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Pediatric Infective Pericarditis Clinical Presentation

  • Author: Poothirikovil Venugopalan, MBBS, MD, FRCPCH; Chief Editor: Stuart Berger, MD  more...
 
Updated: Jan 07, 2016
 

History

Viral pericarditis

Fever and chest pain are usual presenting symptoms. Low-to-moderate fever usually occurs but may be absent at the time of presentation. Patients generally appear less toxic than those with bacterial pericarditis but may shows signs of shock if significant myocarditis is present.

Pain in the chest or left shoulder is often present and is aggravated or relieved by changes in physical position. Patients usually feel better in a sitting position. The pain is usually substernal and accompanied by a sensation of chest constriction. Any movement of the chest, including respiratory motion, increases the pain. Sitting up and leaning forward may reduce the pain. Therefore, a child may refuse to lie down for examination. Palm pressure applied to the sternum markedly increases the pain.

A hacking cough is occasionally a presenting symptom. The cough varies with position. Sitting up and leaning forward improves the cough.

Preceding symptoms of viral illness are present in 40-75% of patients and include the following:

Bacterial pericarditis

Patients are acutely ill and exhibit symptoms of sepsis. Acute purulent pericarditis in an infant is a medical emergency. Rapid evaluation, diagnosis, and treatment are 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. Precordial chest pain is 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.

Most patients have preceding or concurrent infection that is the source of pericarditis. These infections include the following:

Pericarditis may rarely complicate neonatal sepsis.

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Physical Examination

Viral pericarditis

Patients with viral pericarditis generally appear less toxemic than those with bacterial pericarditis. However, some patients appear ill, especially if the accompanying myocarditis is clinically significant.

Physical signs in the absence of tamponade or clinically significant myocarditis are minimal and may be limited to a pericardial friction rub, which is audible in 80% of patients. Sounds may occur in 3 phases of the cardiac cycle. Ventricular contraction is the first phase and occurs during systole. Ventricular filling and atrial contraction are the second and third phases and occur during diastole.

Rub sounds are best heard with the diaphragm of the stethoscope. The sounds may seem close to the ear. They are caused by the inflamed pericardial surfaces rubbing against each other. This rubbing sound may be misinterpreted as movement of the stethoscope on the chest surface. Pericardial friction rub may sound like 2 leather surfaces rubbing together or like hair being rubbed between the fingers. With a large effusion, the loudness of a rub may decrease or even disappear because the pericardial surfaces separate.

Cardiac tamponade is seen in infants but can also occur in older children.[6] Cardiac tamponade is a unique form of obstructive shock with symptoms of venous congestion and low cardiac output. Signs of low cardiac output include weak peripheral pulses, cool and clammy extremities, low blood pressure, and tachycardia. With cardiac tamponade, heart sounds seem distant. The pulse pressure is also narrow. Signs of venous congestion include distend neck veins, pulmonary edema, or hepatomegaly. The patient may report abdominal pain due to acute hepatic distension.

Physical signs of venous congestion, such as elevated nonpulsatile jugular venous pulse and peripheral or pulmonary edema, mimic those of congestive heart failure (CHF). However, do not misinterpret this event as heart failure because drugs commonly used to treat heart failure may cause vascular collapse in a patient with cardiac tamponade. Likewise, avoid administering diuretics because intravascular depletion can increase cardiac compression.

Pulsus paradoxus may be documented by observing an inspiratory decrease in BP of more than 10 mm Hg. In healthy individuals, inspiration causes systolic BP to decrease slightly as a result of the increased 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 systolic BP decreases further (>10 mm Hg). This exaggerated decrease in systolic BP with inspiration is referred to as pulsus paradoxus, an important sign of cardiac tamponade. On occasion, severe respiratory distress of any cause (eg, asthma, emphysema, pleural effusion) may cause this sign.

A chronic, large pericardial effusion may cause ascites and peripheral edema. Pulmonary edema is unusual because pericardial effusion limits the amount of blood that can enter the heart. No rales are heard in the lungs, and the patient does not have dyspnea or tachypnea. With myocarditis, evidence of left-heart failure may be observed.

Signs and symptoms of viral pericarditis can mimic those of systemic lupus erythematosus.

Bacterial pericarditis

Infants with bacterial pericarditis are generally very ill and can present with signs of severe sepsis and shock. A high index of suspicion is required. Purulent pericarditis should be suspected in any infant who appears to have sepsis and has an abnormal cardiovascular examination. Tachypnea and tachycardia out of proportion to fever is characteristic of both purulent pericarditis and acute myocarditis.

