Vascular Radiology

Arteries and veins comprised of 3 layers:

  • Intima – Single layer endothelial cells. Interacts with blood to prevent thrombosis
  • Media – Separated by intima by internal elastic lamina; from adventitia by external elastic lamina. Smooth muscle with elastic fibres (elasticity becomes lost over time). Medium and large vessels with more muscle have vasa vasorum to nourish the outer portions.
  • Adventitia – Connective tissue with nerves and vasa vasorum.

Relative amounts of each layer differ mostly in media and adventitia depending on function. Large/elastic arteries include aorta and large branches, pulmonary arteries; extensive elastic media which is less with age (becomes tortuous and ectatic). Medium/muscular aa include other aortic branches (eg coronary, renal); muscular media allowing vasoconstriction or vasodilatation. Small arteries (<2mm) and arterioles (20-100μm) are branches within organs; also have muscular media controlled by autonomic system. Resistance to flow is inversely proportional to the forth power of diameter, so halving diameter increases resistance 16x. Capillaries (7 to 8 μm, ~RBC diameter) have no media. Vascular leakage from inflammation preferentially occurs in postcapillary venules. Veins have larger lumens, thinner walls, valves.

Vasculogenesis is vessel formation during embryogenesis. Angiogenesis (neovascularisation) is new vessels in mature individuals. Arteriogenesis is remodelling of existing arteries from change in pressure/flow.

Intimal thickening – Any vascular insult (dysfunction or endothelial cell loss) stimulates formation of a neointima by proliferation of smooth muscle cells (originating from circulating precursor cells) and extracellular matrix, usually covered by endothelial cells. Over time the intimal smooth muscle cells stop dividing, but intimal thickening is permanent. This process is also normal with aging.

Doppler Imaging

Doppler frequency shift is proportional to velocity of moving RBCs, frequency of transmitted beam and cosine of angle between beam and direction of flow (Doppler angle). As angle > 90deg, Cosine > 0, hence need to keep <60deg to reduce error (keeping Cosine and hence frequency shift as high as possible). Duplex US is simultaneous greyscale and Doppler scanning (spectral or colour). On spectral display, negative frequency shift (flow away from probe) displays below zero baseline.

Different vessels have different Doppler spectral waveforms (Doppler signature), affected by cardiac contraction, vessel compliance, downstream resistance.

  • High-resistance waveforms have sharp increase in velocity at systole, rapid decrease then little or no forward flow in diastole. Triphasic wave – early diastolic reversal of flow. High pulse pressure with minimal flow to capillary bed from constricted arterioles. Includes vessels feeding skeletal muscle at rest (iliac, femoral, popliteal, subclavian, brachial, ECA), SMA at fasting.
  • Low-resistance waveforms have relative slower increase in velocity at systole, gradual decraese with continued forward flow throughout. Include vessels feeding vital organs (ICA, hepatic, renal aa), CCA (70% of flow goes to ICA), SMA after eating, muscle at exertion.

Laminar flow has narrow spectrum (with window beneath spectral trace) of velocities. Most normal aa and large vens have velocity highest at centre, diminishing closer to vessel walls. Large arteries eg aorta have ‘plug’ flow with uniform flow from centre to near vessel wall. At bifurcations, normal small area of reversed flow near vessel wall opposite flow divider. Tortuous vessles have slower flow on inner aspect of curve and acceleration at outer aspects; laminar distribution returns at short distance downstream.

Disturbed blood flow and turbulence causes increased velocity (proportional to stenosis), spectral broadening, simultaneous forward and reverse flow and fluctuation of velocities with time. Turbulence most pronounced just downstream from a stenosis where eddy currents occur.

Doppler velocity ratios can be used even when doppler angle (hence correct velocity) not known.

  • A/B ratio (systolic/diastolic ratio) = peak systolic / end-diastolic.
  • Resistance Index (RI)/Pourcelot Index (PoI) = (peak systolic – end diastolic) / peak systolic.
  • Pulsatility Index (PI) = (peak systolic – end diastolic) / temporal mean velocity.

Stenoses are assessed proximally (lamina flow), at maximum stenosis (increased V but lamina; highest V obtained correlates best with severity) and 10-20mm downstream (turbulence, eddy currents). Downstream from >50% stenoses causes dampened tardus-parvus waveforms (slow/tardus upstroke with low/parvus velocity). Proximal to complete or nearly complete occlusions are stump-thump waveforms (knocking, small blunt) with little/no diastolic flow, may have some reversed diastolic flow.

Colour Doppler imaging (CDI) superimposes Doppler flow (colour) on greyscale B-mode. Colour Doppler energy (CDE)/Power Doppler superimposes number of moving RBCs (rather than velocity). Colour velocity imaging (CVI) is not Doppler, but instead tracks movement of structure over time. Usually flow towards transducer is red, away is blue; faster flow is lighter, dependent on mean (not peak) velocity. True colour changes distinguised from aliasing by a surrounding black border (zero velocity). Aliasing prevented by increasing PRF to at least twice frequency of detected signal (limited by depth of object; Nyquist limit = half of PRF), reduced with lower frequency transmission, increased Doppler angle. Corect Doppler gain set by turning up until noise appears then slightly lowering. Colour flash (relative motion of transducer) accentuated in cysts, GB, hypoechoic nonvascular structures (most instruments suppress flash in hyperechoic areas). Wall filters set to remove low velocity noise, but may obscure slow flow. Tissue vibration artifact seen in perivascular tissues, from bruits, AVFs, shunts.

Hypertension (HTN)

95% of hypertension is idiopathic (essential HTN). Secondary causes includes renal disease (including renal artery stenosis, vasculitis), endocrine, cardiovascular (including coartation, vasculitis), or neurogenic causes. Low pressure at the juxtaglomerular cells of kidneys induces renin secretion converting angiotensinogen to angiotensin I; is is converted to angiotensin II by ACE; this stimulates aldosterone secretion (increasing tubular reabsportion of sodium) and peripheral resistance (vasoconstriction). Other vasoconstrictors include catecholamines. Vasodilators include kinins, prostaglandins and NO. Complications include:

  • Hyaline arteriolosclerosis – Pink hyaline thickening of arterioles from plasma protein leakage across endothelial cells, intimal thickening.
  • Hyperplastic arteriolosclerosis – Severe/malignant HTN causing onion-skin lesions with concentric mural thickenings with fibrinoid deposits and wall necrosis (necrotising arteriolitis).


Arteriosclerosis (‘hardening of the arteries) is arterial thickening and loss of elasticity; patterns include arteriolosclerosis, Monckeberg medial sclerosis (muscular aa calcification which may ossify, usually doesn’t cause stenosis), and atherosclerosis (most common).

Atherosclerosis is formation of intimal atheromas (atheromatous/atherosclerotic plaques) consisting of yellow lipid core (cholesterol) covered by white fibrous caps. Increased risk with age, postmenopausal F>M>premenopausal F, FHx, hyperlipidemia (esp hypercholesterolemia LDL), HTN, smoking, diabetes, inflammation (esp CRP), hyperhomocystinaemia, metabolic syndrome, lack of exercise, stress, obesity. Involved vessels include (in descending order) lower abdominal aorta, coronary, popliteal, ICAs, circle of willis. Upper extremities, mesenteric and renal arteries usually spared; except the ostia. Multifocal diffuse luminal irregularity by plaques with variable stenosis/occlusion, variable calcification. Stenosis/occlusions @ vesel origins. Diabetic vascular disease – dramatic vascular calcification in arteries of all sizes, more distal with relative proximal vessel sparing.

