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2.3 · Atlas: Extremity Arteries
a
153
b
2
c
. Fig. 2.91a–e (Atlas) Adventitial cystic disease.
a The popliteal artery (red) is surrounded by hypoechoic cystic lesions, which produce slight indentation of the patent lumen but no hemodynamically signicant narrowing. The Doppler waveform shows triphasic ow. The patient reports intermittent claudication with a highly variable
walking distance.
b Seven days after the rst examination, the patient presents with severe claudication and a maximum walking distance of 30m. Ultrasound
shows a markedly increased cyst volume with high-grade stenosis of the popliteal artery (middle section: longitudinal view; right section: transverse view). Color duplex ultrasound depicts a small residual lumen between the cysts with accelerated ow and aliasing. The corresponding
Doppler waveform is presented in the inverted mode with arterial ow displayed below the baseline. The waveform indicates stenosis with monophasic ow and a ow velocity of >3m/s.
c Angiography performed 2weeks later: Fairly inconspicuous popliteal artery with only slight anterior indentation, identied on a lateral view.
The duplex ultrasound examination performed at this time (not shown) demonstrates a markedly increased cyst size without hemodynamically
signicant stenosis, similar to the situation depicted in a.
d Intraoperative view of cystic adventitial degeneration (arrow). Blue slings are placed around the popliteal artery proximal and distal to the diseased arterial segment.
e The therapy of choice is surgical resection of the cyst-bearing arterial segment or enucleation of the cysts if the intima is still intact. In the
patient presented here, gross inspection of the surgical specimen shows the adventitial cysts to be lled with gelatinous material
154
ab
Chapter 2 · Extremity Arteries
2
. Fig. 2.92a, b (Atlas) Adventitial cystic disease– treatment by ultrasound-guided aspiration.
a 40-year-old patient with intermittent foot pain resembling that of polyneuropathy. Arterial duplex imaging of the popliteal fossa reveals large
cysts causing only mild luminal narrowing of the popliteal artery without signicant hemodynamic eects. The patient reported no episodes of
typical intermittent claudication but variable neurologic signs and symptoms. The neurologic examination revealed slightly reduced peripheral
nerve conduction velocity. In patients with adventitial cystic disease, the symptoms vary with the number, size, and location of cysts within the
narrow connes of the popliteal fossa. An occasional patient may present with (intermittent) pain due to nerve compression by a large cyst, while
the popliteal artery is not compromised. The patient shown has a large cyst (Z), but neither the color duplex images (transverse view on the left,
longitudinal view on the right) nor the spectral Doppler interrogation (not shown) suggest signicant narrowing of the arterial lumen.
b Because the patient refused an operation, the cyst was drained and sclerosed under ultrasound guidance (transverse and longitudinal views on
the left); histologic examination of the gelatinous cyst uid conrmed adventitial cystic disease. Following ultrasound-guided drainage using a
1.8-mm needle, the cyst was sclerosed with 1mL of 95% ethyl alcohol to prevent recurrence (needle tip identied by bright echo). The patient’s
symptoms disappeared after treatment. Right image: Follow-up after 1month reveals no recurrent or residual cyst; popliteal vein with blue-coded
ow lateral to the artery
. Fig. 2.93 (Atlas) Adventitial cystic disease– dierentiation from
dissection.
Patients with adventitial cystic disease can have single or multiple cysts
with involvement of a long segment of the popliteal artery. When a
long segment is involved, as in the case shown here, the condition may
be dicult to dierentiate from dissection with complete thrombosis
of the false lumen (see . Figs.2.97a and 5.74 (both Atlas)). The popliteal artery (A.POP) is shown in transverse orientation on the left and in
longitudinal orientation on the right with the cyst (Z) narrowing a long
segment of the artery. There is aliasing as a result of cystic luminal narrowing. The popliteal vein (V.POP) is depicted closer to the transducer
with ow coded in blue. The diagnosis of adventitial cystic disease was
conrmed intraoperatively
2.3 · Atlas: Extremity Arteries
155
2
a
c
. Fig. 2.94a–d (Atlas) Entrapment syndrome.
