MR Venography

MR venography is a group of MRI techniques that show veins. It is used to detect thrombosis, stenosis, compression, anomalies and collateral channels in the cerebral venous system, the neck, the chest, the abdomen and pelvis, and the limbs.

Contrast enhanced MR venography uses an intravenous gadolinium bolus (0.1 mmol each kg) with a 3D gradient echo sequence acquired in the venous phase, at 60 to 90 seconds after injection for most body veins, with delayed imaging for slow flow.

Intravascular contrast agents with long blood half life allow steady state imaging, but they are not widely available.

Non-contrast methods include two dimensional and three dimensional time-of-flight (the inflow technique, tuned to venous flow direction), phase contrast (velocity encoded, for cerebral sinuses), balanced steady state free precession (bright blood, flow independent), and quiescent interval or flow sensitive methods for the limbs and pelvis.

Slices are 1 to 3 mm thick, and the examination takes 15 to 45 minutes. In the brain, the study is often combined with MRI of the brain and MR angiography.

Cerebral venous thrombosis affects about 3 to 4 in a million people each year, with a female predominance, and it is under recognised because it presents with headache, seizures or focal deficits.

Deep venous thrombosis and pulmonary embolism together affect about 1 to 2 in 1000 people each year. MR venography has a sensitivity and specificity of over 90 to 95% for cerebral venous thrombosis and for pelvic and central vein thrombosis.

Indications.

• Suspected cerebral venous thrombosis: headache, seizures, papilloedema, focal deficits, or intracranial haemorrhage in unusual locations.
• Idiopathic intracranial hypertension, to exclude venous sinus stenosis.
• Neck and central veins: jugular, subclavian, brachiocephalic and superior vena cava obstruction, effort thrombosis of the subclavian vein, and catheter related thrombosis.
• Pelvic and iliac veins: iliac vein compression syndromes, pelvic congestion, and thrombosis extending from the leg.
• Inferior vena cava: congenital anomalies, thrombosis, tumour invasion and filters.
• Hepatic, portal and renal veins: Budd-Chiari syndrome, portal vein thrombosis, and renal vein thrombosis.
• Lower and upper limb: deep vein thrombosis when ultrasound is inadequate (pelvic veins, calf in obese patients), venous malformations and varicose disease.
• Venous malformations and anomalies, and access planning for dialysis.
• Pulmonary vein anatomy before ablation and stenosis after ablation.
• Patients who cannot have iodinated contrast or radiation.

Not as the first test for suspected leg deep vein thrombosis (ultrasound is first), or for acute pulmonary embolism (CT).

Contraindications and precautions.

• The usual MRI safety screen. Inferior vena cava filters and stents are mostly conditional. Metal causes artefact.
• Gadolinium: avoid in severe renal impairment with linear agents. Non-contrast methods are used.
• Pregnancy: non-contrast MR venography only, which is particularly useful in pregnancy with suspected cerebral venous thrombosis or pelvic vein thrombosis.
• Claustrophobia and inability to stay still.
• Severe pain or oedema in the limb may limit positioning.

Preparation and technique.

No fasting is needed. A cannula is placed in a vein (for upper limb studies, the contralateral arm or foot). The patient lies supine.

For the cerebral venous system, time-of-flight or phase contrast sequences cover the superior sagittal, transverse, sigmoid and straight sinuses, internal cerebral veins and jugular bulbs. Contrast enhanced imaging is added for subtle thrombosis, and post-contrast T1 images show filling defects.

For the body, a contrast enhanced 3D sequence is acquired in the venous phase in a breath hold. For the lower limb, a station-by-station approach covers the calf, thigh, pelvis and inferior vena cava. In pelvic venous disease, a delayed and prone or straining phase may show reflux.

Black blood T1 and T2 sequences show thrombus and wall abnormalities.

Normal appearances.

Dural venous sinuses show uniform flow signal, and the superior sagittal sinus, straight sinus, transverse sinuses and sigmoid sinuses are continuous. The transverse sinuses are often asymmetric, with a hypoplastic left or right transverse sinus in many people, which is a common variant.

Arachnoid granulations cause small rounded filling defects within the sinuses. The deep cerebral veins drain to the straight sinus. The jugular veins are variable in size.

Body veins are bright in the venous phase, smooth and continuous. The inferior vena cava is oval and enhances uniformly, and mixing artefact from unenhanced renal vein blood may appear in early phases.

Interpretation.

