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PATHOGENESIS

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The pericardium consists of two layers, the inner layer, or visceral pericardium, which is continuous with the outer tissue of the myocardium, and the parietal pericardium, which lines the surrounding mediastinal structures. Between the layers is a space that contains 10 to 15 mL of clear fluid in healthy children and 15 to 20 mL in adults. The pericardial tissue normally is thin and semitransparent. With inflammation, there is influx of fibrin, polymorphonuclear and mononuclear cells, and exudation of fluid into the pericardial space. Pericardial inflammation results in proliferation of fibrous tissue, neovascularization, and scarring, with consequent loss of elasticity and restriction of cardiac filling.
Purulent pericarditis frequently results from contiguous extension of pneumonia, empyema, suppurative mediastinal lymphadenitis, liver abscess, or cardiac conditions, such as myocarditis, myocardial abscess, and infectious endocarditis. Bacterial pericarditis also results from inoculation during bacteremia, as is commonly the pathogenesis in pericarditis due to S. aureus infection.
Enteroviruses are transmitted primarily by the fecal-oral route. After initial proliferation in the lymphoid tissues of the intestine, viremia can lead to disseminated or focal infection in skin, brain, meninges, heart, and pericardium. Pericarditis can be the sole manifestation of enteroviral infection or part of multiorgan infection. During an enteroviral epidemic there is a wide range of expression of disease; pericarditis affects only a small proportion of infected children.
Regardless of cause, acute pericarditis results in collection of fluid in the space between the visceral and parietal pericardium. Small increases in fluid production are clinically insignificant because they are effectively reabsorbed. Large increases in fluid secretion that exceed resorptive capacity may result in significant cardiac dysfunction. The mediastinal structures are so elastic that collections of 1 L or more of fluid in adults may not interfere with cardiac function. However, 200 to 300 mL of fluid accumulation, if rapid, can exceed maximal distensibility

TABLE 40-1 -- Causes of 163 Cases of Purulent Pericarditis, 1950–1977
Causative Organism
Number of Isolates (%)
Staphylococcus aureus
72 (44)
Haemophilus influenzae type b
35 (22)
Neisseria meningitidis
14 (9)
Streptococcus pneumoniae
9 (6)
Salmonella spp.
4 (3)
Escherichia coli
3 (2)
Othera
7 (5)
Unknown
17 (10)
Data from Feldman WE. Bacterial etiology and mortality of purulent pericarditis in pediatric patients: A review of 162 cases. Am J Dis Child 1979;133:641.

a Includes isolates of Klebsiella spp., S. pyogenes, “Paracolon spp.,” P. aeruginosa, S. epidermidis, Bacteroides spp., anaerobic streptococci, singly or in combination.

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of the pericardial sac. When this occurs, small incremental fluid accumulation causes a sharp increase in intracardiac pressure, which interferes with cardiac filling, leading to decreased stroke volume (cardiac tamponade); death from low cardiac output occurs if fluid is not removed.
Tuberculous pericarditis results from lymphatic spread from a focus in the lung or lymph nodes, or by hematogenous spread from a distant site. Granulomas of the pericardium containing M. tuberculosis develop initially and are followed by a serous or serosanguineous effusion containing lymphocytes and monocytes. The healing of tuberculous pericarditis results in deposition of fibrin and collagen, often leading to constrictive pericarditis.

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