a Isolated popliteal artery occlusion due to malformation of the medial head of the gastrocnemius muscle forcing the artery to course around
the head on the medial side. In this type of malformation, the medial head of the muscle is located between the popliteal artery and vein– which
thus do not pass through the popliteal fossa together– and compresses the artery against the femur with each plantar exion. Intermittent
compression damages the vessel wall with deposition of thrombotic material, which may ultimately progress to occlusion. In the case presented,
no color duplex signal is obtained from the popliteal artery (A.POP). Posterolateral to the head of the gastrocnemius, the patent popliteal vein
(V.POP) is depicted closer to the transducer with a blue ow signal. Posterior to it, the artery (red) supplying the soleus muscle and serving as a
collateral and the vein are shown. The arteries recruited as collaterals are markedly dilated due to the chronic occlusion process and may thus
be confused with the popliteal artery. The sonoanatomic situation (transverse section on the left and longitudinal section on the right) is as follows: the popliteal artery courses anterior to the popliteal vein and is depicted farther away with the transducer placed posteriorly. The musclesupplying arteries recruited as collaterals arise from the posterior aspect of the popliteal artery and course posterior to the popliteal vein and are
thus closer to the transducer than the vein.
b In this case with good collateralization of a chronic occlusive process, the ow prole in the relled tibiobular trunk does not show the typical
postocclusive monophasic ow but is triphasic, though damped. Peak systolic velocity (PSV) is just under 20cm/s. Additional collaterals enter
distally. There is no postocclusive peripheral dilatation at rest.
c Angiogram: Short occlusion of the left popliteal artery with relling at the level of the knee joint cleft (lateral collateral).
d The intraoperative site conrms the ultrasound ndings. The popliteal artery and vein do not pass through the popliteal fossa together because
the medial gastrocnemius head (transparent sling) attaches between the artery (red sling placed around distal segment) and the vein (at lower
margin). The proximal popliteal artery (on the right) gives o the collateral already identied sonographically and coursing parallel to the vein
b
d
156
Chapter 2 · Extremity Arteries
2
abc
. Fig. 2.95a–c (Atlas) Entrapment syndrome.
a Calf swelling with occasional pain in a young patient caused by external compression of the vessels in the popliteal fossa due to a hypertrophied
head of the gastrocnemius with normal attachment. The popliteal artery and vein pass through the popliteal fossa together and the vein is already
compressed by the relaxed muscle (see . Fig. 3.98b, c (Atlas)). The popliteal artery is not stenosed, and a normal, triphasic waveform is obtained.
b Progressive compression of the popliteal artery occurs with increasing plantar exion, producing a stenosis signal in the Doppler waveform with
loss of triphasic ow and a peak systolic velocity (PSV) of 300cm/s.
c Further plantar exion leads to complete occlusion of the popliteal artery through muscular compression (see . Fig. 3.98 (Atlas) for popliteal
entrapment syndrome with arterial and venous compression). This form of entrapment syndrome (type VI; see classication in . Fig.2.30) occurs
without malformation and is solely due to a well-developed gastrocnemius muscle (which may result from anabolic intake)
ab
. Fig. 2.96a, b (Atlas) Entrapment constellation.
a The image shows the characteristic abnormality of popliteal fossa anatomy predisposing an individual to popliteal entrapment: muscle structures (X) lying between the popliteal artery (A.P) and vein (V.P). This anatomic constellation may be present even if no compression of vascular
structures can be elicited by plantar exion of the ankle. In the literature, only little attention has been paid to this anatomic deviation in asymptomatic individuals, but it explains why popliteal entrapment is much more commonly encountered at autopsy than in the clinical setting. An
examiner may see this anatomic constellation during a careful sonographic evaluation of the popliteal fossa in patients examined for other reasons (e.g., suspected venous thrombosis, chronic venous insuciency). The identication of musculotendinous structures (attachment of medial
head of gastrocnemius) between the artery and vein in the popliteal fossa is pathognomonic of this constellation.
b In this case, neither color duplex imaging nor Doppler interrogation shows popliteal artery (A.POP) narrowing during provocative maneuvers
(maximum plantar exion of the ankle). There is normal triphasic ow and peak systolic velocity (PSV) is not increased. The longitudinal view
obtained during plantar exion shows the head of gastrocnemicus (M.GC) between the popliteal artery (A.POP) anteriorly (closer to transducer)
and the popliteal vein (V.POP) posteriorly
ab
2.3 · Atlas: Extremity Arteries
157
a b
. Fig. 2.97a, b (Atlas) Dissection.
a Dissection of the popliteal artery with complete thrombosis of the false lumen (TH) following blunt trauma to the popliteal fossa. Longitudinal
view (left) and transverse view (right) show the patent residual lumen of the artery (A.P), which is narrowed by the thrombosed false lumen.
b Peak systolic velocity (PSV) in the compromised popliteal artery segment is increased to 220cm/s. Calipers indicate the popliteal artery lumen
and the thrombosed false lumen in the color ow image. When high-grade luminal narrowing aects a long arterial segment, friction loss is
greater and the PSV increase is less marked than in a focal stenosis. The same phenomenon occurs when there is marginal ow in thromboembolic obstruction (see . Fig.2.85 (Atlas))
2
. Fig. 2.98a, b (Atlas) Progressive ischemia due to venous outow obstruction (extensive venous thrombosis).
