Cerebral Venous Thrombosis

1. Dr. AMIT ANAND
JR1 MEDICINE

2.  Introduction & Epidemiology
 Anatomy of cerebral venous sinuses
 Risk factors
 Pathogenesis
 Clinical presentation
 Suppurative thrombophlebitis
 Diagnosis and Imaging
 Treatment

3.  Thrombosis of the cortical veins & draining Dural venous sinus either alone or in
combination.
 An uncommon and frequently unrecognised type of stroke that
affects approx. 5 per million annually and accounts for 0.5% to1% of
all strokes.
 CVT is more commonly seen in young individuals.
 EPIDEMIOLOGY
 • 3-4 cases per million in adults
 • Most common in 3rd decade of life
 • 75% are female
 • Older studies show no difference in gender and it is believed that use of oral contraceptive have
played a role
 • Accounts for 50% of strokes during Pregnancy and Peri partum period & imp. Cause of maternal
morbidity and mortality in India.

8. • Thrombotic disorders.
• Factor V Leiden Mutation – mc.
• Protein C and Protein S deficiency.
• Antithrombin III deficiency
• Antiphospholipid syndrome
• Lupus anticoagulant
• Nephrotic syndrome
• Chronic inflammatory diseases such as IBD (felt to be mediated by
endotoxins and abnormalities of the fibrinolytic system, platelet count
and functions)
• Collagen vascular diseases – Lupus, Wegeners, Behcet’s syndrome
• Hyper-homocysteinaemia .

9.  • Pregnancy and peripartum period
 • Polycythemia Vera
 • Paroxysmal Noctural Hemoglobinuria
 • Oral Contraception use (estrogen containing)
 • Infection - Meningitis, otitis media, sinusitis, mastoiditis
 • Direct injury to the venous sinuses
 Dehydration
 Moderate to severe Anemia Hb < 10
 Genetic cause- Polymorphism in MTHFR 677C >T , Prothrombin
(factor 2 ) gene.

10.  • Formation of blood clots in the veins as well as venous sinuses of the
brain d/t Hyper- coagulable state , decrease Fibrinolytic activity , slowing of
circulation , damage to endothelium& others.
 • Thrombosis of the veins cause infarcts to associated brain tissue and can
result in cerebral oedema.
 • Infarcts can lead to Haemorrhages (40% can progress to hemorrhagic
infarcts)
 • Sinus thrombosis leads to decreased resorption of the CSF leading to
increased intracranial pressure
 • Most cases of cerebral venous sinus thrombosis are due to
hypercoagulability
 • Thrombosis can lead to embolization and Pulmonary Embolism (occurs
in 10% of patients)

11. CLINICAL PRESENTATION:-
Depend upon on the – which sinuses involved , speed of occlusion ,
involvement of the cortical veins and presence of collaterals.
• Headache (sudden or gradual ) – in 90% of patients.
• Focal nuerological signs esp. paraparesis – in 50% of patients
• Seizures (usually affect only one part of the body) – in 40-70% of patients.
• Increased intracranial pressure leading to visual changes, papilloedema
• Other: nausea/vomiting, vestibular neuropathy, pulsatile tinnitus, double
vision, unilateral deafness, facial weakness.

12.  Septic venous thrombosis of cortical veins and sinuses.
 The cortical veins and sinuses have no valves so blood within
them can flow in either directions leading to spread of
infections from meninges, Subdural Empyema or Epidural
abscess.
 Septic transverse/sigmoid venous thrombosis – can be a
complication of otitis media or mastoiditis.
 Cavernous sinus – receives blood from facial veins via superior
and inferior ophthalmic veins.
 Sphenoid and ethmoid sinus are the most common sites
of primary infection resulting in Septic cavernous sinus
thrombosis. Infection spreads via emissary veins.

