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2.1 · Pelvic andLeg Arteries
93
2
characterized by a fairly homogeneous content of the
occluded lumen and good delineation of the wall without
major plaque. rombotic aneurysms accounted for 27.5% of
the isolated popliteal artery occlusions and an entrapment
syndrome for the remaining 4%.
e dierential diagnosis includes advential cystic disease and entrapment syndrome. Advential cystic disease has
an incidence of 1 per 1200 to 2000 patients presenting with
intermittent claudication (Choschzick etal. 1997) but rarely
causes popliteal artery occlusion. A similar incidence is
reported for entrapment syndrome.
Our analysis of 12,500 duplex ultrasound examinations
of the popliteal fossa (1993–2004) in patients with typical
symptoms of PAOD identied the following rare vascular
conditions:
5 Entrapment syndrome: 12 patients (0.1%), including:
5 Occlusion of the popliteal artery: four patients,
among them three with malformation of the medial
head of the gastrocnemius muscle or popliteal artery
(Insua I) and one with poststenotic aneurysm and
additional compression of the popliteal vein due to
atypical attachment of the popliteal muscle
5 Compression and stenosis of the popliteal artery
during plantar exion: seven patients (Insua I)
5 Compression of the popliteal artery and vein through
hypertrophic heads of the gastrocnemius muscle
without malformation: one patient
5 Adventitial cystic disease: six patients (0.05%)
5 Traumatic intimal dissection: two patients (0.02%)
5 Tumor compression: one patient (0.01%)
5 AV stula of the popliteal artery (traumatic, large ow
volume): one patient (0.01%)
5 Large pseudoaneurysm with compression of artery and
vein (iatrogenic aer arthroscopic meniscal resection):
one patient (0.01%)
2.1.6.4.1 Adventitial Cystic Disease
Adventitial cystic disease is a rare condition in which cystic
structures in the outer wall layer of arteries close to joints
(Leu etal. 1977) and very rarely of veins cause variable stenosis according to their state of lling. A total of 400 cases of
adventitial cystic disease have been reported in the literature.
An understanding of the etiology and pathophysiology of
this rare condition is necessary to ensure adequate treatment
and minimize the risk of recurrence. While various underlying mechanisms have been proposed, there appears to be
agreement that adventitial cysts arise from mesenchymal cell
formations dispersed to the arterial adventitia near joints
during embryonic development. e most likely candidates
are ectopic synovial cells, and the popliteal artery is the most
commonly aected vessel. Adventitial cysts are lled with a
mucinous, viscous uid and resemble articular ganglions in
terms of uid and wall composition (Flanigan et al. 1979;
Vasudevan etal. 2005; Levien and Benn 1998).
Isolated or multiple adventitial cysts can occur and they
may be uniloculated or multiloculated. e
clinical manifes-
tation and ischemic symptoms vary widely
there is a rapid succession of asymptomatic intervals and episodes during which the walking distance is reduced to a few
meters. is pattern is due to the variable vessel compression
resulting from changes in cystic lling (. Fig. 2.29). As a
result, there are periods during which the clinical examination
is normal, and patients may have a long history before the correct diagnosis is made. An early report postulated a communication with the knee joint to explain the variable lling of
adventitial cysts (Flanigan etal. 1979), and some later investigators identied a channel-like communication on imaging
studies (Chiche etal. 1994; Ortmann et al. 2009) or during
surgery (Tsilimparis etal. 2007; Campbell and Milliar 1985).
We may assume, though, that most advential cysts do not
communicate with the joint space. Ultrasonography provides
direct evidence of the cysts and thus conrms the preliminary
diagnosis made on the basis of the clinical presentation and/or
angiographic ndings. Moreover, ultrasound identies the
cysts and their variable size even during asymptomatic periods, and spectral Doppler interrogation enables precise determination of the degree of stenosis. e ultrasound ndings
thus provide the basis for therapeutic decision making.
In the (color) duplex examination, other hypoechoic
lesions in the popliteal fossa must be dierentiated from
adventitial cysts by carefully evaluating their relationship to
the vessel wall:
5 Aneurysm of the popliteal artery (true/false)
5 Hematoma, seroma, abscess
5 Hemangioma
5 Baker’s cyst
5 Dissection with thrombosis of false lumen
5 Tumor
5 Venous aneurysm
e typical hourglass conguration characterizing the
angiographic appearance of arterial stenosis caused by an
adventitial cyst may be absent or just barely visible as a
subtle impression during asymptomatic periods. erefore,
a luminographic technique such as angiography is of limited diagnostic value in patients with suspected adventitial cystic disease, and other modalities including duplex
ultrasound, magnetic resonance imaging (MRI), and CT
angiography have higher diagnostic accuracy when this
condition is suspected. With its high spatial resolution and
exibility, duplex ultrasound is the method of choice and
is even superior to MRI (Brodmann etal. 2001; Schäberle
1996). In CT, problems may sometimes arise in dierentiating adventitial cystic disease from other conditions such as
popliteal artery aneurysm (Brodmann etal. 2002), arterial
dissection with a thrombosed false lumen, or even atypical
Baker’s cysts. A very rare dierential diagnosis is adventitial
cystic disease of the popliteal vein (see . Fig. 3.96 (Atlas);
Dix etal. 2006).
