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Acute myocarditis is a serious but relatively uncommon diagnosis in the emergency department. Symptoms can progress from those of a nonspecific respiratory illness to those of cardiovascular collapse and death in a short period of time. Some patients present with fulminant disease, whereas others have an indolent course that progresses over time to dilated cardiomyopathy with chronic congestive heart failure. Signs and symptoms may point to an obvious cardiac etiology, but subtler and misleading presentations require the clinician to have a high index of suspicion.
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The incidence of myocarditis in the United States is not known because of patients with subclinical infection and difficulties in precise diagnosis. Myocarditis was found at autopsy in between 3% and 40% of infants and children with sudden death.3–7 Frequently, a diagnosis of myocarditis is suspected but never confirmed. More recently, in a survey of the incidence of pediatric cardiomyopathy in two regions of the United States, the incidence of myocarditis as a cause of dilated cardiomyopathy was approximately 0.2 per 100,000 children.6
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In cases of suspected myocarditis, an etiologic agent is identified in less than one-third of the time.8 Laboratory techniques include observing acute and convalescent titer for specific viruses, viral cultures from fluid or tissue, and PCR amplification of viral genome. Viral etiologies predominate, however bacteria, rickettsia, fungi, and parasites are known agents (Table 41-1).
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Clinical Presentation
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Myocarditis may be difficult to diagnose because signs and symptoms may mimic other very common disorders. Frequently, it is not until later in the clinical course that these symptoms are noted to be of cardiac origin. The clinical presentation can be divided into specific symptom complexes based on presentation (Table 41-2). In general, the pathophysiology of the symptom complexes follows the gradual onset of congestive heart failure to frank cardiogenic shock. The patient may present with tachycardia and rhythm disturbances.
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Complaints include cough, wheeze, congestion, fever, or tachypnea. Tachypnea may be compensation for metabolic acidosis. Bronchospasm responding poorly to conventional therapy may suggest early myocarditis. Red flags include the child who is tachypneic, but lack symptoms of wheezing or supporting evidence for the diagnosis of pneumonia. Other signs and symptoms include those associated with congestive heart failure, poor feeding, cyanosis, and grunting. Murmur, gallop rhythm, rales, or organomegaly may confirm the diagnosis (Table 41-3). Myocarditis should be considered in any child who deteriorates despite aggressive treatment for bronchospasm or reactive airway disease.9
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The onset of metabolic acidosis secondary to severe hypoperfusion (cardiogenic shock) accounts for some of the symptoms seen. Metabolic acidosis can cause tachypnea, retractions, and grunting.10,11 Gastrointestinal symptoms arise because of viral processes but also because of gastrointestinal hypoperfusion. Severe acidosis may also affect mental status causing lethargy and coma.
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Diagnosis requires a high index of suspicion. Unfortunately, standard laboratory, radiographic, and electrocardiographic testing is nonspecific. Chest radiograph is positive in only 42% to 75% of cases (Fig. 41-3).9–11 All patients should receive ECG testing. Electrocardiographic changes include nonspecific ST-T wave and axis changes. Rarely, heart block or infarct patterns may emerge.
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Elevations in creatine phosphokinase, lactate dehydrogenase, troponin,12 and brain natriuretic peptide lack specificity.8 Indicators of inflammation such as erythrocyte sedimentation rate and c-reative protein are nonspecific. Patients who may have myocarditis should receive echocardiography. Findings include increased end-diastolic chamber dimensions, reduced shortening fraction, atrioventricular valve regurgitation, and regional wall abnormalities (Fig. 41-4).
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Children with acute myocarditis should be admitted to a pediatric intensive care unit (PICU) for continuous monitoring because of the risks of ventricular ectopy and cardiogenic shock. Preferably, the PICU should have the ability to provide aggressive mechanical cardiac support if needed. Initial management includes the treatment of cardiogenic shock or congestive heart failure. Consider use of invasive monitoring. Ionotropic support with dopamine, dobutamine, epinephrine, or milrinone may be necessary. An aggressive approach to dysrhythmias may prevent sudden death. Heart block is an indication for transvenous pacing. Meticulous supportive care of acid–base derangements, metabolic abnormalities, and fluid status is mandatory. The use of corticosteroids and other immunosuppressants is not well supported by current studies.13 The use of intravenous immunoglobulin remains unproven but is frequently used.14 Patients with fulminant myocarditis should receive aggressive mechanical support of the circulation with extracorporeal membrane oxygenation (ECMO) because of the excellent long-term prognosis if these patients can survive the initial period of cardiogenic shock.15,16 Ultimately, transplantation may be required for end-stage cardiomyopathy secondary to myocarditis.