The contemporary atherogenesis response-to-injury hypothesis is chronic inflammation and healing to endothelial injury:

  • Endothelial injury – Esp haemodynamic disturbances (turbulance at branches, posterior abdominal aorta exaggerated by HTN and stenoses), ROS from oxidised LDL, smoking, immune complexes, radiotherapy etc. Causes permeability, leukocyte adhesion, thrombosis.
  • Accumulation of lipoproteins (esp LDL), become oxidised by local ROS (macrophages, endothelial cells).
  • Monocyte adhesion, migration into intima, transformation into macropahges that ingest oxidised LDL becoming foam cells. Recruited T cells generate chronic inflammation, elaborating cytokines.
  • Platelet adhesion
  • Smooth muscle proliferation and ECM production (esp collagen, produced mostly by the smooth muscle cells) in response to cytokines released from activated platelets, macrophages, endothelium. The immature fatty streak is converted into a mature atheroma, with collagin stabilising the plaque.
  • Lipid accumulation in and outside macrophages and muscle cells.

Mophological features:

  • Fatty streak – Subendothelial foam cells that coalesce. In almost all aortas >10yo, coronary arteries after adolescence. Not all fatty streaks evolve to atherosclerotic plaques.
  • Atherosclerotic plaque – Intimal thickening and lipid accumulation, patchy, rarely circumferential but coalesce and become more diffuse with time. Varying proportions of cells (smooth muscle, macropahges, T cells), ECM (collagen, elastin, proteoglycans) and lipids (intracellular and extracellular). Superficial fibrous cap of smooth muscle and collagen. Shoulders of the cap (under and at the sides) contain macrophages, T cells and smooth muscle. The deeper necrotic core contains lipid, dead cell debris, foam cells, fibrin, variably organised thrombus and other plasma proteins. Neovascularity at the peripheries. Generally progressively enlarges with cell death, degeneration, remodeling, thrombus organisation, may undergo calcification., usually with retention of central core of foam cells and fatty depris tham may calcify.

Plaque complications:

  • Rupture/fissuring or ulceration/erosion – Exposure of internal plaque or subendothelial basement membrane respectively, with thrombosis formation that may occlude or emboli; and/or possible leak of plaque lipid or calcified debris into the lumen (atheroembolism). Plaque disruption is common, often clinically silent without oclusion/emboli. Ulceration may be seen as a penetrating niche; DDx depression between adjacent plaques, intraplaque haemorrhage, luminal bulging from destroyed media with intact intima. Best to describe as irregular or smooth and only call ulcer if there is an undermining niche.
  • Haemorrhage into plaque – From rupture of fibrous cap or neovascularity. May expand or induce plaque rupture.
  • Aneurysms – Damage of media causing weakening.

Plaques that rupture are unable to withstand the vascular shear forces. Strength of the fibrous cap is mostly from collagen syntehsized by smooth muscle cells, which is continuously being remodelled with balance of synthesis and degradation. Inflammation increases degradation, reducing the thickness of the cap hence becoming vunerable/unstable (may warrant therapy despite degree of stenosis). Thick fibrous caps suggest stability. Increased shear forces are from increased blood pressure, vasoconstriction.


Localised dilatation of vessel or heart, congenital or acquired. True aneurysms lined by intact all 3 layers, false aneurysms (pseudoaneurysms, pulsating haematoma) are defects in the wall which free communicates, contained by extravascular connective tissue. Saccular aneurysms are spherical outpoucings, fusiform are diffuse circumferential. Causes include:

  • Atherosclerosis – Atheroma increases distance from vascular supply, inducing ischamia hence loss of smooth muscle cells and collagenous ECM (glycosaminoglycan instead) = cystic medial degeneration (also seen in Marfan disease, scurvy). Common in aorta, iliac, femoral, popliteal, SCA.
  • Connective tissue disease – Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, vitamin C deficiency.
  • Inflammation – Infection (mycotic aneurysm) or inflammation (vasculitis), with proteases causing collagen degradation greater than synthesis. Mycotic aneurysm have bizzare architecture, rare in extremities.
  • Trauma (pseudoaneurysm).

Arteriomegaly (diffuse vascular ectasia, arteria magna, ectatic atherosclerosis) – diffuse generalised dilated aortoiliac and femoral vessels, tortuous iliac aa. Associated with multiple aneurysms.

Popliteal aneurysm ?atherosclerosis, most common peripheral aneurysm, >20mm. 2/3 symptomatic with Cx distal embolism, aneurysmal thrombosis/occlusion (claudication), rupture uncommon (threatened leg viability, mortality). Tx surgical ligation and bypass.

Abdominal Aortic Aneurysm (AAA)

Normal aortic diameter 20-25mm (tapers distally), ectatic 25-30mm, aneurysm >30mm or if the aorta enlarges distally. Usually from atherosclerosis and hypertension; others infection (rare), pseudoaneurysm (rare). >90% are infrarenal, 2/3 extend into CIAs (N CIA <15mm, aneurysmal >20mm, EIAs uncommon) most fusiform. Most enlarge at 2-4mm/year, but 20% are more rapid. US maximum AP diameter in transverse (overestimates) and longitudinal (underestimates) planes, 3.5-5MHz. CT maximum short axis diameter. Thrombus generally hypoechoic, may be isoechoic to blood. Complications include rupture, obstruction of branch vessels, embolisation or impingements on adjacent structures.

  • Inflammatory aneurysm – Periaortic fibrosis (hypoechoic) containing inflammation with macrophages, unknown aetiology. Can adhere to D3 with increased mortality. IVC and ureters drawn into aorta, may be associated with hydronephrosis. Otherwise same growth rate and risk of rupture as non-inflammed AAA. On spectrum of retroperitoneal fibrosis.
  • Mycotic aneurysm – Saccular, irregular. Rapid growth rate, constitutional Sx. Most commonly strep pneumonia (cf Salmonella elsewhere). Surgical emergency.

Rupture rate 1%/yr 40-50mm, 10% 50-60mm, 25% >60mm. Prophylactically treated if >50mm (rupture rate 8%/yr, lifetime 25-50%) or rapid expansion >10mm/yr. Small AAA surveillance if >30mm every 4yrs, >45mm every 6/12. Open surgery or stent graft; operative mortality 1-3% for unruptured, 50% ruptured. Large CFA access (up to 30F) requiring surgical access. Grafts may have an open segment to anchor above renal aa, bifurcation into iliacs. 25% require additional endovascular procedures. Repaired AAA reviewed with US for patency, perigraft collections (>3/12 indicates haemorrhage or infection), anastomotic stenosis/aneurysm. Endoleak type 1 around sup/inf attachment; type 2 filling via a patent sidebranch (lumbar, IMA); type 3 loss of integrity of graft; type 4 leak through porous graft material.

99% of iliac aneurysms are associated with AAA. CIA treated with stent graft. IIA usually Tx with embolisation (Cx buttock claudication, male impotence).

Thoracic Aortic Aneurysm

Ascending aorta (60%) from Marfan, Ehlers-Danlos, syphilis (usually die from aortic incompetence), atherosclerosis; arch and descending aorta from atherosclerosis; isthmus from trauma. Complications include local mass effect (mediastinum, lungs/airways, oesophagus, recurrent larygneal nerves with cough, bone with erosion and pain), cardiac disease (aortic reguirgitation or narrowing of coronary ostia), or rupture. Rate of rupture/dissection is 2%/y <5cm, 4%/y 5-6cm, 7%/y >6cm, worse in descending aorta.


Syphilitic aortitis in 12% untreated syphilis with 10-25y latent period. Direct effect of spirochetes on wall with chronic inflammation of media and adventitia. Aneurysm (ascending, may > arch), fine dystrophic calcification exclusively in ascending aorta (40%), aortic insufficiency. Risk of rupture ++.

Mycotic/nonsyphilitic aortitis from staphylococclus, streptococcus, Salmonella, many others. Bacteria detroy wall, media destruction > iregular saccular aneurysms in 40%. Asc aorta, may > arch and descending aorta.


Interuption of the intima and inner media with blood splaying/cleaving laminar plans of the media (false lumen). May or may not be associated with dilatation. Increased risk of disection in aorta or branches (including coronaries) during or after pregnancy. Hypertrophy causes media hypertrophy of the vasa vasorum, with reduced flow causing ischaemia and loss of vessel media smooth muscle cells. Most have cystic medial degeneration. Trigger for intimal tear is unknown.