• Cerebral venous thrombosis: absent flow signal in a sinus or vein, with a filling defect on contrast enhanced images. The thrombus signal evolves: isointense on T1 and dark on T2 in the first days, bright on T1 and T2 in the subacute phase (days 5 to 30), and variable later with recanalisation. A thrombosed cortical vein appears as a linear dark or bright cord.
• Secondary brain findings: venous infarction (not in an arterial territory, often haemorrhagic), cortical or subcortical oedema, parasagittal haemorrhage, and raised pressure.
• Venous sinus stenosis: focal narrowing of the transverse sinus, often bilateral, in idiopathic intracranial hypertension. Pressure gradients are measured at venography to decide on stenting.
• Hypoplasia versus thrombosis: a small sinus with a normal flow signal and a smooth tapered course suggests hypoplasia, while loss of signal in a normal size sinus suggests thrombosis.
• Deep vein thrombosis: filling defect in the vein, expanded vein with absent flow, perivenous oedema and loss of normal flow related signal. Acute thrombus is bright on T1 (methaemoglobin) in some cases. Chronic thrombus shows a thickened wall, small calibre, synechiae and collaterals.
• Iliac vein compression: narrowing of the left common iliac vein where it is crossed by the right common iliac artery, with collateral veins and a fibrous web. Often found in young women with left leg swelling and in left leg deep vein thrombosis.
• Central venous obstruction: stenosis or occlusion of the brachiocephalic, subclavian veins or superior vena cava, with chest wall collaterals. Causes include catheters, tumour compression, fibrosing mediastinitis and radiation.
• Inferior vena cava: thrombus, congenital anomalies (double or left sided cava, interrupted cava with azygos continuation), tumour thrombus (from renal cell carcinoma, hepatocellular carcinoma, adrenal tumour) that enhances, and filter position.
• Hepatic and portal veins: thrombosis and occlusion (Budd-Chiari syndrome), cavernous transformation of the portal vein, and portosystemic collaterals. Renal vein thrombosis causes an enlarged kidney with delayed enhancement.
• Pelvic congestion: dilated gonadal and parauterine veins (over 6 mm) with reflux.
• Venous malformations: slow flow lesions, very bright on T2, with phleboliths (signal voids) and septa, and gradual enhancement.
• Varicose veins and perforators: dilated tortuous veins with incompetent perforators on dynamic images.
• Pulmonary veins: number, ostial size, and stenosis after ablation (narrowing, flow loss and downstream congestion).
• Dialysis access: central venous stenoses and arteriovenous fistula flow.
• Incidental: tumours, nodes, haematomas, cysts and other masses compressing veins.

Critical values and findings needing immediate action.

• Cerebral venous thrombosis, particularly with haemorrhage, coma, or raised pressure: anticoagulation (even with haemorrhage), neurological review, and endovascular treatment in selected severe cases.
• Superior vena cava obstruction with airway compromise or cerebral oedema: urgent stenting, radiotherapy or chemotherapy as appropriate.
• Extensive iliofemoral deep vein thrombosis, phlegmasia: anticoagulation and consideration of thrombolysis or thrombectomy.
• Budd-Chiari syndrome or acute portal vein thrombosis: anticoagulation and hepatology review.
• Inferior vena cava tumour thrombus: surgical and oncological planning.
• Renal vein thrombosis with renal impairment: anticoagulation and nephrology review.
• Pulmonary vein stenosis with symptoms: cardiology review.

Limitations and artefacts.

• Slow or turbulent venous flow causes signal loss that mimics thrombosis, particularly in time-of-flight methods. Contrast enhanced or phase contrast imaging helps.
• Inflow of unsaturated blood in the first slices of a time-of-flight stack gives false bright signal, and in plane flow gives false signal loss.
• Normal variants (hypoplastic or absent transverse sinus, arachnoid granulations, a high flow jugular bulb) mimic disease. Source images and multiplanar review are needed.
• Subacute thrombus is bright on T1 and can mimic flow on time-of-flight images, producing false normal appearances. Phase contrast or contrast enhanced sequences resolve it.
• Mixing of enhanced and unenhanced blood in the inferior vena cava and iliac veins mimics thrombus in early phases. Delayed images clarify.
• Metal (inferior vena cava filters, stents, coils) causes artefact.
• Respiratory and cardiac motion degrade body venous images.
• Chronic thrombus and web like stenoses are difficult to separate from normal collapsed veins.
• Ultrasound is more accurate for leg proximal deep vein thrombosis and more available.

Special groups.

• Pregnant patients: non-contrast MR venography is the preferred test for cerebral and pelvic vein thrombosis.
• Women using oral contraceptives, with thrombophilia or in the postpartum period: higher risk of cerebral venous thrombosis.
• Children and neonates: cerebral sinus thrombosis with dehydration, infection (mastoiditis) and congenital heart disease. Sedation may be needed.
• Patients with cancer: tumour thrombus, hypercoagulable states, and catheter related thrombosis.
• Patients with renal impairment: non-contrast sequences.
• Regions: cerebral venous thrombosis from puerperal causes, dehydration, infection and Behçet disease; superior vena cava obstruction from tuberculosis and lymphoma; schistosomiasis and portal vein thrombosis; and Budd-Chiari syndrome are common. MR venography is rarely available, so CT venography, ultrasound and clinical diagnosis are used, with anticoagulation started early.

Follow up tests.

• Compression ultrasound with Doppler for limb veins, and ultrasound of hepatic, portal and renal veins.
• CT venography or CT of the brain with contrast for cerebral venous sinuses and when MRI is not possible.
• Catheter venography with pressure measurement for venous stenosis.
• D-dimer for exclusion in low risk patients, full blood count, platelet count, coagulation tests.
• Thrombophilia screen when indicated: antiphospholipid antibodies, factor V Leiden, prothrombin gene mutation, protein C, protein S, antithrombin, JAK2 mutation, paroxysmal nocturnal haemoglobinuria screen.
• Lumbar puncture opening pressure for idiopathic intracranial hypertension.
• Cancer screening where thrombosis is unprovoked and suspicion is high.
• Referral to haematology, neurology, vascular surgery, interventional radiology or hepatology.