Ultrasound-Guided Treatment
z
Local surgical enucleation
and resection of the aected arterial segment with replacement
of the cysts from the arterial wall
, and occasionally
94
cd
Chapter 2 · Extremity Arteries
2
a
. Fig. 2.29a–d Adventitial cystic disease. a–c Variable cyst size. a This patient with intermittent claudication of variable severity due to
adventitial cystic disease (Z) shows a highly variable cyst size over a period of 2weeks. The transverse view (left) demonstrates compression of the popliteal artery with a residual lumen of 20–30%. Aliasing in the longitudinal image and a peak systolic velocity (PSV) of 3m/s
confirm stenosis due to cystic compression. b, c The cyst has become so small that it is easily overlooked on routine ultrasound if one is
unaware of the earlier findings (b, longitudinal view on the left, transverse view on the right). The diameter of the cyst has decreased from
1cm to 2.7mm, and the arterial lumen is no longer compromised (not seen angiographically). The Doppler waveform is normal. d Patient
with multiple adventitial cysts. The composite B-mode image shows compression of the popliteal artery (P3 segment) by multiple cysts
anterior and posterior to the affected segment. The cysts cause occlusion of a 3-cm segment of the popliteal artery, indicated by absence
of color flow (<<). This sonographic finding is an indication for resection of the compromised arterial segment and insertion of a venous
bypass graft. The anterior tibial artery (KOL) is filled by collaterals and in turn provides collateral flow to the tibiofibular trunk (T.TF) through
retrograde flow proximally
b
by a venous bypass gra have the best outcome with the lowest
recurrence rates. ere is no evidence that one is superior to
the other (Tsilimparis etal. 2007; Hong etal. 2007).
Percutaneous aspiration of the cyst uid guided by ultra-
sound or CT is controversial. On the one hand, aspiration is
low in complications, and several authors report successful
treatment without recurrence (Do et al. 1997; Colombier
etal. 1997; Schäberle 1996, Schäberle etal. 2013) for followup periods of up to 11years (Keo etal. 2007). On the other
hand, the cyst uid may be too viscous for aspiration (Wilbur
and Spigos 1986; Cassar and Engeset 2005) or the cysts recur
aer initially successful aspiration (Ortiz etal. 2006; Sys etal.
1997; Holden etal. 2008; Sieunarine etal. 1991). Recurrence
is not surprising considering that aspiration alone does not
eliminate the postulated communication of adventitial cysts
with the knee joint (Cassar and Engeset 2005). Even if the
communication is obliterated or does not exist, synovial cells
in the cyst wall can secrete uid that rells the cyst.
Pretherapeutic ultrasound and other imaging modalities
can help the physician select the most suitable treatment from
the dierent options available and identify patients in whom
ultrasound-guided aspiration may be justied. Enucleation
without resection of the aected popliteal segment is promising only when high-frequeny ultrasound demonstrates a single
cyst without signs of secondary intimal damage or even small
thrombotic deposits. Otherwise, resection of the aected segment with vein gra interposition is preferable. In the author’s
experience,
ultrasound-guided aspiration is promising only if
the following conditions are met (Schäberle etal. 2013):
5 Presence of one or at most two adventitial cysts without
secondary intimal damage (thickening) of the aected
arterial segment and sonographic exclusion of a communication between the cyst and the knee joint space
(using a high-resolution transducer)
5 Aspiration with a large needle (14G) to maximize the
chance of completely removing the cyst uid
5 Injection of a small amount of sclerosing agent (e.g.,
2–3mL of 96% ethanol) might be considered to lower
the risk of recurrence (aer a communication with the
knee has been ruled out)
2.1 · Pelvic andLeg Arteries
95
2
Ultrasound- or CT-guided aspiration aims at relieving compression-related symptoms, leaving the mucin- producing
cyst wall and a possible communication with the joint in
place. erefore, the available evidence regarding freedom
from recurrence aer aspiration treatment must be interpreted with caution. On the other hand, spontaneous resolution conrmed by imaging has been reported (Pursell
etal. 2004) and may be attributable to cyst rupture (Lossef
etal. 1992). e author also saw a patient with spontaneous
resolution of both reactive eusion and advential cyst uid
aer arthroscopy with repair of a bucket handle meniscal
tear. As a result, the moderate luminal narrowing of the
popliteal artery caused by the cyst resolved as well, leaving
the patient without symptoms for a follow-up period of
5years. Two of three patients in whom the author performed
initially successful ultrasound-guided aspiration (Schäberle
1996) were asymptomatic for a 5-year follow-up period (see
. Fig. 2.92 (Atlas)). e third patient had recurrence with
marked relling of the cysts at 6months and underwent
surgical enucleation.
