Dural sinus thrombosis, also known as cerebral venous sinus thrombosis, is a type of stroke caused by a blood clot in the dural sinuses or cerebral veins. It accounts for 0.5-1% of all strokes and affects 5 people per million. Risk factors include oral contraceptive use, genetic mutations, pregnancy, infections, and thrombophilic conditions. Patients typically present with headaches and may experience focal neurological deficits, seizures, or altered mental status due to increased intracranial pressure or brain infarction. Diagnosis involves imaging such as CT, MRI or angiography to detect the clot. Treatment consists of anticoagulation with heparin or warfarin for 3-12 months depending on risk factors

1. BY DR. SYED MUHAMMAD ADNAN
TMO MEDICAL A WARD
ATH
Dural Venus Sinus
Thrombosis

2. Contents
 Introduction
 Epidemiology
 Pathogenesis
 Clinical features
 Investigations
 Treatment
 Prognosis

3. Introduction
 Dural sinus thrombosis also called cerebral venus
sinus thrombosis.
 It refers to presence of blood clot inside Dural
sinuses or cerebral veins.
 DST is a form of cerebrovascular accident and is least
common of all.

4. Epidemiology
 DST accounts for 0.5 -1 % of all strokes
 Affects 5 people/1 million
 Commonest in middle east (due high prevalence of
 Behcet’s disease)
 Young > old 5:1
 Women > men 3:1

5. Etiology
. The exact mechanism is not known
.How ever it can be linked to Virchow’s triade
Thrombosis
Vessel wall
injury
Stasis
Hyper
coagulability

6. Risk Factors
 Exogenous Hormones; e.g. OCPs ( estrogen types)
 Genetic ; e.g. Inherited thrombophilia
 Mutation: Factor V Leiden Gene mutation and
Prothrombin G 20210A mutation
 Pregnancy and Puerperium specially 3rd trimester
 Malignancy

7. Risk Factors
 Infections; sinusitis, meningitis, ear/ face infection
 Trauma to head
 Thrombophilic conditions e.g.
a) Anti thrombin III, protein C and S deficiency
b) Antiphospholipid and anticardiolipin antibodies
c) Polycythemia

8. Risk Factors
 Nephrotic syndrome
 Bechet’sdisease
 Iron deficiency anemia
 Multiple myeloma
 IBD ( inflammatory bowel disease)
 Sickle cell disease

9. Pathogenesis
 IN DST blood clot is formed inside the veins of brain
and venus sinuses.
 Formation of clot results in increased venus pressure
congestion and engorgement of blood vessels and
near by brain tissue.
 This leads to decrease capillary perfusion, BBB
disruption, and cerebral edema

10. Cont:Pathogenesis
 Thrombosis of sinuses also results dec CSF
resorption and increased intracranial pressure and
could lead to intracranial hypertension

11. Clinical features
 Clinical findings fall in to 2 categories
1. Those due to increased ICT
 Headache 90% (Headache is diffused, and often progress
in severity over days to weeks)
 Minority of pts present wit thunderclap headache
 May be associated with vomiting , papilledema and visual
disturbances

12. Cont:Clinical features
2. Those due to brain infarction/hemorrhage
 Focal signs ; monoparesis/hemiparesis,Aphasia, cranial nerve
involvement, seizure
 Encephalopathy ( confusion, psychiatric like presentation)
 Drowsiness , stupor , coma

13. Cont:Clinical features
3. Others
 fever
 Elevated BP
 Tachycardia / bradycardia

14. Investigations
 Blood tests
a) Baseline blood
b) Septic screen/ viral screen
c) D-dimmers for DIC
d) Clotting profile; PT/PTT
e) Screening for potential prothrombotic condition ;
TTP etc
f) LP; elevated opening pressure in > 80%, Elevated
cell counts ( 50%) and proteins (35%) can be seen

15. Cont: Investigations
Imaging
1. Non Invasive
 CT
 MRI
 Ultrasonography
2. Invasive Imaging
 Cerebral angiography
 Direct cerebral venography

16. Treatment
 Seizures present in 37% of adults and 48% in
children diagnosed with DST
 Treatment is recommended after single episode of
seizure
 Prophylactic antiepileptics may be harmful

17. Cont: Treatment
 Medication like Mannitol , And Acetazoleamide can be used
 Neurosurgical intervention like shunting and
Decompressive Hemicraniectomy may be offered if
necessary.

18. Cont Treatment
1. Anticoagulation:
 Heparin or low molecular weight heparin followed by
warfarin.
 Dose for Heparin is 5000 units iv bolus followed by 1000
units /hour contineous infusion.
 LMW heparin is preferred over unfractionated heparin
 Presence of ICH is not contraindicated
 Adjust dose to achieve INR of 2-3

19. Cont: Treatment
• Anticoagulation therapy lasts 3-6 month for provoked DST
associated with transient risk factors e.g. hormonal
replacement therapy , pregnancy
• Anticoagulate for 6-12 month for unprovoked Cebrovenus
thrombosis, No known risk factor
• Indefinite anticoagulation is recommended for recurrent
DST, DST with severe thrombophilia or venus
thromboembolosm after DST

20. Cont: Treatment
 Thrombolysis
 European Federation of Neurological Society
guideline recommends thrombolysis only if patient
deteriorate despite adequate treatment
 Thrombolytic agents are given either systemically
via vein or directly into the clot during angiography
 The commonest drug used are Urokinases and tpA(
tissue plasminogen activator

21. Cont: Treatment
 Mechanical thrombolysis is done using Balloon
assisted thrombectomy
 Surgical thrombectomy is rarely done

22. Cont: Treatment
Other treatments:
Steroids incase of vasogenic edema
Antibiotics ( incase of associated infection)
Aspirin has no place in treatment of DST

23. Prognosis
 About 80 %pts with DST recovers completely
 It has 5 % mortality rate in early phase and 10 % in
late phase
 Main cause of death in early phase is herniation of
brain, diffuse brain edema, pulmonary embolism
 Death in later phase is generally due to underlying
cause like CNS infection or carcinoma

24. Predictors of Poor Prognosis
 CNS infection
 Any malignancy
 Thrombosis of deep venus system
 Intracranial hemorrhage
 GCS <9 on admission
 Age > 37
 Male gender

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