Why does cortical venous thrombosis occur during pregnancy?

Why Cortical Venous Thrombosis Occurs in Pregnancy

Cortical venous thrombosis occurs in pregnancy due to the convergence of all three components of Virchow's triad—pregnancy-induced hypercoagulability, venous stasis from mechanical compression and hormonal effects, and vascular injury during delivery—creating a prothrombotic state that begins at conception and persists through the puerperium. 1, 2

Hypercoagulability Mechanisms

Pregnancy creates a profound hypercoagulable state starting from conception, which is an evolutionary adaptation to reduce hemorrhage during childbirth or pregnancy loss. 2 This involves multiple specific coagulation changes:

• Increased procoagulant factors: Fibrinogen, factor VII, VIII, X, and von Willebrand factor all increase by the third trimester 1
• Decreased natural anticoagulants: Free protein S levels decrease, and acquired activated protein C resistance develops 1
• Impaired fibrinolysis: Plasminogen activator inhibitor type 1 (PAI-1) levels rise, reducing the body's ability to break down clots 1
• Persistence beyond delivery: These changes do not normalize until at least 6 weeks postpartum 2

Venous Stasis Mechanisms

Mechanical and hormonal factors combine to create significant venous stasis:

• Anatomical compression: The enlarged uterus compresses the inferior vena cava and pelvic veins, particularly affecting the left iliac vein, which explains why deep vein thrombosis is more frequent on the left side 1
• Reduced venous flow: Femoral venous blood flow decreases significantly during pregnancy due to both mechanical compression and decreased venous tone from hormonal modifications 1
• Hormonal effects: Pregnancy hormones reduce venous tone, further contributing to stasis 1

Vascular Injury Component

The third element of Virchow's triad is completed by:

• Delivery trauma: Both vaginal delivery and cesarean section cause endothelial damage 2
• Volume depletion: Hypercoagulability worsens after delivery due to volume depletion and trauma 1
• Surgical interventions: Cesarean delivery and instrumental delivery increase risk through direct vascular trauma 1

Timing and Risk Distribution

Most pregnancy-related cortical venous thrombosis occurs in the third trimester or puerperium, with the postpartum period carrying the highest risk. 1

• Seven of 8 cerebral venous thromboses among 50,700 deliveries in Canada occurred postpartum 1
• In one Mexican study, 50% of all cerebral venous thrombosis cases occurred during pregnancy or puerperium 1
• The frequency of cerebral venous thrombosis in the puerperium is estimated at 12 cases per 100,000 deliveries 1

Additional Risk Factors That Amplify Baseline Pregnancy Risk

Beyond the universal pregnancy-related mechanisms, specific factors further increase risk:

• Genetic thrombophilias: Factor V Leiden heterozygosity (7.3-19.5% of cases), prothrombin G20210A mutation, and MTHFR polymorphisms 3, 4
• Acquired prothrombotic states: Hyperhomocysteinemia (34% of cases) and elevated factor VIII levels (14.6%) 4
• Clinical factors: Increasing maternal age, cesarean delivery, hypertension, infections, and excessive vomiting in pregnancy 1
• Dehydration: Traditional puerperal water restriction practices significantly increase risk (P < 0.02) 4
• Multiple prothrombotic markers: Mortality increases by odds of 1.3 for every additional prothrombotic marker present 4

Critical Clinical Pitfalls

The most common pitfall is delayed diagnosis, which is associated with significantly poorer prognosis. 5

• Headache is the most frequent presenting symptom and should not be dismissed in pregnant or postpartum women 1, 5
• Focal neurological symptoms and cerebral infarction occur more frequently during pregnancy than postpartum 5
• Epileptic seizures, hemiparalysis, and aphasia are less frequent but important warning signs 5
• Status epilepticus (OR 13.2), deep venous system involvement (OR 9.64), midline shift (OR 24.7), and diffuse cerebral edema (OR 14.5) are associated with increased mortality 4