Myocarditis in Children
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Direct answer
A previously well child with a short viral prodrome who then develops tachypnoea, a gallop rhythm, hepatomegaly and arrhythmia has myocarditis until echocardiography proves otherwise: inflammation of the myocardium, most often viral (enteroviruses, classically coxsackie B, plus parvovirus B19 and adenovirus, with post-SARS-CoV-2 immune syndromes overlapping). Diagnosis rests on a compatible illness with raised troponin and natriuretic peptides, ECG changes (disproportionate sinus tachycardia, low voltages, ST-T changes) and an echo showing a dilated, poorly contracting left ventricle; endomyocardial biopsy remains the gold standard, with the Dallas criteria defining histological myocarditis. Management is supportive — diuretics, afterload reduction, rhythm control and intensive care — since most children recover ventricular function, though fulminant cases may need mechanical circulatory support.
What you must remember
- Aetiology: viruses dominate — coxsackie B historically, now parvovirus B19 and adenovirus by polymerase chain reaction of biopsy tissue; diphtheritic myocarditis, rheumatic carditis, Kawasaki and drug hypersensitivity sit in the differential.
- Troponin and ECG: troponin I or T elevation with sinus tachycardia disproportionate to fever, low QRS voltages, ST-segment and T-wave changes, or occasional ventricular ectopy form the recognisable pattern.
- Echo versus biopsy: echocardiography shows regional or global hypokinesis with a dilated, thin-walled left ventricle; biopsy is reserved for deteriorating or unexplained cases but remains the definitive diagnostic standard.
- Dallas criteria: an inflammatory infiltrate with myocyte necrosis or damage on endomyocardial biopsy distinguishes true myocarditis from borderline changes and from infiltration.
- Treatment is supportive: loop diuretics, angiotensin-converting enzyme inhibitors, intravenous immunoglobulin 2 g/kg in many centres (evidence debated), and avoidance of non-steroidal anti-inflammatory drugs in the acute phase; steroids and other immunosuppression are reserved for giant-cell, eosinophilic or biopsy-proven immune disease.
- Fulminant myocarditis: rapid onset, severe haemodynamic compromise but often smaller ventricles with thick walls and preserved or hyperdynamic recovery if the child is bridged — extracorporeal membrane oxygenation is the rescue.
- Sport and death: arrhythmia is the leading cause of death, and competitive exercise is restricted, commonly for three to six months, until function and Holter monitoring normalise.
Walking through a suspected case
Take an eight-year-old with fever and myalgia for four days, now breathless at rest with a heart rate of 150, a third heart sound and a liver edge two centimetres below the costal margin. The emergency sequence runs: secure the airway and circulation, obtain an ECG and troponin, run the echo, and simultaneously exclude the mimics — pericarditis with effusion (which muffles rather than gallops), septic shock (which has culture and wider vasopressor needs) and a primary dilated cardiomyopathy presenting acutely. Chest radiography shows cardiomegaly with pulmonary venous congestion; brain natriuretic peptide is markedly raised. The child with poor perfusion goes to intensive care, where the quietly decisive interventions are judicious fluid avoidance, diuresis, inotropy with milrinone or dopamine, and continuous rhythm monitoring, because a previously stable myocarditic child can declare ventricular tachycardia without warning.
In the recovering phase the question changes to how long dysfunction will last: myocarditis is defined clinically by the acute inflammatory illness, whereas dysfunction persisting beyond about three months without inflammation enters dilated cardiomyopathy territory, which changes follow-up, family counselling and transplant discussion.
Where candidates slip
The classic error is anchoring on cough and fever and treating pneumonia while missing the gallop, the hepatomegaly and the disproportionate tachycardia — myocarditis masquerades as respiratory infection in children more often than any exam question admits. The second slip is over-reliance on troponin alone: troponin confirms myocyte injury but not its cause, and the combination of a pericarditic pain, rub and ST elevation belongs to myopericarditis, which has a different prognosis. Viva examiners like the boundary question — when does myocarditis become dilated cardiomyopathy — and expect the three-month convention plus the point that immunosuppression decisions, unlike supportive care, genuinely require biopsy-proven histology in most current practice.
Frequently asked questions
Which virus is classically blamed for paediatric myocarditis?
Enteroviruses, especially coxsackie B, remain the textbook answer, though molecular studies now identify parvovirus B19 and adenovirus frequently, and post-viral immune syndromes including MIS-C overlap the picture.
What are the Dallas criteria?
Histological criteria on endomyocardial biopsy: an inflammatory infiltrate in the myocardium with myocyte necrosis or degeneration, distinguishing active myocarditis from borderline disease.
Which investigations support the diagnosis?
Raised troponin and brain natriuretic peptide, an ECG showing disproportionate sinus tachycardia, low voltages or ST-T changes, and an echocardiogram demonstrating ventricular dysfunction.
Is intravenous immunoglobulin routinely indicated?
Many centres give 2 g/kg, but randomised evidence is unconvincing; management remains primarily supportive with diuresis, afterload reduction and intensive monitoring.
When may an affected child return to competitive sport?
Usually after three to six months of restriction, once ventricular function, arrhythmia screening on Holter monitoring and exercise parameters have normalised.