a 75-year-old woman with a history of PAOD and occlusion of the supercial femoral artery with very good collateral circulation. The Doppler
waveform shows triphasic ow with a peak systolic velocity (PSV) of 68cm/s in the popliteal artery. The most salient feature of postocclusive ow
seen in this case is a delayed systolic upstroke with an acceleration time of 136ms.
b The patient developed secondary peripheral thrombosis ascending to the common femoral vein (level of the inguinal ligament) and presenting
with swelling and acute ischemic pain in the forefoot and classic signs of ischemia as well as early ischemic toe necrosis. Duplex imaging reveals
no macroangiopathic changes in perfusion compared with her status prior to the onset of thrombosis. Below the knee, the posterior tibial and
dorsalis pedis arteries are patent to just below the ankle joint. The Doppler waveform from the posterior tibial artery (same as in the dorsalis pedis
artery) is presented, conrming a largely normal PSV (44cm/s). The longer acceleration time of 145ms is consistent with postocclusive ow. However, in a patient with foot ischemia, the Doppler waveform should also reect the ow eects of peripheral dilatation; the pulsatile ow prole
seen in this case is due to venous outow obstruction caused by extensive venous thrombosis. For illustration, the two thrombosed veins (V) are
depicted above and below the arteries (venous wall indicated by arrow); also seen is the posterior tibial artery (A.TIB.P). The veins are dilated and
no ow signals are obtained despite a low PRF.The dorsalis pedis vein was also thrombosed (not shown).
The ultrasound and Doppler ndings show that disease progression with toe necrosis in this patient is attributable to venous obstruction with
concomitant extensive thrombosis including the arterioles. This condition cannot be remedied by a femoropopliteal bypass graft. Nevertheless, a
bypass procedure was performed in the acute situation, but no improvement ensued. In summary, in this case of stage IIa PAOD, extensive thrombosis led to the clinical and sonographic picture known as phlegmasia coerulea dolens
158
ab
Chapter 2 · Extremity Arteries
2
. Fig. 2.99a, b (Atlas) Cardiac causes of abnormal spectral Doppler ndings.
a Patient with low peak systolic velocities (PSV) at multiple Doppler sampling sites in the leg. As no stenosis is identied, one should consider cardiac insuciency with reduced cardiac output as a possible underlying cause. If this is the case, PSV will be reduced in all arterial segments. In the
example, a PSV of 25cm/s is measured in the proximal supercial femoral artery and there is plaque, while no stenosis or occlusion is detectable
down to the ankle joint.
b In a patient with a higher-grade aortic stenosis, a Doppler tracing from a peripheral artery will show the same poststenotic pattern as distal to
a stenosis of a peripheral artery: delayed systolic upstroke, reduced PSV (32cm/s in the case shown), and monophasic ow. In this case, a foot
phlegmon further contributes to the changes in the spectral waveform from the popliteal artery
. Fig. 2.100a–c (Atlas) Vasculitis.
a Vasculitis of the femoral artery
(longitudinal view on the right,
transverse view on the left) with
concentric hypoechoic inammatory thickening of the media
in a patient with concomitant
atherosclerosis. The atherosclerotic
plaques on the luminal side are
seen as hyperechoic deposits on
the thickened wall.
b Calf artery (posterior tibial
artery) in polyarteritis nodosa
with circumferential wall thickening (conventional longitudinal
view and power mode images
in longitudinal and transverse
orientation).
c Angiogram of the same artery
as in b (Figs. b and c courtesy of
K.Amendt)
a
b
c
2.3 · Atlas: Extremity Arteries
. Fig. 2.101 (Atlas) Inammatory vascular disease.
Vascular inammation– Takayasu’s arteritis of the subclavian and common carotid arteries or polyarteritis nodosa of the extremity arteries–
leads to concentric wall thickening with a centrally perfused lumen. It
is identied on ultrasound by the macaroni sign. There is a normal echo
reected from the wall interface while the remainder of the arterial
wall is depicted as a concentric, hypoechoic structure (wall thickening)
over a long segment without signs of atherosclerotic plaques. Progressive inammatory wall thickening may ultimately lead to occlusion of
the aected vessel. Aneurysmal changes may also occur. The longitudinal view on the left and the transverse view on the right show the
concentric wall thickening of an artery below the knee in a patient with
polyarteritis nodosa. (Due to reux caused by postthrombotic venous
changes, the veins depicted to the left and right of the artery are likewise displayed in red)
159
2
abc
. Fig. 2.102a–c (Atlas) Subclavian artery stenosis due to atherosclerosis.