Cyst aspiration can be performed when desired by the
patient or justied on the basis of clinical considerations
even if the above conditions are not met. Percutaneous cyst
aspiration is uncomplicated and can be performed as an outpatient procedure. Prior aspiration treatment has no eect on
the outcome of subsequent surgical resection (Asciutto etal.
2007; Keo et al. 2007). While the exact recurrence rate is
unknown due to the rarity of advential cysts, a rough estimate is that recurrence-free cure can be achieved in approx.
60% of cases.
In patients presenting with knee problems (simultaneous
Baker’s cyst), diagnostic arthroscopy with therapeutic management of other conditions should be performed prior to
vascular surgery and may also lead to shrinkage of adventitial
cysts. e postulated communication between adventitial
cysts and the knee joint space is not compatible with the high
intracystic pressure (i.e., higher than systolic blood pressure)
that is required to compress the arterial lumen (valve mechanism, inammatory secretion of the cyst wall?).
2.1.6.4.2 Popliteal Artery Entrapment Syndrome
Entrapment of the popliteal artery was rst described in
1879 by a medical student in Edinburgh. Few data are available on the incidence of this syndrome, but it seems to be
more common than assumed in the past. A study performed
in members of the Greek army reported an incidence of
0.17% (Bouhoutsos and Daskalakis 1981), while an autopsy
study found an incidence of 3.5% (Gibson 1977). In the
above-quoted analysis of our group (7 Sect. 2.1.6.4), the incidence was 0.1% in symptomatic patients with clinical stage
II or III disease. e lower incidence of popliteal entrapment
in symptomatic patients appears to be attributable to the fact
that the malformation of the medial head of gastrocnemius,
which causes the entrapment constellation (see . Fig.2.96
(Atlas)), may be present without causing symptoms. Close
examination of the popliteal fossa occasionally reveals an
entrapment constellation as an incidental nding in patients
evaluated for other reasons (e.g., suspected thrombosis, preoperative vein mapping prior to varicosis surgery). ese
individuals are completely asymptomatic, and even extreme
plantar exion does not compress the popliteal artery (no
published data on such cases exist). Consequently, there is no
risk of arterial wall damage or popliteal artery occlusion, and
no treatment is required.
Intermittent claudication, chiey associated with walk-
ing uphill, is the cardinal clinical symptom. Paresthesia and
rest pain or trophic disorders have been observed but are
uncommon. Both our results and published data indicate
that thrombosis or segmental arterial occlusion is already
present at the time of diagnosis in 50–70% of patients.
Bilateral involvement was reported to occur in 30–50% of
cases but was seen in only one patient (9%) of our series.
e popliteal artery courses through the center of the
intercondylar fossa together with the popliteal vein and the
tibial nerve and gives o a variable number of branches along
this course (sural arteries). An atypical course of the popliteal
artery, and possibly of the popliteal vein as well, or abnormal
attachment of the medial head of the gastrocnemius muscle
can lead to compression of the vessels during muscle contraction.
Compression of the popliteal artery during plantar exion temporarily reduces distal blood ow. is in turn can
cause intermittent claudication, oen becoming apparent
only during activities involving extreme plantar exion, such
as walking upstairs. Compression can cause secondary vessel
wall damage with intimal and medial proliferation. Intimal
damage may give rise to the formation of mural thrombi with
subsequent complete occlusion, while compression of the
artery may lead to poststenotic dilatation. e mural thrombi
developing in the aneurysm may cause arterial embolism
with occlusion of peripheral vessels.
Insua et al. (1970) distinguish four types of popliteal
artery entrapment syndrome based on the relationship
between artery and muscle:
5 In types I and Ia, the popliteal artery courses on the
medial side of the medial head of the gastrocnemius
muscle. Type I refers to a malformation of the artery
. Fig.2.30: I), type Ia to the malformation of the medial
(
head of the gastrocnemius (. Fig.2.30: II), which attaches
to the femur more laterally and cranially than under
normal conditions, thereby displacing the artery from its
normal path. Sonographically, these two types are
suggested by the demonstration of muscle tissue between
the artery and vein, which usually course through the
popliteal fossa together (see . Fig.2.94 (Atlas)).
5 In types II und IIa, the artery and vein have a normal
course but are compressed by structures crossing the
popliteal fossa (. Fig.2.30: III and IV) (abnormal
attachment of a lateral extension of the medial gastroc-
nemius head, abnormal course of plantar muscle).
Rarely, a well-developed gastrocnemius can cause intermittent
claudication. During contraction, the hypertrophied heads
compress the popliteal artery and occasionally the vein as well.
