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Pediatric Viral Myocarditis Clinical Presentation

  • Author: Edwin Rodriguez-Cruz, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
Updated: Aug 26, 2015


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 usually weeks after the initial viral infection and prodromal symptoms.

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, diuretic therapy, 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 typically a compensatory mechanism in patients with myocardial dysfunction, 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
  • Diaphoresis

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.


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 (see the Cardiac Output calculator). 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 in older patients.


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.


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.


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.

Contributor Information and Disclosures

Edwin Rodriguez-Cruz, MD Director, Section of Cardiology, Department of Pediatrics, San Jorge Children’s Hospital, Puerto Rico; Private Practice in Interventional Pediatric Cardiology and Internal Medicine, Centro Pedíatrico y Cardiovascular

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

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: St Jude's Medical Co.<br/>Received grant/research funds from NOVARTIS for investigator; Received consulting fee from St. Jude Medical Corp. for speaking and teaching.


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, Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.


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.

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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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