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284
Chapter 4 · Arteriovenous Fistulas
4
a b
c d
efg
. Fig.4.11a–g (Atlas) Aneurysm of hemodialysis access– puncture aneurysm, suture aneurysm, degenerative dilatation.
a A puncture aneurysm is a pseudoaneurysm with little tendency to thrombose spontaneously. It is frequently due to obstructed venous outow
(see . Figs.4.15 and 4.20 (Atlas)). In the case presented here, puncture aneurysm developed 6years after creation of an AV stula in the bend of
the elbow. Color duplex and spectral Doppler show the typical features of a pseudoaneurysm: systolic inow through the aneurysm neck and
outow from the sac throughout diastole. The standard treatment is surgical repair. In rare cases, it is possible to treat a stula-related pseudoaneurysm by thrombin instillation. This requires very condent identication of the aneurysm neck and very strict precautions to minimize the risk
of thrombin spillage. The measures to be taken include temporary complete manual compression of the stula (blue) (conrmed by ultrasound)
downstream of the aneurysm (red) to prevent escape into the outow vein and throttling of inow by placement of a tourniquet upstream of the
aneurysm. With these precautions, thrombin instillation begins near the wall in the portion away from the neck using ultrasound to monitor
correct needle placement. To avoid thrombosis, compression of the stula must be released immediately after clotting of the aneurysm sac has
occurred.
b Following thrombin injection, ultrasound conrms complete thrombosis of the puncture aneurysm (PA) with some residual pulsation in the
aneurysm neck (red). The hemodialysis access (S, blue) is patent.
c Woman with a long history of hemodialysis and a loop in the thigh following loss of hemodialysis stulas in both arms due to multiple complications. A posterior puncture aneurysm was suspected, due to iatrogenic piercing of the far wall of the access segment (SHUNTAN). The Doppler
waveform obtained with the sample volume placed in the leak between the loop and the aneurysm shows the changes characteristic of a
pseudoaneurysm: ow into the aneurysm (below the baseline, away from transducer) during systole (S) and back into the loop as a result of the
changed pressure during diastole (above the baseline, toward transducer). In inconclusive cases, a spectral Doppler measurement can thus help
dierentiate between severe ectasia of the stula (only in a direct AV stula without an interposed conduit) and puncture aneurysm (pseudoaneurysm).
d Suture aneurysm and anastomotic stenosis in a patient with an AV stula in the bend of the elbow (A.B=brachial artery, S=stula vein). The
sonographic ndings include a PSV>500cm/s, aliasing, and turbulent ow.
e–g Brescia-Cimino stula (> 10years) with aneurysmal dilatation and partial thrombosis (e). The longitudinal image (f) shows that, due to
thrombosis, the patent lumen of the dilated portion is of the same diameter as the adjacent normal segment (which is why this aneurysm would
escape detection by angiography). There is a patent accessory branch vessel, and downstream of its origin, the access vein is occluded. At sites of
frequent needle puncture, the access vein is narrowed due to scarring (left part of f). As a result of the long use of the stula for hemodialysis, the
feeding brachial artery is also dilated (g) and shows triphasic ow due to partial obstruction of the access vein. Based on these ndings, the
indication for creation of a new hemodialysis access can be established without additional diagnostic tests or prior attempts to revise the existing
stula
4.9 · Atlas: Arteriovenous Fistulas
abc
d
285
4
. Fig.4.12a–d (Atlas) Stenosis of proximal feeding artery.
a Brachial artery with the typical, monophasic ow prole of an artery feeding an AV stula (left portion of waveform). With manual stula
compression (right portion of waveform, SHUNTKOMP), ow becomes triphasic (as in a peripheral artery without an AV stula), and the indirect
criteria can be used to rule out upstream (proximal) stenosis. (Without manual stula compression, a triphasic waveform in the feeding artery of a
hemodialysis access indicates occlusion of the access vein or high-grade venous outow obstruction.)
b Patient with ischemic nger pad necrosis and higher-grade subclavian artery stenosis. Manual compression of the stula results in decreased
ow velocity in the axillary artery, and the spectral Doppler display (right portion of waveform, SHUNTKOMP) shows the indirect signs of upstream
stenosis: delayed systolic upstroke (prolonged rise time) and monophasic ow prole.
