How does a dural venous sinus thrombosis (DVST) lead to an intracerebral hemorrhage (ICH)?

Mechanism of Intracerebral Hemorrhage in Dural Venous Sinus Thrombosis

Dural venous sinus thrombosis (DVST) causes intracerebral hemorrhage (ICH) primarily through venous hypertension, which leads to increased pressure in cerebral veins, capillary rupture, and subsequent hemorrhagic transformation of venous infarcts. 1

Pathophysiological Sequence

1. Initial Venous Obstruction

   • Thrombosis blocks normal venous drainage in dural sinuses
   • Most commonly affects lateral dural venous sinuses (73%) and superior sagittal sinus (35%) 1
   • Obstruction prevents normal cerebral venous outflow

2. Venous Pressure Elevation

   • Blocked outflow causes retrograde pressure increase in the venous system
   • Pressure is transmitted backward to smaller cortical veins and capillaries
   • This creates venous congestion in brain tissue

3. Venous Infarction Development

   • Persistent venous congestion leads to:
     • Decreased cerebral perfusion pressure
     • Impaired blood-brain barrier integrity
     • Cytotoxic and vasogenic edema
     • Ischemic injury to brain tissue

4. Hemorrhagic Transformation

   • The combination of:
     • Increased venous and capillary pressure
     • Damaged vessel walls from venous congestion
     • Compromised blood-brain barrier
     • Results in rupture of venous structures and hemorrhage into brain parenchyma

Characteristics of DVST-Related Hemorrhages

• Hemorrhagic infarction occurs in approximately 40% of cerebral sinovenous thrombosis cases 1
• Higher incidence in neonates (72%) compared to older children (48%) 1
• Often located in proximity to the thrombosed venous sinus 1
• Frequently crosses usual arterial boundaries, which is a distinguishing radiological feature 1
• May appear as multiple, sometimes bilateral hemorrhages

Risk Factors for Hemorrhagic Transformation

Several factors increase the risk of hemorrhagic transformation in DVST:

• Thrombosis of the deep cerebral venous system (5.4× higher risk) 2
• Right lateral sinus thrombosis (2.6× higher risk) 2
• Male gender (3.3× higher risk) 2
• Older age (5% increased risk per year of age) 2
• Presence of motor deficit 2
• Delayed or inadequate anticoagulation 2

Clinical Implications

• Despite the presence of hemorrhage, anticoagulation remains the standard treatment for DVST 1
• Patients with ICH due to DVST have worse outcomes than those without hemorrhage 2
• Rapid diagnosis and treatment are essential to prevent progression of venous congestion and reduce risk of hemorrhagic transformation
• In cases with severe mass effect from hemorrhage, decompressive surgery may be necessary 1

Imaging Findings

• CT may show hyperdense thrombosed sinuses and hemorrhagic infarcts 1
• MRI with MR venography is more sensitive for detecting both the thrombosis and associated parenchymal changes 1
• Key diagnostic feature: hemorrhagic lesions that cross typical arterial territories, especially near venous sinuses 1

Understanding this pathophysiological mechanism helps explain why DVST-related hemorrhages can be extensive and why anticoagulation, despite the presence of hemorrhage, remains the cornerstone of treatment to prevent further thrombosis and venous hypertension.