CVST work up

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Cerebral Venous Sinus Thrombosis (CVST) — Workup

Clinical Suspicion: Who to Work Up

CVST accounts for 0.5–1% of all strokes. Consider it in any patient with:

Progressive headache over days–weeks (most common symptom), or thunderclap headache
Elevated ICP signs: papilledema, transient visual obscurations, vomiting
Seizures (~40% of patients), focal neurological deficits, altered consciousness, or coma
Hemorrhagic infarctions — especially multifocal, bilateral, involving gray matter and subcortical white matter simultaneously
Presumed idiopathic intracranial hypertension (pseudotumor cerebri) — must rule out CVST first
Any headache + elevated LP opening pressure without obvious explanation

High-risk groups: Women in the peripartum period; OCP/HRT users; patients with hypercoagulable states; patients post-surgery; those with active malignancy, head/neck infection, or inflammatory disease.

Step 1 — Initial Labs

Test	Purpose
CBC with differential	Polycythemia, thrombocytosis, leukemia
BMP / CMP	Dehydration, metabolic causes
PT/INR, aPTT	Baseline coagulation prior to anticoagulation
D-dimer	A normal D-dimer has high NPV for CVST in low-probability cases; elevated D-dimer supports the diagnosis (not specific)
ESR, CRP	Septic/inflammatory etiology
Blood cultures	If septic thrombosis suspected (cavernous sinus, lateral sinus)
Pregnancy test	In women of childbearing age
Hemoglobin electrophoresis	If sickle cell suspected

Step 2 — Thrombophilia Workup

All patients with CVST should be screened for underlying thrombophilia:

Factor V Leiden (most common hereditary thrombophilia)
Prothrombin G20210A mutation
Protein C and Protein S levels
Antithrombin III level
Antiphospholipid antibodies (anticardiolipin IgG/IgM, anti-β2-glycoprotein I, lupus anticoagulant)
Homocysteine level
JAK2 V617F mutation (if myeloproliferative disorder suspected)

Note: Protein C, Protein S, and antithrombin III levels are affected by acute clot and anticoagulation — ideally recheck 3 months after stopping anticoagulation for definitive interpretation.

Step 3 — Neuroimaging

CT Head (Non-contrast) — First-Line in the ED

Fast and widely available, but sensitivity for CVST alone is poor
May show:
- Hyperdense sinus sign — direct visualization of thrombus in the superior sagittal sinus (SSS) or other dural sinuses
- Empty delta sign (on contrast CT) — filling defect within the sinus after contrast, pathognomonic but only present in ~30%
- Low-density areas of venous infarction, hemorrhagic transformation, small ventricles
A normal CT does not exclude CVST

MRI Brain + MR Venography (MRV) — Gold Standard

MRV has replaced conventional angiography for diagnosis of CVST
MRI sequences to obtain:
- T1/T2: Abnormal signal within the sinus (variable by thrombus age)
- FLAIR: Venous infarction/edema
- DWI: Ischemic venous infarct (may have restricted diffusion)
- SWI or GRE (T2*): Blooming artifact from thrombus — highly sensitive for cortical vein thrombosis
- T1 post-contrast: Empty delta sign
- MRV (time-of-flight or phase-contrast): Non-visualization or filling defect in dural sinuses

Fig. 65.35 — Sagittal T1 MRI showing increased signal and enlargement of the superior sagittal sinus throughout most of its course, consistent with SSS thrombosis:

Sagittal T1 MRI showing SSS thrombosis with increased signal throughout the superior sagittal sinus

Fig. 65.36 — Bilateral hemorrhagic parietal infarctions (GRE, Panel A) and MRV showing SSS thrombosis (sagittal, Panel B) in a 14-year-old on L-asparaginase therapy:

GRE MRI showing bilateral hemorrhagic parietal infarctions (A) and sagittal MRV showing SSS thrombosis (B)

CT Venography (CTV)

Alternative to MRV when MRI is unavailable or contraindicated
Excellent sensitivity and specificity; requires IV contrast and radiation
Head ultrasound with color Doppler is used in neonates/infants

Conventional Angiography

Rarely needed; reserved for cases where non-invasive imaging is indeterminate or when intervention is planned

Step 4 — Lumbar Puncture

LP can be safely performed in CVST (no herniation risk from the diffuse venous pathology)
Findings: elevated opening pressure (often >25 cmH₂O), may show xanthochromia or mild pleocytosis
An elevated LP opening pressure in a patient with severe headache should specifically prompt MRV to rule out CVST
LP also helps rule out meningitis/SAH if the diagnosis is unclear

Step 5 — Workup for Underlying Cause

Category	Investigations
Infection	Blood cultures, throat swab, ENT exam, CT sinuses/mastoids (septic CVST from otitis, mastoiditis, sinusitis, facial infection)
Malignancy	CT chest/abdomen/pelvis, tumor markers
Inflammatory	ANA, ANCA, anti-dsDNA (lupus, Behçet, IBD-associated)
Hematologic	Peripheral smear, bone marrow biopsy if myeloproliferative disorder
Medications	Review OCP, HRT, tamoxifen, L-asparaginase, corticosteroids

Summary of Key Imaging Points

Finding	Modality	Significance
Hyperdense sinus	Non-contrast CT	Acute thrombus
Empty delta sign	Contrast CT	Filling defect in SSS, ~30% sensitive
Absent flow void in sinus	MRI T2	Loss of normal "black" flow signal
Blooming artifact	GRE/SWI	Highly sensitive for cortical vein thrombosis
Non-visualization of sinus	MRV	Diagnostic of CVST
Hemorrhagic infarct, multifocal, bilateral	MRI	Characteristic venous pattern

Anticoagulation Note (not to delay workup)

Once CVST is confirmed, IV heparin or LMWH is first-line, even in the presence of hemorrhagic infarction. Transition to warfarin for 3–12 months. DOACs are being studied but evidence remains limited. Anticoagulation should not be withheld pending the full thrombophilia workup — send labs before starting heparin when possible.

Sources: Bradley and Daroff's Neurology in Clinical Practice; Tintinalli's Emergency Medicine: A Comprehensive Study; Rosen's Emergency Medicine: Concepts and Clinical Practice

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