CEREBRAL VENOUS THROMBOSIS

1. DR. DIVAKAR REDDY M
MBBS;( DNB GENERAL MEDICINE)
CEREBRAL VENOUS
THROMBOSIS(CVT)

2. • Thrombosis of dural sinus and/or cerebral veins
• Uncommon form of STROKE
• 0.5% to 1% strokes
• CVT has diversity of causes and presenting scenarios
• YOUNG>>> OLD
• F:M- 3:1.. Pregnancy/peurepreum/ocp

4. ETIOPATHOGENESIS
• Predisposing conditions of CVT are multiple
• Risk factors for venous thrombosis In
general are linked clasically to VIRCHOWS TRIAD
Among all risk factors imp.. Prothrombotic conditions
• Important mechanisms involved in development of c/f..
a) Thrombosis of cerebral/dural sinuses leading to cerebral
parenchymal leisons/dysfunction
b) Occlusion of dural sinus leading to decreased CSF
absorption and raised ICT

5. RISK FACTORS
• INHERITED THROMBOPHILIA
Factor V leiden mutation
Prothrombin gene mutation
Protein S deficiency
Protein C deficiency
Anti thrombin deficiency
Homocysteinemia
Dysfibrogenemia
ACQUIRED DISORDERS
Malignancy CHF APLA
surgery IBD PNH
Trauma Nephrotic syndrome Polycythemia vera
Pregnancy HIV Multiple myeloma
OCP’ s HRT Myeloproliferative d/s
Hyperviscocity

6. Pathogenesis

9. CLINICAL FEATURES
• CVT has a highly variable clinical presentation
• It can present as… Acute, Subacute, Chronic
• Presentation as TIA also repoted
• Signs and Symptoms can be grouped into 3 main syndromes
• 1) ISOLATED INTRACRANIAL HYPERTENSION SYNDROME( Headache +/-
vomitings,papilledema,visual disturbances)
• 2) FOCAL SYNDROME( focal deficits, seizures, both)
• 3) ENCEPHALOPATHY( mutlifocal signs, mental status changes, stupor or
coma)
• Variables affecting presentation and course
Age
Presence of parenchymal leisons
Site and number of occluded sinuses and veins
Gender
Interval from CVT onset and presentation

10. HEADACHE
most frequent symptom
common in young pts and women
usually gradual in onset, often localised than diffuse but site of
headache has no relation to site of occluded vessel/ parenchymal leison
if due to ict.. Dull difuse and increases with valsalva and recumbency
SEIZURES
Focal/generalised
more common compared to other forms
ENCEPHALOPATHY
FOCAL SYMPTOMS AND SIGNS

11. INVESTIGATIONS
1) NEURO IMAGING
a) NON INVASIVE- CT,CTV, MRI ,MRV , ULTASOUND
b) INVASIVE - CEREBRAL ANGIOGRAPHY, DIRECT CEREBRAL
VENOGRAPHY
NON INVASIVE
CT,CTV
CT is initial modality in new onset neurological symptoms, often
normal
only around 30% cases abnormal
signs in CT associated with CVT
Dense triangle sign/Empty delta sign/ Cord sign
other fidings.. Hemorrhagic leisons/ non-hemorrhagic leisons like
edema venous infarction

12. MRI, MRV
MRI using gradient echo T2* susceptibility-
weighted sequences in combination with MR
venography is the most sensitive imaging
In the first five days, the thrombosed sinuses appear
isointense on T1-weighted images and hypointense on T2-
weighted images
Beyond five days, venous thrombus becomes more
apparent because signal is increased on both T1 and T2-
weighted images
After the first month, thrombosed sinuses exhibit a
variable pattern of signal, which may appear isointense
MRV, usually performed using the time-of-flight (TOF)
technique, is useful for demonstrating absence of flow in cerebral
venous sinuses, though interpretation can be confounded by
normal anatomic variants such as sinus hypoplasia and
asymmetric flow

13. • CEREBRAL INTRA ARTERIAL ANGIOGRAPHY is recommended
mainly when the diagnosis of CVT is uncertain, such as in the rare
suspected cases of isolated cortical vein thrombosis, or when
the clinical suspicion for CVT is high but CT venography or MR
venography are inconclusive
• Anatomic variations, such as variability of number and
location of cortical veins, hypoplasia of the anterior part of the
superior sagittal sinus, duplication of the superior sagittal sinus,
and hypoplasia or aplasia of the transverse sinuses, may make
the diagnosis of CVT by all types of angiography difficult
2) LAB INVESTIGATIONS
Role of D-DIMER- negative predictive value
Role of LP- to r/o meningitis, to measure csf pressure
ROUTINE LAB TESTS
TESTING FOR THROMBOPHILIA SHOULDNOT BE DONE IN ACUTE
STATE

18. TREATMENT
ANTICOAGULATION
OTHER TREATMENTS
FIBRINOLYTIC THERAPY
DIRECT CATHETER ABLATION
MECHANICAL THROMBECTOMY/ THROMBOLYSIS
SURGERY
• STEROIDS.. Useful in vasogenic edema but not recommended
routeinly. steroid medications are not recommended, even in the
presence of parenchymal brain lesions on CT/MRI, unless needed for
another underlying disease
ANTIBIOTICS
Local infection can cause CVT so appropriate antibiotics should
be adminsitered if needed surgical intervention should be done

