Bacterial, fungal, and viral infections may involve the pericardium (pericarditis), although viral pericarditis is more common than bacterial pericarditis in both children and adults.  Awareness of this disease has increased because of the introduction of noninvasive diagnostic techniques, such as echocardiography, computed tomography (CT), and cardiac magnetic resonance (CMR). The disease can be severe and even lethal, especially in children with immunosuppression. The infection may also involve the myocardium (myopericarditis).
The infection involves the pericardium and leads to accumulation of pericardial effusion that, if untreated, can lead rapidly to hemodynamic collapse, tamponade, and death. The fluid is generally purulent but can be serosanguineous; however, the causative agent can usually be identified from the pericardial fluid by culture or more sensitive tests (eg, polymerase chain reaction (PCR) or from samples of pericardial biopsy in cases that require open drainage of the fluid.
Workup of the patient with infective pericarditis may include laboratory studies, imaging studies (CT and CMR), electrocardiography (ECG), pericardioscopy, and pericardial biopsy. (See Workup.)
Management of pediatric infective pericarditis is influenced by the cause of the pericarditis. It may involve supportive care, pain control, and antibiotic therapy if necessary, as well as pericardiocentesis (indicated in symptomatic patients or when the etiology is in doubt and essential in suspected tamponade), pericardial drainage, or pericardiectomy as required. (See Treatment and Management.)
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The pericardium consists of 2 layers: the visceral pericardium (epicardium) and the parietal pericardium. These layers enclose the pericardial cavity (a potential space) between them. In healthy adults, this cavity contains approximately 20 mL of serous fluid, which has the appearance of a plasma ultrafiltrate and serves to lubricate the space. The pericardium provides a membrane barrier that protects the heart from infection, limits acute myocardial distention, decreases friction, and modulates ventricular interdependence.
Inflammation of the pericardium secondary to an infection leads to an increase in permeability to proteins and inflammatory cells, and fluid accumulates between the visceral and parietal layers (pericardial effusion). Because the pericardium has a limited ability to stretch acutely, rapid accumulation of fluid leads to increased intrapericardial pressure and hemodynamic compromise. The capacity of the pericardial space is influenced by its natural stiffness, and infection is known to increase this stiffness, contributing to the symptomatology. Studies show that persistent pericarditis triggers an autoimmune reaction to the myopericardial cells. The clinical manifestations may be due to the inflammatory process or the effusion or may be related to the underlying cause. Chest pain is related to pericardial inflammation and acute distention.
Significant collection of fluid in the pericardial cavity is a potentially dangerous accompaniment of infective pericarditis. The normal pericardium does not limit filling of the cardiac chambers either at rest or during exercise. When pericardial effusion occurs, chamber capacity may be reduced. Venous return may be severely limited and, therefore, cardiac output may be severely limited. Rapid accumulation of fluid is poorly tolerated, whereas slow accumulation may allow large amounts of pericardial fluid to collect without producing symptoms. Tamponade occurs when pericardial fluid accumulates rapidly enough or in sufficient volume to impair diastolic filling. During tamponade, all 4 cardiac chambers compete for space within the pericardium, producing increased systemic venous, pulmonary venous, and atrial pressures. Therefore, the clinical features result from limitation of cardiac output and elevated venous pressures.
Initially, an increased ejection fraction and tachycardia maintain cardiac output. When these mechanisms fail, systemic vascular resistance rises to maintain BP, and the pulse pressure narrows. Any further increase in pericardial volume compromises ventricular filling, producing systemic hypotension and cardiovascular collapse. Volume and rapidity of fluid accumulation both determine whether a pericardial effusion produces tamponade.
In healthy individuals, inspiration causes the systolic blood pressure (BP) to fall slightly, as a result of the greater volume of blood accommodated by the pulmonary vascular bed. This occurs despite inspiratory increase in venous return to the right heart.
In cardiac tamponade, right ventricular filling is maintained at the expense of restricted left ventricular filling, and the systolic BP falls further (>10 mm Hg). This exaggerated fall in systolic BP with inspiration is referred to as pulsus paradoxus. It is an important sign of cardiac tamponade; however, occasionally, severe respiratory distress of any cause (asthma, emphysema, pleural effusion) may give rise to this sign.
Often, a specific etiologic agent is not identified. These cases are often considered viral in origin. Common viral causes include the following:
Coxsackievirus B (most common cause)
Viral hepatitis B
Human herpesvirus 6
Hepatitis C virus 
Primary infection of the pericardium is rare. Bacterial pericarditis most commonly occurs as a direct extension of an infection from an adjacent pneumonia or empyema. Alternatively, a distant infection can hematogenously seed the pericardium. Patients recovering from thoracic, cardiac, or esophageal surgery are at risk for purulent pericarditis. Purulent pericarditis has been reported in patients recovering from traumatic injury.
