Middle East respiratory syndrome-coronavirus
Herpes simplex virus
Hepatitis B virus
Human immunodeficiency virus
Staphylococcus aureus a
Streptococcus pneumoniae a
Haemophilus influenzae a
Neisseria meningitidis a
Mycobacterium avium complex
|Collagen vascular diseases|
|Systemic lupus erythematosus|
|Acute myocardial infarction|
Chest trauma (penetrating or blunt)
|Familial Mediterranean fever|
Microbial pathogens may gain entry into the pericardial space by direct extension from the chest (e.g., in the context of pneumonia or mediastinitis), through direct extension from the heart itself (e.g., endocarditis), through hematogenous or lymphatic spread (bacteremia or viremia), or via direct inoculation (e.g., surgery, trauma). The presence of an adjacent or otherwise concurrent infection, as well as a history of recent surgery or trauma, may provide significant clues to specific pathogens. For example, purulent pericarditis due to N. meningitidis has been diagnosed in patients with concurrent bacterial meningitis. In a review of 162 children with purulent pericarditis, all but 10 patients had at least one additional site of infection, suggesting that isolated cardiac disease occurs infrequently in those with purulent pericarditis. In cases where either S. aureus or H. influenzae type B was the responsible pathogen, pneumonia, osteomyelitis, and cellulitis were the most frequently identified additional sites of infection. Tuberculous pericarditis, however, usually occurs in the absence of identifiable pulmonary disease, suggesting that the pathogenesis involves the spread of mycobacteria from adjacent mediastinal lymph nodes into the pericardium.
The inflammatory response in the pericardial space leads to extravasation of additional pericardial fluid, polymorphonuclear white blood cells, and monocytes. During bacterial or fungal pericarditis, the inflammatory process may be sufficient to lead to loculation and fibrosis. Significant fibrosis may lead to constrictive pericarditis, which is manifest by signs and symptoms associated with compromised ventricular filling. The rapid accumulation of exudative fluid, as is often seen in purulent pericarditis, frequently leads to hemodynamic changes. Cardiac tamponade occurs when increased fluid within the pericardial space prevents adequate right atrial filling and leads to reduced stroke volume, low output cardiac failure, and shock. If the accumulation of pericardial fluid occurs more slowly, as is common with viral pericarditis, large amounts may be present without hemodynamic effect.
Symptoms and clinical manifestations
Chest pain is the most common presenting symptom of acute pericarditis. Due to the relationship between the phrenic nerve and pericardium, pain resulting from inflammation of the pericardium may be retrosternal with radiation to the shoulder and neck or may localize between the scapulae. Often, the pain is worsened by swallowing or deep inspiration or is positional and worsened when the patient is supine but lessened by leaning forward while sitting. Dyspnea is also a common presenting symptom. If pericarditis has resulted from contiguous spread of bacteria or fungi from an adjoining structure, the signs and symptoms of the primary infectious process may predominate. Purulent pericarditis due to a bacterial pathogen tends to be more acute and severe in nature, whereas viral pericarditis is typically of lesser severity. Symptoms of tuberculous pericarditis tend to be insidious in presentation.
In infants, the presenting signs and symptoms of pericarditis may be nonspecific and include fever, tachycardia, and irritability. Older children may complain of chest and/or abdominal discomfort. A study by Carmichael et al. in 1951 showed that more than half of patients diagnosed with “nonspecific” pericarditis of presumed viral origin described a respiratory illness preceding the diagnosis of pericarditis by 2 to 3 weeks.