19. ANTICOAGULATION
Initial anticoagulation by.. LMWH/ UFH( dose adjusted with a goal of
2-3 times control APTT)
Later.. oral Vit K Antagonists
Target INR- 2.0-3.0
DURATION..
1) Povoked CVT- 3-6 mon
(associated with transient risk factor)
2) Unprovoked CVT- 6-12 mon
3) recurrent/ CVT with severe THROMBOPHILIA / VTE after CVT-
indefinite anticoagulation
severe thrombophilia- deficeincy of protein c/ protein S/
antithrombin, APLA, homozygous factor V leiden, homozygous
prothrombin G20210A

20. • Testing for protein C,protein S, and antithrombin deficiency is
generally indicated 2 to 4 weeks after completion of
anticoagulation.There is a very limited value of testing in the acute
setting or in patients taking warfarin
• Special situation of CVT with cerebral hemorrhage on presentation
Anticoagulants appear to be safe to use in adult patients with
CVT who have intracranial hemorrhages, either intracerebral or
subarachnoid

21. • ENDOVASCULAR THROMBOLYSIS
Some patients with CVT worsen despite anticoagulant therapy.
Direct endovascular thrombolysis has been used as an
alternative treatment in such cases.
Direct thrombolysis aims to dissolve the venous clot by
delivering a thrombolytic substance (urokinase or rt-PA) within the
occluded sinus through an intravenous catheter.
In some cases, mechanical endovascular disruption of the
thrombus has also been used
• DECOMPRESSIVE HEMICRANIECTOMY
In patients with neurological deterioration due to severe mass
effect or intracranial hemorrhage causing intractable intracranial
hypertension, decompressive hemicraniectomy may be considered

23. COMPLICATIONS
EARLY
LATE
1)EARLY..
a)SEIZURES-
37% cases
Rx.. Controversial.. To initiate or await initial seizures before treatment
RECOMMENDATIONS
Early initiation of AED in pts with CVT and single seizure with
parenchymal leisons for definite period is recommended to prevent furthur
seizure
CVT with seizures withOUT parenchymal leison AED initiation is
probably recommended
Pts withOUT seizures routine use of AED not recommended
b) HYDROCEPHALUS
Communicating/ Obstructive
If obstructive- ventriculostomy/ VP shunt

24. c) INTRACRANIAL HYPERTENSION
40%
Rx.. Anticoagulation
LP
Acetazolamide
Decompressive craniotomy
LATE
HEADACHE
50%
Common complaint in follow up
Persistent/severe headache- r/o recurrence or intracranial HTN
In patients with a history of CVT who complain of new, persisting,
or severe headache, evaluation for CVT recurrence and intracranial
hypertension should be considered
VISUAL LOSS
SEIZURES
DURAL ARTERIOVENOUS FISTULA

25. CVT and PREGNANCY
one of risk factor because of hypercoaguable state
• The greatest risk periods for CVT include the third trimester and the
first 4 postpartum weeks
• Cesarean delivery appears to be associated with a higher risk of CVT
• women with a history of VTE appear to have an increased risk of
thrombotic events
• CVT is not a contraindication for future pregnancies
• Recommendations
1. For women with CVT during pregnancy, LMWH in full
anticoagulant doses should be continued throughout pregnancy,
and LMWH or vitamin K antagonist with a target INR of 2.0 to 3.0
should be continued for at least 6 weeks postpartum (for a total
minimum duration of therapy of 6 months)
2. It is reasonable to advise women with a history of CVT that
future pregnancy is not contraindicated. Further investigations
regarding the underlying cause and a formal consultation with a
hematologist and/or maternal fetal medicine specialist are
reasonable.

26. 3. It is reasonable to treat acute CVT during pregnancy with
full-dose LMWH rather than UFH
4. For women with a history of CVT, prophylaxis with LMWH
during future pregnancies and the postpartum period is
probably recommended

27. PROGNOSIS
CVT is associated with a good outcome (complete recovery or minor
residual symptoms or signs) in close to 80 % of patients.
Nevertheless, approximately 5% of patients die in the acute phase of
the disorder, and longer-term mortality is nearly 10%.
The main cause of acute death with CVT is neurologic, most often
from brain herniation.
After the acute phase, most deaths are related to underlying
disorders such as cancer
Causes of death in acute phase… TranstentorialHerniation, Diffuse
brain edema, Statusepilepticus, Medicalcomplications,
Pulmonaryembolism
cause of death in later phase is generally due to underlying cause
like cancer
• Neurological worsening may occur in 23% of patients, even
several days after diagnosis. Approximately one third of patients with
neurological deterioration will have new parenchymal lesions when
neuroimaging is repeated

28. Predictors of mortality at 30 days
• Depressed consciousness
• Altered mental status
• Thrombosis of the deep venous system
• Right hemisphere hemorrhage
• Posterior fossa lesions
Predictors of poor long-term prognosis
• Central nervous system infection
• Any malignancy
• Thrombosis of the deep venous system
• Hemorrhage on head CT or MRI
• Glasgow coma scale score <9 on admission
• Mental status abnormality
• Age >37 years
• Male gender

29. • Recanalization
In a systematic review of 5 small studies, recanalization rates of
CVT at 3 months and 1 year of follow-up were 84% and
85%,respectively.
The highest rates of recanalization are observed in deep
cerebral veins and cavernous sinus thrombosis and the lowest rates
in lateral sinus thrombosis.
In adults, recanalization of the occluded sinus is not related to
outcome after CVT.
A follow-up CTV or MRV at 3 to 6 months after diagnosis is
reasonable to assess for recanalization of the occluded cortical
vein/sinuses in stable patients
Recurrence
The risk of recurrent CVT is approximately 2 -4 %, while the risk of
recurrent venous thromboembolism in other locations ranges from 4
- 7 %

30. THANK YOU