Serum ferritin and cardiogenic shock in severe pediatric dengue: pathophysiology, evidence and clinical correlation - a narrative review

Abstract

Severe dengue infection in children can lead to life-threatening shock classically attributed to plasma leakage. However, emerging evidence links hyperinflammation – often reflected by extreme elevations in serum ferritin – with myocardial dysfunction and cardiogenic shock in dengue. Ferritin, an acute-phase reactant, is markedly elevated in hyperinflammatory syndromes such as hemophagocytic lymphohistiocytosis (HLH), which is increasingly recognized as a complication of severe dengue. This narrative review critically examines the pathophysiology connecting dengue virus infection, hyperferritinemia, and cardiac dysfunction. We summarize key studies demonstrating that serum ferritin levels correlate with dengue severity and outcomes, including recent pediatric cohorts where ferritin >10,000 ng/ml portended higher mortality. Myocardial involvement in dengue – ranging from transient functional impairment to fulminant myocarditis – is discussed in light of cytokine-mediated injury and HLH-like immune activation. We also outline clinical implications, recommending vigilance for “dengue-HLH” in severe cases with unexplained shock and very high ferritin, and considering adjunctive immunomodulatory therapy in addition to standard supportive care. State-of-the-art evidence is presented to guide clinicians in early identification of hyperinflammatory dengue cases, prompt cardiac support (inotropes, fluid management, and extracorporeal life support when needed), and potential interventions to improve outcomes. This review provides a comprehensive, evidence-based update on the role of serum ferritin as both a biomarker and a clue to pathogenic processes (including HLH) that can culminate in cardiogenic shock in pediatric dengue.