Journal of the Association of Physicians of India
JAPI
Editor : Dr. Siddharth N. Shah
Journal of the Association of Physicians of India
JAPI
Editor : Dr. Siddharth N. Shah
Current Issue • July 2018 • Vol. 66
Original Article
Spectrum of Cerebral Venous Thrombosis in Uttarakhand
Sunil Jee Bhat1, Priyanka Vikas Kashyap2*
1
Senior Resident, 2
Assistant Professor, Shri Mahant
I n d i re s h H o s p i t a l, D e h ra d u n , U t t a ra k h a n d ;
*
Corresponding Author
Received: 02.07.2016; Accepted: 13.04.2018
Abstract
Background: CVT is an uncommon but important cause of stroke that is
often misdiagnosed delaying its treatment. High suspicion is essential in early
recognition and treatment.
Objective:To study the clinical features and etiology of patients with Cerebral
Venous Thrombosis (CVT) and relation between septic and non septic CVT if any.
Patients and Methods: A prospective study was done in SMIH that enrolled 40
patients of CVT in 2 years duration (Jan 2014 to Dec 2015). The patients were
diagnosed as CVT according to Magnetic Resonance Venogram (MRV) and clinical
status.
Results: Forty (40) patients of CVT were enrolled during 2 years period, most
were females (22/30) and aged between 18-50 years (mean age 30.2+4.9). Most
common presentation was headache followed by seizures and focal deficit.
Other symptoms encountered were cranial nerve palsies, meningeal signs,
papilloedema. Most common headache type was tension type headache.
Most common cranial nerve involvement was abduscens nerve. Superior Sinus
Thrombosis (SSS) involvement was most commonly thrombosed followed by
its involvement with other sinuses. Isolated lateral sinus involvement also seen.
On screening for cause, non septic CVT outnumbered septic CVT (22/8) and the
most common cause of non septic CVT was unknown followed by coagulation
defect. Among septic CVT group puerperial sepsis in females and mastoiditis in
males were the dominant cause.
Conclusion:Septic CVT prognosis had better than non septic CVT. Hence, CVT
presents with wide range of presentations and anticoagulation is the treatment.
Septic CVT if intervened timely with proper antibiotics have better prognosis.
Antibiotics are the mainstay of therapy for septic CVT.
Introduction
Cerebral venous thrombosis (CVT)
is an uncommon cerebrovascular
disease presenting with a remarkably
wide spectrum of signs and mode
onset.1
It was first described by Ribes
in 1825. The disease is characterized
by headache, papilloedema, seizures
a n d f o c a l n e u r o l o g i c a l d e f i c i t
culminating to coma and death and
pathophysiologically by hemorrhagic
infarction. 2 Advent of conventional
angiography and more recently MRV
allowed frequent recognition of CVT
cases. We present a series of CVT
patients with varied etiology.
CVT may occur as a complication of
infectious or noninfectious processes.
Although the majority of CVT is
actually due to non infectious causes,
however septic thrombosis is still a
potential life threatening complication
that needs to be recognized and treated
on emergency basis. The incidence
of CVT has dropped dramatically in
recent years. In the past, before the
introduction of antibiotics, infection
was the main cause of CVT, early
suspicion and recognition is very crucial
to reduce mortality and morbidity rates
of this potentially fatal disease. Unlike
non septic CVT, intravenous wide
spectrum antibiotics and early surgical
drainage of primary site of infection
whenever possible are essential in
septic CVT.
In this series, we highlight the
early use of antibiotics for CVT. The
vast majority of cases of septic CVT
have an acute presentation associated
with prominent features of sepsis. The latent period between symptoms
of the predisposing infection and the
clinical features of septic CVT varies
between one and twenty-one days,
but averaged about five to six days
in one series 3
.In our series, patients
presented within 3-5 days of the initial
infection. Pyrexia occurs in over 90
per cent of cases, which is usually
severe, and has a ‘picket fence’ pattern
suggestive of thrombophlebitis. Other
features of sepsis may be the presence
of tachycardia, vomiting, hypotension,
confusion, rigors and comatose. 3
Headache has been reported in about 52
– 90 percent and is typically unilateral,
with a retro-orbital or fronto-temporal
area distribution.4
The series highlights
that signs of infection in form of high
grade pyrexia, tachycardia and sick
appearance and evidence of local
infection in form of furuncle, ear
discharge or vaginal discharge are core
features of septic CVT which should be
taken in account during history taking
Material and Methods
We studied 40 patients of CVT
from January 2014 to December 2015
of 2 years period in Department of
Neurology, Shri Mahant Indiresh
Hospital, Dehradun. The patients
were enrolled both from Out Patient
Department and In Patient Department.