Acute Aortic Syndrome

Includes aortic dissection (85%), intramural haematoma (10%), penetrating aortic ulcer (5%). If CT contrast is contraindicated and MRI could be performed with dark blood imaging (IMH) and bright blood SSFP imaging ± cine.

  • Dissection – Usually spirals downstream and variably upstream in false lumen. Typically HTN in M 40-60yo, or younger patient with cocaine, congenital disease (Marfan, Turner, Ehlers-Danlos, bicuspid aortic valve); other causes aortitis, blunt/iatrogenic trauma (including catheterisation, intra-aortic balloon pump). Unusual in presence of atherosclerosis or other media scarring (eg syphilis). Most tears are within 10cm of the aortic valve, with <1/4 starting beyond the arch. Stanford type A (proximal) involves the ascending aorta and extend distally (DeBakey I) or in isolation (DeBakey II); type B (distal/DeBakey III) arises beyond the subclavial artery. Pain is typically anterior in type A; posterior type B; painless in <10%. True or false lumen may have blood flow (with re-entry points) or thrombose. Rupture usually at site of primary entry, mortality 1% per hour. Typically false channel is on the right/ant ascending (->RCA), superior arch (->great vessels), left/post descending (->L renal a, into L iliacs). True lumen is usuall smallher, enhances more, central. False lumen has convex tips (beak sign), may have ‘cobwebs’.  Neurological symptoms in 20%. Almost all abdominal aortic dissections are extensions from thoracic. Double-barrel aorta if second re-entry intimal tear distally; false channel may be endothelialised creating a chronic dissection. There is a shared adventitial sheath with the PA, so IMH/dissection may extend around the PA. Tx for Type A is primary intimal taer; type B usually medical (surgery if complication, intractable pain, >55mm or growth >5mm in 12 months). DDx pulsation artifact (motion artifact in a slow scanner).
  • Intramural haematoma (IMH) – Localised haematoma within wall. Usually elderly, HTN. ?Controlled dissection without identifiable entry/re-entry point, ?haemorrhage from vasa vasorum. May only be able to see on the non-contrast scan as non-circumferential hyperdensity. DDx atherosclerosis, vasculitis. May progress to full dissection. Tx similar to dissection.
  • Penetrating aortic ulcer (PAU) – Ulceration of atherosclerotic plaque into media beyond the expected borders of the aorta (intimal breach); compared to an ulcerated plaque which is confined to the aortic border. Usually elderly, HTN, marked atherosclerosis. May cause IMH, dissection, pseudoaneurysm or complete rupture. In acute setting, high risk of rupture; Tx stent graft or open surgery.
  • Intramural blood pool (branch artery pseudoaneurysm) – localised contrast filled pouch communicating with the aortic lumen from an intimal disruption. At an intercostal or lumbar artery origin.

Open surgery for proximal dissection to prevent rupture into pericardium, surgery for distal (arch/desc) is controversial (except if there is abdominal involvement or mesenteric ischaemia), which usually progress to chronic dissection. Endovascular stent grafting for entry site closure is limited to the descending aorta, causing false lumen thrombosis. Endovascular fenestration – long needle puncture of the intimal flap via US with balloon dilatation to equalise pressure, preserving side branch patency; for emergencies only.

Carotid Artery Dissection

Traumatic, inflammatory, degenerative or spontaneous. Tapering occlusion on angiogram. ‘mural crescent sign’ surrounding true lumen in expanded artery.

Carotid ‘wind-sock’ pseudoaneurysm is expanded ‘blind ending branch’.


Blunt, penetrating or iatrogenic. Vasospasm, intimal iregularity, pseudoaneurysm, extravasation, AV fistula.

  • Hypothenar hammer – Repetitive palmar trauma injuring ulnar artery as it passes hook of hamate > aneurysm, thrombosis or emboli to digital arteries.
  • Dislocation of the knee – 30-40% have vascular injury, highest in posterior dislocation. Small intimal tear to complete thrombosis.
  • Fractures prone to vascular injury in upper tibia/fibula, pelvic brim (10% have persistent arterial bleed).

Embolotherapy – Occlusion of bleeding/parent vessel with coils, sacrificing non-essential vessels (branches of internal iliac, profunda femoris, geniculate branches, SCA/brachial a branches except vertebral). Exclusion of injury with preservation of parent vessel with stent grafting or surgery (CIA, EIA, CFA, SFA, pop a, SCA, ax a, brach a).

Traumatic Aortic Injuries

Typically blunt trauma from crushing of vascular structures and sudden deceleration with tearing at junction of fixed and mobile portions, aortic isthmus (in 95%, just distal to LSCA) or just above diaphragm. 80-90% die at the scene (likely from an aortic root or diaphragmatic rupture.

Mediastinal haemorrhage – poorly defined fat planes, perivascular haematoma, increased density relative to aorta (on CXR), loss of sharp aortic contour, loss of AP window, left apical cap (haematoma extending along L SCA), right displacement of trachea/oesophagus, drepression of left main bronchus, widened paravertebral line. Direct signs – abnormal contour, change in calibre, intraluminal irregularity/intimal flap, active extravasation.

Aortography for questionable cases esp proximal extent of injury or planning endovascular repair. Irregular outpouching @ isthmus (pseudoaneurysm bounded by thin adventitia or supported by mediastinum), aortic insufficiency (pseudoaneurysm just above valve), intimal tear, frank extravasation rare. DDx normal ductus bump (very smooth, convex without acute margins, rapid contrast washout), atherosclerotic plaques.

Tx surgical grafting (mortality 30%, paraplegia 10%), endovascular stent graft (difficult maintaining patent LSCA). If left and tissues strong enough > chronic saccular/fusiform pseudoaneurysm with calcification.

Minimal aortic injury – injury isolated to intimal layer, which may resolve with time.

Thoracic Aorta Mobile Thrombus

Pedunculated filling defect, usually at inferior aspect of aortic arch. Middle aged, minimal atherosclerotic disease, rare source of thromboemboli.


(Angiitis, arteritis). Precise mechanisms unknown. Causes of vasculitis include:

  • Immune complex-associated vasculitis – Typically small or medium sized vessels. Antigen-antibody complexes and/or complement. Includes SLE, PAN, Henoch-Scholein purpura, cryoglobulin, Goodpastures, drug hypersensitivity (bound do serum proteins), viruses.
  • Antineutrophil cytoplasmic antibodies (ANCA) – Antibodies against enzymes of neutrophil granules, monocyte lysosomes and endothelial cells. Raised ANCA also seen in IBD, PSC, RA.
    • Anti-myeloperoxidase (MPO-ANCA, perinuclear pANCA) against lysosome granules. Raised in Churg-Strauss (in 50%), microscopic polyangiitis, PAN (occasionally), UC (in 50% with high specificity), PSC (in most), RA, some glomerulomephritis.
    • Anti-proteinase-3 (PR3-ANCA, previously cytoplasmic c-ANCA) against neutrophil azurophilic granule. Raised in Wegener granulomatosis (in 90%).
  • Anti-endothelial antibodies – Includes Kawasaki disease
  • Infectious vasculitis – Direct invasion, usually bacterior or fungi esp Aspergillus, Mucor.