c The Doppler waveform from the brachial artery distal to the venous anastomosis shows to-and-fro ow due to arterial steal; manual stula
compression elicits increase in ow (right portion of Doppler waveform, SHUNTKOMP) and features of poststenotic ow (monophasic prole with
delayed systolic upstroke).
d The subclavian artery stenosis, the underlying cause of ischemia in this patient, can only be graded while the stula is being compressed. During
compression, a PSV of 450cm/s is measured, indicating >75% stenosis. (Fistula compression allows the examiner to use both the direct and
indirect criteria for peripheral artery stenosis grading also in individuals with an AV stula)
. Fig.4.13 (Atlas) Anasto-
motic stenosis.
Forearm loop AV graft with
higher-grade stenosis at the
venous anastomosis (PSV of
5m/s). The stenosis (indicated by
arrow in the angiogram) is
dicult to evaluate or grade in a
single angiographic projection
286
bc
Chapter 4 · Arteriovenous Fistulas
4
abc
de
. Fig.4.14a–e (Atlas) Hemodialysis access complication– peripheral ischemia, arterial steal.
a A patient with a hemodialysis access in the bend of the elbow which functioned for many years developed ischemic necrosis of the nger pads.
The AV stula was found to be patent and showed a high ow rate with a peak systolic velocity (PSV) of 186cm/s and end-diastolic velocity (EDV)
of 94cm/s.
b Without compression of the stula, no ow is detected in the radial artery by color duplex or spectral Doppler. The transverse view of the radial
artery on the left demonstrates marked medial sclerosis with posterior acoustic shadowing obscuring ow. The image on the right shows blood
ow coded in blue in the radial artery upon compression of the stula. Angiography also requires compression of the stula to visualize the distal
radial artery (not shown).
c Banding of the stula causes stenosis in this area with a PSV of 280cm/s and EDV of 100cm/s.
d As a result of banding, there is a decrease in blood ow in the stula (PSV of 95cm/s and EDV of 60cm/s).
e Although visualization is impaired by medial sclerosis, ow with a PSV of 50cm/s is detectable in the radial artery (A) after banding. However,
only isolated spot-like ow signals are depicted in the radial artery despite a high gain (indicated by posterior artifacts due to overmodulation)
and a low PRF.The calcied plaques and medial sclerosis cause acoustic scattering and shadowing (S)
a
. Fig.4.15a–c (Atlas) Hemodialysis access complication– reduced stula ow, terminal cephalic vein stenosis.
a In a patient with a long-standing Brescia-Cimino stula, there is increased pulsatility of arterial inow, shown here in the axillary artery. Color
bruit (PV, perivascular vibration) is seen in the tissue adjacent to a high-grade stenosis at the termination of the cephalic vein (VC) (see c).
b The hemodialysis access is patent and shows normal ow, but pulsatility is increased as well (reduced diastolic ow velocity), consistent with
increased venous drainage resistance more centrally.
c In this patient, reduced ow with increased pulsatility in the stula is due to a high-grade stenosis of the terminal cephalic vein (V.CEP) (which
takes an arched course and is dicult to image in a single plane) with a PSV >420cm/s. This hemodialysis access problem can present with arm
swelling (V.ax=axillary vein)
bc
de
4.9 · Atlas: Arteriovenous Fistulas
a
287
4
. Fig.4.16a–e (Atlas) Hemodialysis access complication– peripheral ischemia.
a Patient with hemodialysis access in the bend of the elbow presenting with peripheral ischemia and hand pain. High ow through the stula causes
to-and-fro ow in the brachial artery distal to the venous anastomosis. The alternating forward and backward ow is demonstrated both by color duplex
(systolic ow away from transducer depicted in blue and diastolic ow toward transducer and stula depicted in red) and spectral Doppler. To-and-fro
ow in the distal feeding artery in conjunction with a high-ow stula does not cause peripheral ischemia when perfusion is maintained via collaterals.
b–e Peripheral ischemia after creation of hemodialysis access– accessory vein ligation.
