AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Purulent pericarditis is a rare but life-threatening bacterial infection. Purulent pericarditis refers to pericardial fluid that is either culture positive regardless of appearance or purulent appearing despite, in some instances, inability to obtain a positive culture. This bacterial infection of the pericardium produces pericardial effusion that, if untreated, can lead rapidly to hemodynamic collapse, tamponade, and death. The signs of bacterial pericarditis are nonspecific; thus, a high index of suspicion is required to institute life-saving therapy. Proper treatment requires appropriate antibiotics and pericardial drainage.

Pathophysiology

The pericardium, which is composed of visceral and parietal layers, envelops the heart and great vessels. The pericardium provides a membrane barrier that protects the heart from infection, limits acute myocardial distention, decreases friction, and modulates ventricular interdependence. In healthy adults, the pericardial space contains approximately 20 mL of fluid, which has the appearance of a plasma ultrafiltrate.

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. Primary infection of the pericardium is rare. With inflammation, the pericardium becomes permeable to protein, and fluid accumulates between the visceral and parietal layers. Because the pericardium has a limited ability to stretch acutely, rapid accumulation of fluid leads to increased intrapericardial pressure and hemodynamic compromise.

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. Initially, an increased ejection fraction and tachycardia maintain cardiac output. When these mechanisms fail, systemic vascular resistance rises to maintain blood pressure, 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.

With treatment, purulent pericarditis usually resolves without sequelae. Some patients may develop constrictive pericarditis.

Frequency

United States

Bacterial pericarditis is a rare disease. Its incidence appears to be decreasing, perhaps because of earlier treatment of primary infections and availability of Haemophilus influenzae immunization.

International

Compared with the United States, bacterial pericarditis may occur more frequently in developing nations. This increased incidence has been associated with delay in diagnosis and treatment of serious bacterial infections, malnutrition, and overcrowding.

Mortality/Morbidity

• Without treatment, the mortality rate of bacterial pericarditis approaches 100%. Treatment with antibiotics and pericardial drainage decreases the mortality rate to 2-20% in modern case series. Treatment without early and adequate pericardial drainage significantly increases the risk of death. Other risk factors for increased mortality include patients presenting with tamponade or myocardial involvement, delays in diagnosis and/or institution of therapy, infection with Staphylococcus aureus, and malnutrition.
• Constrictive pericarditis is an infrequent sequel of purulent pericarditis. Signs can develop as early as 15 days after onset of the acute illness. Pericardiectomy usually resolves the symptoms.

Sex

Purulent pericarditis affects both sexes nearly equally.

Age

• Most cases of purulent pericarditis occur in children younger than four 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.

CLINICAL

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History

• Patients are acutely ill and exhibit symptoms of sepsis. Acute purulent pericarditis in an infant is a medical emergency. Rapid evaluation, diagnosis, and treatment is essential.
• • Symptoms are often nonspecific and include fever, respiratory distress, and tachycardia out of proportion to the degree of fever.
  • Children may complain of abdominal discomfort.
• Most patients have preceding or concurrent infection that is the source of pericarditis. These infections include the following:
• • Pneumonia
  • Meningitis
  • Acute osteomyelitis
  • Acute arthritis
  • Soft tissue infections
  • Pericarditis rarely can complicate neonatal sepsis.
• Precordial chest pain in not a frequent symptom, especially in young children.
• • The pain, if present, may be sharp or dull.
  • Supine position, chest wall motion, or coughing may worsen the pain.
  • Sitting forward may relieve the pain.

Physical

Infants with bacterial pericarditis generally are very ill and can present with signs of severe sepsis and shock. A high index of suspicion is required.

• Tachypnea and tachycardia out of proportion to fever is characteristic of both purulent pericarditis and acute myocarditis.
• Purulent pericarditis should be suspected in any infant who appears to have sepsis and has an abnormal cardiovascular examination.
• Cardiac auscultation
• • Classic findings of pericarditis include muffled heart sounds and a friction rub.
  • A friction rub is a high-pitched scratchy sound that can occur in any combination of systole, mid diastole, and late diastole.
  • A friction rub is unlikely in the presence of a large pericardial effusion.
  • Rub may vary with patient position or the respiratory cycle, and it may be transient.
  • Infants with purulent pericarditis seldom demonstrate a rub.
  • Diastolic filling sounds may be heard.
• Signs of venous congestion may be present, including hepatomegaly and jugular venous distention. Jugular veins are difficult to assess in infants.
• Tamponade
• • Tamponade occurs when enough pericardial fluid accumulates to impair diastolic ventricular filling and, subsequently, cardiac output.
  • Tamponade can present rapidly with hypotension, soft heart tones of poor quality, and signs of venous congestion indicating acute cardiac decompensation.
  • Alternatively, tamponade can develop more insidiously, presenting a picture of right heart failure.
  • Signs of tamponade include dyspnea, tachycardia, narrow pulse pressure, pulsus paradoxus, and venous congestion.
• Pulsus paradoxus
• • Pulsus paradoxus is a decrease in systolic blood pressure more than 10 mm Hg with inspiration.
  • Any significant pericardial constriction produces this finding. Other causes of pulsus paradoxus include hypovolemia and either a large or small airway obstruction like with epiglottitis or asthma.