The diagnosis of CVT was made
on basis of history of unremitting
headache, focal deficit and confirmed
by MR venography. Patients more than
15 yrs of age were included in the study.
Patients whose radiological workup
does not confirm CVT were excluded
from the study. Institutional Ethical
Committee clearance was obtained for
conducting the study.
I n i t i a l A s s e s s m e n t i n c l u d e d
history taking of the patients who
presented with clinical manifestations
suggestive of CVT, such as headache,
altered mental status, seizures, focal
neurological deficits, especially in
the absence of the usual vascular risk
factors were considered for inclusion
into study. Past medical history was
obtained for each case. All medications
that were used by patients including
contraceptives use were noted.
All the participants were subjected
to a detailed physical examination,
including general physical examination,
a detailed neurological examination,
Glasgow coma scale 5 and examination
of other systems.
In all the patients, the following
l a b o r a t o r y t e s t i n g we r e c a r r i e d :
complete haemogram, coagulation
profile [bleeding time, clotting time,
prothrombin time with international
normalized ratio (INR) and activated
partial thromboplastin time]; workup
for other prothrombogenic disorders
(protein C and S, homocysteine levels);
rheumatological work-up including
rheumatoid factor (RF), antinuclear
antibody (ANA), anti-double stranded
deoxyribonucleic acid antibody (antidsDNA),
anticardiolipin antibody
(AcLa); and serological testing for
human immunodeficiency virus (HIV)
infection.
All patients were subjected to
Magnetic Resonance Imaging (MRI)
of the brain [T2 weighted (T2W) and
diffusion weighted (DWI) images] and
MR Venogram. Patients whose scans
were suggestive of other pathologies
such as arterial infarcts, tumors, arteriovenous
malformations were excluded
from the study. All the patients were
m a n a g e d a c c o r d i n g t o s t a n d a r d
guidelines.6
All the patients who have
definite evidence of CVT were admitted
in the neurology Intensive Care Unit.
The treatment included management of
predisposing/precipitating conditions,
antithrombotics, lowering intracranial
pressure and symptomatic treatment
for seizures, headaches. Patients with
CVT without contraindications for
anticoagulation were treated with doseadjusted
intravenous heparin with
an at least doubled activated partial
thromboplastin time.
Analogous to patients with a first
episode of CVT, oral anticoagulation
was given for 3 months if CVT was
secondary to a transient risk factor,
for 6–12 months in patients with
idiopathic CVT and in those with
mild thrombophilia. Indefinite oral
anticoagulation was given in patients
with two or more episodes of CVT
and in those with one episode of
C V T a n d s e ve r e t h r o m b o p h i l i a .
Other symptomatic measures such
as intravenous mannitol (100 ml, 6th
hourly), were instituted. Antiepileptic
drugs were started based on need. Large
haemorrhages and infarcts associated
with extensive cerebral oedema with
progressive deterioration in sensorium
were managed with decompressive
craniectomy. Further course of illness,
from hospital admission to the time of
discharge, was assessed by progression
of presenting complaints, neurological
deficits and mental status assessment
by Glasgow Coma Scale. We also
assessed the treatment outcome in
Septic versus non septic group. All
the patients recruited in the study
were assessed for functional status at
the end of their hospital stay using
Modified Rankin Scale (mRS)7
which
were classified as complete recovery - 0
to 1, partial recovery independent - 2,
partial recovery dependent - 3 to 5 and
death - 6.
Statistical Analysis
D a t a w e r e r e c o r d e d o n a
predesigned proforma and Excel 2007
(Microsoft Corporation, Redmond,
WA, USA) was used. All the entries
were double-checked for any possible
error. Descriptive statistics for the
categorical variables was performed by
computing the frequencies (percentage)
in each category. For the quantitative
variables, approximate normality of
the distribution was assessed. Variables
following normal distribution were
summarized by mean and standard
deviation.
40 patients of CVT were enrolled, 10
were excluded not satisfying inclusion
criteria. Thirty patients satisfying the
inclusion criteria were included in the
study.