96
IV VVI
Popliteal
artery
Popliteal
muscle
Chapter 2 · Extremity Arteries
2
Popliteal
vein
Popliteal
artery
III III
Popliteal
vein
Popliteal
vein
Popliteal
artery
Medial head
of gastrocnemius muscle
Popliteal
vein
Popliteal
artery
Medial head
of gastrocnemius muscle
Popliteal
vein
Popliteal
artery
Popliteal
vein
Popliteal
artery
. Fig. 2.30 Classication of popliteal artery entrapment syndrome (modied from Insua). I The popliteal artery courses medially over the posterior
aspect of the normal attachment of the medial head of the gastrocnemius to return to its normal course in front of the muscle (corresponding to
Insua type I). II The medial head of the gastrocnemius attaches more cranially and laterally, thus forcing the popliteal artery to take an abnormal
course around the head (see . Figs.2.31 and 2.94 (Atlas); corresponding to Insua type Ia); the popliteal vein may be compressed as well. III The
attachment of the medial head of the gastrocnemius has an accessory lateral extension, or the plantar muscle takes an abnormal course. The path of
the popliteal artery is normal, but the artery and vein may be compressed to variable degrees, depending on the strength of the muscle bers (see
. Figs. 3.98a (Atlas)) coursing to the lateral femoral condyle (corresponding to Insua types II and IIa). IV The popliteal artery and vein can be com-
pressed by the popliteal muscle, an abnormal branch of the tibial nerve, or a brous ligament (according to Rich). V In rare cases, the popliteal vein
follows the artery along its abnormal path and is compressed as well. Only one case of an isolated abnormal course of the popliteal vein has been
reported so far. VI Normal course of the popliteal artery and vein through the popliteal fossa with compression of both vessels by a well- developed
gastrocnemius muscle during muscle contraction, giving rise to intermittent claudication or venous congestion (see . Figs.2.95 and 3.98b
(bothAtlas))
Younger persons presenting with typical claudication
should be examined for the presence of popliteal entrapment.
is is done sonographically by carefully following the course
of the popliteal artery, evaluating its relationship to muscular
structures (. Fig.2.30) and performing the plantar exion
test.
e latter is done using real-time ultrasound to observe
the eects of increasing plantar exion: these may include
displacement of the artery from its course in the B-mode and
hemodynamic signs of luminal narrowing due to compres-
sion of the artery in the spectral Doppler tracing (. Table2.13;
. Fig.2.31).
A complete examination always includes the (asymptom-
atic) contralateral popliteal fossa since the condition is bilat-
eral
in up to 80% of cases.
Angiography does not yield any relevant additional information that may aect therapeutic management (. Table2.14),
especially since ultrasound also demonstrates secondary wall
damage and longer-term complications of intermittent vascu-
cde
2.1 · Pelvic andLeg Arteries
97
2
. Table 2.13 Nonatherosclerotic vascular disease: dierent
sites of involvement compared with atherosclerotic disease
(intima)
Feature Site and type of vascular disease
Wall thickening with
luminal narrowing
(adventitia, media)
Focus of ultrasound examination: morphology (hemodynamics)
Vessel compression (by
perivascular structures)
Focus of ultrasound examination: hemodynamics in functional
tests (morphology)
Adventitial cystic disease:
adventitial cysts in arteries near
joints
Preferred site: popliteal artery
Arteritis: wall thickening, media
(concentric)
Medium-sized and large arteries
Popliteal artery entrapment
syndrome
Thoracic outlet syndrome
(subclavian artery, axillary artery,
axillary vein)
lar compression, which are as follows (. Figs.2.31 and 3.98a
(Atlas)):
5 Mural thrombus formation secondary to local vessel wall
lesions
5 Poststenotic aneurysm
5 rombotic occlusion of the damaged or dilated vessel
segment
e diagnosis of popliteal artery entrapment syndrome
relies on a high index of suspicion when assessing a young
patient with isolated popliteal artery occlusion or dilatation
(see . Fig. 3.98a (Atlas)). Other ndings in patients with
arterial stenosis due to vascular compression syndrome or
other nonatherosclerotic conditions may include poststenotic aneurysmal dilatation caused by increased wall pressure downstream of the stenosis (see . Figs.2.105 and 2.106
(Atlas)).
erapeutic management consists in division of the
structure compressing the popliteal artery. At a later stage,
when occlusion has occurred, surgery includes reconstruction of the damaged artery (Steckmeier etal. 1989). In Insua
type I popliteal artery entrapment syndrome, the atypically
attaching medial gastrocnemius head is divided.