Causes

• Most cases of purulent pericarditis are associated with a preexisting or concurrent infection such as pneumonia with or without empyema, meningitis, osteomyelitis, arthritis, or other soft tissue infections.
• 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 are Staphylococcus aureus, H influenzae, Neisseria meningitidis, and Streptococcus pneumoniae.
• Less common organisms include gram-negative enteric bacilli, Pseudomonas aeruginosa, Salmonella species, Francisella tularensis, and anaerobic bacteria and fungi (Histoplasma species, coccidioidomycosis, blastomycosis, Aspergillus species, Candida species).
• S aureus
• • This is the most common organism in children, causing approximately 40% of cases.
  • Pericarditis occurs concomitantly with pneumonia with empyema and less often 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.
  • Within the first 3 months after cardiac surgery, S aureus is the most common cause of purulent pericarditis.
• H influenzae
• • This 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: At one time, S pneumoniae was the leading cause of purulent pericarditis, but it has become much less common perhaps because of widespread use of antibiotics.
• Other organisms
• • 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.

DIFFERENTIALS

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Other Problems to be Considered

Diseases associated with pericardial effusion and tamponade
Infectious pericarditis (fungal pericarditis)
Malignancy
Autoimmune disorders
Connective tissue diseases (see Mixed Connective Tissue Disease, Undifferentiated Connective Tissue Disease)
End-stage renal disease (uremic pericarditis)
Chest trauma (see Penetrating Chest Trauma, Blunt Chest Trauma)
Extravasation from central venous catheter

WORKUP

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Lab Studies

• CBC
• • CBC usually shows leukocytosis with predominance of immature polymorphonuclear leukocytes.
  • Lymphocytosis suggests viral or idiopathic etiology.
• Blood culture: Results are positive in more than one half of patients with bacterial pericarditis.
• Erythrocyte sedimentation rate (ESR) and other acute phase reactants are elevated with purulent pericarditis.

Imaging Studies

• Chest radiography
• • A rapidly enlarging cardiac silhouette with a water-bottle appearance without accompanying increase in pulmonary vascular markings strongly suggests a pericardial effusion.
  • Consider purulent pericarditis in an infant or child with sepsis and cardiomegaly.
• Echocardiography
• • Echocardiography is the imaging modality of choice for rapid accurate identification of a pericardial effusion and its size and distribution.
  • By 2-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 exist, but none are completely sensitive or specific. The echocardiogram must be considered in relation to the clinical picture when making the diagnosis of tamponade.
  • Common criteria of tamponade on echocardiograph include right atrium (RA) collapse at end diastole that continues into systole, right ventricle (RV) 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.
  • Echocardiography is useful in guiding pericardiocentesis. 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 echocardiogram.

Other Tests

• Electrocardiography
• • Most patients exhibit at least 1 ECG abnormality. ECG abnormalities depend on the amount of effusion and the presence of superficial myocardial injury. A normal ECG does not exclude the diagnosis of acute pericarditis. Typical findings include ST segment elevation and low voltage QRS complexes.
  • Pericardial fluid can produce low voltage QRS complexes because of a dampening effect of the fluid between the chest wall and myocardium.
  • Most patients have ST elevation (usually in leads I, II, V5, and V6).
  • 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.
  • Four classic stages of ECG changes are described in acute pericarditis; however, many patients will not exhibit all 4 stages. The stages are as follows:
    1. ST segment elevation and PR segment may be depressed.
    2. ST segment still is elevated but returning 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.