b When banding or any other type of stula revision including closure is contemplated, the course of the stula vein should be evaluated to
search for accessory branches or communications with deeper veins. If ow in such an accessory vein is high, it can divert blood away from the
access vein. In the example shown, the cephalic vein, which is the access vein (S), is only slightly dilated with a diameter of 1.2cm, but ow is high
with a peak systolic velocity (PSV) of approximately 2.5m/s (upstream of the origin of the accessory vein).
c There are two dilated accessory veins (V) with diameters of 8 and 7mm. The Doppler waveform from one of the veins shows a PSV of 123cm/s
and an end-diastolic velocity (EDV) of 60cm/s with similar velocities in the second vein (waveform not shown).
d There is to-and-fro ow in the proximal radial artery shortly after its origin from the brachial artery: slow orthograde ow during systole with a
PSV of 20cm/s and diastolic backward ow (D) with an EDV of 8cm/s. Compression of the stula (right) results in systolic and diastolic forward
ow (into the periphery, away from transducer) with a postischemic increase in the diastolic component (PSV of 40cm/s and EDV of 10cm/s).
e The accessory veins described in c were sonographically marked and exposed for ligation to improve hand perfusion and salvage the dialysis access.
Following revision, the improved hemodynamic situation is demonstrated by repeat spectral Doppler measurement at the same site as in d: orthograde
ow is restored (without backward ow), and the PSV is 35cm/s (compare the waveform in d). The patient’s symptoms resolved after the intervention
288
bc
Chapter 4 · Arteriovenous Fistulas
. Fig.4.17a–c (Atlas) Peripheral ischemia– arterial steal with
retrograde ow in palmar arch.
a Patient with a dilated Brescia- Cimino stula in the wrist (12mm
diameter) and ischemic pain in the nger pads but with an otherwise
well-functioning access (stula not shown). There is high ow in the
proximal radial artery (not shown) with retrograde ow in the distal
segment (coded in red, toward transducer). The Doppler waveform
conrms retrograde ow with reduced systolic ow velocity (S) and a
high end-diastolic ow velocity (EDV) of 75cm/s (D). Compression of
4
the stula elicits ow reversal (KOMP SHUNT) with an orthograde ow
direction (away from transducer) and a large diastolic ow component
(postischemic) in the radial artery.
b The ulnar artery shows high orthograde ow (aliasing in the color
ow image) toward the periphery (coded in blue, away from transducer; below the baseline in the waveform). The Doppler waveform is
that of an artery supplying an AV stula with a large diastolic component (EDV of 44cm/s) and a high PSV of 100cm/s. Upon compression
of the stula (KOMP SHUNT), the ow pattern normalizes (triphasic
ow characteristic of peripheral arteries) with a PSV of 45cm/s. These
ndings are consistent with arterial steal due to a high-ow stula;
arterial blood ow is insucient, and the ulnar artery is recruited to
also supply the stula via the palmar arch, which explains the
retrograde ow in the radial artery distal to the stula. Based on these
sonographic ndings, the patient underwent ligation of the radial
artery distal to the stula. This measure eliminated arterial steal and
restored adequate blood supply to the hand through the ulnar artery.
c Drawing illustrating blood ow in this situation (arrows indicate ow
direction)
a
b
c
a
. Fig.4.18a–c (Atlas) Outow obstruction– central vein thrombosis downstream of hemodialysis access.
In patients with a stenotic lesion upstream of a hemodialysis access, the Doppler waveform from the stula is less pulsatile with a delayed systolic
upstroke and an increased diastolic ow component (resembling venous ow). Conversely, impaired venous drainage (thrombosis, stenosis,
compression) results in a more pulsatile ow prole.
a The Doppler waveform from the hemodialysis access lacks a diastolic component, suggesting an increased ow resistance (ow obstruction)
downstream of the site of sampling.
b Color duplex imaging demonstrates thrombosis of the axillary vein with some residual ow near the walls coded in red. The lumen of the vein
(V) is nearly completely lled by the thrombus.
