What is the cause of bleeding in cerebral venous sinus thrombosis (CVST) patients who have not received low‑molecular‑weight heparin (LMWH)?

Causes of Bleeding in CVST Without Anticoagulation

Bleeding in CVST patients who have not received LMWH or any anticoagulation occurs due to the underlying pathophysiology of venous thrombosis itself—specifically, venous congestion leads to elevated venous pressure, which causes rupture of small vessels and hemorrhagic venous infarction. 1, 2

Primary Mechanism: Venous Hypertension and Congestion

The fundamental cause of hemorrhage in untreated CVST is the thrombotic occlusion of cerebral veins and sinuses, which creates a cascade of pathologic events:

• Venous outflow obstruction from the thrombus causes blood to back up in the cerebral venous system, dramatically increasing local venous pressure 3, 4
• Elevated venous pressure forces blood through the walls of small capillaries and venules that cannot withstand the increased hydrostatic force, resulting in hemorrhagic transformation 1, 3
• Venous infarction develops when the congestion becomes severe enough to impair tissue perfusion, leading to ischemic injury that subsequently becomes hemorrhagic 4

Secondary Contributing Factors

Beyond the direct mechanical effects of venous obstruction, several additional mechanisms contribute to bleeding:

• Disruption of the blood-brain barrier occurs as venous congestion damages endothelial tight junctions, allowing blood extravasation into brain parenchyma 4
• Vasogenic edema develops around the thrombosed vessels, creating mass effect that can further compress adjacent vessels and worsen venous drainage 3, 4
• Increased intracranial pressure from both edema and impaired CSF resorption (when major sinuses are involved) can lead to additional vascular injury 5, 3

Clinical Evidence from Untreated Cases

The natural history of CVST without anticoagulation demonstrates the hemorrhagic tendency:

• In pediatric populations, observational data showed 3 deaths among 8 untreated children with CVST, highlighting the severity of untreated disease 1
• Historical case series prior to routine anticoagulation documented hemorrhagic complications in a substantial proportion of CVST patients, even without any antithrombotic therapy 3, 6
• The case report of spontaneous intracranial hypotension precipitating CVST demonstrated hemorrhage development before any anticoagulation was initiated, with a 3.1 × 3.8 × 3.1-cm left posterior parietal hemorrhage appearing over a thrombosed cortical vein 5

Hemorrhage as a Presenting Feature

Intracranial hemorrhage is present at diagnosis in approximately 30-40% of CVST cases, occurring before any treatment is given:

• These hemorrhages are typically hemorrhagic venous infarctions rather than primary arterial bleeds 3, 4
• The hemorrhages tend to be located in areas drained by the thrombosed venous structures 4
• Presence of baseline hemorrhage does not contraindicate anticoagulation, as the bleeding is a consequence of ongoing thrombosis rather than a separate process 5, 1, 2

Critical Distinction: Hemorrhage is a Complication of Thrombosis

A crucial concept is that hemorrhage in CVST represents a complication of the thrombotic process itself, not a separate bleeding disorder:

• Without anticoagulation, the thrombus continues to propagate, worsening venous congestion and increasing hemorrhage risk 1, 3
• Anticoagulation actually reduces the risk of hemorrhagic progression by preventing thrombus extension and facilitating recanalization 5, 1
• Meta-analysis data suggest anticoagulation is associated with 108 fewer deaths per 1,000 cases at 90 days, despite theoretical bleeding concerns 5

Common Pitfall to Avoid

The most dangerous error is withholding anticoagulation due to presence of intracranial hemorrhage in CVST. The hemorrhage is caused by the venous thrombosis, and anticoagulation is the treatment that prevents further thrombotic propagation and additional hemorrhagic complications 5, 1, 2, 3. Even when hemorrhage expands after anticoagulation initiation (as in the case described in 5), guidelines recommend continuing anticoagulation because the underlying thrombotic process poses greater risk than the hemorrhage itself 5.