Procedures

• Pericardiocentesis
• • Definitive diagnosis of purulent pericarditis requires direct examination of pericardial fluid.
  • Pericardiocentesis is safest when performed in a controlled environment, such as the catheterization laboratory or ICU.
  • ECG, blood pressure, and oximetry monitoring is necessary.
  • The procedure is associated with morbidity and should be performed or supervised by an experienced physician.
  • Sedation is desirable unless the patient is unconscious or extremely unstable. Pericardiocentesis in a struggling patient is dangerous.
  • Some operators prefer to use ECG monitoring of needle advancement by clipping the V₁ lead to the needle. This technique is cumbersome and is not often employed. If visualization is desired, echocardiography or fluoroscopy guidance is preferred.
  • A pericardial pigtail catheter may be placed using a modified Seldinger technique. The use of a pigtail catheter reduces the risk of dislodgment and myocardial puncture. Additionally, the pigtail catheter may be left in place to provide continuous and potentially definitive pericardial drainage.
  • During pericardiocentesis, bloody fluid often is obtained that may be blood from a myocardial puncture or bloody pericardial fluid. Pericardial fluid fails to clot and has a hematocrit that is much lower than the patient's hematocrit.
  • Potential complications of pericardiocentesis include arrhythmias, laceration of coronary arteries with subsequent hemopericardium and tamponade, pneumothorax, and myocardial perforation.
  • Careful handling of pericardial fluid is required to properly identify etiologic agents for pericardial effusion.
  • Culture fluid for aerobic and anaerobic organisms, fungi, miliary tuberculosis, and viruses.
  • Approximately 50-60% of patients with purulent pericarditis have positive pericardial fluid cultures.
  • Antigen detection tests can be helpful in patients who have received antibiotics.
  • If malignancy is suspected, other studies include cell count and differential, Gram stain, and cytology.
  • The effusion of purulent pericarditis usually has a high WBC with predominately polymorphonuclear cells.
  • Viral pericarditis produces a lymphocytic picture. Protein and lactate dehydrogenase (LDH) often are sent, although both usually are elevated in most types of pericarditis.

TREATMENT

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Medical Care

Proper treatment of life-threatening illness requires proper antimicrobial therapy, pericardial decompression and drainage, and intensive supportive care.

• Antibiotics
• • Until a definitive agent is identified, empiric therapy includes antibiotics to treat both S aureus and gram-negative bacilli.
  • Initial antibiotics should include a combination of penicillinase-resistant penicillin and third-generation cephalosporin.
  • In areas of high antibiotic resistance, consider the use of vancomycin and a third-generation cephalosporin.
  • Include an aminoglycoside if the patient is postoperative from cardiac surgery, is immunocompromised, or has a genitourinary coinfection.
  • Duration of therapy is empiric but generally continues for 3-4 weeks with an antibiotic specific to the organism isolated.
• Pericardial drainage
• • Although needle pericardiocentesis may be life saving in tamponade and confirming the diagnosis, it rarely provides complete and long-lasting resolution of the effusion.
  • Avoid repeated attempts at needle pericardiocentesis because they are associated with increased morbidity rates.
  • Open surgical drainage has been used in most cases of purulent pericarditis.
  • Continuous drainage using specialized pericardial catheters and echographic monitoring has had reported success in treating bacterial pericarditis. However, the pericardial fluid may be too thick or loculated to be drained adequately by a catheter.
  • Delay in adequate pericardial drainage is associated with increased mortality rates.
• Supportive care
• • Almost all patients require intensive supportive care.
  • In patients with tamponade, supportive therapies are of little or no benefit until emergent pericardial drainage is performed.
  • Drugs that depress the heart rate, produce vasodilatation, or decrease intravascular volume are contraindicated because they further compromise cardiac output. Do not administer digoxin to an infant with purulent pericarditis who shows signs of congestive heart failure.
  • Application of positive pressure mechanical ventilation and positive end-expiratory pressure (PEEP) must be performed carefully because the increased intrathoracic pressure can lead to lethal falls in ventricular preload and worsened shock.
  • Although systolic function of the heart may not be depressed, inotropic agents may be required to treat hypotension that persists after pericardial drainage.
  • Plasma volume expansion is helpful in maintaining cardiac output.

Surgical Care

• Pericardial drainage
• • If pericardiocentesis is unsuccessful in resolving tamponade, emergent surgical drainage is indicated.
  • Surgical drainage is indicated in most patients after the acute emergency resolves.
  • Delay in adequate pericardial drainage is associated with increased mortality rates.
  • A variety of surgical procedures have been employed to provide adequate pericardial drainage, and optimal approach is controversial. Techniques for drainage include placement of a large bore subxiphoid drainage tube (with or without irrigation), creation of a pericardial window and placement of a drain, or pericardiectomy.
  • Proponents of pericardiectomy argue that thick clots and fibrin will not be removed through a tube and that it prevents the possibility of late pericardial constriction and recurrent tamponade.
• Pericardiectomy: Late pericardiectomy may be required in the rare patient who develops constrictive pericarditis as a complication of the infection.

Consultations

• Critical care medicine: Most patients with bacterial pericarditis present with severe hemodynamic compromise. Patients should be referred to specialists proficient in the use of vasoactive agents and mechanical ventilation.
• Cardiology: Patients with cardiomegaly and cardiovascular compromise require cardiology consultation and echocardiography to rule out myocardial or pericardial disease.
• Cardiovascular surgery: Emergent consultation with a cardiovascular surgeon is warranted in patients who have incomplete resolution of pericardial tamponade despite pericardiocentesis. Consultation should be considered in patients with recurrent effusions or constrictive pericarditis.

Activity

No activity restrictions are required in patients who have recovered from bacterial pericarditis.

