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2. CASE - 1
• 16/F , 10th std student
• kannur
• c/o headache
vomiting 20 days .
• HOPC : Insidious onset of right sided headache which was associated
with multiple episodes of vomiting.
• No history of seizures, altered sensorium, loss of consciousness,
weakness, bowel or bladder symptoms, neck pain, visual blurring.
There was no head in-jury/trauma/ear discharge/fever, cough,
breathlessness, chest pain , myalgia.
• Referred from a local hospital as anemia & thrombocytosis was
detected .
3. • Past history :No known comorbidities
normal birth and developmental history .
• Family history :No family h/o similar history/significant
neurological disease.
• Personal history :Mixed diet , sleep , appetite normal .bowel
/bladder normal
• Menstrual history : Irregular menses , h/o menorrhagea .
• GENERAL EXAMINATION
• BP-120/80 ; PR-73/mt ; T-afebrile ; GRBS-96
• Pallour present . No ICCLE
• CNS –NO FND , CVS –S1S2 Normal , RS- nvbs b/l , P/A-No hsm
5. CT Brain- No evidence of any ICSOL or focal parenchymal
lesions , Normal ventricles and subarachnoid spaces ,clear
paranasal sinuses.
• P.smear – microcytic hypochromic anemia, Leucocytosis
• Coagulation profile – normal
• USG-wnl
• Fundus- normal
• Iron -2.1(9-21.5) ,TIBC-84.1(39-85) ,ferritin-8.45(13-150)
• MRI Brain with MRV- s/o dural sinus thrombosis in right
transverse and sigmoid sinuses extending to proximal IJV.
6. ANA, Anti ds DNA
P and c ANCA negative
Protein c
Protein s
Factor V laiden mutation
S.Homocysteine – within normal range
Final diagnosis
Dural venous sinus thrombosis in right transverse and sigmoid sinuses
extending to proximal IJV.
Possibly due to anemia secondary thrombocytosis.
Pt started on heparin and later bridged with OAD.
7.
8.
9.
10. CASE-2
• 33/M
• kannur
• Bus conductor
• His complaints started as chest discomfort associated with
profuse sweating and was admitted in sahakarana hridayalaya .
He was diagnosed with inferior + posterior + lateral wall MI .
PTCA done , post procedure he was stable .
• 3 days later he developed excruciating headache feeling as if a
belt was tightened around his head . Pain worsened mainly on
coughing . Initially he was managed with analgesics which gave
him mild relief , but intensity and duration worsened over next
four to five days .
• He was shifted to dept of medicine for headache evaluation.
11. • No history of seizures, altered sensorium, loss of consciousness,
weakness, bowel or bladder symptoms, neck pain, visual blurring. There
was no head injury/trauma/ear discharge/fever, cough, breathlessness.
• Past History :detected with diabetes and hypertension two months
before presenting to hospital.
• Family History : No f/h/o diabetes hypertension , cardiac diseases.
• Personal history : consumes alcohol since last 8 years. mixed diet, sleep
appetite-normal
• Examination :
• Bp : 120/80 ; PR : 86 regular ; Afebrile
• No PICCLE
• CNS : HMF – wnl ; no fnd
• CVS – S1 S2N , no murmur.
• RS – AEBE ; NVBS b/l
• P/A : soft ; no organomegaly
16. • Patient was started on heparin infusion after consultation with
neurologist.
• Daily fundus examintion was done. Therapeutic csf drainage
was done thrice on alternate days to reduce csf pressure
below 25 cm of csf.
• Patient conditon improved. OAD started and was discharged.
17. CASE -3
• 25/M
• payyanur
• IT professional, Referred from Jubilee Hospital
• c/o Headache - 3days
weakness of Left UL - 1 day
• HOPC: His symptoms began as toothache of 3 days which subsided on
taking analgesics . 2 days later he developed progressively worsening
headache in right side of forehead not subsiding with medications . No h/o
radiation of headache or associated vomiting, diplopia, .He had to travel to
thrissur, and on the way from the car he developed sudden onset of
weakness of left upper limb associated with deviation of angle of mouth to
right side and slurring of speech . Consulted in jubilee mission hospital and
was referred to our centre.
• He developed multiple episode of focal seizure with secondary
generalisation from EMD.
18. • No history of seizures, altered sensorium, loss of consciousness,
weakness, bowel or bladder symptoms, neck pain, visual blurring.
There was no head in-jury/trauma/ear discharge/fever, cough,
breathlessness, chest pain , myalgia , loc , seizure .
• No h/o similar episode in the past , no any other known
comorbidities .
• No significant family history
• Personal H – mixed diet , bowel and bladder normal .
• EXAMINATION
• BP-130/60 , PR -88 , AFEBRILE , NO PICCLE
• Appeared moderately dehydrated.
• CNS- conscious , oriented , slurring of speech present
power – 5/5 , 0/3 . Plantar – bilateral extensor .
No neck stiffness , Left UMN Facial palsy present, Left conjugate gaze
palsy
• CVS , P/A , RS - wnl
21. • MRV S/o thrombosis of superior sagital sinus and right
transverse sinus . No parenchymal oedema or hemorrhage.
• Diagnosis
dural venous sinus thrombosis –sss and right transverse sinus
d/t ? Severe dehydration .
• Patient started on LMWH , anti epileptics and anti edema
measures.
