The presentation and course of inflammatory pericarditis depend on its cause, but most syndromes have associated chest pain, which is usually pleuritic and postural (relieved by sitting). The pain is substernal but may radiate to the neck, shoulders, back, or epigastrium. Dyspnea may also be present and the patient is often febrile. A pericardial friction rub is characteristic, with or without evidence of fluid accumulation or constriction. The presentation of tuberculous pericarditis tends to be subacute, but nonspecific symptoms (fever, night sweats, fatigue) may be present for days to months. Pericardial involvement develops in 1–8% of patients with pulmonary tuberculosis. Symptoms and signs of bacterial pericarditis are similar to those of other types of inflammatory pericarditis, but patients appear toxic and are often critically ill. Uremic pericarditis can present with or without symptoms; fever is absent. Often neoplastic pericarditis is painless, and the presenting symptoms relate to hemodynamic compromise or the primary disease. At times the pericardial effusion is very large, consistent with its chronic nature. Post-MI or postcardiotomy pericarditis (Dressler syndrome) usually presents as a recurrence of pain with pleural-pericardial features. A rub is often audible, and repolarization changes on the ECG may be confused with ischemia. Large effusions are uncommon, and spontaneous resolution usually occurs in a few days. Dressler syndrome occurs days to weeks to several months after MI or open heart surgery, may be recurrent, and probably represents an autoimmune syndrome. Patients present with typical pain, fever, malaise, and leukocytosis. Rarely, other symptoms of an autoimmune disorder, such as joint pain and fever, may occur. Tamponade is rare with Dressler syndrome after MI but not when it occurs postoperatively. The clinical onset of radiation pericarditis is usually within the first year but may be delayed for many years; often a full decade or more may pass before constriction becomes evident.
The diagnosis of viral pericarditis is usually clinical, and leukocytosis is often present. Rising viral titers in paired sera may be obtained for confirmation but are rarely done. Cardiac enzymes may be slightly elevated, reflecting an epicardial myocarditis component. The echocardiogram is often normal or reveals only a trivial amount of extra fluid during the acute inflammatory process. The diagnosis of tuberculous pericarditis can be inferred if acid-fast bacilli are found elsewhere. The tuberculous pericardial effusions are usually small or moderate but may be large when chronic. The yield of mycobacterial organisms by pericardiocentesis is low; pericardial biopsy has a higher yield but may also be negative, and pericardiectomy may be required. If bacterial pericarditis is suspected on clinical grounds, diagnostic pericardiocentesis can be confirmatory. In uremic patients not on dialysis, the incidence of pericarditis correlates roughly with the level of blood urea nitrogen (BUN) and creatinine. The pericardium is characteristically “shaggy” in uremic pericarditis, and the effusion is hemorrhagic and exudative. The diagnosis of neoplastic pericarditis can occasionally be made by cytologic examination of the effusion or by pericardial biopsy, but it may be difficult to establish clinically if the patient has received mediastinal radiation within the previous year. Neoplastic pericardial effusions develop over a long period of time and may become quite huge (more than 2 L). The sedimentation rate is high in post-MI or postcardiotomy pericarditis and can help confirm the diagnosis. Large pericardial effusions and accompanying pleural effusions are frequent. Myxedema pericardial effusions due to hypothyroidism usually are characterized by the presence of cholesterol crystals within the fluid.
The ECG usually shows generalized ST and T wave changes and may manifest a characteristic progression beginning with diffuse ST elevation, followed by a return to baseline and then to T-wave inversion. Atrial injury is often present and manifested by PR depression, especially in the limb leads. The chest radiograph is frequently normal but may show cardiac enlargement (if pericardial fluid is present), as well as signs of related pulmonary disease (eFigure 10–79). Mass lesions and enlarged lymph nodes may suggest a neoplastic process. About 60% of patients have a pericardial effusion (usually mild) detectable by echocardiography. MRI and CT scan can visualize neighboring tumor in neoplastic pericarditis. A screening chest CT or MRI is often recommended to ensure there are no extracardiac diseases contiguous to the pericardium. A consensus statement from the American Society of Echocardiography proposes adding an elevated CRP and late gadolinium enhancement of the pericardium to confirmatory criteria for the diagnosis of pericarditis. There are data that the degree of quantitative delayed enhancement of the pericardium is associated with a higher rate of recurrent pericarditis. PET scanning can also be used to help define pericardial inflammation.