Chapel Hill classification:

  • Large-vessel vasculitis – Aorta and large branches.
    • Giant-cell arteritis (GCA, temporal arteritis) – Granulomatous inflammation with immune response against unknown antigen (?vessel wall). Medium to large vessels in head (temporal, opthlamic aa), neck (carotid aa), arms (brachial aa), aorta (giant cell aortitis). F>M, >50yo, may be associated with polymyalgia rheumatica. Nodular, segmental, intimal thickening, media granulomas, multinucleated giant cells.
    • Takayasu arteritis – Granulomatous transmural inflammation. F:M 10:1, <50yo. Esp thoracic aorta (arch) and proximal branches, upper limbs (pulseless disaese), PAs in 1/2, coronaries, renal aa. Histologically similar indistinguishable from GCA. Acute phase mural thickening and enhancement; late phase narrowing of descending thoracic and abdominal aorta, dilated ascending aorta, irregular long segment severe stenoses ± abrupt occlusions with collaterals
  • Medium-vessel vasculitis – Main visceral arteries and branches
    • Polyarteritis nodosa (PAN) – Segmental transmural necrotising vasculitis of muscular arteries esp renal (85%) and hepatic (65%). Lesions of different ages. Immune complex-mediated; 30% have chronic hepatitis B. Multiple saccular microaneurysms (usually at branch points), occlusions and irregular stenosis throughout viscera. Tx when >20mm. DDx microaneurysms is PAN, Wegener’s, SLE, rhematoid vasculitis, drug abuse.
    • Kawasaki disease – Usually children, self-limiting. Mucocutaneous lymph node syndrome with conjunctival, oral erythema/erosion, hand/feet oedema, palm/soles erythema, rash, cervical lymphadenopathy. Predilection for coronary aa. May form anuerysms and/or thrombosis.
    • Thromboangiitis obliterans (Buerger disease) – Segmental thrombosing acute and chronic inflammation of medium and small arteries. Esp tibial and radial aa, may extend into veins and nerves of extremities. Exclusively heavy smokers, usually <35yo. ?Direct endothelial toxicity or immune response to a tobacco component. Thromboses contain sterile microabscesses. ‘Corkscrew’ appearance (collaterals around occlusion), absence of atherosclerosis, multiple segmental occlusions of palmar and digital aa.
  • Small-vessel vasculitis – Arterioles, venules, capillaries, occasionally small arteries. Typically immune complex or ANCA vasculitis
    • Wegener granulomatosis – Granulomatous necrotising inflammation of respiratory tract and necrotising vasculitis of small vessels incl glomeruli. PR3-ANCA.
    • Churg-Straus syndrome (allergic granulomatosis) – Eosinophil-rich granulomatous inflammation of respiratory tract and necrotising vasculitis. Vasculitis involves the lungs, GIT, peripheral nerves, heart, skin, kidneys. Associated with asthma and eosinophilia, arthralgias, gastritis/colitis, neuropathy, sinusitis, random consolidation/GGO. MPO-ANCA.
    • Microscopic polyangiitis (hypersensitivity or leukocytoclastic vasculitis) – Necrotising (nongranulomatous), commonly glomeruli and pulmonary capillaries. All lesions of same age. MPO-ANCA.
    • Raynaud phenomenon – Exaggerated vasoconstriction of digital arteries and arterioles. Primary is response to cold or emotional stress, 3-5% of population, young, F>M, usually benign but may cause skin/muscle atrophy. Secondary is from vascular insufficiency due more proximal arterial disease (SLE, scleroderma, Buergers, atherosclerosis).

Vasculitis associated with other disorders include RA, SLE, cancer, cryoglobulinaemia, antophospholipid antibody syndrome, Henoch-Schonlein purpura.

Chest and Neck Vascular

Thoracic Aorta Variants

Normal in 70% (R branchiocephalic, LCCA, LSCA). Variants/congenital anomalies include:

  • Common R brachiocephalic and L CCA (bovine anatomy) in 20%
  • Aberrant RSCA in 2%, distal to LSCA > posterior to oesophagus in 80%, between trachea and oesophagus in 15%, anterior to trachea in 5%. Diverticulum of Kommerell is dilatation at origin, may cause posterior oesophageal narrowing and dysphagia.
  • L vertebral from arch in 1%
  • Ductus bump (ductus diverticulum) in 9%, fusiform dilatation ant/med proximal descending aorta
  • R-sided arch with mirror-image branching. 98% associated with congenital heart disease (most ToF)
  • R arch with aberrant LSCA
  • Coarctation of aorta (10 media abnormal) from infolding of aortic wall near ligamentum arteriosum. 70% associated with congenital cardiac anomaly (most bicuspid aortic valve)
  • Pseudocoarctation (aortic kink) is mild coarctation, asymptomatic, pressure gradient <10mmHg. Asc aorta elongated, high transverse arch distal to kink. Associated with bicuspid aortic valve. <br>
  • Double arch

Pulmonary Vascular

See Heart and Pulmonary Vascular

Carotid Artery Stenosis

Normal CCA usually 6-8mm diameter between thyroid and jugular. Distances from echogenic intima, through hypoechoic media to echogenic adventitia (intima-media complex) normally <1.1mm thick. normal bifurcation at carotid bulb at C3-4 (but anywhere from C1-T2). ECA (N 3-4mm) anteromedial in 70%, intermediate in 20%, reversed/lateral in 10%. ICA (N5-6mm) usually post-lat course. Flow divider = arterial wall between ICA and ECA at origin. ICA has no branches, courses posterior to mastoid, low-resistence and has carotid bulb at origin. ECA has branch vessels, courses anterior to face, high-resistance and ‘temporal tap’ (superficial temporal or preauricular branch) positive. L VA same size or larger than R in 75%; VAs often have spectral broadening due to small size and poor visualisation. Ultrasound evaluation made on longitudinal 5-10MHz, head rotated away, grayscale, colour Doppler and sepctral Doppler; findings confirmed on transverse. Angle of insonation must be between 30 and 60deg. Normal flow reversal is seen in the carotid bulb opposite the flow divider.

Intimal hyperplasia if intima-media thickness (IMT) >1.1mm, indeterminate 0.8-1.1. Increased risk of atherosclerosic vascular disease (TIA, stroke, coronary artery disease).

Carotid plaques usually within 20mm of bifurcation from endothelial injury > fatty streak in wall > plaque grwoth from deposition of lipids, proliferation of smooth muscle, migration of fibrocytes. ‘Vunerable’ plaques have lipid core with variable fibrous cap, as it increase in size > repeated fissuring and intraplaque haemorrhage/healing ± rupture > emboli. Surface may be smooth, irregular or ulcerated (US unreliable but may show undercutting, lucent area extendign to surface, divot/crater ± flow into crater with reversal). Density is hypoechoic/anechoic (increased lipid content), isoechoic (smooth muscle) or hyperechoic (fibrous tissue). Texture is homogeneous or heterogeneous (lucent areas intraplaque haemorrhage). All ulcerated plaques are heterogeneous, but not all heterogeneous plaques ulcerate. Calcification is nonspecific. Plaque characteristics significance controversial, Doppler and diameter stenosis most important.

ICA stenosis. Peak systolic velocity (PSV) most accurate for stenosis 50-90% (exponential increase). <50% more accurate with grayscale/colour Doppler in transverse. ICA/CCA PSV ratios should be used instead of ICA PSV when CCA velocities are abnormal/assymetric eg significant hypertension. Bilateral ICA disease causes flow alterations complicating determination of the more significant side.

  • 0-29% stenosis – PSV <100cm/s
  • 30-49% stenosis – PSV 110-130cm/s, EDV <40cm/s, PSV ICA/CCA ratio <3.2, plaque <50% of diameter,
  • 50-69% stenosis – PSV 130-230cm/s, EDV 40-110cm/s, PSV ICA/CCA 3.2-4.0, plaque >50% of diameter
  • 70-95% stenosis (high grade) – PSV >230cm/s, EDV 110-140cm/s (for 70-79%) or >140 (80-95%), PSV ICA/CCA >4.0, lumen <1.5mm.
  • 95-99% stenosis – PSV falls as stenosis approaches occlusion. String/trickle flow, PSV may be high, low or undetectable. Sensitivity reduced with calcified plaque due to shadowing.
  • 100% stenosis (occluded) – No flow, may have small diameter filled with echogenic thrombus. Brief systolic pulse followed by reversal may be seen from thumping of blood against occlusion. CCA high resistance with reduced diastolic velocity (‘externalisation of the CCA’), unless there is well-developed intracranial ECA-ICA collateralisation causing ‘internalisation of the ECA’. Must be differentiated from ‘trickle flow’ in near-occlusion stenosis as they are still candidates for endarterectomy. This is not seen in 5-7% of USS/MRA, hence catheter or CT angiography may be needed to exclude ‘string sign’.