Out of 30 patients, 8 were males,
22 were females, and their age ranged
from 18 to 50 years. Their mean age was
27.67±9.1 years. Most of the patients
were in the third decade of life; majority
was women (70%). Headache was
the predominant and first symptom
to bring patients to medical services,
in 90% of patients. Headache was
moderate to severe in 70%, and in rest it
was mild but nagging and not relieving
by any measures like sleep, analgesics
or rest. 10% of patients had seizures
and focal deficit in 16% of patients as
shown in Table 1.
Headache was tension type in 40%,
migrainous in 30% patients, 10% had
mixed type and 20% had Chronic Daily
Headache. Visual blurring was seen in
12 cases (40%). Focal neurologic deficit
was seen in form of hemiparesis was
noted in 2 patients (6%), aphasia in 2
(6%) and 1 had hemisensory loss. Cranial
nerve involvement was seen in 4 (13%)
patients and 3 (10%) had unilateral
VI palsy and on had associated VII
nerve along with abduscens palsy.
Seizures seen in 3 (10%) patients
and all had focal with secondary
generalization. The mode of onset of
symptoms was also highly variableacute
(<30 hrs) headache in 16 (53%)
patients, subacute (>1 month) headache
along with visual blurring and cranial
nerve involvement in 8 (26%) patients
and progressive in 6 (20%) patients
over months and had exacerbation
of headache intermittently. Neuro
imaging in form of Magnetic Resonance
Imaging of Brain with venogram was
done in all patients. The results were as
follows. Venous sinus thrombosis was
present in all the patients. Hemorrhagic
infarction was seen in 22/30 (73%)
patients, non hemorrhagic infarct was
present in 8/30 (26%) patients. Saggital
Sinus Thrombosis (SSS) was the most
common sinus involved (78%) with
either partial or complete occlusion.
Its involvement with other sinuses
was seen in 14 % patients and isolated
lateral sinus thrombosis was seen
in 5% and lateral and straight sinus
thrombosis was seen in rest 3% patients
as shown in Table 2.
Etiology
A m o n g t w e n t y - t w o f e m a l e s
patients, contraceptive pills were
used by 5 females and rest 6 were
in post partum state with duration
varying from 2 weeks to 8 weeks.
Evidence of puerperial sepsis was
seen in three postpartum females,
diagnosis made on basis of history of
foul smelling discharge per vaginum,
lower abdomen pain and culture of
vaginal swab. Culture from vaginal
swab grew staphylococcus aureus and
pseudomonas aueroginosa.
Among all 30 CVT patients, 8 had
septic cause, 5 were females and 3
were males. One male had mastoiditis
and rest two males had furuncle over
face area. Three females had puerperial
sepsis as mentioned above and 2 had
furuncle over upper lip region. These
septic CVT patients presented with
high grade fever, facial erythema
and swelling and headache. Among
non CVT patients, no cause could be
attributed in 14 patients and 4 were
found to have coagulation disorder,
most common being antithrombin III
(3 patients) and protein S deficiency
(1patient). Collagen vascular profile
was negative in all patients so as anti
phospholipid antibody workup as
shown in Table 3.
Septic CVT patients had more
acute presentation, more severe, they
responded to treatment early and
dramatic than non septic CVT pts. Two
patients among non-septic CVT died
of raised Intracranial pressure (ICP)
and cerebral herniation underwent
d e c o m p r e s s i v e c r a n i o t o m y b u t
developed ICU complication in form
aspiration pneumonitis.
Septic CVT patients had sudden
onset erythema of eyelids and limitation
of ocular movements which alerted
the possibility of CVT. All patients
received heparin. Septic CVT patients
received antibiotics in addition to
anticoagulants and short duration steroids and improved.
Discussion
Septic CVT can occur at any age
but typically affect young adults,
most commonly in the 3rd decade of
life. The incidence is approximately
15% of all the cases of CVT8 that
is 3 - 4 /1,000,000 with 3:1 female
predominance.9
Although rare, septic
vein thrombosis (SVT) remains a
potentially lethal complication of
infections that involve the sinuses,
face, ears and oral cavity. The early
recognition and differentiation from
other diseases are keys to reducing
mortality rates and long term sequelae.
The dural sinuses and the cerebral and
emissary veins have no valves, which
allow blood to flow in either direction
according to pressure gradients in
the vascular system. This makes this
venous system vulnerable to septic
thrombosis resulting from spreading of
infection from adjacent locations. Septic
CVT involves mainly the cavernous
sinus followed by lateral and then
sagittal sinus.10 Infection may trigger
the thrombosis directly by causing
septic thrombosis or indirectly by
precipitating thrombosis in people who
suffer from a prothrombotic illness.
