## Pathophysiology of Hemorrhagic Manifestations in Dengue **Key Point:** Thrombocytopenia is the primary mechanism of bleeding in dengue fever, occurring in 50–80% of hospitalized children. The platelet count typically falls to <100,000/μL during the critical phase (days 3–7). ### Mechanism of Thrombocytopenia 1. **Bone marrow suppression** — Direct viral replication in bone marrow progenitor cells (particularly megakaryocytes) leads to decreased platelet production. 2. **Peripheral consumption** — Immune complex deposition and complement activation cause platelet activation and aggregation. 3. **Increased peripheral destruction** — Antibody-mediated destruction of infected platelets. **High-Yield:** The degree of thrombocytopenia correlates with disease severity. Platelet counts <50,000/μL carry higher risk of spontaneous bleeding. ### Why Other Mechanisms Are Secondary | Mechanism | Role in Dengue | Frequency | |-----------|---|---| | Platelet dysfunction | Occurs but not primary cause | Rare, only in severe cases | | DIC | Seen only in dengue hemorrhagic fever (DHF) Grade III–IV | <5% of dengue cases | | Vasculitis/capillary leak | Important in shock phase but not primary bleeding cause | Secondary phenomenon | **Clinical Pearl:** Bleeding in dengue is typically mucosal (petechiae, gum bleeding, epistaxis) rather than deep tissue, reflecting the platelet-mediated mechanism rather than coagulopathy. **Warning:** Do not confuse thrombocytopenia-mediated bleeding with DIC. In uncomplicated dengue, PT/INR and aPTT are normal; DIC develops only in severe dengue with shock. [cite:Nelson Textbook of Pediatrics 21e Ch 273]
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