c The outow obstruction leads to high-resistance ow in the brachial artery feeding the hemodialysis stula, which is indicated by a return to a
triphasic waveform (i.e., the ow prole characteristic of normal peripheral arteries). When inadequate blood ow during hemodialysis is due to
impaired venous drainage, this is suggested by spectral Doppler interrogation of the feeding artery or of the access vein and then conrmed by
continuous evaluation of venous outow to identify the site of obstruction. In the case presented here, thrombosis of the axillary vein was
revealed. In patients with a synthetic loop graft, the dierential diagnosis of a triphasic waveform includes stenosis of the venous anastomosis
cd
4.9 · Atlas: Arteriovenous Fistulas
ab
289
4
. Fig.4.19a–d (Atlas) Peripheral ischemia– to-and-fro ow, anastomotic stenosis, accessory vein.
a Patient with AV stula (S) in the bend of the elbow (A.B=brachial artery) presenting with peripheral ischemia and mild swelling of the hand. The
ultrasound examination reveals high-grade anastomotic stenosis (aliasing, peak systolic velocity (PSV) of >6m/s, peak end-diastolic velocity (EDV)
of 2.5m/s).
b Despite the high-grade anastomotic stenosis, there is to-and-fro ow in the brachial artery distal to the venous anastomosis. During manual
stula compression, forward ow is restored in this segment.
c Close evaluation of the stula vein (displayed in blue; S) identies a large accessory vein (red; SAV) with blood ow into the hand.
d Color ow imaging and spectral Doppler interrogation demonstrate a large ow volume in the accessory vein (PSV of 80cm/s, diameter of 1cm)
with blood ow to the periphery (red). The accessory vein was marked, and subsequent ligation led to resolution of peripheral pain and hand
swelling. The anastomotic stenosis was left untreated
290
Chapter 4 · Arteriovenous Fistulas
Loop
Artery
Vein
4
a
b
c
34
2
1
d
. Fig.4.20a–e (Atlas) a–c Hemodialysis access complication– progressive swelling of forearm and hand.
Patient with a history of interposition of a synthetic graft (onto basilic vein) to replace a failing AV stula 1 year before presenting with progressive
swelling of the forearm and hand.
a Duplex ultrasound with a peak systolic velocity (PSV) of up to 5.5m/s indicates high-grade stenosis (ST) of the basilic vein (V.B) just central to
the venous anastomosis (ANAST).
b The stenosis causes ow toward the hand in the dilated basilic vein distal to the anastomosis (red, ow toward transducer). Venous drainage to
the hand is the cause of hand swelling in this patient. As a result of this reversed venous drainage, the more central stenosis (see . Fig.4.15)
causes neither increased pulsatility in the access segment nor a drop in blood ow below the limit required for adequate hemodialysis function.
However, the stenosis may cause dilatation, prolonged bleeding after hemodialysis, and puncture aneurysm.
c The PTA angiogram obtained on the basis of the ultrasound ndings provides an overview of the complex ow situation with central stenosis of
venous drainage and dilatation of the vein peripheral to the anastomosis (right).
d Diagram of late morphologic changes in an AV stula for hemodialysis (right drawing): stenosis at venous anastomosis (3); dilatation of access
vein and scarring due to frequent puncture (2); dilatation of distal draining vein (4); stenotic changes of feeding artery due to progressive
atherosclerosis (1) (From Scholz 1998).
e Normal hemodialysis ow despite high-grade stenosis of the access vein central to the anastomosis (a). Normal ow is ensured due to venous
drainage via retrograde ow in forearm veins. Aliasing in the center of the image (yellow and red colors at the origin of the draining vein, which
shows red-coded, retrograde ow) is due to a very small Doppler angle at this site (with the beam tangential to the direction of blood ow) (see
. Figs.1.18b and 1.50b)
e
. Fig.4.21 (Atlas) Failure of stula maturation due to stenosis close to anastomosis.