MEDICATION

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Drug Category: Antibiotic agents

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Initial empiric coverage requires a combination of a penicillinase-resistant penicillin and third-generation cephalosporin. In areas of high antibiotic resistance, substitute vancomycin for the penicillin antibiotic.

FOLLOW-UP

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Further Inpatient Care

• Almost all patients have critical illness and require admission to an ICU.

Further Outpatient Care

• Once the patient has recovered from the acute infection, follow-up with a cardiologist is recommended to monitor for the development of constrictive pericarditis.

Transfer

• Critically ill patients with suspected purulent pericarditis require transfer to a tertiary pediatric center with cardiac, cardiac surgical, and critical care medicine expertise. Bacterial pericarditis is a life-threatening disease requiring a full complement of pediatric subspecialty care.
• Do not delay treatment of a critically ill infant in shock. Every hospital with echocardiographic capability should have someone who can perform an emergency pericardiocentesis.

Deterrence/Prevention

• Pericarditis often is preceded by other severe bacterial infections such as pneumonia with empyema. Proper treatment of those infections will prevent some cases of pericarditis.
• Immunization against H influenzae has led to dramatic decreases in the incidence of invasive H influenzae disease, including pericarditis.

Complications

• Acutely, serial ECGs may indicate the presence of occult arrhythmia, suggesting additional myocardial involvement.
• Most patients recover without significant complications.
• Constrictive pericarditis
• • Constrictive pericarditis is a rare complication. Acute constriction has been reported as early as 8 days but generally develops within weeks of diagnosis.
  • Patient symptoms include increased systemic venous pressure, weight gain, hepatomegaly, dyspnea, and decreased urine output. Presence of continued heart failure without a large cardiac silhouette suggests constriction.
  • After recovery from the acute infection, patients should have follow-up with a cardiologist to monitor for the development of constrictive pericarditis. Once identified, pericardiectomy is indicated.

Prognosis

• Bacterial pericarditis is a life-threatening infection with a high mortality rate unless timely therapy with antibiotics and pericardial drainage is instituted. Despite optimal therapy, the mortality rate can be as high as 20%.
• Patients who survive the acute infection generally do well, without long-term sequelae. Patients infrequently develop constrictive pericarditis requiring pericardiectomy.

Patient Education

• The following items should be disguised with patients and/or their families:
• • 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.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Bacterial pericarditis is a life-threatening illness that requires proper antibiotics and adequate pericardial drainage. The signs and symptoms are often nonspecific and subtle; thus, a high index of suspicion is required. Consider the diagnosis in any infant or young child with septic shock and abnormal cardiovascular physical findings.

MULTIMEDIA

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Media file 1:  15-lead ECG from a patient with bacterial pericarditis demonstrating marked ST elevation in multiple leads.
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Media type:  ECG

Media file 2:  Left: Chest radiograph in a patient with bacterial pericarditis showing 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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Media type:  X-RAY

Media file 3:  Apical 4-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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Media type:  Photo

Media file 4:  This ECG shows markedly decreased QRS voltage and electrical alternans (especially in lead V1)
	View Full Size Image
Media type:  ECG

REFERENCES

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• Dupuis C, Gronnier P, Kachaner J, et al. Bacterial pericarditis in infancy and childhood. Am J Cardiol. Oct 15 1994;74(8):807-9. [Medline].
• Feldman WE. Bacterial etiology and mortality of purulent pericarditis in pediatric patients. Review of 162 cases. Am J Dis Child. Jun 1979;133(6):641-4. [Medline].
• Jayashree M, Singhi SC, Singh RS, Singh M. Purulent pericarditis: clinical profile and outcome following surgical drainage and intensive care in children in Chandigarh. Ann Trop Paediatr. Dec 1999;19(4):377-81. [Medline].
• Kocheril AG, Luttmann C, Sadaniantz A. Pneumococcal pericarditis successfully treated with catheter drainage and intravenous antibiotics. Cathet Cardiovasc Diagn. Dec 1991;24(4):286-7. [Medline].
• Morgan RJ, Stephenson LW, Woolf PK, Singh M. Surgical treatment of purulent pericarditis in children. J Thorac Cardiovasc Surg. Apr 1983;85(4):527-31. [Medline].
• Sinzobahamvya N, Ikeogu MO. Purulent pericarditis. Arch Dis Child. Jul 1987;62(7):696-9. [Medline].
• Strauss AW, Santa-Maria M, Goldring D. Constrictive pericarditis in children. Am J Dis Child. Jul 1975;129(7):822-6. [Medline].
• Zahn EM, Houde C, Benson L, Freedom RM. Percutaneous pericardial catheter drainage in childhood. Am J Cardiol. Sep 1 1992;70(6):678-80. [Medline].

Article Last Updated: Mar 30, 2006