a
. Fig. 2.31 a Popliteal artery entrapment syndrome– functional test. 38-year-old athletic man with entrapment syndrome caused by an abnor-
mal gastrocnemius muscle (Insua type I). The transverse images from left to right show progressive compression of the popliteal artery by the gastrocnemius muscle (M.GC) with increasing plantar exion. The muscle attaches between the popliteal artery and popliteal vein (V.POP) and forces
them apart, resulting in subtotal occlusion of the artery (right image). b–e Popliteal entrapment syndrome in an 18-year-old male. The examination shows progressive compression of the popliteal artery (A.P) by the medial head of the gastrocnemius muscle (M.GC) with increasing plantar
exion. b With the calf muscles relaxed, there is no evidence of popliteal artery stenosis. c With the patient beginning to raise the heels o the
oor, compression begins to induce stenosis with a PSV of 3m/s. d With the patient standing on tiptoes (full plantar exion), compression causes
occlusion of the popliteal artery. The patient refused surgery. e Two years later, the ultrasound examination shows intimal thickening (arrow) of
the popliteal artery segment exposed to intermittent compression
b
98
Chapter 2 · Extremity Arteries
. Table 2.14 Role of ultrasound in the diagnostic workup of
nonatherosclerotic vessel disease prior to surgical repair
2
Findings/Diagnosis Diagnostic information provided by
ultrasound/supplementary imaging
tests
Vascular compression syndrome,
adventitial cystic
disease
Duplex ultrasound with assessment of
morphology and hemodynamics during
provocative maneuver: most accurate
diagnostic test, method of choice,
mandatory in patients with clinical
suspicion
Optional: angiography– not necessary in:
- Adventitial cystic disease without
occlusion
- Popliteal artery entrapment syndrome
without occlusion
May be supplemented by MRI, CT
angiography
must be dierentiated from vascular disorders of the larger
proximal vessels as well as from arterial embolism (popliteal
artery aneurysm, aortic aneurysm, thoracic outlet syndrome
with poststenotic subclavian aneurysm). is is especially the
case if color duplex demonstrates occlusion of interdigital
arteries and the clinical picture of trash foot is present.
2.1.6.4.4 Paraneoplastic Disturbance
ofAcral Perfusion
A tumor can compromise blood ow by the following pathomorphologic and pathophysiologic mechanisms:
5 Local displacement and compression (tumors of so
tissue, nerves, vessels, and bones as well as metastases)
or tumor inltration of the vessel wall, which may give
rise to arterioarterial embolism
5 Paraneoplastic vasculitis
5 Paraneoplastic hyperviscosity of the blood and hyperco-
agulable state
Inammatory
vascular disease
Duplex ultrasound to conrm the diagnosis and prevent unnecessary and contraindicated vessel repair (supplementary
CT angiography; sonographic follow-up
of immunosuppressive treatment)
Duplex ultrasound can identify the site of external compression or inltration of the arterial wall by the tumor and provides information on the hemodynamic signicance of the
narrowing, which is important for therapeutic decision making. Arteries, with their strong muscle coat and intramural
2.1.6.4.3 Raynaud’s Disease
Raynaud’s disease is characterized by intermittent attacks of
pressure, are much less susceptible to local tumor compres-
sion than veins.
ischemia of the ngers and toes, typically brought on by cold
and enhanced by emotional stress, local compression, and
conditions that are associated with an increased sympathetic
tone. e vasospasm is relieved by heat or drug treatment.
Primary or idiopathic Raynaud’s disease (no underlying disease; no occlusion of nger arteries) is distinguished from a
secondary form (e.g., in patients with scleroderma or simultaneous nger artery occlusion). Ischemic attacks oen occur
bilaterally, aecting the second to h ngers while in most
cases sparing the thumb. e toes are involved in only about
2% of cases. Women are aected two to ve times more commonly than men, primarily between the ages of 20 and 50.
e diagnosis of Raynaud’s disease chiey relies on the
typical clinical presentation, while further diagnostic tests are
only required to identify vasospasm as the underlying cause of
the clinical symptoms. Here again, duplex ultrasound has
turned out to provide useful information. e examination is
performed with exposure to cold to provoke the vasospasm
and exposure to heat to relieve the spasm. When exposed to
cold, the systolic nger artery pressure in Raynaud’s disease
drops markedly by 20–50% compared with only up to 10% in
healthy persons. Duplex scanning typically demonstrates
residual perfusion in the common digital arteries, while there
is no or reduced ow in the distal nger arteries during spasm.
e vasospasm produces a markedly pulsatile ow pattern
with a short systolic peak and absence of diastolic ow in the
hand arteries and the common digital arteries. Heat exposure
induces vasodilatation with hyperemia, which results in pronounced diastolic ow in the proximal nger arteries and distinguishes Raynaud’s disease from occlusion of the distal nger
arteries. Other helpful diagnostic tests are oscillography and
pressure measurement in the nger arteries. Raynaud’s disease
2.1.6.4.5 Buerger’s Disease
Buerger’s disease, or thromboangiitis obliterans, is a chronic
nonatherosclerotic endarteritis characterized by inammation with thrombosis. It has an intermittent course and leads
to segmental and multiple occlusions of small and mediumsized arteries of the extremities. As a panangiitis, it can be
dierentiated from atherosclerosis and other inammatory
vascular diseases. ough the etiology of Buerger’s disease is
unknown, there is an association between the onset and progression of the disease and cigarette smoking– 93–99% of
the patients smoke. Remission is seen in most patients who
quit for good. e severity and frequency of disease episodes
correlate with the patient’s smoking habits.
