Stenosis

Vessels

Aorta, Arteries

Anomalies and Variant Positions

Dilatation

Stenosis

Wall Thickening

Intraluminal Mass

Perivascular Mass

Vena Cava, Veins

Aortic Stenosis

Arterial Stenosis

Aortic/Arterial Embolism

Arteriosclerotic Aortic/Arterial Occlusion

Anastomotic/Bypass Stenosis

Tumor Stenosis/Infiltration

Aortic Stenosis

Arteriosclerotic stenotic lesions also exhibit complex protuberances that produce luminal stenosis of varying significance. Generalized sclerosis of the aorta will lead to severe narrowing of the aortic lumen (Fig.1.21).

Fig. 1.21

a Arteriosclerotic sclerosis of the aorta: severe narrowing of the distal aortic lumen (AO) due to complex calcified plaques with posterior shadowing (S).

b Disseminated arteriosclerotic sclerosis of the aorta. Multiple stenoses of the aorta (AO) due to complex calcified plaques with posterior shadowing (S).

c Thickening of the aortic wall with multiple consecutive stenoses and turbulence-induced color changes. Arrow: color change at the origin of the iliac artery.

c Fibromuscular dysplasia of the internal carotid artery with alternating zones of vasoconstriction and vasodilation in an extracranial vascular segment far above the bifurcation.

d Hypoechoic wall thickening at the carotid bifurcation in the case of idiopathic carotidynia.

e Typical vasculitis finding of the common carotid artery in Takayasu arteritis: long hypoechoic wall thickening visualized in the color Doppler image as a dark halo around the vascular lumen.

The sonographic criteria of proximal renal artery stenosis are ( 1.3j–l):

● Demonstration of a localized thickening of the wall, and in the B-mode image narrowing of the lumen (quite often not identifiable)

● Turbulence before and after the stenosis with color changes (“confetti phenomenon”)

● Increased velocity of more than 180 cm/s; increase in the end-diastolic velocity to above 50 cm/s

● Poststenotic drop in the velocity presents a higher diastolic plateau, indicating a reduced resistance

● Decrease in the resistance ratio below 0.5 or a difference of more than 5% ( RI 0.05) when comparing both sides (poststenotic or at the intrarenal arteries)

1.3 shows typical examples of splanchnic and renal artery stenosis.

Carotid artery. Ultrasonography of the carotid arteries and possibly the aortic arch may be of vital importance in internal medicine and neurology. B-mode imaging will demonstrate any stenosis and thrombosed plaques, while the severity is ascertained by duplex scanning. This is mainly relevant to the consequences of arteriosclerosis. The other most important nonarteriosclerotic diseases of the cervical arteries are (see Arning8) dissection, fibromuscular dysplasia, vasculitis, and idiopathic carotidynia (Fig.1.22a–e).

1

Vessels

1

Aorta, Arteries

Fig. 1.23

a Small, soft plaque (arrow) in the CCA: faint, smoothly curved area of luminal narrowing without an acoustic shadow.23

Dissection. Dissection (predominantly of the internal carotid or vertebral artery) is spontaneously caused by the diversion of blood into the artery wall, either following intimal tear or due to bleeding of the vasa vasorum. It may be also caused by a Stanford type A aortic dissection with spreading into the supraaortic vessels or vascular injury including an iatrogenic lesion due to puncture or surgery.

The sonography of a spontaneously occurring dissection as an intramural hematoma without intimal rupture shows an extended and distal asymmetrical localized hematoma without a double-layer lumen.

Dissections of the ICA with severe stenosis (associated with a high risk of stroke) and dissections including milder stenosis can be detected with an overall sensitivity of 70–96%, depending on the degree of stenosis and a specific search for dissections.8

Fibromuscular dysplasia. This is a nonatheromatous, noninflammatory arteriopathy of unclear etiology with segmental manifestation at medium-sized arteries, the renal arteries and the ICA, often with alternating zones of

b Luminal narrowing in the region of the carotid bulb: complex lesion (cursors) with secondary calcification, shadowing.

vasoconstriction and vasodilation in an extracranial vascular segment far above the bifurcation.

Vasculitis. Two forms of immunovasculitis can manifest at the large extracranial vessels and be detected with ultrasound: Takayasu arteritis and giant-cell arteritis (Horton disease).

Takayasu arteritis manifests with stenoses and secondary thrombotic occlusion, or with aneurysms at the aortic arch and the supraaortic arteries. Since the subclavian artery is often affected to a greater extent than other vessels, hypoperfusion of the arms can be the main symptom (“pulseless disease”). In typical cases, the CCA exhibits long, homogeneously hypoechoic, concentric wall thickening (the “macaroni sign”), resulting in lumen narrowing. On color Doppler imaging the thickened, hypoechoic wall appears as a dark halo surrounding the colorful lumen.

Giant-cell arteritis manifests in mediumsized and large arteries, particularly the supraaortic arteries and their branches, the abdominal and pelvic arteries and vessels. Sonography shows long, concentric, homogeneously hypo-

c Luminal narrowing in the internal carotid artery by hard plaque with zones of turbulent flow behind the stenosis (red, yellow, blue).

echoic wall thickening visualized on the color Doppler image as a dark halo surrounding the bright lumen (for diagnosis on the temporal artery, see Fig.1.41, p. 21).