Early diagnosis can be facilitated by
prompt recognition of the clinical
and radiological findings that are
suggestive of venous occlusion of the
cavernous sinus. Bacterial meningitis
and paranasal sinusitis can be a
Complication of superior sagittal
thrombosis, resulting in an 80 %
mortality rate.11
Septic CVT patients are more toxic
with features of facial infection. They
would present with acute onset of
headache, fever, and vomiting, facial
redness and painful eyelid edema.
Fever is a constant finding as was
in our patients as well as orbital
symptoms may start in one side then
very shortly within 24-48 hours become
bilateral. Patients usually have the
triad of chemosis, proptosis (due to
orbital vein congestion) and painful
ophthalmoplegia (due to involvement
of III, IV, VI) with occasional ophthalmic
branch of trigeminal cranial nerve
involvement. Papilloedema is seen
in some patients and is usually mild
and late. It was present in 8 patients
in our series. Decreased visual acuity
is reported in less than 50% cases,
pupils can be dilated (parasympathetic involvement) or smaller and immobile
(both parasympathetic and sympathetic
dysfunction). Impaired vision is
uncommon. Nevertheless, visual loss
may be caused by corneal ulceration
secondary to proptosis and loss of the
corneal reflex, occlusion of the internal
carotid, ischemic optic neuropathy,
orbital congestion, toxic neuritis of the
optic nerve, or embolic phenomena.12
In our series, septic thrombosis
patients were much sicker than those
with non septic thrombosis. The illness
is almost always acute in nature and
patients were sick, toxic and febrile.
Some had focal symptoms and signs
suggestive of raised intracranial
pressure varying on site of CVT, but
responded early and better with lesser
morbidity and mortality as compared
to non septic group.
Clinically, the differential diagnosis
includes meningoencephalitis, orbital
cellulitis, orbital apex syndrome and
non septic CVT. In Sebire et al series,
23/42 patients had infection precipitated
venous thrombosis emphasizing that
people with prothrombotic conditions
may develop thrombosis after having
any systematic infection13 and blood
culture was positive in 70% of cases.
Reviews of large single center series
from the pre-antibiotic and early
antibiotic era had documented that
infections of the middle third of the
face were responsible for most cases of
Septic CVT. It was seen in 4 patients of
Septic CVT in our series. Approximately
60 to 80% of these nasal furunculosis
accounts for the most common cause.14
Organisms may reach the cavernous
sinus from the face by an anterograde
route along the ophthalmic veins,
which is connected to the angular
veins, or by a retrograde route along
the emissary veins that are connected
to the pterygoid venous plexus. In up
to 25 percent of cases where a facial
furuncle is responsible, it has either
been previously manipulated by the
patient or incised by the surgeon.15
Staphylococcus aureus is the most
frequently cultured organism in these
infections accounting for 70 %, followed
by Streptococcus species at 20 %.16 In our
cases, patients had different source of
infections like furunculosis, puerperial
sepsis, mastoiditis. The most sensitive
i n ve s t i g a t i o n o f i n t r a c a ve r n o u s
occlusive defects is venography.
Previously, Cerebral angiography
with late venous views was considered to be gold standard in the diagnosis
of CVT. but nowadays, it has been
reserved for the definitive assessment
of intracavernous aneurysms after they
have been detected and monitored using
CT or MRI.17 Diagnosis of cavernous
sinus thrombosis is usually made with
MRI scan with venogram; or contrast
enhancement Computed Tomography.