e clinical symptoms depend on the extent and site of
occlusions. Pain at rest and acral necrosis occur at an early
stage, while typical intermittent claudication of the calf muscles
is less common. e duplex examination can rule out other
disorders such as arterial embolism, aneurysms of the aorta
and popliteal artery, popliteal artery entrapment syndrome,
atherosclerosis, and macroangiopathy. B-mode imaging with a
high-resolution transducer will show normal walls of the large
arteries without hyperechoic atherosclerotic plaques or thickening. Occlusions primarily involve the arteries below the knee
including the pedal arteries, and disseminated occlusion of the
interdigital arteries may also be seen. e occluded lumen has
low echogenicity. Venous involvement is seen as segmental
phlebitis. Demonstration of
channels
is diagnostic of thromboangiitis obliterans. e char-
corkscrew-like revascularization
acteristic variation in color is due to tortuosity and merely
reects changing ow direction relative to the transducer rather
than true ow reversal (. Fig.2.32). is ow pattern is also
2.1 · Pelvic andLeg Arteries
a
99
2
b c
. Fig. 2.32 a Occlusion of the posterior tibial artery in thromboangiitis obliterans (hypoechoic artery without plaque). The patent vein (V) with
ow coded red is seen deep to the occluded artery. A tortuous, recanalized collateral (with sample volume) is depicted close to the transducer with
red and blue indicating ow toward and away from the transducer; this is also reected in the waveform obtained from a short segment of the artery.
This ow pattern is typical of a corkscrew collateral and characterizes recanalization in thromboangiitis obliterans. b Gray-scale image illustrating poor
demarcation of a revascularized artery in thromboangiitis obliterans from surrounding connective tissue and muscle (rather high echogenicity due to
septum-like internal structures). Both the color ow image and the spectral Doppler waveform reect the blood ow pattern in the tortuous transmural revascularization channel. c Angiographic appearance of corkscrew collaterals
reected in the Doppler waveform. Otherwise, there are no
specic sonomorphologic ndings in Buerger’s disease.
active stage of vascular inammation, most patients have a
markedly elevated erythrocyte sedimentation rate (typically
above 100 during the rst hour) with only a slight increase in
2.1.6.4.6 Vascular Inammatory Disease
Inammatory vascular disease may be localized or generalized. Primary vasculitis arises in the vessel wall, while sec-
ondary vasculitis
occurs on the background of other
systemic diseases (rheumatoid arthritis, collagen disease).
e following primary inammatory vascular diseases are
distinguished according to the vessels aected:
5 Inammation of large vessels (giant cell arteritis,
Takayasu’s arteritis)
5 Inammation of medium-sized vessels (polyarteritis
nodosa, Kawasaki’s disease)
5 Inammation of small vessels (Wegener’s granulomato-
sis, microscopic polyangiitis, Schoenlein–Henoch
purpura, Churg–Strauss syndrome)
C-reactive protein. Additional ndings are anemia, mild to
moderate leukocytosis, and marked thrombocytosis.
Supplementary tests include protein electrophoresis, complement determination, and antibody serology.
Duplex ultrasound allows localization and quantication
of vascular constriction, but its foremost role is to noninvasively demonstrate
the vessel wall
the typical inammatory thickening of
. is is done using a high-resolution trans-
ducer (7–10MHz), which will depict the characteristic “mac-
aroni sign
” (. Fig. 2.33) consisting of a higher-level echo
from the lumen/intima interface surrounded by a concentric,
homogeneous tube-like structure of lower echogenicity
(intima-media complex) (see . Fig. 2.100 (Atlas)) (Maeda
etal. 1991). If the scanner resolution is not high enough, the
macaroni sign may be visualized only in large and medium-
e clinical diagnosis is suggested by the symptoms and
changes in the organ or body region supplied by the inamed
arteries. ese can range from pathognomonic local skin
lesions with palpable purpura to organ loss (kidney) or acral
ischemia when peripheral arteries are involved. During the
sized vessels. With disease progression, wall thickening will
lead to the development of concentric and rather long stenoses with subsequent obliteration (. Fig.2.49).
Polyarteritis nodosa is segmental inammation of
medium-sized arteries and is characterized by circumferential
100
Chapter 2 · Extremity Arteries
In color ow imaging, dissection may present with dierent
ow directions or dierent ow velocities in the true and
false lumen, indicated by dierent colors and dierent levels
2
of brightness, respectively (
. Fig.2.34). e diagnosis of dis-
section is conrmed when dierent waveforms (with dierent PSVs) are obtained from the same artery (i.e., the true
and false lumen). In addition, waveforms from a dissected
artery may reect superimposed artifacts resulting from
oscillation of the dissection membrane. A thrombosed false
lumen has low echogenicity and causes eccentric luminal
narrowing of a long arterial segment (see . Fig. 5.74 (Atlas)).
e severity of ow obstruction can be estimated by spectral
. Fig. 2.33 In polyarteritis nodosa, inammatory thickening of the
wall causes circumferential luminal narrowing, which may at times
alternate with dilated segments. The diagrams illustrate circumferential
arterial wall thickening in longitudinal and transverse orientation
(courtesy of K.Amendt)
Doppler interrogation distal to the dissection (. Fig. 5.45).