13. Septic thrombosis of superior sagittal sinus :-
 Headache, fever, nausea, vomiting, confusion, focal or generalised seizures
 Rapid development of stupor and coma.
 Weakness of lower extremities with B/L Babinski’s sign positive and hemiparesis.
 In meningitis- nuchal rigidity, Kernig’s sign, Brudzinski’s signs present.
Septic cavernous sinus thrombosis:-
 Fever, headache, frontal and retro orbital pain, diplopia
 Classic signs – Ptosis, Proptosis, Chemosis ,and Extraocular dysmotility due to
3,4,6 cranial nerve involvement.
 Hyperaesthesia of ophthalmic and maxillary division of the 5th nerve and
decreased corneal reflexes.
 Dilated tortuous retinal veins and papilloedema.

14. Classic signs of Cavernous Sinus
Thrombosis

15.  Transverse sinus thrombosis:-
 Headache and earache – most frequent symptom
 Gradenigo’s syndrome : *Otitis media
*Sixth nerve palsy
*Retro-orbital or facial pain
 Sigmoid sinus and int jugular vein thrombosis –
may present with neck pain

16.  • CBC & blood cultures , sinus culutres.
 • Antiphospholipid and anticardiolipin
antibodies
 • Protein S • Protein C
 • Antithrombin III
 • Lupus anticoagulant
 • Factor V Leiden
 • Hb Electrophoresis
 • ESR
 • ANA
 • Urine protein
 • LFT

17. • Most sensitive - MRI and MR Venography
 Diagnosis of septic venous sinus thrombosis is suggested by ‘absent flow void’ within
the affected venous sinus on MRI.
 confirmed by MR Venography.
• DSA :- is gold standard & it shows– filling defects.
• Cerebral Angiography – may be able to demonstrate smaller clots than MRI and CT.
• On CT :- shows Directs signs of CVT like- a. Cord sign b. Dense Delta sign c.
Empty Delta sign.
• Indirect signs :- venous stasis and hyperemia d/t occlusion of SS & SSS lead to intense
enhancement of the falx cerebri & tentorium.

23.  Main priority to stabilise the pt. Condition & to prevent or reverse cerebral
herniation.
 Riased ICT :- Rx.- Osmotic agents such as Mannitol , Acetazolamide with
supportive ventilation.
 Antiepileptic medication.
 Treatment of underlying cause.
 SEPTIC THROMBOPHLEBITIS :-
 Antibiotics – antimicrobial based on bacteria responsible for associated condition.
Duration – atleast 6 weeks or till radiologic evidence of resolution of thrombosis.
 Hydration – IV fluids.
 Removal of infected tissue and thrombus in lateral / cavernous sinus thrombosis.
 Anticoagulant therapy with Iv heparin given in those patient with progressive
neurologic deterioration despite antimicrobial and iv fluid therapy. Given even in
small intracerebral haemorrhages.

24.  Aseptic venous sinus thrombosis
 IV Heparin is the mainstay of treatment, regardless of intracerebral
haemorrhages
 It reduces morbidity and mortality and long term outcome is generally
good.
 Heparin prevents further thrombosis and reduces venous hypertension
and ischemia.
 Surgical embolectomy
 Catheter directed urokinase therapy
 Combination of intrathrombus rtPA and iv heparin.
 If hypercoagulable state not found, Vitamin K antagonists
given for 3-6 months then convert to Aspirin
 If thrombophilia diagnosed, Anticoagulation is continued for
lifetime.

26. CVT DURING PREGNANCY :-
Rx. – LMWH in full anticoagulation doses continued throughout pregnancy &
LMWH OR Vitamin K antagonist should continued at least 6 weeks postpartum
with target INR of 2-3 for a total minimum duration of therapy of 6 month.
Course and Prognosis :- > 80% have good neurological outcome.
Poor Prognostic Factor:-
1. Prolonged deep coma.
2. Massive Haemorrhagic infarction with midline shift & Brainstem
compression.
3. Rapidly progressive course
4. Involvement of Deep venous sinuse.
5. Infection & cancer