Pediatric Viral Myocarditis Clinical Presentation

  • Author: Edwin Rodriguez-Cruz, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Dec 6, 2011
 

History

Clinical presentation of viral myocarditis widely varies. In mild forms, few or no symptoms are noted. In severe cases, patients may present with acute cardiac decompensation and progress to death.

Heart failure is the most common presenting picture in all ages. The condition of patients who present with heart failure may rapidly deteriorate even with supportive care. Neonates and young children have higher mortality rates than older patients. Rapid supportive care with blood pressure support, afterload reduction, and control of arrhythmia may prevent early death.

Although rare in young children, chest pain may be the initial presentation for older children, adolescents, and adults. Chest pain may be due to myocardial ischemia or concurrent pericarditis.

Patients can present with any type of dysrhythmia, including atrioventricular conduction disturbances. Sinus tachycardia is typical, and the rate is faster than expected for the degree of fever present, which is typically low-grade. Junctional tachycardia is also seen and can be difficult to control medically.

The debate continues over whether myocarditis progresses to dilated cardiomyopathy. Many investigators believe that dilated cardiomyopathy is a direct result of a previously burned-out myocarditis episode.

Initial symptoms in infants include the following:

  • Irritability
  • Lethargy
  • Periodic episodes of pallor
  • Fever
  • Hypothermia
  • Tachypnea
  • Anorexia
  • Failure to thrive

Older children present with similar symptoms and may experience lack of energy and general malaise. Parents of pediatric patients may refer to a recent, nonspecific, flulike illness, gastrointestinal (GI) symptoms, poor feeding, or rapid breathing.

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Physical Examination

Signs of diminished cardiac output, such as tachycardia, weak pulse, cool extremities, decreased capillary refill, and pale or mottled skin, may be present. Heart sounds may be muffled, especially in the presence of pericarditis. An S3 may be present, and a heart murmur caused by atrioventricular valve regurgitation may be heard. Hepatomegaly may be present in younger children. Rales may be heard in older children. Jugular venous distention and edema of the lower extremities may be present.

Neonates

Neonates may seem irritable, be in respiratory distress, and exhibit signs of sepsis. Somnolence, hypotonia, and seizures can be associated if the central nervous system (CNS) is involved.

Hypothermia or hyperthermia, oliguria, elevated liver enzymes, and elevated blood urea nitrogen (BUN) and creatinine levels caused by direct viral damage, low cardiac output, or both may be present.

Infants

Signs include failure to thrive, anorexia, tachypnea, tachycardia, wheezing, and diaphoresis with feeding. End-organ damage may develop because of direct viral infestation or because of low cardiac output. CNS involvement may also develop. In severe cases, low cardiac output may progress to acidosis and death.

Adolescents

The presentation of viral myocarditis may be similar to that in younger children but with a more prominent decrease in exercise tolerance, lack of energy, malaise, chest pain, low-grade fever, arrhythmia, and cough. End organ damage and low cardiac output may be present.

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Contributor Information and Disclosures
Author

Edwin Rodriguez-Cruz, MD  Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Pediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico

Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, American Society of Echocardiography, Puerto Rico Medical Association, Society of Cardiac Angiography and Interventions, and Society of Pediatric Echocardiography

Disclosure: NOVARTIS Grant/research funds INVESTIGATOR

Coauthor(s)

Robert D Ross, MD  Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Children's Hospital of Michigan; Professor of Pediatrics, Wayne State University School of Medicine

Robert D Ross, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, and Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital 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, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

Ameeta Martin, MD Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine

Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

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.

References
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Hypersensitivity myocarditis. High magnification of myocardium with perivascular infiltrates rich in eosinophils. This patient had a clinical history compatible with drug-induced hypersensitivity myocarditis.
 
 
 
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