Patient with a persistent thin access vein (2mm) 5 weeks after creation of an AV hemodialysis access. Ultrasound identies high-grade stenosis as
the underlying cause (arrow; with a peak systolic velocity (PSV) ratio>4; calculated from an intrastenotic PSV of 437cm/s and a prestenotic PSV of
98cm/s). The stenosis is not apparent morphologically (B-mode image), only in the waveform. The possible cause is an intimal ap or intraoperative trauma (for intimal ap see . Fig.4.4)
291
Extracranial Cerebral Arteries
5.1 Normal Vascular Anatomy andImportant Variants – 293
5.1.1 Carotid Arteries – 293
5.1.2 Vertebral Arteries – 295
5.2 Examination Technique andProtocol – 296
5.2.1 Carotid Arteries – 296
5.2.2 Vertebral Arteries – 299
5.3 Documentation – 301
5.4 Normal Findings – 301
5.4.1 Carotid Arteries – 301
5.4.2 Vertebral Arteries – 302
5.5 Clinical Role ofDuplex Ultrasound – 302
5.5.1 Carotid Arteries – 302
5.5.1.1 Stenosis Grading – 305
5.5.1.2 Plaque Morphology – 307
5.5.2 Vertebral Arteries – 309
5
5.6 Ultrasound Criteria, Measurement Parameters,
andDiagnostic Role – 309
5.6.1 Carotid Arteries – 309
5.6.1.1 Plaque Evaluation andMorphology – 309
5.6.1.1.1 Intima-Media Thickness – 309
5.6.1.1.2 Plaque Features – 311
5.6.1.1.3 Plaque Dierentiation – 312
5.6.1.1.4 Plaque Thickness – 314
5.6.1.1.5 Plaque Morphology: Plaque Surface – 314
5.6.1.1.6 Plaque Echogenicity: Inuencing Factors – 316
5.6.1.1.7 Gray-Scale Analysis: Potential andLimitations – 317
5.6.1.1.8 Carotid Plaque Characterization Using Contrast-Enhanced
Ultrasound – 318
5.6.1.2 Stenosis Quantication/Grading – 319
5.6.1.2.1 Primary andSecondary Criteria forCarotid Stenosis Grading – 322
5.6.1.3 Occlusion – 332
5.6.1.3.1 Persistent Primitive Hypoglossal Artery – 333
5.6.1.4 Postoperative Follow-Up – 334
5.6.1.4.1 Carotid Endarterectomy (CEA) – 334
© Springer International Publishing AG, part of Springer Nature 2018
W. Schäberle, Ultrasonography in Vascular Diagnosis, https://doi.org/10.1007/978-3-319-64997-9_5
5.6.1.4.2 Carotid Artery Stenting (CAS) – 337
5.6.1.4.3 Scientic Discrepancies Regarding Restenosis Grading
After CAS – 337
5.6.1.4.4 Stenosis Grading Based onthe Continuity Equation – 340
5.6.1.4.5 Stent Dislocation – 342
5.6.2 Vertebral Arteries – 343
5.6.2.1 Stenosis – 343
5.6.2.2 Occlusion – 344
5.6.2.3 Dissection – 344
5.6.2.4 Subclavian Steal Syndrome – 345
5.7 Diagnosis ofBrain Death – 346
5.8 Rare (Nonatherosclerotic) Vascular Diseases
oftheCarotid Territory – 346
5.8.1 Dissection – 346
5.8.2 Vasculitis – 348
5.8.2.1 Ultrasound Findings inTakayasu’s Arteritis – 348
5.8.2.2 Ultrasound Findings inHorton’s Disease – 349
5.8.3 Fibromuscular Dysplasia – 350
5.8.4 Aneurysm – 350
5.8.5 Arteriovenous Fistula – 351
5.8.6 Idiopathic Carotidynia – 351
5.8.7 Vasospasm – 352
5.8.8 Compression by Tumor, Carotid Body Tumor – 352
5.9 Diagnostic Role ofDuplex Ultrasound inEvaluating
theExtracranial Cerebral Arteries – 352
5.10 Atlas: Extracranial Cerebral Arteries – 356
5.1 · Normal Vascular Anatomy andImportant Variants
293
5
Cardiovascular disease is the most common cause of death
in Western industrialized countries. e most serious cerebrovascular manifestation is stroke with its complications,
which is fatal in one third of cases. Patients who survive
cerebral infarction oen suer from irreversible damage
and paralysis and require permanent care. With atherosclerosis of the carotid artery circulation becoming more common with age, cerebral infarction gains relevance as the
population ages (Fabres etal. 1994; Mannami et al. 2000;
Roederer etal. 1984). Over 60–70% of all ischemic cerebral
infarctions are caused by arterial embolism, typically arising
from the carotid artery (Bock etal. 1993; Evans 1999; Roederer etal. 1984).
