Management of Acute Decompensated Heart Failure in a 12-Year-Old Boy With Chronic Rheumatic Multivalvular Heart Disease and Severe Pericardial Effusion: A Case Report

Introduction: Acute heart failure (AHF) in children is a life-threatening clinical syndrome whose aetiological spectrum differs markedly between high-income and low- and middle-income countries. In Indonesia and other endemic regions, chronic rheumatic heart disease (RHD) remains a leading acquired cause of paediatric heart failure, frequently presenting late with advanced multivalvular disease, ventricular dysfunction and pericardial involvement. Early recognition, haemodynamic stabilisation and timely referral are decisive for survival, particularly in district hospitals with limited diagnostic resources. Case Illustration: A 12-year-old boy presented with progressively worsening dyspnoea for three days, accompanied by cough, bilateral leg oedema, orthopnoea and palpitations, on a background of intermittent dyspnoea for one year. Thirteen months earlier, an outside M-mode echocardiogram had documented left-sided chamber enlargement, a reduced ejection fraction (27.5%), mild pericardial effusion and suspected RHD. On admission he had diaphoresis at rest, scleral icterus, tachycardia, a cardiac murmur with gallop rhythm, tachypnoea, rhonchi and wheezing, hepatomegaly, ascites and pedal oedema, yielding a modified Ross score of 11 (severe heart failure). Electrocardiography showed sinus tachycardia, right axis deviation, biatrial enlargement, prolonged PR interval (197 ms), Q waves in the high lateral leads and electrical alternans; chest radiography demonstrated marked cardiomegaly. He received inotropic support with dobutamine and dopamine together with furosemide and spironolactone, and improved clinically. After stabilisation he was referred through the outpatient clinic to the provincial referral hospital, where echocardiography confirmed chronic RHD with mitral, tricuspid and aortic regurgitation and a severe pericardial effusion. He was hospitalised for approximately seven days under a paediatric cardiology consultant, recovered, and was discharged home with long-term follow-up. Discussion: This case illustrates the typical late presentation of RHD in an endemic setting, the pathophysiological interplay of chronic volume overload, ventricular dysfunction and pericardial effusion, and the practical value of bedside severity scoring, electrocardiography and radiography where echocardiography is not immediately available. Inotropes combined with loop diuretics and a mineralocorticoid receptor antagonist achieved decongestion, while the severe pericardial effusion mandated exclusion of tamponade physiology before aggressive preload reduction. The missed opportunity 13 months earlier underscores the importance of registry-based follow-up, secondary antibiotic prophylaxis tailored to cardiovascular risk, and early referral for definitive valve intervention. Conclusion: Paediatric AHF due to chronic RHD can be stabilised successfully at district level through structured clinical assessment, judicious inotropic and diuretic therapy and prompt referral. Long-term outcome depends on secondary prophylaxis, guideline-directed heart failure therapy, nutritional rehabilitation and access to surgical valve repair.