Fine -cut CT scan is less sensitive.11
Because it is often difficult to
distinguish septic and non-septic
causes of CST, the initial management is
the same. Only when a septic etiology is
ruled out definitively can antibiotics be
withdrawn. Antibiotics are the mainstay
of CST therapy. Anticoagulation,
c o r t i c o s t e r o i d s , a n d s u r g e r y a r e
adjunctive treatment in appropriately
s e l e c t e d p a t i e n t s . U n d o u b t e d l y ,
antibiotics have the greatest impact
on the prognosis of SVT.18 The overall
mortality and morbidity associated
with cavernous sinus thrombosis (CST)
continue to be high. Consequently,
institution of intensive treatment
at the earliest suspicion of disease
should be emphasized. Postmortem
studies have shown that there is
less extensive thrombosis within the
cavernous sinuses since the advent of
antibiotics.10 Case reports and expert
opinion recommends antibiotics have
the greatest impact on the prognosis
of septic CST. High-dose intravenous
a n t i b i o t i c s s h o u l d b e i n s t i t u t e d
emergently at the earliest suspicion of
this diagnosis. Appropriate selection
of empiric antibiotic regimens should
be directed at the probable organisms
implicated as the primary source of
infection. Complications such as brain
or orbital abscesses, meningitis or
subdural empyema should be kept in
mind as these need surgical intervention
at the earliest. 19,3 Staphylococcus
aureus is the most common pathogen
identified in approximately 70% of
cases and is seen in nearly all cases
of facial infections and sphenoid
sinusitis.20 Our series also found this
pathogen common in septic CVT
group. Less common is Streptococci
(including S pneumoniae, S milleri,
and S viridans group). Infections
of nasal sinus, dental, or tonsillar
infections show anaerobes. Fungal
infections from Aspergillus fumigatus
or mucormycosis have been implicated
rarely in CST. Therefore, empiric
therapy should include vancomycin to
cover for potential methicillin-resistant
Staphylococcus aureus (MRSA) until
the actual culture results are available
plus a third-generation cephalosporin,
such as ceftriaxone. Quinolones should
be used in patients allergic to penicillin.
Intravenous metronidazole should
be added if dental or sinus infection
is suspected. Antifungal therapy has
been advocated only in cases of biopsyconfirmed
invasive fungal infection.
Vancomycin is used routinely until
culture results negate MRSA. It is
also indicated for patients who have
failed to respond to penicillins and
cephalosporins. Empiric antibiotics
can be switched to specific antibiotic
therapy once culture sensitivities
reports are available. Intravenous
a n t i b i o t i cs a r e r e q u i r e d b e c a u se
thrombus may limit penetration of
antibiotics. Bacteria, sequestered within
the thrombus, may not be killed until
the dural sinuses have started to
recanalise. Antibiotics also need to be
administered over an extended period,
for at least 2 weeks beyond the time of
clinical resolution and in high doses.
This insures complete sterilisation and
prevents relapses. Supportive therapy is
includes resuscitation, oxygen support,
and local eye care. Considerable
controversy exists concerning the
efficacy of anticoagulation in the
treatment of CST. As the condition
is rare, prospective trials to establish
any benefit from anticoagulation
a r e u n l i k e l y t o b e p e r f o r m e d .
Anticoagulation carries the risk of
hemorrhage, especially in patients
with concomitant complications (e.g.,
cortical venous infarction, necrosis
of intra-cavernous portions of the
carotid artery, and cerebral or intraorbital
haemorrhages). 11,21 Tw o
retrospective reviews examining the
use of anticoagulation for septic CST
produced varying results (Level C
evidence). However, some evidence
says that the use of anticoagulation
prevents propagation and contributes
to re-canalisation of the thrombus.
These are potentially beneficial effects,
partly because the thrombus itself can
harbour bacteria and sustain their
growth.
Two controlled trials comparing
the use of placebo to anticoagulants
in patients with cerebral sinus venous
thrombosis. European Federation
of Neurological Societies (EFNS)
guidelines recommend either low
molecular weight subcutaneous or
intravenous heparin for aseptic dural
venous thrombosis. European Paediatric
Neurology Society (EPNS) in 2012
recommend the use of anticoagulants
for dural venous thrombosis to lessen
the risk of death and other sequelae.
However, it should be noted that
septic CST and aseptic dural venous
thrombosis differ in many respects
and that anticoagulation may be more
hazardous in patients with septic
CST. The differences include the
presence of infective etiology, the
site of the thrombosis, the acuteness
of the process, and the presence of
associated haemorrhagic complications.
Anticoagulation should be cautiously
used in patients with bilateral CST
a n d / o r c o n c u r r e n t i n t r a c r a n i a l
haemorrhage. The types and protocols
f o r a n t i c o a g u l a t i o n h a ve va r i e d
considerably in research protocols.
I n t r a v e n o u s a n d i n t r a m u s c u l a r
unfractionated heparin, subcutaneous
low molecular-weight heparin (LMWH),
and oral coagulation have all been used.