a Scanning of the left subclavian artery from the supraclavicular position demonstrates direct signs of stenosis: increased peak systolic velocity
(PSV), aliasing, and perivascular vibration artifacts. Atherosclerotic stenosis of the arm arteries typically occurs at the origin of the subclavian
artery and cannot always be identied directly. Instead, the diagnosis has to rely on indirect criteria such as monophasic postocclusive ow.
b Angiogram showing stenosis of the left subclavian artery.
c The additional aneurysm (AN) of the right subclavian artery (longitudinal view on the left, transverse view on the right) is not depicted angio-
graphically (see b) due to thrombosis
160
ab
cd
Chapter 2 · Extremity Arteries
2
. Fig. 2.103a, b (Atlas) Axillary artery stenosis due to atherosclerosis.
a High-grade axillary artery stenosis due to a hypoechoic plaque, revealed by ultrasound with the transducer placed in the infraclavicular fossa.
This is a rare case of atherosclerotic plaque distal to the subclavian artery causing peripheral embolism with occlusion of interdigital arteries
( ischemia of the 4th and 5th ngers).
b Angiogram showing axillary artery stenosis before PTA.
Distal axillary artery stenosis in arteritis.
c A 69-year-old patient with an 11-year history of immunosuppressive treatment for histologically proven Horton’s arteritis developed ischemic
symptoms of the hand during long-term cortisone treatment at a dose of 10mg. Color duplex ultrasound shows only mild concentric wall thickening of the proximal axillary artery but a fairly localized high-grade stenosis with a PSV of 4m/s (not typical of an acute episode of vasculitis).
d Examination of a temporal artery branch (prior temporal artery biopsy on the same side 10years earlier) shows concentric wall thickening
characteristic of vasculitis. Application of pressure with the transducer (right image) reveals incomplete compressibility of the thickened wall
(1.6mm) and is highly diagnostic of vasculitis
2.3 · Atlas: Extremity Arteries
a b
161
2
c
e
. Fig. 2.104a–e (Atlas) Cervical rib syndrome.
a A cervical rib (HR) forces the subclavian artery (supraclavicular transducer position) to take an abnormal, arched course (“the artery is riding the rib”).
The patient presented here has moderate stenosis with a peak systolic velocity (PSV) of 2.5m/s. Due to its abnormal course, the artery is not depicted
completely in a single scan plane. Mirror artifacts (with superimposed vibration artifacts) are seen posterior to the proximal subclavian artery.
b Diagram of the mechanism causing the cervical rib syndrome: Displacement and compression of the subclavian artery by the cervical rib (from
Heberer and van Dongen 1993).
c–e Subclavian artery compression by cervical rib.
c Strand-like extensions from a cervical rib compress the subclavian artery, resulting in stenosis with a PSV of >3m/s (sample volume in the com-
pressed arterial segment).
d Flow velocity is reduced in the subclavian artery upstream of the compressed segment.
e Hyperabduction results in more severe compression of the subclavian artery (arrow) by the strand-like extension of the cervical rib with a PSV of
>6m/s indicating subtotal occlusion
d
162
Chapter 2 · Extremity Arteries
2
a
b
. Fig. 2.105a–d (Atlas) Aneurysm of subclavian/axillary artery.
a 62-year-old patient presenting with acute onset of a sensation of cold and pallor of the right hand and increasing pain unrelated to exercise. The
radial and ulnar arteries are not palpable. Duplex imaging identies an occluded brachial artery (A) as the cause of the patient’s complaints with
the absence of plaques and the hypoechoic homogeneous lumen suggesting an embolic mechanism. The veins (V) are coded red.
b The brachial occlusion in this case is caused by emboli from a 14-mm aneurysm of the subclavian artery at the junction with the axillary artery.
Due to mural thrombosis, the patent lumen is only slightly dilatated compared to the proximal, normal vessel segment (hypoechoic rim around
the blue, patent lumen of the artery on the transverse scan, right section). The longitudinal view on the left shows the proximal end of the aneurysm with retrograde ow components (eddy currents).
c Angiogram: Due to mural thrombosis, only mild dilatation of the subclavian artery at the junction with the axillary artery is seen angiographically. The aneurysm in this patient is caused by mechanical irritation due to an exostosis of an old clavicular fracture.
d Intravascular pressure on the arterial wall increases downstream of a stenosis. In an artery without pre-existing atherosclerotic damage (e.g.,
patients with vascular compression syndrome), this increase in pressure can lead to dilatation of the poststenotic segment (see . Fig.2.106
(Atlas))
c
d