2.1.6.4.8 Arteriovenous Fistulas
An arteriovenous (AV) stula is a congenital or acquired
abnormal direct communication between an artery and a
wall thickening with luminal narrowing or constricted arterial
segments alternating with dilated segments (. Fig.2.33).
e sonomorphologic dierentiation of intimal thickening and sclerotic changes (calcication) from circumferential
thickening of long vessel segments (macaroni sign) in inammatory disease has important clinical implications. It is
highly accurate in supercial vessels (carotid, subclavian,
axillary, and femoral arteries), which can be examined with a
high-frequency transducer.
Computed tomography (CT) and magnetic resonance
imaging (MRI) are the reference methods for the diagnostic
evaluation of the vessel wall. Angiographic mapping can
identify the segments aected by inammatory constriction
but does not demonstrate wall thickening (see . Table2.14).
Duplex ultrasound thus makes an important contribution to
the correct diagnosis and treatment of steno-occlusive disease caused by vasculitis, thereby providing a sound basis for
initiating proper treatment and sparing patients unnecessary
interventions or surgery.
Hypersensitivity vasculitis (antigen-induced immune
complex vasculitis) is typically caused by drugs or occurs in
association with an infection. It is an arteritis of small arteries
and therefore not amenable to sonographic evaluation because
medium-sized and large arteries are not involved. In the legs,
the clinical manifestations include painful ulcerations, oen
located on the lateral calf, urticaria, and hemorrhagic necrosis.
vein. Congenital micro- and macrostulas occur in association with vascular malformations (hemangiomas). Acquired
AV stulas can develop aer penetrating vascular injuries
that damage an artery and a vein lying side by side or as iatrogenic complications of interventional procedures or
surgery. Spontaneous AV stulas can develop in the presence
of a tumor or aneurysm (large aneurysm penetrating an adjacent vein). ese abnormal short circuits between the arterial
and venous system are distinguished from AV stulas created
surgically for hemodialysis or other therapeutic purposes
(
7 Chap. 4).
Over time, increasing blood ow through an AV stula
can lead to dilatation of the feeding artery and draining vein
with arterial complications such as aneurysm formation and
venous stasis as late sequelae. Venous stasis leads to edema
with tissue damage and crural ulcers. Additionally, large ow
volumes across an AV stula can cause an increased heart
rate and cardiac output to maintain arterial pressure, and
some patients develop cardiac failure.
Duplex ultrasound identies an AV stula by increased
blood ow
in the feeding artery (low-resistance ow) and
draining vein. e increase varies with the stula volume and
is most pronounced during diastole. Spectral Doppler imaging will demonstrate arterialized, more pulsatile ow in the
draining vein. Ultrasound allows very accurate determination of volume ow through the stula (calculated from the
cross-sectional area of the feeding artery and time-averaged
2.1.6.4.7 Dissection
Causes of dissection of the peripheral arteries are:
5 Spontaneous dissection (very rare)
5 Distal extension of an aortic dissection into the pelvic
arteries
5 Trauma (typically in the popliteal fossa, oen involving
posterior impact with compression of the artery against
bone)
5 Iatrogenic injury occurring during catheter-based
interventions
blood ow velocity in comparison to the contralateral artery
of the same name). e exact site of an AV stula can be
identied by the presence of perivascular tissue vibration,
seen as a mosaic of colors in color duplex imaging, and by the
transition from low-resistance to high-resistance ow in the
spectral Doppler waveform from the feeding artery (for
details see
2.1.6.4.9 Chronic Recurrent Compartment
7 Sects. 4.1, 4.2, and 4.4 and . Figs.4.7 and 4.8).
Syndrome oftheCalf
Chronic recurrent compartment syndrome of the calf most
Gray-scale ultrasound will demonstrate a thin membrane
uttering in the lumen at dierent phases of the cardiac cycle.
commonly involves the anterior compartment. It is an overuse condition causing a rise in intracompartmental pressure
ab
2.1 · Pelvic andLeg Arteries
101
2
c
e
. Fig. 2.34 a, b Dissection of the external iliac artery after catheter intervention. The lumen of the artery is narrowed by the dissection mem-
brane, and dierent waveforms are obtained by selectively placing the sample volume in the true and false lumen. c–e The dissection ap (D)
extends into the proximal supercial femoral artery. Dierent waveforms are obtained from the false lumen (c) and the true lumen (d). The artery
is occluded distal to the origin of collaterals (K) at the mid-thigh level (e)
with subsequent microvascular compromise. Patients present
with swelling, tension, and severe pain. Foot pulses are palpable. Muscle damage can lead to an increase in creatine
kinase, and intracompartmental pressure, which even during
activity is normally below 20 mmHg, can increase two- to
fourfold. When duplex imaging is performed aer activity to
reproduce increased compartmental pressure, the calf veins
d
of patients with chronic compartment syndrome will appear
compressed or may be collapsed (at pressures >30mmHg). At
pressures >50mmHg, arterial ow becomes more pulsatile.
With a further increase in pressure, the orthograde diastolic
ow component disappears, and nally a line-like artifact will
appear in the waveform in late diastole. B-mode imaging will
show intrafascial edema in the anterior compartment.