Idiopathic carotidynia. Affected patients complain of severe pain on one side in the upper cervical region that responds well to cortisone or nonsteroidal anti-inflammatory drugs (NSAIDs). Sonography shows hypoechoic thickening of the vascular wall resulting not only in minimal lumen narrowing but also a pronounced hypoechoic thickening of either the cranial CCA, or the junction to the ICA. Because spontaneous dissection is more cranially located, hemodynamic signs of stenosis are not detectable.8

Arteriosclerotic stenoses. According to Neuer- burg-Heusler and Hennerici6 and Widder et al.,9 stenosis of the common, external, and internal carotids may be classified according to five possible degrees of severity (Table 1.1,

Fig.1.23, Fig.1.24).

c Doppler spectrum sampled in the stenosis: Vmax is increased to 140 cm/s, indicating 50% stenosis.

Fig. 1.25 Color-flow duplex scan with spectral analysis and measurement of the pulsatility index. ATP = posterior tibial artery.

a A solely neuropathic foot (plantar ulcer): normal arterial spectral profile, pulsatility index 7.67.

b A neuroischemic foot (deep plantar ulcer Wagner grade II): marked decrease in the peak systolic velocity (10 cm/s), high diastolic plateau, pulsatility index 0.87; critical ischemia of the lower extremity.

Fig. 1.26 Pulsatility index (PI) and velocity as a function of the severity of the obstruction in normal and pathological extremity flow pulses. The PI is computed by dividing the difference between peak and minimum flow velocity (h) by the mean flow velocity (Vm) (see Neuerberg-Heusler and Hennerici6).

sclerosis of the media, where the pedal pulses are not palpable, even in the absence of any clinically significant obstruction, and the parameters generated by Doppler ultrasound are meaningless. Here, a subtle search for obstruction may be called for to differentiate and assess the status of the ischemic leg in the presence of any concomitant neuropathy. In our studies the diabetic foot, solely neuropathic and without any vascular obstruction, will yield a pulsatility index (PI) greater than 4, while in the neuroischemic foot PI lies between 4 and 1.2; in critical ischemia of the lower extremity the PI drops below 1.2 (Fig.1.25).10

Determination of the peak and minimum flow velocities as well as the PI of Gosling and King in the poststenotic segment of the artery is easier to perform. This will resemble the curves illustrated in Fig.1.26 (after Gosling as quoted in Neuerberg-Heusler and Hennerici6). Figures 1.27 and 1.28 are images of iliac and femoral artery stenoses, respectively.

Fig. 1.27 Stenosis (AID) of the right iliac artery. AO = aorta.

a B-mode image: severe narrowing of the origin (arrow) of the iliac artery.

b Color-flow Doppler scan: stenosis (arrow), the color changes signifying turbulent flow.

Fig. 1.28 Stenosis (arrow) of the femoral artery (AF), colorflow Doppler scan: prestenotic color changes denoting turbulence. The stenosis is due to a massive calcified plaque (note the shadowing, S) encroaching on the lumen.

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Aorta, Arteries

Aortic/ArterialEmbolism

atrial fibrillation (see Fig.1.44; the incidence of embolism at the various sites of the arterial tree is given in the schematic Fig.1.45).11

In ultrasound imaging, arteriosclerotic occlusion of the aorta and the other arteries is demonstrated by a complete loss of continuity in the lumen and no flow in color-flow Doppler scanning. Adjacent collateral vessels become

visible. Spectral analysis identifies decreased systolic and diastolic flow velocity proximal to the occlusion, with no flow (or collaterals) or decreased systolic velocity combined with a high end-diastolic flow velocity distal to the

obstruction. Sensitivity for stenosis and occlusions is 100%, and specificity is 98% (Fig.1.29,

Fig.1.30).

Fig. 1.29 Aortic occlusion.

a The interrupted color flow is caused by the shadowing due to wall calcification.

b Occlusion of the superior mesenteric artery: no arterial flow. AO = aorta; TR = celiac trunk (see 1.3 d–g).

c Acute thrombotic occlusion of the common femoral artery (AFC).

dand e Chronic limb ischemia.

dHigh-grade stenosis of the left iliac artery (AIS).

e Following complete occlusion of the superficial femoral artery (AFS). Stenosis of the profound femoral artery (AFP).

Fig. 1.30 Chronic long segment occlusion of the femoral artery (AF).

a Slowed preocclusive flow, absence of color flow distally, slight increase of echogenicity.

b Collaterals refill the popliteal artery (AP). VP = popliteal vein.

Stenosis within a bypass, at its proximal segment, or at the anastomosis is easily identified sonographically by localized thickening of the

wall with encroachment of the lumen, while color-flow Doppler scanning will demonstrate increased peak systolic velocity. An insufficient

bypass is assumed when flow velocity decreases below 40 cm/s (Fig.1.31).

Fig. 1.31 Stent in the CCA (a and b)23 and in the region of the ECA.

a The stent (arrow) appears as an interrupted echogenic band.

b Carotid stent. Segments are devoid of color flow due to acoustic shadowing.

c Carotid stent for external carotid artery stenosis. Vmax indicates 70% stenosis.