• Condition improved dramatically such that he was symptom
free in 2 days.
22.
23. CASE-4
• 22/M
• vilayancode
• College student
• c/o headache – 3 days
• HOPC : His symptoms started as progressively worsening headache
mainly in right frontal side over 3 days .It was associated with
multiple episodes of vomiting , and also c/o diplopia .
• Past history : VZ virus infection 3 months ago .
• Family history – nil significant
• EXAMINATION :
• Bp -120/70 PR – 70/mt , Afebrile
• NO PICCLE
• CNS- drowsy .right eye appears adducted
• CVS- S1 S2 normal no murmur
• P/A – soft .no hsm
• RS – AEBE , Nvbs b/l .
25. • IDV- negative
• HCV- negative
• HBsAg- negative
• VDRl – negative
• VEP – normal in both eyes
• ANA – negative
• Anti DS – DNA – negative
• APLA profile – negative
• Hereditary thrombophilic workup – negative
• Vasculitic workup – P.ANCA- borderline positive
• Fundus - papilloedema
26. MRI BRAIN –s/o ethmoidal and sphenoidal sinusitis.
MRV – superior sagittal and rt lateral sinus thrombosis.
Diagnosis
Dural venous sinus thrombosis – sss and right lateral sinus
thrmobosis
d/t ethmoidal and sphenoidal sinusitis and ? Chicken pox.
Vasculitic workup planned.
27. • Patient treated with heparin, anti edema measures.
Therapeutic csf draining done.
• Patient improved and was dicharged with OAD.
28.
29. To summarize….
• All 4 case were dural venous sinus thrombosis
• Main highlight of this case series is that all were young individuals
,Less than 35 yrs.
• Case 1 ,patient had low hb and thrombocytois.
• case2 alcoholism ,diabetes, hypertension and h/o vascular
thrombosis in the form of MI
• Case3had history of dental infection with high Hb and features of
dehydration .
• Case4chickenpox,ear infection and had P-ANCA borderline
positivity with high hb.
• Incidence of CST is showing an increasing trend nowadays which can
be attributed to increased detection by radiological measures.
30.
31. BACKGROUND
Knowledge of the anatomy of the venous
system is essential in evaluating patients with
cerebral venous thrombosis (CVT), since
symptoms associated with the condition are
related to the area of thrombosis.
Diagnosis is missed because of the
heterogeneity in clinical presentation and
etiological factors.
43. CAUSE AND RISK FACTORS
thrombosis is almost never due to a single etiological
factor, it occurs only when several etiological factors
come together accidentally or incidentally. In normal
state the fluidity of blood is maintained by the
following factors
(1) normal intact endothelium; (2) prostacycline;
(3) antithrombin III (4) heparan sulfate;
(5) thrombomodulin; (6) protein C and Protein S;
(7) fibrinolytic System; (8) normal flow of blood;
(9) absence of a prethrombotic/hypercoagulable state
(thrombophilic state).
44. (thrombophilic states) to be routinely looked for
1)dehydration (even subclinical),
2)unusual postures in travel or sleep,
3)Prolonged immobilisation,
4)Surgery or trauma,
5)Focus of infection/inflammation/abscess adjacent to
the sinuses or in its drainage areas,
6)Pregnancy/postpartum period,
7)Hyperhomocysteinemia,
8)Polycythemias,
9)Thrombocytosis,
10)Obesity,
11)Diabetes,
12)Oral contraceptives,
13)Head Injury
46. hereditary thrombophilia- like
1)Factor V Leiden (APCR),
2)Prothrombin gene mutation,
3)Hereditary hyperhomocysteinemia,
4)deficiency of Protein C, Protein S,
5)Antithrombin deficiency,
6)Increased factor VIII, and
7)Dysfibrinogenemia
8)Resistance to activated Protein c
9)Prothrombin G20210A mutation
47. symptoms
Depending on the site, size, duration, and rapidity
of development of thrombus, it can present as
seizure alone,
space occupying lesion,
benign intracranial hypertension,
subarachnoid haemorrhage,
unexplained altered sensorium, or
meningoencephalitis
48.
49.
50. workup
• Cbc with esr - ? Polycythemia , TTP , sepsis
• APLA , Anti cardiolipin Antibody
• Protein c, s , antithrombin III , lupus anticoagulant , factor V
Laiden mutation
• Hb Electrophoresis , Urine protein , LFT ,RFT ,SE,CXR,RBS
• Anti Ds DNA , ANCA .
• D-dimer
• Lumbar Puncture
• EEG
• CT
• MRI with MRV
51.
52.
53.
54.
55.
56.
57.
58. A Per the European Stroke Organization (2017) , recommendations
include the following:
1)MRI or CT angiography is recommended for confirming the
diagnosis of CVT
2)Use parenteral anticoagulation in acute CVT and decompressive
surgery to prevent death due to brain herniation.
3)Use low-molecular-weight heparin in the acute phase and not
direct oral anticoagulants.
4)Do not use steroids and acetazolamide to reduce death or
dependency.
5)Antiepileptics are recommended in patients with an early seizure
and supratentorial lesions to prevent further early seizures.
6)Avoid contraceptives containing oestrogens in women who have
suffered a previous CVT.
7)Subsequent pregnancies are safe, but use of prophylactic low-
molecular-weight heparin should be considered throughout
pregnancy and puerperium