North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Stenosis Trial (ECST) showed benefit of endarterectomy for ICA stenoses >70% (only modest benefit 50-69% in selected cases), no benefit <50%. NASCET (‘gold standard’) measured by ratio between diameter of stenosis to normal ICA distally; ECST compared stenotic diameter to approximation of original vessel diameter. 50% NASCET ~equivalent to 70% ECST stenosis. Benefits of carotid angioplasty and stenting (CAS) still being determined, currently only recommended in patients with severe stenoses not fit for endarterectomy.

Postendarterectomy (vein or polytetrafluoroethylene PFTE patch) sutures may remain visible along arterial wall. Patulous artery at site common. Complications include restenosis (10-15% in 1st yr from intimal hyperplasia), intimal flap, clamp strictures.

CCA low velocities (<50cm/s) in low cardiac output, wide arteries, severe proximal stenosis, severe distal stenosis/occlusion, long segment stenosis. CCA high velocity (>100cm/s) in high cardiac output, narrow arteries, technical issues (eg tortuous), CCA stenosis, contralateral severe stenosis. CCA stenosis PSV ratio (from stenosis to velocity proximally) can be used to estimate degree where 50% stenosis is 2:1, 75% 3.5:1 and 90% 7:1. CCA occlusion causes retrograde flow through ipsilateral ECA to supply the ICA.

ECA stenoses don’t affect clinical management/stroke, but significant stenosis may elevate ICA velocities. Vertebral artery stenosis determination difficult and treatment limited; assesment usually confined to presence and direction of flow.


  • Takayaso arteritis – Concentric wall thickening.
  • Radiation fibrosis – Concentric wall thickening.
  • Fibromuscular dysplasia – Irregular intimal thickening over full length of CCA.
  • Carotid dissection
  • Carotid body tumours
  • Vascular invasion from metastases
  • Significant aortic stenosis – Bilateral parvus-tardus.
  • Aortic insufficiency – Bisferious pulse with second peak higher than first.

Subclavian Steal Syndrome

Innominate or subclavian artery occlusion proximal to origin of the vertebral artery. Upper extremity receives blood from the CCA via circle of Willis, retrograde flow through vertebral artery. Partial subclavian steal causes reversed flow only during systole (bidirectional flow), from severe stenosis.

Superior Vena Cava (SVC) Syndrome

Extrinsic compression of SCV -> thrombosis. From bronchogenic carcinoma (in 80%), granulomas (histoplasmosis, TB), lymphoma, intravascular foreign body (pacemaker leads, central venous catheter), venous stenosis (chronic dialysis, venous HTN). Tx of carcinoma is radiotherapy; thrombosis is venopasty and stenting.

Thoracic Outlet Syndrome

Spectrum of dissorders causing compression of upper limb neurovascular bundle (a, n or v) @ level of scalene and 1st rib. Sx arterial insufficiency, venous obstruction, painless wasting of intrinsic hand muscles, pain.

Arterial form diagnosed by placing arm in position creating most Sx cf neutral position and various degrees of abduction, but occlusion may occur in normal subject with arm position. Compression causes cease of flow or dampening of waveform. Arterial injury (70% from cervical rib) > aneurysm, stenosis, thrombosis and embolism.

Paget-von Schroetter syndrome ( effort thrombosis) – compression of SCV by cervical rib, soft tissue or scar tissue after clavicle fracture > thrombosis, arm swelling. Stenting should be avoided prior to surgery as persistent extrinsic compression > stent fracture.

Pulmonary Artery Aneurysm

Rare. From TB (Rasmussen aneurysm), iatrogenic (pseydoaneyrysm from PA/Swan-Ganz catheter).

Abdominal Vascular

Mesenteric Ischemia

Acute 75% from arterial embolism/thrombosis. Mortality 70%.

  • Embolism usually cardiac origin. Abrupt SMA cutoff ~40-60mm from origin with reverse meniscus appearance (contrast partially enveloping embolus).
  • Arterial thrombosis background severe atherosclerotic disease. Postprandial abdo pain, weight loss, altered bowel habit. Tx intra-arterial thrombolysis, surgery if infarction.
  • Nonocclusive ischaemia (10%) – Low flow states from hypotension, dehydration, low CO > disproportionate vasoconstriction > iscahemia. Alternating areas of vasospasm (sausage link narrowings). Tx vasodilators (papaverine).
  • Mesenteric venous occlusion (10%) – Medium-sized veins of mid SB. Tx catheter-directed thrombolysis via arterial or portal venous with perc or transjugular access.

Chronic mesenteric ischaemia from occlusion/high-grade stenosis of >/= 2 of the 3 mesenteric aa. Atherosclerosis, FMD, vasculitides. Postprandial pain.Tx angioplasty with stenting or surgical bypass.

  • Median arcuate syndrome (coeliac artery compression syndrome, Dunbar syndrome) – Fibres from median arcuate ligament causing stenosis of coeliac axis controversial (?splanchnic nerve compression, ?delayed gastric emptying). Superior impression proximal coeliac worse with expiration. Variable results with surgery.

GI Haemorrhage

Upper GI bleeding (proximal to ligament of Treitz) > gastric aspiration, upper endoscopy. Mallory-Weiss tear, haemorrhagic gastritis, gastric/duodenal ulceration, recent surgery, tumour. Duodenal bleed > embolisation of GDA by trapping bleeding site (retrograde filling from pancreaticoduodenal aa_. Gastric > L or R gastric embolisation. Proximal agents unlses tumour. Post-surgical patients high risk of infarction (collateral supply may be compromised).

Lower GI bleeding (jejunum to rectum) > colonoscopy, radionucline, CTA or angiography (>0.5mL/min). Contrast extravasation > amorphous persisting through venous phase, may outline mucosal folds. Pseudovein sign = linear contrast between mucosal folds simulating enlarged vein.

Small bowel

  • SB Tumour (20-50%) – Neovascularity (enlarged, bizarre irregular vessels with AV shunting).
  • Vascular malformations (20%) – Solitary or multiple (eg Rendu-Osler-Weber syndrome). Chronic recurrent bleeds.
  • Aortoenteric fistula (10%) – Cx >3/52 posterior AAA surgery. 80% in duodenum with anterior nipple-like projection from aortic graft. Visualised extravasation rare.
  • Diverticula of SB – Uncommon cause. Mesenteric border of bowel. Slow and difficult to manage angiographically.
  • Meckel diverticulum – Painless bleeding from heterotopic gastric mucosa.
  • Inflammatory bowel disease – Diffuse hyperaemia, AV shunting, oozing.

Large bowel Tx superselective embolisation in arcuate branches beyond marginal aa with coils or particles, preserving collateral flow. Clinical failure inc with coagulopathy, multiorgan failure, shock, corticosteroids. Vasopressin infusion more time consuming with higher Cx rates.

  • Colonic diverticula (most) – Diverticula more common on left, but bleeding diverticula 3x more likely on R. May bleed despite active diverticulitis.
  • Angiodysplasia – Early and persistent opacification of enlarged draining vein, vascular tufts along antimesenteric border cauecum/asc colon. Tx embolic or surgical.
  • Colorectal tumour – Slow with anaemia, infrequeintly massive. Tx selective/superselective embolisation if not surgical candidate.

Blunt Abdominal and Pelvic Trauma

Aortic trauma rarely survivable.

Pelvic fractures causing bleed usually controlled with fixation. Arterial bleed usually from branches of internal iliac > embolisation with proximal agents.

Splenic Artery Aneurysm

Most common aneurysm after aortic and iliacs. 3rd-6th decate, F>M. Congenital high rate of rupture. Pseudoaneurysms from pancreatitis. Multiple aneurysms of main and branch vessels in cirrhosis. Tx coil obliteration or trapping of arterial segment (coils, occlusion balloons; distal collaterals from short gastric).

