CVST Flashcards

(20 cards)

1
Q

Epidemiology

A
  • Accounts for ~1% of all strokes.
  • Affects young patients, 20–50 years old.
  • 3-fold female predominance
    =>CVST is primarily a disease of young, often female, hypercoagulable patients.
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2
Q

Risk factors

A

=>Thrombophillic states:
* Pregnancy
* Hormone therapy- HRT/ OCPs
* Heriditary thrombophilic states
* Autoimmune diseases- APLA;
* Malignancy
* Drugs- Chemotherapy; Heparin

=>Head and Neck infections:
* Sinusitis
* Otitis media
* Mastoiditis
* Meningoencephalitis
* Cerebral abcess

=>Mechanical causes:
* Trauma- base of skull fractures
* EVD
* I J CVC
* Dural A-V fistula

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3
Q

Risk factors

A

=>Thrombophillic states
=>Head and Neck infections
=>Mechanical causes

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4
Q

Clinical Features

A

=>Presentation is often progressive rather than hyperacute (unlike arterial stroke).
Median delay to diagnosis ≈ 1 week
=>Evolution may be:
* Acute
* Subacute (several days)
* Chronic (>1 month)

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5
Q

Clinical Features

A

=>Depend upon the site of thrombosis
1️⃣=>Headache-> May worsin lying flat/ Valsalva
->Pain localization:
* Sigmoid sinus → occipital / neck pain
* Lateral sinus → mimics ear infection

2️⃣=>Features of raised ICP:
* Nausea, vomiting
* Vision changes
* Diplopia
* Papilledema (~30%)
* CN VI palsy
* Encephalopathy

3️⃣=>Focal Neurological Deficits
* Hemiparesis (most frequent)
* Dysarthria
* Aphasia
* Visual impairment
* Cranial neuropathies–>Especially with cavernous sinus thrombosis

4️⃣=>Seizures
* Usually focal ± secondary generalization
Seizures are more common than in arterial stroke.

5️⃣=>Diffuse Encephalopathy / Reduced LOC
->Mechanisms:
1. Communicating hydrocephalus
2. Deep venous system occlusion
* Bilateral thalamic dysfunction
* May cause:
* Mutism
* Amnesia
3. Intracranial hemorrhage
4. Cerebral edema → herniation
* Fever-+/-

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6
Q

Cavernous sinus thrombosis
Clinical Features

A
  • Painful ophthalmoplegia
  • Proptosis
  • CN III, IV, VI palsies
  • V1/V2 sensory loss
  • Fever (if septic)
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7
Q

Symptoms in detail

A

1️⃣ Oculomotor palsies
* CN III→ Ptosis (CN III)
* CN IV
* CN VI
→ Ophthalmoplegia
→ Diplopia
CN VI is often affected early (medial position within the sinus).


2️⃣ Trigeminal sensory loss–>Facial numbness due to involvement of:
* V1 (ophthalmic)
* V2 (maxillary)


3️⃣ Headache->severe, periorbital pain common


4️⃣ Ocular findings
* Orbital pain
* Conjunctival redness
* Proptosis
* Loss of visual acuity

Mechanism:
* Impaired venous drainage of orbit
* Raised orbital venous pressure

5️⃣ Fever
* May occur in septic cavernous sinus thrombophlebitis

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8
Q

Causes of Cavernous Sinus Thrombosis

A

=>Most common:
* Infection- Facial infection, Sinusitis, Orbital cellulitis

=>Inflammatory / autoimmune

=>Structural / mechanical:
Trauma, Meningioma

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9
Q

Pathophysiology

A

=>Dural venous sinuses lack valves, allowing multidirectional flow.
* Venous anastomoses permit partial rerouting of blood around a thrombus, hence compensate to an extent

=>If venous pressure rises:
1). Cerebral edema
* Elevated capillary pressure
* Reversible if occlusion resolves
2). Ischemic infarction
* Due to tissue blood stasis
* May become irreversible
* Elevated venous pressure + infarct → hemorrhagic transformation

=>CSF physiology:
* Venous sinuses drain CSF via arachnoid granulations (into superior sagittal sinus).
* Sinus thrombosis → impaired CSF absorption.
* May cause communicating hydrocephalus (ventricular dilation + ↑ ICP).
* Most problematic with superior sagittal sinus thrombosis.