Intravenous unfractionated heparin
is rapidly reversible agent hence,
advocated in the early stages of disease,
followed by conversion to longer-acting
agents, such as warfarin, when the
patient’s condition has stabilized. 22
New anticoagulants, including direct
thrombin inhibitors and factor Xa
inhibitors has a more predictable
anticoagulant effect and an absence
of induction of immune-mediated
heparin-induced thrombocytopenia
(HIT). But there is a paucity of reported
cases of CST or other forms of dural
sinus thrombosis that have been
treated with these agents. The use of
direct thrombin inhibitors, such as
argatroban, can be considered as an
alternate form of anticoagulation to
heparin in patients with HIT (Heparin
Induced Thrombocytopenia) or those
at risk of HIT. Regarding duration
of anticoagulation, some authors
have suggested that anticoagulation
should be continued until clinical or
radiological evidence of complete
r e s o l u t i o n o r u n t i l s i g n i f i c a n t
improvement of infection and thrombus.
If a patient is considered suitable for
anticoagulation but deteriorates despite
this therapy, they may be considered
for thrombolysis. This therapy is
usually reserved for progressive,
aseptic CST and carries with it the
risks of intracranial haemorrhage,
stroke, and the inability to re-cannalise.
Patients commenced on anticoagulants
are usually still in an unstable clinical
c o n d i t i o n a n d a r e t h e r e f o r e n o t
candidates for surgical management.
However, if the patient’s condition
stabilises and surgical management
i s i n d i c a t e d , r a p i d l y r e ve r s i b l e
anticoagulants can be discontinued
to allow surgery. Corticosteroids has
controversial role in many cases of CST
because of their potentially harmful
immunosuppressive effects. However,
they are absolutely indicated in cases of
pituitary insufficiency and Addisonian
crisis secondary to ischaemia or necrosis
of the pituitary that complicates CST.
Steroids may be essential in the acute
setting to prevent Addisonian crisis 15
as well as in replacement doses in the
long-term. 23 Corticosteroids reduce
intraorbital congestion in patients
with orbital oedema and cranial nerve
inflammation in patients with cranial
nerve dysfunction. There are only a
few anecdotal reports concerning the
use of corticosteroids in CST in general
and their efficacy has not been proved
by these reports. Studies in which
the use of corticosteroids has been
reported, other treatments have been
used concurrently. In one case, reported
in 1962, cranial nerve dysfunction and
orbital oedema failed to improve after
37 days of antibiotic and anticoagulant
therapy but regressed dramatically 2
days after the addition of corticosteroid
therapy, with eventual complete
resolution in eye signs and symptoms.
Prompt drainage of the primary site
of infection (such as the para-nasal
sinusitis, dental abscess) or other
concurrent closed-space infection
is advisable once patient condition
permits. Different operations have been
performed to decompress the sinuses,
including transeptal sphenoidectomy,
e n d o s c o p i c s p h e n o i d e c t o m y a n d
ethmoidectomy and external frontoethmoido-sphenoidectomy.
In cases
of otogenic CST, mastoidectomy has
been performed, with decompression of
sigmoid sinus thrombophlebitis.
Summary
To summarize, CVS is associated
with significant mortality, which is
estimated at 30% but can range from 14
- 79 % according to some case reviews.
Approximately half of patients will
suffer a residual morbidity, typically
from associated cranial neuropathies.24
Overall therapeutics for CVT need
larger randomized controlled trials. Anticoagulation with heparin is the
only modality with reasonable evidence
to support its use in CVT, even in
patients with cerebral hemorrhage.
E n d o va s c u l a r t h r o m b o l y s i s i s a
promising option for patients with a
severe form of CVT or following a failure
of anticoagulation therapy. Mechanical
thrombectomy is reserved for selected
cases and decompression surgery
for malignant CVT with impending
herniation.25 With increasing awareness,
not only is CVT being diagnosed more
frequently, but less clinically severe
cases of CVT are also being detected
presently. However, despite substantial
improvements, the diagnosis of CVT is
often missed because of the remarkable
variations in the clinical presentation
and neuroimaging signs. Furthermore,
existing studies on CVT patients are
often limited by small numbers; their
retrospective nature and short term
follow-up periods.26 Thus, CVT remains
a diagnostic and therapeutic challenge,
and scanty information still exists
on the natural history and long-term
prognosis of this disease. Most patients
with CVT have a benign prognosis.26
Only a minority of patients die during
the acute phase or in the following
months. Most patients surviving CVT
recover completely, or have only mild
functional or cognitive deficits.
Limitation of the study
The number of CVT patients was less
and that of Septic CVT group further
less which limits the definite conclusion
on etiology causes and treatment
guidelines.
But, inspite of lower number, the
study strengthens the fact that septic
CVT should be kept as high index of
suspicion and timely management with
antibiotics and steroids can decrease
the mortality in these patients.
Acknowledgement
We are thankful to the statistical
department and computer department
for their valuable help.
References
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