Pediatric Infective Pericarditis Workup

Workup of the patient with infective pericarditis may include laboratory studies, imaging studies, electrocardiography (ECG), pericardioscopy, and epicardial biopsy. Echocardiography and cardiac magnetic resonance imaging have key roles in the diagnosis, management, and prognostic outlook of pediatric inflammatory and/or infectious cardiac conditions. ^[2]

See Infective Endocarditis for more detailed information on this topic.

A complete blood cell (CBC) count  is performed. In cases of viral pericarditis, the CBC is usually within the reference range but may show relative lymphocytosis. In cases of bacterial pericarditis, the CBC usually reveals leukocytosis with predominance of immature polymorphonuclear leukocytes. Lymphocytosis may also reflect an idiopathic etiology.

Nasopharyngeal aspirate and stool samples should be obtained for viral isolation, and blood samples should be obtained for acute and convalescent viral titers.

Blood culture should be performed to help confirm or exclude bacterial infection. Cultures are positive in more than half of patients with bacterial pericarditis. Erythrocyte sedimentation rate (ESR) and other acute phase reactant levels are elevated in purulent pericarditis.

Other blood tests (eg, blood gas analysis and electrolyte, blood urea nitrogen, and glucose tests) may be required for acute-stage management.

Elevated troponin I levels have been reported in young adults with pericarditis, especially with effusion. This may indicate the coexistence of varying degrees of underlying myocarditis; however, it may not be prognostic. ^[19]

Laboratory examination of pericardial fluid should include cell count, Gram stain, and culture. Cytologic examination should be considered for patients with suspected malignancy or systemic lupus erythematosus. Polymerase chain reaction (PCR) tests for virus and Mycoplasma allows for more rapid identification in some cases.

Radiography demonstrates cardiomegaly, depending on the amount of fluid and presence of underlying myocarditis. A typical saclike appearance of the cardiac silhouette is characteristic of large effusions (see the image below).

Plain chest radiograph in a 2-year-old boy with viral pericarditis and massive pericardial effusion.

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Chamber enlargement is not observed.

A rapidly enlarging cardiac silhouette with a water-bottle appearance without accompanying increase in pulmonary vascular markings strongly suggests a pericardial effusion (see image below).

Left: Chest radiograph in a patient with bacterial pericarditis reveals cardiomegaly and left lower lobe infiltrate with marked increase in pulmonary vascular markings. Right: The same patient after placement of a pigtail pericardial catheter and pulmonary artery catheter.

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Consider purulent pericarditis or myocarditis in an infant or child with sepsis and cardiomegaly.

Echocardiography is the imaging modality of choice for rapid, accurate identification of a pericardial effusion and determination of its size and distribution (see the image below). ^{[2, 20]} The thickness of the pericardium and the amount of fluid can be quantified, and the effect of fluid on cardiac hemodynamics can be assessed. However, limitations of this imaging modality include a limited ability to characterize myocardial tissue anomalies (eg, inflammation, fibrosis), and limited quantitative evaluation of cardiac output and valve function. ^[2]

Two-dimensional echocardiograph shows a large pericardial effusion.

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On two-dimensional echocardiography, pericardial fluid appears as an “echo-free” space. With small effusions, fluid first appears posteriorly in the dependent portion of the pericardial sack. With larger effusions, fluid is found both anterior and posterior to the heart. Echogenic material may be observed in the pericardial fluid and may represent adhesions, clots, or fibrinous material.

Multiple echocardiographic indicators of cardiac tamponade are recognized, but none is completely sensitive or specific. Echocardiography findings must be considered in relation to the clinical picture when making the diagnosis of tamponade.

Common criteria of tamponade on echocardiography include right atrium collapse at end diastole that continues into systole (see the image below), right ventricle compression during diastole (especially with expiration), and marked respiratory variation in transvalvular flow velocities by Doppler echocardiogram. Reversal of systemic venous return flow can occur during diastole.

Apical four-chamber view from a patient with bacterial pericarditis. The large pericardial effusion (EF) appears as an echo clear space in this view surrounding the right atrium (RA) and left ventricle (LV). The RA wall is collapsed, indicating tamponade. The longer the duration of RA inversion into systole correlates with increasing hemodynamic severity.

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Echocardiography is useful in guiding pericardiocentesis. (See Treatment.) Visualizing the tip of the needle is helpful because echographic artifacts arising from the shaft of the needle may mislead the operator to the actual location of the needle tip. If needle position is uncertain, 5 mL (or less) of agitated saline may be injected for a contrast echocardiography.

Echocardiography is also helpful to assess for coexisting congenital heart defects and vegetations from infective endocarditis. ^{[9, 12]}

Computed tomography (CT) scanning of the chest can help confirm the thickness of the pericardial effusion, assess pericardial thickening, and also help to identify other abnormalities, such as mediastinal lymph nodes, that may point to an etiology.

