Cerebral Venous Sinus Thrombosis (CVST) — Workup

When to Suspect CVST

Consider CVST in any patient with:

New headache (progressive over days–weeks, or thunderclap) — especially without a clear etiology
Signs of elevated ICP: papilledema, nausea/vomiting
Seizures (present in ~40%)
Focal neurologic deficits not following an arterial territory
Altered mental status or coma (14%)
Unexplained stroke symptoms in a young female under 50
Elevated LP opening pressure without another explanation

High-risk presentations: female gender, peripartum state, OCP use, recent head/neck surgery, hypercoagulable state.

— Rosen's Emergency Medicine, p. Cerebral Venous Thrombosis section; Tintinalli's Emergency Medicine, p. 1293

Risk Factors to Elicit on History

Category	Examples
Hormonal	OCP, HRT, pregnancy/peripartum
Thrombophilia	Factor V Leiden, protein C/S deficiency, antithrombin III deficiency, lupus anticoagulant
Infection/local	Sinusitis, otitis media, mastoiditis, oropharyngeal infection
Systemic disease	SLE, IBD, malignancy, nephrotic syndrome, sickle cell disease
Drugs	Asparaginase, estrogen, cocaine
Other	Dehydration, trauma, recent surgery

— Harriet Lane Handbook, p. 726; Grainger & Allison's Diagnostic Radiology, p. 1453–1454

Laboratory Workup

Send on all suspected CVST:

Test	Purpose
CBC	Polycythemia, thrombocytosis, hematologic disorder
PT/INR, PTT	Coagulopathy baseline; guides anticoagulation
BMP/Electrolytes, BUN, Cr	Metabolic contributors, dehydration
ESR, CRP	Inflammatory/infectious cause
D-dimer	A normal D-dimer can exclude CVT in low-risk patients (no thromboembolic risk factors, normal neuro exam, no papilledema)
Pregnancy test	Women of childbearing age
Antithrombin III activity	Thrombophilia

Thrombophilia screen (ideally after acute anticoagulation phase or before starting):

Protein C and S activity
Antithrombin III
Factor V Leiden (PCR)
Prothrombin gene mutation (G20210A)
Lupus anticoagulant / antiphospholipid antibodies
JAK2 mutation (if polycythemia/essential thrombocythemia suspected)

Note: thrombophilia screening in the acute phase or while on anticoagulation may yield false results; can be deferred but should still be ordered.

— Rosen's Emergency Medicine, p. Diagnostic Testing; Harriet Lane Handbook, p. 726

Imaging Workup

Step 1 — Non-contrast CT Head (initial screen)

Often normal or non-specific — insensitive alone
May show:
- Hyperdense sinus/vein (hyperdense cord sign for cortical vein, dense triangle sign for SSS)
- Infarct, hemorrhage, or edema — often not conforming to an arterial territory
- Parasagittal hemorrhagic infarcts (superior sagittal sinus thrombosis)
Does NOT rule out CVST

Step 2 — MRI Brain + MR Venography (MRV) ← Gold Standard

MRI: loss of normal flow void in the sinus; T1/T2 hyperintensity in thrombosed vessel; parenchymal edema, hemorrhagic infarct
MRV: loss of flow signal / nonvisualization of sinus
SWI/GRE: "blooming" hypointensity in thrombosed sinus; prominent engorged draining veins (venous congestion pattern)
DWI + FLAIR also recommended to characterize parenchymal injury
MRI/MRV is the test of choice when available

Step 3 — CT Venography (CTV) — Alternative if MRI contraindicated

At least as sensitive as MRV for major dural sinus thrombosis
Shows "delta sign" (hypodense thrombus + peripheral rim enhancement) on contrast CT
Faster; less susceptible to motion artifact

Step 4 — Digital Subtraction Angiography (DSA)

Now rarely required for diagnosis
Reserved for: equivocal MRI/MRV/CTV, prelude to endovascular therapy if deteriorating despite anticoagulation

Parenchymal lesion patterns by sinus involved:

Sinus Thrombosed	Parenchymal Lesion Location
Superior sagittal sinus	Bilateral parasagittal cortical/subcortical (often asymmetric)
Internal cerebral veins / straight sinus	Bilateral thalami ± basal ganglia
Vein of Labbé / lateral sinus	Posterolateral temporal lobe, inferior parietal

— Grainger & Allison's Diagnostic Radiology, p. 1453–1454; Rosen's Emergency Medicine, p. Diagnostic Testing; Bradley & Daroff's Neurology, p. MRV section

CVT imaging: CT and MRI findings including hemorrhagic infarcts, venous congestion, and parenchymal signal changes in cerebral venous sinus thrombosis

Fig. 56.28 — Cerebral Venous Thrombosis. CT (A, B, D) and MRI (C, E–J) demonstrating hemorrhagic infarcts, venous congestion, and parenchymal edema/signal abnormalities from Grainger & Allison's Diagnostic Radiology.

Lumbar Puncture

Can be performed safely in CVST (no contraindication)
Elevated opening pressure in the setting of a new headache type should raise suspicion and prompt MRV
CSF may show elevated RBCs or protein; results are non-specific
Useful if infection (meningitis) is in the differential

Workup Summary (Quick Reference)

Suspected CVST
    │
    ├── Labs: CBC, BMP, PT/PTT, ESR, CRP, D-dimer, pregnancy test
    │         Thrombophilia panel (antithrombin III, protein C/S,
    │         factor V Leiden, prothrombin mutation, lupus anticoag)
    │
    ├── Imaging:
    │     1. Non-contrast CT head (initial; can miss CVST)
    │     2. MRI brain + MRV ← Gold standard
    │        (DWI, FLAIR, SWI/GRE, T1, T2)
    │     OR CTV if MRI contraindicated
    │     3. DSA if equivocal or endovascular planned
    │
    └── LP if opening pressure elevated or infection suspected

Differential Diagnosis

Idiopathic intracranial hypertension (IIH) — early CVST mimics IIH
Brain tumor
Ischemic or hemorrhagic arterial stroke
Meningitis / encephalitis / brain abscess
SAH (thunderclap presentation)
PRES, RCVS
SLE, sarcoidosis

— Rosen's Emergency Medicine, p. Differential Diagnoses

Initial Management (ED)

Anticoagulation — LMWH preferred over UFH (weak recommendation); start regardless of intracranial hemorrhage
Antiepileptics (levetiracetam or phenytoin) if seizures
Admission to stroke unit
Thrombectomy/thrombolysis in refractory, deteriorating cases at expert centers

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