Carotid endarterectomy (CEA), rst performed by De
Bakey in 1953, is a highly eective surgical procedure for
reducing the risk of stroke in patients with atherosclerosis of
the carotid system. is has been conrmed in several large
trials in individuals with symptomatic carotid artery stenosis
performed in Europe (European Carotid Surgery Trial
(ECST)) and the USA (North American Symptomatic
Carotid Endarterectomy Trial (NASCET)) as well as in an
asymptomatic population (Asymptomatic Carotid Atherosclerosis Study (ACAS)) (
. Table 5.1). ese studies com-
pared the natural history with the morbidity and mortality
aer carotid surgery stratied by clinical stage and degree of
carotid artery stenosis. e results of all three studies suggest
that carotid reconstruction is benecial in individuals with
symptomatic high-grade stenosis (>70%) and in selected
cases of 60–70% symptomatic stenosis. In high-grade asymptomatic stenosis, however, surgical repair is benecial only in
individuals with a low risk of perioperative morbidity and
plaque morphology predictive of a high risk of embolism.
Suitable diagnostic tests are necessary for identifying
those patients who will benet from the therapeutic measures conrmed in these large trials to be advantageous.
More specically, this involves identifying individuals with
carotid stenosis who are at a high risk of embolism and will
benet from CEA.Color duplex ultrasound is a noninvasive
method that can be repeated at any time and has evolved into
a highly accurate method for quantifying the degree of
carotid stenosis (the risk of embolism increases with the
degree of stenosis). Moreover, sonography also provides
information on plaque morphology, the second major factor
aecting the risk of embolism. Another feature associated
with the risk of embolism and inammatory activity is plaque
neovascularization, which can be evaluated by contrastenhanced ultrasound (CEUS).
e supercial course of the carotid arteries, without
interfering structures, enables detailed sonographic evaluation of the arterial segment accounting for the majority of
cerebral infarctions. Given these ideal scanning conditions
and the fact that the vast majority of carotid stenoses occur at
the origin of the internal carotid artery (ICA), continuous
wave (CW) Doppler ultrasound alone is already highly accurate in detecting higher-grade carotid stenosis.
(Color) duplex ultrasound provides both morphologic
and blood ow information, thus enabling precise evaluation
of arterial lesions and their locations in conjunction with
determination of their hemodynamic relevance based on the
measurement of angle-corrected spectral Doppler velocities.
Sonographic assessment of plaque morphology contributes
further information for estimating the risk of embolism.
Taken together, the sonographic ndings are sucient to
identify candidates for surgery or medical management of
carotid artery stenosis without the need for additional invasive tests.
5.1 Normal Vascular Anatomy
andImportant Variants
. Table 5.1 Results of randomized multicenter trials
comparing surgical versus medical treatment of symptomatic
(NASCET, ECST) and asymptomatic carotid artery stenosis
(ACAS)
Parameter NASCET ECST ACAS
No. of patients
– Surgical management
– Medical management
Perioperative stroke rate 2.1% 6.6% 1.4%
Morbidity/mortality rate
(natural history)
Risk reduction (relative)
– Men
– Women
NASCET North American Symptomatic Carotid Endarterectomy
Trial, ECST European Carotid Surgery Trial, ACAS Asymptomatic
Carotid Atherosclerosis Study
659
328
331
5.8% 7.5% 2.3%
65% 43% 53%
778
455
323
1659
825
834
66%
17%
5.1.1 Carotid Arteries
e brain derives its blood supply from the two carotid arteries and the two vertebral arteries. e latter unite at the inferior border of the pons to form the basilar artery. In over 70%
of individuals, the le common carotid artery (CCA) arises
directly from the aortic arch before the origin of the subclavian artery (
. Fig.5.1a). e right CCA originates from the
brachiocephalic trunk or artery (innominate artery), which
arises from the aortic arch and additionally gives o the subclavian artery. e most important variants of the supraaortic arteries, which originally developed from the branchial
arches, are:
5 Common origin of the brachiocephalic trunk and le
CCA from the aortic arch (13%)
5 Persisting communicating trunk arising from the aortic
arch and giving o rst the le CCA and then the
brachiocephalic trunk (9%)
5 Bilateral brachiocephalic trunk dividing into the CCA
and the subclavian artery (1%)
5 Situs inversus (very rare).