Cardiac magnetic resonance imaging (CMRI) reveals similar findings and helps to assess cardiac function (especially right ventricular function) in the presence of coexisting myocarditis. Thus, CMRI is superior to echocardiography for characterizing myocardial tissue anomalies (eg, inflammation, fibrosis) quantitatively evaluating cardiac output and valve function. ^[2]

Most patients exhibit at least one electrocardiographic (ECG) abnormality. ECG abnormalities depend on the amount of effusion and the presence of superficial myocardial injury. Normal ECG findings do not exclude the diagnosis of acute pericarditis. Typical findings include ST-segment elevation and low-voltage QRS complexes.

Generalized elevation of the ST segment in leads with an upright T wave is the typical pattern of pericarditis, although this finding may not be apparent (see the image below).

A 12-lead ECG from a patient with bacterial pericarditis demonstrating marked ST elevation in multiple leads.

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Pericardial fluid can produce low-voltage QRS complexes because of a dampening effect of the fluid between the chest wall and myocardium. Such complexes may occur in the presence of a large effusion. However, an adult study showed greater frequency of low P-wave and T-wave voltages than low QRS voltages. ^[21]

Similarly, differentiation of ST-segment elevation on ECG from acute pericarditis could prove difficult from the normal variant early repolarization and early repolarization of left ventricular hypertrophy, ^[22] but clinical features could help.

Electrical alternans (ie, changes in the P, QRS, and T wave voltages) is very specific, although not sensitive, for large pericardial effusions. Electrical alternans results from the heart swinging in a large effusion (see the image below).

This ECG shows markedly decreased QRS voltage and electrical alternans (especially in lead V1)

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Four classic stages of ECG changes are described in acute pericarditis; however, many patients do not exhibit all four stages. The stages are as follows:

1. ST-segment elevation and PR segment may be depressed.

2. ST segment is still elevated, but the PR segment returns to baseline with decreased T-wave amplitude. PR segment is depressed.

3. ST segment returns to normal with T-wave inversion (may be incomplete in some cases).

4. ECG normalization occurs. T-wave changes may persist and do not necessarily indicate active disease.

Pericardiocentesis is required for all patients who have clinical evidence of cardiac tamponade or suspected bacterial pericarditis and for some patients with immunocompromise. Pericardiocentesis is also used as a diagnostic test in patients with a pericardial effusion of unknown cause. The volume of fluid present should be sufficient to allow for the removal of a reasonable portion for diagnostic purposes.

However, note the procedure is associated with morbidity and therefore should be performed by or supervised by an experienced physician. Pericardiocentesis is safest when performed in a controlled environment, such as the catheterization laboratory or intensive care unit (ICU). Electrocardiography (ECG), blood pressure, and oximetry monitoring is necessary. (See Pericardiocentesis for a description of the procedure.)

Laboratory examination of pericardial fluid should include a cell count, Gram stain, and culture. Cytologic examination should be considered for patients with suspected malignancy or systemic lupus erythematosus. Polymerase chain reaction (PCR) tests for virus and Mycoplasma allows for more rapid identification in some cases. Lactate dehydrogenase (LDH) and protein levels are often sent but are generally elevated in most types of pericarditis and do not add much diagnostic utility. Many times, bloody fluid is obtained and raises a concern for intracardiac puncture. Several findings can help exclude cardiac puncture, including echocardiographic images, a hematocrit value of the effusion lower than peripheral blood, and failure of the fluid to clot.

Pericardioscopy with epicardial biopsy is rarely required by may yield diagnostic information in tuberculous pericarditis. Instead, it is used to macroscopically visualize alterations of both the epicardium and the pericardium. The macropathology of the epicarditis and pericarditis can be observed in vivo.

The prerequisite is documentation of a large pericardial effusion. This procedure requires a separation of at least 5 mm between the epicardial and pericardial layers in diastole at the anterior side of the heart when echocardiographic imaging is performed from the subxiphoidal or third intercostal space.

After the pericardial effusion is punctured, introduce a 9-ft sheath using a guidewire under echocardiographic or fluoroscopic control. Aspirate the fluid and infuse 100-150 mL of saline warmed to body temperature into the pericardial sac. Use a flexible 8-ft fiberglass instrument (eg, Vantec, Baxter, Storz) and a rigid 110°, 8-ft endoscope (Storz) to visualize the pericardium and epicardium.

Fibrinous strands or increased vascular injection can be observed in viral, autoimmune, or idiopathic pericarditis or in idiopathic perimyocarditis. In the last three forms of pericardial effusion, only inflammatory cells are observed when the pericardial fluid is analyzed. Pericardial biopsy findings may reveal a viral etiology using antigen detection techniques. Definitive diagnosis of purulent pericarditis requires direct examination of pericardial fluid.