Portal Hypertension

N portal venous pressure 5-10mmHg with portosystemic gradient 3-6mmHg. Varices (portosystemic collaterals) form when portosystemic gradient >11-12mmHg. Risk of variceal haemorrhage, ascites, spontaneous bacterial peritonitis, coagulopathy, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome. ‘Uphill’ varices incl coronary veins anast with azygos v in submucosal distao oesophagus and gastric cardia (thin overlying mucosa, project into lumen). Tx medical management, endoscoic control of variceal bleeding, TIPS if these are no longer effective.

Renal Artery Stenosis

(Renal artery occlusive disease). 99% from atherosclerosis, FMD, other causes include disection, vasospasm, vasculitis, coarctation syndromes, neurofibromatosis. Renal transplant artery narrowing from surgical factors (acute), intimal hyperplasia (late) or atherosclerosis (very late).

  • Fibromuscular disease (FMD) – Most common cause of renovascular HTN <40yo. Initimal (7-8%), medial (85%, beaded) or periarterial/adventitial (7-8%, smooth/linear) forms. In mid, distal renal or segmental renal aa. Associated with NF1, or may be condition similar to FMD. Rarely causes extrarenal aneurysms. Medial fibroplasia – ‘string of beads’ (alternating webline stenoses and aneurysms), mostly middle and distal main renal a. Progressive. Rx angioplasty with success rates 98%.
  • Atherosclerotic renal stenosis – HTN, renal failure, usually >60yo. Aortic and proximal renal a disease, rarely extrarenal aneurysms. Rx stenting (angioplasty alone poor) with variable unpredictable outcomes, most HTN is essential with renal insufficiency multifactorial. Elevated renal vein renin tend to correlated with positive outcome, pressure grandients not predictive. 20% cured, 50% improved.
  • Neurofibromatosis causes extrinsic compression from neurofibromata or disorganised intimal/medil proliferation origin/proximal renal a. Smooth or nodular stenoses ± aneurysms.

Renal artery angioplasty Cx in 5-10% including worse renal function, renal a injury.

Aortoiliac Occlusive Disease

Usually atherosclerotic, less commonly Takayasu arteritis (long segment smooth narrowing), hypoplastic aortic syndrome (congenital long-segment narrowing, young female), neurofibromatosis, fibromuscular disease (iliac aa). Claudication incl bilateral buttock, impotence, absent femoral pulses, blue toe syndrome. Leriche syndrome – aortic occlusion. Pressure gradient >10mmHg significant, augmented with intra-arterial vasodilators. Isolated aortic lesion rare.

Rx angioplasty with ‘kissing’ ballons at bifurcation from each CFA. Any posterior angioplasty residual gradient, vessel irregularity or intimal flap > stent.

IVC Thrombosis

Normal waveform saw-tooth from transmission of RA pulsatations. Leg oedema ± pain, renal failure, bowel ischaemia. Thrombosis usually extends from peripheral veins, occasionally from extrinsic compression, Budd-Chiari, tumour. Clot often expands the IVC (also seen in CHF wehrer there may also be slow-flowing blood). Partial thrombosis spectral waveform blunted with loss of pulsatility and respiratory phasicity. Tumour thrombus (RCC, hepatoma, adrenal carcinoma, pheo, lymphoma, angiolipoma, atrial myxoma) if arterial flow seen in IVC lumen within mass.

Budd-Chiari Syndrome

Occlusion of hepatic veins, from hepatic venous or IVC obstruction. 70% have predisposing factors (hypercoagulable states, posttraumatic, tumour invasion, membranous/web/diaphram obstruction of suprahepatic IVC). Post-sinusoidal portal hypertension. Sx acute or chronic hepatic failure or portal HTN. Echogenic thrombus in narrowed veins with monophasic waveform. ‘Steeple’/’pencil point’ intrahepatic IVC from compression by swollen liver. May thrombose. ‘Spiderweb’ pattern of collateral hepatic veins and lymphatics. Caval webs or segmental IVC occlusion > venoplasty, frequent venography followup required. Other Tx IVC/hepatic vein stent, transjugular intrahepatic portosystemic shunt (TIPS).

Fibromuscular Dysplasia (FMD)

Focal irregular thickenings from media and intimal hyperplasia and fibrosis. Most young women. Medium and large arteries including renal, carotid, splanchnic, vertebral, SCA, axillary, brachial, iliac, femoral, and popliteal arteries. Subclassified into intimal, medial (most common) or adventitial hyperplasia. F>M, 20s-30s. May be single well-defined constriction or series of constrictions. Beaded appearance ± Cx including aneurysm, dissection, thrombosis, distal embolism.

DDx standing waves – corrugated luminal contour in medium-sized aa, unknown aetiology, appearances change between angiographic injections.

Peripheral Vascular

Normal high-resistance triphasic – high velocity systole, postsystolic reversal then low level forward late diastolic flow from elastic recoil of vessel wall. PSV reduces distally, ~110cm/s CFA and SCA, 85cm/s ax a, 70cm/s pop a. PSV not reliable for grading stenoses. Velocity ratios more predictive; stenotic PSV / normal PSV proximal to stenosis, where > 2:1 severe/haemodynamically significant with >50% stenosis, monophasic waveform; 3.5:1 75% stenosis, 7:1 90% stenosis.

Intermittent claudication in lower limbs:

  • Atherosclerotic peripheral vascular disease (ASPVD).
  • Popliteal artery entrapment
  • Endofibrosis
  • Cystic adventitial disease
  • FMD
  • Trauma, esp popliteal fossa

Intermittent claudication in upper limbs:

  • ASPVD, uncommon distal to SCA
  • Thoracic outlet syndrome
  • Takayasu arteritis
  • Radiation vasculitis
  • Iatrogenic injury

Chronic ischaemia/vascular insufficiency Fontaine classification I assymptomatic/coldness/numbness, II intermittent claudication, III rest pain, IV ulcer/gangrene. Critical limb ischaemia is advanced stage. Physical exam includes colour, temperature, pulses and tissue loss. Ankle-brachial pressure index (ABPI) >1 N, 0.5-0.95 intermitent-severe claudication, <0.5 rest pain and tissue loss. Most common atherosclerosis, in SFA adductor canal, CIA, popliteal, tibioperoneal trunk, tibial aa origins, symptomatic upper limb uncommon. (prox LSCA > subclavian steal, digital aa). <br>

Endovascular angioplasty/stent success 83-98% with 5-yr patency 48-75% better in larger/greater blood flow aa. Cx access haematoma, thrombosis, rupture. Below knee revascularisation usually for limb salvage.

Synthetic grafts are Dacron (polyester fibre, corrugated) or PTFE (two parallel echogenic lines), rarely used below the knee. Failure usually at anastomosis with native aa, being stenosis, pseudonaeurysm (DDx patulous anastomosis) usually within 2 yrs. Fibrointimal hyperplasia within graft lumen usually 5-10yrs.

Autologous vein grafts from reversed saphenous of in situ graft (only proximal and distal saphenous vv mobilised, venous valves lysed). Pre-op vein mapping can be done, most commonly greater saphenous vein (or other vein asl long as >3mm without varicosities); course of vein marked on skin and all branch points labeled. Surveillance increases 5-yr patency rate from 60-85% to 82-93%, done every 2-3/12 for 1st year then every 6-12/12. Cx in 1st/12 incl perivascular fluid collections, anastomotic failure, poor vein selection, AVF, residual valves, occlusion. At 1/12-2yr intimal hyperplasia causes focal stenoses in 20%, usually at site of venous valves; doubled velocity ratio (PSV cf 20-40mm prox) suggests 50% stenosis, ~PSV 180cm/s; intervention considered with ratio triples. Proximal anastomosis velocity ratio cf 40-60mm prox, distal anastomosis to native artery in ‘normal’ segment distally. Fract velocity <45cm/s indicates impending failure. <br>

Acute Lower Limb Ischaemia

From emboli being cardiac (AF, MI) or noncardiac (atheromatous debri, aneurysm) or in situ thrombosis (severe atherosclerosis, coagulopathy, trauma). Rutherford classification I (viable) – audible arterial doppler; IIa (marginally threatened) – minimal/no sensory loss, ± arterial but audible venous Doppler; IIb (immediately threatened) – partial paralysis and sensory loss, rarely audible arterial Doppler; III (irreversible, amputation required) – complete paralysis and sensory loss, inaudible venous Doppler. Abrupt transition, often at bifurcation (if embolic), poorly developed collaterals. Blue toe syndrome – microemboli to foot digital arteries, mostly from abdo aortia/iliac a stenosis/aneurysm.

