Acute Fulminant Myocarditis Presenting as Cardiogenic Shock in a Previously Healthy Child
A previously healthy 4-year-old male presented to the emergency department with 24 hours of fever (38.5°C), vomiting, and progressive lethargy. Vital signs showed tachycardia at 165 bpm, hypotension (78/42 mmHg), tachypnea (36 breaths/min), and oxygen saturation 94% on room air. Physical examination revealed cool extremities, delayed capillary refill >4 seconds, hepatomegaly 4 cm below the costal margin, and no murmur or pulmonary crackles. Glasgow Coma Scale (GCS) was 13.
Initial laboratory evaluation demonstrated metabolic acidosis (pH 7.22, lactate 6.5 mmol/L), elevated cardiac troponin I (2.8 ng/mL), and BNP 3100 pg/mL. Complete blood count and infectious workup, including blood cultures and viral panel, were obtained. Electrocardiogram showed sinus tachycardia with low voltage QRS complexes. Chest radiograph revealed mild cardiomegaly without pulmonary edema.
Given concern for cardiogenic shock, the patient was fluid-restricted after a cautious 10 mL/kg crystalloid bolus worsened respiratory effort. Peripheral epinephrine infusion (0.05 µg/kg/min) was initiated. Point-of-care echocardiography demonstrated globally depressed left ventricular systolic function with an estimated ejection fraction (EF) of 25%, consistent with severe myocarditis.
The patient was intubated for worsening work of breathing and initiation of mechanical ventilation to optimize oxygen delivery and reduce cardiac workload. Milrinone was added (0.3 µg/kg/min) to improve myocardial contractility. Broad-spectrum antibiotics and intravenous immunoglobulin (IVIG, 2 g/kg) were administered due to suspected immune-mediated myocarditis. Serial cardiac biomarkers and echocardiograms were performed to monitor therapeutic response.
Over the next 72 hours, hemodynamics gradually improved, lactate normalized, and inotropic support was weaned. Extubation occurred on hospital day five. Viral studies later returned positive for enterovirus. Repeat echocardiography on day seven displayed EF 55% with resolved wall motion abnormalities. The patient was discharged on day ten with low-dose ACE inhibitor therapy and scheduled cardiology follow-up. At three-month review, he demonstrated normal exercise tolerance and echocardiographic findings indicative of full cardiac recovery.
Introduction
Acute fulminant myocarditis (AFM) is a rare but life-threatening inflammatory condition of the myocardium, often triggered by viral pathogens. Children may initially present with non-specific symptoms resembling benign infections, making early recognition challenging. Rapid deterioration into cardiogenic shock requires timely diagnosis and aggressive hemodynamic support to reduce mortality [placeholder citation]. This case highlights diagnostic complexity, the role of point-of-care ultrasonography, and the importance of multidisciplinary management in pediatric intensive care.
Discussion
AFM can mimic sepsis, pneumonia, or dehydration, delaying appropriate therapy. Elevated cardiac biomarkers and early bedside echocardiography were crucial in distinguishing primary cardiac dysfunction from other shock etiologies. Immunomodulatory therapy with IVIG is frequently used despite mixed evidence; its rapid initiation in this case coincided with clinical improvement [placeholder citation]. Avoiding excessive fluid resuscitation was important due to the risk of worsening pulmonary and systemic congestion in cardiogenic shock. Early mechanical ventilation and inotropic support optimized preload and afterload conditions. Multidisciplinary collaboration facilitated timely intervention and favorable neurologic and cardiac outcomes.
Conclusion & Learning Points
Early echocardiography in shock, cautious fluid management, and prompt inotropic and immunomodulatory therapy are critical to optimize survival in pediatric AFM.