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10
Q

Invx for CVST

A

=>D dimer
=>Imaging-

->Non-enhanced CT / MRI
* Sensitivity ≈80%
* Non-enhanced MRI is superior to non-enhanced CT

->CT Venography (CTV)
* Sensitivity ≈ 99%
* Specificity ≈ 88%

->MR Venography (MRV)
* Slightly superior for:
* Isolated cortical vein thrombosis
* Deep venous thrombosis
* MRI/MRV = gold standard if available

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11
Q

Direct Signs of the Clot on Imaging

A

=>Non-contrast CT
* Dense triangle sign–>Superior sagittal sinus thrombosis
* Dense cord sign–>Cortical or deep vein thrombosis

=>CT Venography
* Filling defect
* Classic: Empty delta sign
* Acute clot may appear dense like contrast

=>MRI Normal:
*	Dural sinuses = flow voids (T2/FLAIR) Abnormal:
*	Loss of flow void → thrombosis
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12
Q

Tt

A
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13
Q

Specific Tt

A

1️⃣ Anticoagulation (Mainstay)
Initial therapy:
* Heparin anticoagulation
* Transition to warfarin or DOAC after ~5–15 days

=>Intracranial hemorrhage–> NOT a contraindication
* Hemorrhage extension uncommon
* Risk of thrombus extension without anticoagulation is greater

=>UFH vs LMWH
* No robust evidence one is superior
->LMWH–>Preferred in mild cases if unlikely to need procedure

->UFH infusion
* Preferred in critically ill
* Easier reversal if EVD/craniectomy required
* Must avoid supra- or subtherapeutic levels

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14
Q

Seizure Mx

A

2️⃣ Seizure Management

=>Risk factors
* Supratentorial cortical lesions
* SAH
* Focal edema or infarct
* Focal neurologic deficits

=>Prophylaxis
* Generally not recommended
* Consider in high-risk individuals
=>EEG if:
* Altered mental status
* Possible non-convulsive seizures

If seizure occurs:
* Treat aggressively
* Even a single seizure → start antiepileptic

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15
Q

3️⃣ Communicating Hydrocephalus & Papilledema

A

=>Mechanism:
* Impaired CSF drainage into venous sinuses → ↑ ICP

=>Clinical:
* Papilledema
* Visual field deficits

=>Mx:
->Acetazolamide
* 500–1000 mg/day-> Reduces CSF production

Cautions:
* Causes bicarbonate wasting → may need supplementation
* Contraindicated in pregnancy

->CSF drainage:
* EVD–> Rarely required
* Lumbar puncture
* Only if no focal lesion on CT
* Often requires serial LPs
* Difficult with anticoagulation

If effective → consider lumbar drain

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16
Q

4️⃣ Focal Cerebral Edema

A

=>Spectrum:
* Mild → improves with anticoagulation
* Severe → herniation risk

=>Supportive measures
* Head elevation
* Osmotherapy

=>Decompressive craniectomy
* Strongly recommended in European guidelines
* No RCT-level evidence

Young CVST patients may be excellent candidates.

Radiologic indications:
* Uncal herniation
* PCA territory ischemia due to herniation
* Midline shift >5 mm
* Persistent severe ICP elevation

=>Steroids: Not useful

17
Q

5️⃣ Treat Underlying Cause

A

=>Infection
* Cultures
* Broad-spectrum antibiotics
* Imaging for focus
* Surgical drainage if needed

=>Autoimmune / Vasculitis
* Steroid therapy if indicated

=>Prothrombotic drugs
* Stop hormonal therapy if possible

18
Q

Role of Catheter-Directed Endovascular Therapy

A

May include:
* Local thrombolysis
* Mechanical clot disruption

RCT evidence:
* No demonstrated benefit

=>Role:
* Rescue therapy only
* When deterioration despite optimal anticoagulation

19
Q

If Neurologic deterioration despite Tt

A

=>Neurologic Deterioration Despite Treatment, Consider:
* Thrombus extension
* Worsening edema
* New hemorrhage
* Deep venous involvement
* Refractory ICP
* Missed underlying infection

=>Escalation pathway:
1. Repeat imaging
2. Optimize anticoagulation
3. Manage ICP aggressively
4. Consider decompressive craniectomy
5. Rescue endovascular therapy

20
Q

Prognosis

A

=>In general better than arterial stroke- Younger pt group, better neuroplasticity
* Mortality ~5%

=>Worst predictors:
* Coma
* Deep venous thrombosis
* Intracerebral hemorrhage