Tx acute transcatheter thrombolysis if pain and pallor, surgery if sensory/motor deficits.

Popliteal Entrapment Syndrome

Intermitent compressive occlusion, exaccerbated by plantarflexion of popliteal artery.

  • Type 1 – Aberrant course of popliteal artery, normal muscles.
  • Type 2 – Aberrant insertion of medial head gastrocnemeus.
  • Type 3 – Accessory slip of muscle.
  • Type 4 – Popliteus coursing posterior to artery (usually anterior) with soleal sling.
  • Type 5 – Both artery and vein entrapped.
  • Type 6 – Physiological. Doesn’t respond to treatment.

Young, athletic men, atraumatic leg ischaemia. Bilateral in 30%. Micrrotrauma > intimal hyperplasia > filling defects. Irregularity of pop artery, confirmed with medial deviation of aa during maneuvers of leg/foot. Reduced pulses/duplex with plantarflexion or passive dorsiflexion, but this is normal in 50%. Angiography/MR/CT in plantarflexion and dorsiflexion. Symptomatic patients treated with division of offending muscle, otherwise may become irreversible with pop a injury (thrombosis, aneurysm) requiring bypass.

Cystic Adventitial Disease

Accumulation of mucin in adventitial layer ?synovial rests > fixed narrowing/obstruction. Popliteal a, EIA, EIV. Young-middle aged male, mimics pop entrapment. Cystic component seen with US/MR/CT. Tx surgical excision ± bypass.

May Turner Syndrome

Compression of left iliac vein by anterior crossing RIA. Some patients arterial pressure > thickening of venous wall > narrowing > thrombosis. Exercise may exacerbate narrowing. Tx angioplasty and stenting.


Almost always elite cyclists, symptomatic at maximum exercise. Intimal thickening in EIA with velocities up to 400-700cm/s (cf normal 150cm/s). ABPI <0.6. Tx venous patch with Cx anurysm requiring followup.

Deep Venous Thrombosis (DVT)

90% of PEs arise in lower extremities, untreated DVT -> PE in up to 50%. Risk factors prolonged immobolisation, age, pregnancy, oral contraceptives, surgery, trayuma, MI, CHF, malignancy, polycythaemia, prior DVT, other hypercoagulable state. Upper limb DVT usually from current or previous catheter, and is only associated with PE in 12%..
Isolated calf DVT do not cause PE, but up to 20% propagate into popliteal of SFV hence if patient remains symptomatic serial evaluation every 3-5/7. Most spontaneously resolve.

Compressive US to coapt and exclude DVT (most accurate, needs enough pressure to deform adjacent aa) for popliteal to CFV, may be augmented with Doppler resp phasicity, augmentation with release of Valsalva, augmented flow with squeezing calf or plantarflexion), colour/power Doppler (confirming patency and unidirectional flow). DVT may also cause venous distension, visualised intraluminal thrombus. If still indeterminate or IVC thrombus likely then CT venography. In the upper limbs need to asses SCV, axillary and IJVs. Compression can be impossible in the SC vein, hence colour Doppler or ‘sniff’ test (sniff -> decreased or collapsed lumen). DDx Baker cyst, cellulitis, pop art aneurysm, oedema (CHF, lymphatic, renal failure etc), chronic venous insufficiency, extrinsic venous compression, superficial thrombophlebitis, haematomas.

Anticoagulation only prevents PE. Embolism from superficial veins is rare. Catheter-directed thrombolysis can be done if clot extends centrally. Offending lesion can be treated with venoplasty or stent. Access via brachial/basilic or popliteal vv. Multiple-sidehole infusion catheter imbedded in thrombus with repeat imaging at 12-24h. Stenting avoided below inguinal ligament due to frequent stent failure and thrombosis. 6/12 posterior DVT, 50% ahve persistent abnormal; chronic clot doesn’t tend to expand the lumen, is more echogenic ± echogenic strands in lumen, thickened irregular echogenic wall, collateral vessels.

Phlegmasia cerulea dolens – arterial comprimise from elevated venous pressures in massive acute DVT. Thromboses in main and collateral drainage > swelling, riased vascular resistence, ischaemia.

Chronic Venous Insufficiency

40-80% of DVT -> postthrombotic syndrome (chronic pain, swelling, cutaneous ulcers) due to chronic venous outflow obstruction and injury to valves, but most patients with DVT have incompetent valves unrelated to DVT. Insufficiency from destroyed/incompetent valves, in 25% of women, 15% men. Flow reversal from deep -> superficial as seen at saph-fem junction for >1 sec during Valsalva or augmentation.

Varicose veins are dilated tortuous veins, from increased intraluminal pressure and loss of wall support. Usually superficial veins of lower limb. 10-33% of adults, increased risk with obesity, F>M, pregnancy, FHx. Dilatation causes incompetent valves. Venous stasis causes oedema, skin ischaemia (poor wound healing, infections, varicose ulcers).

Vascular Tumours

Tumours are from endothelium or support cells. Benign tumours tend to have obvious vascular channels; malignant tumours do not form well-organised vessels. Haemangiomas are true benign neoplasms with cellular proliferation, small or absent at birth. Vascular malformations are always present at birth and enlarge with the child, persiste through life.


True benign neoplasm of large (cavernous) or small (capillary) endothelium lined spaces filled with blood.Very common (1-3%), F:M 7:1, most are localised, but some are large (angiomatosis). Usually superficial, 60% H&N, 25% trunk, can be deep. Rarely malignant transformation. May have closely packed tortuous vessels (‘can of worms’ appearance) with high signal or flow voids depending on flow rate. Enhancement excludes lymphangioma. If slow-flowing may have fluid-fluid levels. Have an associated mass, distinguishing it from a vascular malformation (no mass). Contain variable amounts of fat (may be extensive mimiking lipoma), smooth muscle, fibrous, myxoid, tissue, haemosiderin, thrombus, bone. Usually high T1 and T2. May have phleboliths. May scallop or extend into adjacent bone. In skeletally immature may cause chronic haeperaemia and focal bone overgrowth.

  • Capillary/infantile/strawberry haemangioma (most common) – Closely packed, thin-walled capillaries, scant connective tissue stroma. Skin, subcutaneous and mucous membranes of oral cavities and lips; may involve liver, spleen, kidneys. May be multiple. 3 phases of 1st year/newborn rapid proliferative phase; 1-10yo involution phase (50% by 5yo); and involuted phase of fibrofatty tissue. Rupture may cause haemosiderin or focal scarring. High flow lesions with vessels on Doppler and flow voids. Pseudopermeative pattern – cortical holes in adjacent bones mimicing permeative/moth-eaten pattern (DDx radiotherapy; true permeative pattern spares the cortex).
  • Cavernous haemangioma – Large dilated vascular channels separated by modest connective tissue stroma. Less circumscribed, more frequently deep. Don’t spontaneously involute, may enlarge over time. May be locally destructive. Most are asymptomatic, may cause mass effect. Multiple in VHL. 75% of osseous vascular malformations, in vertebral bodies, skull, facial bones. In vertebral bodies reduced trabeculae leaving only vertical compressive which a less and thickened causing vertical striated appearance or ‘polka dot’ on transverse CT, may cause mild expansion, occasionally soft tissue mass; variable fatty stroma (high T1 and T2), halo sign – rim of high T1. Skull lesions more commonly expansile esp outer table with coarsened trabeculae radiating in sunburst pattern towards outer table (pathognomonic). Other bones geographic lytic, may have radiating/spoke-wheel ossification.
  • Cystic angiomatosis – Rare multicentric haemangiomatosis or lymphangiomatosis.
  • Gorham’s disease (massive osteolysis, vanishing bone disease) – Multicentric angiomatosis with rapid regional dissolution of bone spreading across joints.

