<p>Intracranial hemorrhage (ICH) represents the most devastating complication of immune thrombocytopenia (ITP), associated with high mortality despite its rarity. We describe four adult patients with ITP who developed diverse forms of ICH at different stages of their disease. Two patients experienced intraparenchymal hemorrhage during initial and relapsed disease, one presented with subarachnoid hemorrhage (SAH) as the first manifestation of ITP, and another developed subacute subdural hemorrhage while on long-term romiplostim therapy. All patients had severe thrombocytopenia (&lt;15 × 10⁹/L) at presentation. Despite appropriate corticosteroid and/or intravenous immunoglobulin therapy, two patients succumbed, while the other two recovered following prompt multidisciplinary management, including TPO-RA initiation and surgical intervention where indicated. These cases highlight the clinical heterogeneity of ITP-associated ICH, spanning newly diagnosed, persistent, and chronic phases, and underscore that catastrophic bleeding can occur even in patients previously deemed stable. The pathophysiology likely extends beyond platelet count alone, involving immune dysregulation, vascular fragility, and cytokine-mediated endothelial injury. Early recognition of neurological symptoms, rapid neuroimaging, and aggressive management remain crucial for favourable outcomes. Given the unpredictability of ICH onset, continuous risk assessment and individualized therapeutic escalation are warranted. Our findings emphasize the need for prospective data to define predictors of catastrophic bleeding and to optimize management algorithms for this rare but life-threatening complication.</p>

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Catastrophic Bleeding in Immune Thrombocytopenia: Insights from Four Adult Cases of Intracranial Hemorrhage

  • Sarthak Wadhera,
  • Rudra Narayan Swain,
  • Aarushi Sahni,
  • Pankaj Malhotra

摘要

Intracranial hemorrhage (ICH) represents the most devastating complication of immune thrombocytopenia (ITP), associated with high mortality despite its rarity. We describe four adult patients with ITP who developed diverse forms of ICH at different stages of their disease. Two patients experienced intraparenchymal hemorrhage during initial and relapsed disease, one presented with subarachnoid hemorrhage (SAH) as the first manifestation of ITP, and another developed subacute subdural hemorrhage while on long-term romiplostim therapy. All patients had severe thrombocytopenia (<15 × 10⁹/L) at presentation. Despite appropriate corticosteroid and/or intravenous immunoglobulin therapy, two patients succumbed, while the other two recovered following prompt multidisciplinary management, including TPO-RA initiation and surgical intervention where indicated. These cases highlight the clinical heterogeneity of ITP-associated ICH, spanning newly diagnosed, persistent, and chronic phases, and underscore that catastrophic bleeding can occur even in patients previously deemed stable. The pathophysiology likely extends beyond platelet count alone, involving immune dysregulation, vascular fragility, and cytokine-mediated endothelial injury. Early recognition of neurological symptoms, rapid neuroimaging, and aggressive management remain crucial for favourable outcomes. Given the unpredictability of ICH onset, continuous risk assessment and individualized therapeutic escalation are warranted. Our findings emphasize the need for prospective data to define predictors of catastrophic bleeding and to optimize management algorithms for this rare but life-threatening complication.