Classic cardiac findings of pericarditis include muffled heart sounds and a friction rub. A friction rub can occur in any combination of systole, mid diastole, and late diastole. It may vary with patient position or the respiratory cycle and may be transient. A friction rub is unlikely in the presence of a large pericardial effusion or in an infant with purulent pericarditis. 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 can present rapidly with hypotension, soft heart tones of poor quality, signs of venous congestion, and signs of low cardiac output, 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. Any significant pericardial constriction produces pulsus paradoxus. Other causes of pulsus paradoxus include hypovolemia and either a large or small airway obstruction like epiglottitis or asthma.

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Complications

Cardiac tamponade may develop from any cause of acute fluid accumulation in the pericardial sac. Severe tamponade may cause cardiac arrest due to electromechanical dissociation. Less severe cases may cause tachycardia, tachypnea, decreased arterial BP, increased central venous pressure, and paradoxical pulse. Patients report dyspnea and chest pain.

Acutely, serial ECGs may indicate the presence of occult arrhythmia, suggesting additional myocardial involvement.

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.

Go to Neurologic Sequelae of Infective Endocarditis for complete information on this topic.

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Contributor Information and Disclosures
Author

Poothirikovil Venugopalan, MBBS, MD, FRCPCH Consultant Pediatrician with Cardiology Expertise, Department of Child Health, Brighton and Sussex University Hospitals, NHS Trust; Honorary Senior Clinical Lecturer, Brighton and Sussex Medical School, UK

Poothirikovil Venugopalan, MBBS, MD, FRCPCH is a member of the following medical societies: Royal College of Paediatrics and Child Health, Paediatrician with Cardiology Expertise Special Interest Group, British Congenital Cardiac Association

Disclosure: Nothing to disclose.

Coauthor(s)

John Berger, MD Associate Professor, Department of Pediatrics, George Washington University School of Medicine, Director, Cardiac Intensive Care and Pulmonary Hypertension Program, Children's National Medical Center

John Berger, MD is a member of the following medical societies: American Academy of Pediatrics, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hugh D Allen, MD Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, Western Society for Pediatric Research, American College of Cardiology, American Heart Association, American Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

Ira H Gessner, MD Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

References
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  7. Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in children: elevated troponin I level does not predict outcome. Pediatr Cardiol. 2012 Oct. 33(7):1040-5. [Medline].

  8. Ananthasubramaniam K, Farha A. Primary right atrial angiosarcoma mimicking acute pericarditis, pulmonary embolism, and tricuspid stenosis. Heart. 1999 May. 81(5):556-8. [Medline]. [Full Text].

  9. Habashy AG, Mittal A, Ravichandran N, Cherian G. The electrocardiogram in large pericardial effusion: the forgotten "P" wave and the influence of tamponade, size, etiology, and pericardial thickness on QRS voltage. Angiology. 2004 May-Jun. 55(3):303-7. [Medline].

  10. Bhardwaj R, Berzingi C, Miller C, et al. Differential diagnosis of acute pericarditis from normal variant early repolarization and left ventricular hypertrophy with early repolarization: an electrocardiographic study. Am J Med Sci. 2013 Jan. 345(1):28-32. [Medline].

  11. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005 Sep 27. 112(13):2012-6. [Medline].

  12. Levy PY, Fournier PE, Charrel R, Metras D, Habib G, Raoult D. Molecular analysis of pericardial fluid: a 7-year experience. Eur Heart J. 2006 Aug. 27(16):1942-6. [Medline].

  13. Adler Y, Finkelstein Y, Guindo J, et al. Colchicine treatment for recurrent pericarditis. A decade of experience. Circulation. 1998 Jun 2. 97(21):2183-5. [Medline].

  14. Yazigi A, Abou-Charaf LC. Colchicine for recurrent pericarditis in children. Acta Paediatr. 1998 May. 87(5):603-4. [Medline].

 
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Two-dimensional echocardiograph shows a large pericardial effusion.
M-mode echocardiograph shows moderate pericardial effusion.
Plain chest radiograph in a 2-year-old boy with viral pericarditis and massive pericardial effusion.
Left: Chest radiograph in a patient with bacterial pericarditis revealing 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.
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.
A 12-lead ECG from a patient with bacterial pericarditis demonstrating marked ST elevation in multiple leads.
This ECG shows markedly decreased QRS voltage and electrical alternans (especially in lead V1)
 
 
 
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