent form is uncommon. Risk factors include immunodeficiency, recent thoracic surgery, pneumonia, meningitis, chest trauma, or malignancy. Staphylococci, meningococci, pneumococci, and Haemophilus influenzae are the most common etiologic agents. Uncommonly, pericarditis can represent extension from endocarditis.
About 5% to 7% of patients with pericardial effusion will bear a neoplastic process involving the pericardial space.42 Metastatic tumors are by far more common than primary pericardial tumors, and lung tumor, breast tumor, and lymphoma are the three prevalent tumors that have a predilection to the pericardium. In cases of primary pericardial mesothelioma or pleural mesotheliomas involving the pericardium, constrictive pericarditis can occur. Cytologic aspirate material and biopsy have a high specificity and moderate sensitivity in cases of effusions unexplained but other causes or in patients unresponsive to medical treatment with NSAIDs.
TABLE 167.2 Causes of Noninfectious Pericarditis | ||||||||||||||
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 FIGURE 167.1 ▲ Chronic fibrinous pericarditis. A. The epicardial surface is shaggy, with a brown exudate. B. The pericardium shows the brown exudate on the visceral surface. |
Pathologic Evaluation of Acute Pericarditis
Pathologic evaluation of pericarditis and pericardial disease includes analysis and cytology of pericardiocentesis fluid and routine histopathology of pericardial biopsies resulting from pericardiotomy with biopsy or percutaneous pericardial biopsy. Biopsy can be undertaken by direct visualization by video or pericardiotomy. Pericardial fluid is analyzed similar to pleural or peritoneal fluid including red blood cell count, white blood cell count with differential, pH, total protein, glucose, lactic acid dehydrogenase, culture for viruses, bacteria and fungi, Gram stain and stain for acid-fast bacilli, and cytologic examination.
The histologic findings of acute pericarditis include acute and chronic inflammation with loss or mesothelial lining and fibrin deposition. Biopsy greatly increases the sensitivity for specific causes such as malignancies and granulomatous processes (sarcoid and infection, especially tuberculosis). Cytologic findings in viral or autoimmune (lymphocytic fibrinous pericarditis) include a paucity of neutrophils, and abundant lymphocytes, macrophages, and reactive mesothelial cells. The differential diagnosis of acute pericarditis includes metastatic carcinoma and other malignancies, which typically result in a hemorrhagic effusion. An abundance of neutrophils or granulomas points to a bacterial or mycobacterial infection, respectively.
In patients with suspected infectious pericarditis, PCR tests for bacterial, mycobacterial, fungal, protozoal, and viral etiologies complement routine culture.43,44,45 Serologic tests to exclude lupus erythematosus, rheumatoid arthritis, and acute rheumatic fever may be performed in selected patients based on history and clinical findings.
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