Glomus Tumour

(Glomangioma). Benign, from modified smooth muscle cells of the glomus body (involved in thermoregulation). Usually <10mm, most distal digits esp under fingernails.


Rare, from pericytes-myofibroblast-like cells around capillaries and venules. Meninges, sinuses or elsewhere in H&N, lower limbs, retroperitoneum. Peak 30s-40s. Nonaggressive to aggressive appearance. Slowly enlarging, painless. 1/2 metastasize, usually lungs, bone, liver.


Spectrum of intermediate-grade/borderline tumours between haemangiomas and angiosarcomas. 20-30% eventually metastasize. Peak 20s-3s. Bone lesions may have osteolysis, occasionally multifocal, oss expansile, variable aggressive margins. No underlying fatty stroma. Multicentric lesions usually several bones of same extremity, tend to have better prognosis than solitary lesions. Mimics angiosarcoma histologically.


Rare, malignant, older adults. Any site, but most involve skin, soft tissue, breast, liver. Hepatic angiosarcomas associated with arsenic, Thorotrast, polyvinyl chloride (PVC) with long latent periods. Others may be associated with lymphoedema (eg axillary dissection, causing lymphagiosarcoma), radiation, rarely foriegn bodies. All degrees of differentiation seen histologically. Locally invasive, readily metastasize. Bone lesions very rare being permeative, aggressive, no matrix, most metaphyseal. Soft tissue lesions may develop in chronic lymphoedema, may be difficult to see a discrete mass. 40% multifocal, regional, better prognosis than if solitary. Solitary lesions poor prognosis with metastases to lungs, bones.

Bacillary Angiomatosis

Vascular proliferation from opportunistic infection (Bartonella henselae, B.quintana) in immunocompromised (esp AIDS). Skin, bone, brain or other organs. Capillary proliferation. Red papules/nodules.

Kaposi Sarcoma (KS)

95% infected with human herpesvirus-8 (HHV-8, KS-assiciated herpesvirus KSHV). Progression requires a cofactor (eg HIV). Latent infection in endothelial cells, local proliferation. Intermediate grade.

  • Chronic/classic/European KS – Older men of Eastern european or Mediterranean descent. Multiple skin plaques/nodules esp legs spreading proximally. Not associated with HIV, common in second malignancy or altered immunity.
  • Lymphadenopathic/African/endemic KS – Same demographics as Burkitt lymphoma, not associated with HIV. Lymphadenopathy, occasionally involves viscera (very aggressive).
  • Transplant-assciated KS – Solid-organ transplant with long-term immunosuppressed. Aggressive with nodal, mucosal, visceral invovlemnt. Often regress when immunosupressives reduced.
  • AIDS-associated/epidemic KS – Now <1% of patients with AIDS (previously 1/3). LN, viscera, may disseminate early. Most die from other disease.

Vascular Malformations

Errors in development resulting in dysplastic vessels. Present at birth, and grow proportionately with the child, may grow more rapidly with hormonal changes (puberty, pregnancy). Subcategorised depending on histological makeup. Slow-flow lesions have veins, lymphatics, capillaries (eg Sturge-Weber) or mixed. Fast-flow malformations include arterial, arteriovenous malformations and fistulas. Malformations may be mixed (eg Klippel-Trenaunay).

Lymphatic Malformations

Sequestered primitive lymphatic tissue that fails to communicate with peripheral drainage pathways. May be mixed lymphatic/venous slow flow malformation. Present at birth and grow with the child. Sudden enlargement from haemorrhage, infection or obstruction. No enhancement, or only enhancement within septa.

  • Microcystic/simple/capillary lymphatic malformation (‘lymphagioma’) – Small lymphatic channels esp H&N, axillary SC. Absence of erythrocytes in capillary endothelium-lined spaces.
  • Macrocystic/cavernous lymphatic malformation – Typically children H&N (cystic hygroma), rarely retroperitoneium. Neck more common in Turner syndrome. May be enormous. Massively dilated lymphatic spaces with intervening lymphoid aggregates in stroma. Cystic with fluid levels, walls enhance. Adjacent veins may be enlarged.

Venous Malformations

Usually large muscles of lower limbs. Enlarge when limb is dependent, decompress with elevation/compression (cf haemangiomas). May be associated with muscle atrophy, local fatty infiltration, phleboliths.

  • Venous malformations of the synovium (‘synovial haemangioma’) – Typically knee, elbow. Repetitive bleeding into joint causing similar appearance to haemophilia.

Arteriovenous Malformation (AVM)

High-flow lesions with large feeding and draining vessels. No associated soft tissue mass or endothelial proliferation (cf haemangiomas). Present at birth and grow with the child. Most in the skin, but can be anywhere, 60% LL, 25% UL. When in deep soft tissues may be associated with limb overgrowth due to increased blood flow. Haemangiomatous, nidus (central network of bypassing vascular channels), single-hole fistulas or combination. Most Peripheral AVMs. Endovascular Tx transcatheter/direct percutaneous embolotherapy with obliteration of nidus, as close to single-hoe fistulas as possible, staged for large extensive AVMs.

Vascular Ectasias

Not true neoplasms (haemangiomas) or malformations. Reactive dilatations of preexisting vessels.

  • Varices – Eg portal venous hypertension, orbital varix (primary/idiopathic/congenital or secondary/acquired from AVM, CCF, DAVF etc).
  • Nevus flammeus (‘birthmark’) – Flat, esp H&N, most regress. Port wine stains tend to grow with the child, may be associated with Sturge-Weber.
  • Spider telangiectasia – Radial, often pulsatile subcutaneous arterioles, esp H&N, upper chest. Most associated with hyperoestrogenaemia eg pregnancy, cirrhosis.
  • Hereditary haemorrhagic telangiectasia (HHT, Osler-Weber-Rendu disease) – AD, dilated capillaries and veins over skin and oral mucous membranes, respiratory, GI and urinary tracts. May rupture causing epistaxis, GI bleeding, haematuria.

Procedural Complications

Ateriovenous Fistula (AVF)

Generally from simultaneous puncture of artery and vein, usually small and resolves spontaneously. In large AVF the feeding artery is low-resistance waveform, distended draining vein with high-velocity pulsatile flow, only within several cm of the AVF. In small AVF the waveforms may be normal. Colour Doppler heterogeneous, disorganised pattern over fistula from soft tissue vibration = ‘colour Doppler bruit’.


Contained rupture with persistent connection/neck. Most commonly complication of arterial puncture, others include surgery, trauma. Echolucent mass, occasionally multilocular ± internal echoes/mural thrombus. Typical colour Doppler ‘yin-yang’ pattern. ‘To-and-fro’ waveform over neck.

DDx haematoma (impossible to distingush from thrombosed pseudoaneurysm, most common post-procedure perivascular mass), seroma, abscess.

US-guided compression of neck from transducer during colour imaging for 20-30min, repeated if required. Cx pain, distal embolisation, rupture, thrombosis, DVT; contraindications infection, pucture above inguinal ligament, large haematomas. Success in 80-90%, if on anticoagulation is ~2/3.

US-guided thrombin injection is less time consuming and better tolerated. 0.5-1mL thrombin 1000iU/mL into cavity avoiding artery or neck. Success 90-100%, including on anticoagulation. Thromboembolic events in 0.8%, occasionally fever (allergic reaction), groin pain at 1/52 in 41%.


From catheter placement, trauma (including only proximity trauma), Tx intra-arterial vasodilator (100mcg nitroclycerin). Systemic vasospasm from ergot alkaloids (ergotism) eg ergotamine stimulates contraction of smooth muscle >long segment aa narrowing esp lower limbs, reverses with discontinuation.