Cerebral Venous Sinus Thrombosis

complete reference · anticoagulate despite hemorrhage · MRV · thrombophilia workup · ICP/seizure mgmt · Full Card

Symptoms / Associated Sx

• Headache is the most common symptom (~90%) — usually subacute and progressive, but can be thunderclap. Highly variable presentation depending on which sinus and whether venous infarction occurs: signs of raised ICP (papilledema, visual obscurations, sixth-nerve palsy), seizures (more common than in arterial stroke), focal deficits that cross arterial boundaries, or a diffuse encephalopathy. Cavernous sinus thrombosis → painful ophthalmoplegia, proptosis, chemosis.

• Think CVST in any young patient with a new persistent headache plus a prothrombotic context, or a "stroke" that doesn't fit an arterial territory.

Neg

• Pt denies an instantaneous thunderclap with blood filling the basal cisterns — argues against aneurysmal SAH (CVST headache is usually gradual; venous blood, when present, is lobar/parenchymal not cisternal)

• No high fever with meningismus and rapid systemic decline — argues against bacterial meningitis (though septic CVST from contiguous infection overlaps — image the venous system)

• Deficit does not localize to a single arterial territory and is not maximal at onset — argues against arterial ischemic stroke (venous infarcts cross territories, are often hemorrhagic, and evolve)

• Papilledema/headache without a sinus thrombus on MRV would instead suggest idiopathic intracranial hypertension (CVST must be excluded before diagnosing IIH)

Social History (SHx)

• Estrogen exposure — oral contraceptives, pregnancy and especially the puerperium; recent head/neck infection (otitis, mastoiditis, sinusitis); dehydration.

• Personal or family history of thrombophilia or VTE; active malignancy; smoking; recent LP, neurosurgery, or jugular line.

Main Etiology

• Prothrombotic states dominate: pregnancy/puerperium, oral contraceptives/hormone therapy, inherited thrombophilias (factor V Leiden, prothrombin G20210A, protein C/S or antithrombin deficiency), antiphospholipid syndrome, malignancy, nephrotic syndrome. Local/septic causes — contiguous infection (mastoid, paranasal sinus, dental, facial). Mechanical — head trauma, neurosurgical procedures, jugular catheterization. Dehydration. Often multifactorial.

RF

• Modifiable: estrogen-containing contraception, dehydration, smoking, treatable infection.

• Non-modifiable: inherited thrombophilia, pregnancy/postpartum state, malignancy, female sex (childbearing age).

Data

• MR venography (or CT venography) (diagnostic — demonstrates absent venous flow / filling defect; the "empty delta sign" on post-contrast imaging is the non-opacified superior sagittal sinus)

• Non-contrast CT (often normal early; may show a dense triangle/cord sign of clotted sinus, or a venous infarct that is frequently hemorrhagic and crosses arterial territories)

• D-dimer (supports the diagnosis when elevated, but a normal value does NOT exclude CVST — do not withhold imaging)

• Thrombophilia panel, antiphospholipid antibodies, β-hCG, CBC, peripheral smear (identify the prothrombotic driver; send thrombophilia studies ideally before/with anticoagulation, interpret some later)

• LP with opening pressure if isolated intracranial hypertension (after imaging excludes herniation risk; elevated pressure, can be therapeutic)

DDx

Aneurysmal SAH (thunderclap, cisternal blood, aneurysm on CTA) · arterial ischemic stroke (single arterial territory, maximal at onset) · idiopathic intracranial hypertension (papilledema but patent sinuses on MRV) · meningitis/encephalitis (fever, CSF pleocytosis) · migraine (recurrent, stereotyped, prior history) · intracranial hemorrhage from other cause (arterial/hypertensive pattern)

Home Meds

• Stop estrogen-containing contraceptives permanently and counsel on alternative contraception.

• Start therapeutic anticoagulation (see plan); reconcile any other prothrombotic medications.

Plan

Consults

• Neurology — diagnosis confirmation and anticoagulation strategy.

• Hematology — thrombophilia workup, malignancy screen, duration of anticoagulation.

• Neuro-interventional — if clinical deterioration despite anticoagulation (endovascular thrombectomy in select centers).