The organisms that most commonly cause purulent pericarditis include the following:
Less common organisms include the following:
Gram-negative enteric bacilli
Fungi ( Histoplasma species, coccidioidomycosis, blastomycosis, Aspergillus species, Candida species)
S aureus is the most common cause of bacterial pericarditis in children, causing approximately 40-80% of cases. Within the first 3 months after cardiac surgery, S aureus is the most common cause of purulent pericarditis.
S aureus pericarditis occurs concomitantly in patients who have pneumonia with empyema and less often in patients with acute osteomyelitis or soft tissue abscess. Rarely, pericarditis is associated with S aureus endocarditis. Necrotizing infection and exotoxin production lead to increased incidence of shock and higher mortality risk.
H influenzae is the second most common organism listed in most reported pediatric case series of purulent pericarditis, although comprehensive data since the introduction of routine immunization is lacking. Infection of the upper or lower respiratory tract frequently precedes pericarditis caused by H influenzae. Purulent pericarditis may occur with H influenzae meningitis. H influenzae produces very thick fibrinopurulent exudate.
N meningitidis pericarditis occurs in approximately 5% of young adults with meningococcemia. The clinical course is often milder than with other causes of purulent pericarditis. Pericardial effusion can be detected at the onset of the illness or later in the course of the infection. Late onset effusions have a purulent appearance but are usually sterile. Whether this late appearing effusion represents an infection, hypersensitivity to an antibiotic, or an immunologic response to the primary infection is unclear.
S pneumoniae was the leading cause of purulent pericarditis at one time, but it has become a much less common cause, perhaps because of widespread use of antibiotics. Like other causes, many cases are associated with respiratory infections but also with S pneumoniae with hemolytic uremic syndrome.
Other unusual organisms, such as gram-negative enteric bacilli and anaerobes or fungi, are rare but should be considered in patients who are immunocompromised.
Aspergillus pericarditis arises as a result of pulmonary infection in patients who are immunocompromised. Patients have a very poor prognosis. Therapy includes long-term amphotericin B or itraconazole. Successful therapy relies on recovery of adequate immune function.
Mycoplasma pneumoniae pericarditis is associated with pulmonary disease. The effusion responds to erythromycin.
The frequency of viral pericarditis is not known; various studies have placed it between 12.5% and 60%. People of all ages are affected, and both sexes are affected. A recent report on acute pericarditis has indicated that the majority of cases (68%) are idiopathic; however, these could very well represent viral or postviral pericarditis.  Bacterial pericarditis is rare. Its incidence appears to be decreasing, perhaps because of earlier treatment of primary infections and the availability of H influenzae immunization, as well as the polyvalent pneumococcal vaccine. Bacterial pericarditis may occur more frequently in developing nations than in the United States. This increased incidence has been associated with delay in diagnosis and treatment of serious bacterial infections, malnutrition, and overcrowding.
Most cases of purulent pericarditis occur in children younger than 4 years. Infants may not present with typical or classic features. For example, in one study, no patient younger than 18 months had a friction rub. In infants, almost all cases of pericarditis have a bacterial etiology. Purulent pericarditis affects both sexes nearly equally.
Almost all patients with viral pericarditis without concomitant myocarditis recover completely if no serious acute complication occurs. Causes of death include cardiac tamponade and systemic involvement by the viral infection or the underlying disease. A small percentage of patients develop a chronic form of pericarditis that resembles chronic idiopathic pericarditis. Constrictive pericarditis rarely occurs after viral pericarditis.
Bacterial pericarditis, on the other hand, is a life-threatening infection with a high mortality rate unless timely therapy with antibiotics and pericardial drainage is instituted. Without treatment, the mortality rate of bacterial pericarditis approaches 100%. Even with optimal therapy with antibiotics and pericardial drainage, mortality rates of 2-20% have been reported in modern case series. Treatment without early and adequate pericardial drainage significantly increases the risk of death.
Other risk factors for increased mortality include tamponade or myocardial involvement, delays in diagnosis or delays in institution of therapy, infection with S aureus, and malnutrition.
Patients who survive the acute bacterial infection generally do well, without long-term sequelae. Infrequently, constrictive pericarditis may develop as a sequel of purulent pericarditis. Signs can develop as early as 15 days after onset of the acute illness. Pericardiectomy usually resolves the symptoms.
Educate the patient on the likelihood of recurrence and about the need to continue medications and for follow-up, as appropriate. In particular, the following items should be discussed with patients and/or their families in children with bacterial pericarditis:
Bacterial pericarditis is a life-threatening disease.
Proper treatment includes a prolonged course of antibiotics and drainage of the pericardium.
If the patient survives, prognosis is good.
If symptoms suggestive of congestive heart failure develop after treatment (eg, dyspnea, fatigue, weight gain), the patient should seek evaluation for possible constrictive pericarditis.
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