102
Chapter 2 · Extremity Arteries
2.1.7 Follow-Up After Surgical
andInterventional Treatment
2
With its proven validity compared with the gold standard
and intraoperative ndings, duplex ultrasound is an excellent
imaging modality for treatment planning in patients with
steno-occlusive disease of the pelvic, femoral, and popliteal
arteries including the trifurcation and also for surveillance
aer surgery or endovascular interventions. e duplex
ultrasound information on the sites and severity of stenosis
or occlusion, in conjunction with the clinical manifestation,
helps the physician decide whether conservative management with walking exercises, a radiologic intervention, or
surgical repair (TEA or bypass graing) is the most suitable
treatment for the patient.
e surgical procedure and revisions in case of complications can be planned in the infrainguinal arteries with the same
accuracy as with angiography (Wain et al. 1999; Ligush et al.
1998). In patients with adequate sonographic visualization, no
pretherapeutic angiography is necessary for planning recon-
. Fig. 2.35 Restenosis of the common femoral artery after TEA.The
gray-scale image demonstrates an intimal ap (arrow) as the underlying cause of stenosis. Spectral Doppler interrogation of this segment
with measurement of peak systolic velocity (PSV) gives a PSV ratio of
3.8 (calculated from intrastenotic PSV of 407cm/s and prestenotic PSV
of 105cm/s), corresponding to 60–70% stenosis
structive procedures in this territory including the P1 segment.
Evaluation of the recipient artery is important both in the preoperative workup and in the examination of patients with restenosis or reocclusion aer surgery. As this can be done very
accurately by duplex ultrasound including evaluation of the
trifurcation and segmental evaluation of the arteries below the
knee, the indication for a P1 femoral artery bypass can be established without preoperative angiography on condition that an
inow obstruction (at the pelvic level) has been ruled out.
2.1.7.2 Percutaneous Transluminal
Angioplasty andStenting
Percutaneous transluminal angioplasty (PTA) is performed
to improve peripheral perfusion by restoring adequate blood
ow through a narrowed arterial segment. In patients with
occlusion, the therapeutic procedure (PTA or bypass surgery) can be planned beforehand once the length of the
occluded segment has been determined. In PTA, atherosclerotic plaques are fragmented and pressed into the arterial
2.1.7.1 Thromboendarterectomy
An important indication for thromboendarterectomy (TEA)
is stenosis of the femoral artery bifurcation, which is easily
accessible to ultrasound examination. e duplex ndings
alone can serve to identify candidates for TEA and plan the
procedure.
Duplex imaging enables very detailed planning of TEA or
profundaplasty for obstructive lesions at the origin of the
profunda femoris artery as well as of repeat interventions in
patients with complications or recurrent stenosis. Moreover,
hemodynamic evaluation by duplex ultrasound provides
more valid diagnostic information in this region, where angiography is limited by superimposition of vessels and in the
evaluation of stenosis caused by posterior wall plaque.
Ultrasound is also a suitable tool for assessing outcome
aer surgery, identifying postoperative complications, and
detecting recurrent stenosis. For example, in a patient who
has undergone surgery for stenosis of the profunda femoris
artery to improve its collateral function in supercial femoral
artery occlusion, the success of surgery can be conrmed by
the sonographic identication of improved ow with higher
peak systolic and diastolic velocities in the relled popliteal
artery (. Fig. 2.59 (Atlas)). Postoperative complications
detectable by high-resolution ultrasound include intimal
aps and constriction at the suture line. Recurrent stenosis
aer surgical repair can be identied by B-mode imaging and
graded by spectral Doppler (. Fig.2.35).
wall (. Fig.2.65 (Atlas)), oen resulting in intimal or medial
tears. e irregular surface is susceptible to the deposition of
thrombotic material. A complication of PTA is recurrent stenosis due to fragmented plaques extending into the lumen,
dissection, elastic recoil (see . Figs. 5.36 and 5.38), intimal
hyperplasia, or progression of atherosclerosis. PTA is also
used to dilate residual stenosis persisting aer intra-arterial
administration of plasmin activators for thrombolytic therapy. Other interventional procedures, apart from standard
PTA, include arterectomy, rotational angioplasty, and laser
angioplasty.
Duplex scanning is the rst-line diagnostic modality to fol-
low up the outcome of vascular repair
in patients aer PTA
(with and without stent implantation) or bypass surgery for
the early identication of those who require reintervention. A
study revealed restenosis in 85% of patients with a postinterventional PSV ratio greater than 2 (Mewissen etal. 1992).
e role of postinterventional duplex ultrasound is to
detect complications (dissection, aneurysm, perforation) and
to identify residual or recurrent stenosis caused by thrombotic deposits or fragmented plaques protruding into the
lumen. e morphologic appearance of the wall in the treated
segment and hemodynamic information are important for
identifying restenosis. Subintimal hemorrhage due to intimal
or medial tears may be seen as hypoechoic wall thickening in
the treated segment while thrombotic deposits appear as
hypoechoic intraluminal areas without color ow.