• Neurosurgery — for large venous infarct with mass effect or impending herniation (decompressive craniectomy is life-saving).

• ICU — if depressed consciousness, status epilepticus, or herniation risk; OB if pregnant/postpartum; ENT if septic source.

Anticoagulation

• Anticoagulate even when there is associated venous hemorrhage — the clot is the cause of the bleed; treating it is beneficial (ISCVT, RCT evidence). Start LMWH enoxaparin (Lovenox) 1 mg/kg SC q12h, or unfractionated heparin gtt (preferred if a procedure or rapid reversibility may be needed).

• Transition to oral: warfarin (Coumadin) bridged to INR 2–3, OR a DOAC — dabigatran (Pradaxa) 150 mg BID has RCT support (RE-SPECT CVT non-inferior to warfarin); other DOACs increasingly used. Duration 3–6 months if provoked, 6–12 months if unprovoked, indefinite for recurrent CVST or high-risk thrombophilia/active malignancy.

Intracranial pressure

• For raised ICP / threatened vision: acetazolamide (Diamox) 250–500 mg PO/IV BID; therapeutic LP or CSF diversion; urgent ophthalmology for progressive visual loss.

Seizures / cause

• Treat seizures with levetiracetam (Keppra) 60 mg/kg IV load then maintenance; give prophylaxis when there is a supratentorial parenchymal lesion plus a seizure (high recurrence). Septic thrombosis → empiric broad-spectrum antibiotics + source control. Rehydrate; stop estrogen.

Always

• PT / OT eval and treat if focal deficits; early mobilization once stable.

• Trend: serial neuro exams; fundoscopy/visual fields for ICP; repeat venous imaging only if deterioration; INR or anticoagulation monitoring.

• Escalation triggers: declining LOC or new/worsening deficit → repeat imaging, ICU · large venous infarct with mass effect/midline shift → neurosurgery for decompressive craniectomy · progression despite therapeutic anticoagulation → neuro-IR for endovascular thrombectomy · status epilepticus → ICU.

• Discharge checklist: oral anticoagulant with defined duration and monitoring plan (warfarin INR 2–3 or DOAC) · permanent discontinuation of estrogen contraception with alternative method counseled · hematology follow-up for thrombophilia results · neurology follow-up with planned repeat MRV (recanalization assessment ~3–6 months) · headache/vision and bleeding return precautions.

Red Flags — ICU / Neurosurgery

• Declining consciousness / large venous infarct with mass effect → decompressive craniectomy can be life-saving; ICU.
• Status epilepticus → ICU, aggressive AED therapy.
• Progressive deficit despite anticoagulation → neuro-interventional endovascular thrombectomy.
• Threatened vision from severe intracranial hypertension → urgent CSF diversion / ophthalmology.
• Septic cavernous sinus thrombosis → emergent antibiotics, source control, often ICU.

Senior IM Resident Pearls

• Anticoagulate even if there's blood. The most counterintuitive point in CVST: a venous hemorrhage is caused by the thrombus, so heparin is the treatment, not a contraindication. RCT and ISCVT data support it.
• A normal D-dimer does NOT rule it out. If the story fits (young patient, prothrombotic state, atypical headache or non-arterial "stroke"), get the MRV regardless of the D-dimer.
• It crosses arterial territories. A bilateral or non-arterial-pattern infarct, especially if hemorrhagic, should make you image the venous system.
• Seizures are common — far more than in arterial stroke. Treat them, and give prophylaxis when there's a supratentorial lesion plus a seizure.
• Always hunt the cause. Estrogen, pregnancy/postpartum, thrombophilia, malignancy, and contiguous infection — the etiology determines the anticoagulation duration and whether you need antibiotics/source control.
• DOACs are now reasonable. RE-SPECT CVT showed dabigatran non-inferior to warfarin — a real option for stable, non-malignancy CVST after initial heparinization.
• Common mistake: diagnosing IIH without excluding CVST — both cause headache and papilledema, but only one needs anticoagulation. The MRV is what separates them.
• Common mistake: withholding heparin because of the hemorrhagic venous infarct — that's exactly backwards.