Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5760_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Preface to the Third English and Fourth German Edition
- •Preface to the Second English and Third German Edition
- •Preface to the First English Edition
- •Preface to the Second German Edition
- •Preface to the First German Edition
- •Contents
- •1: Fundamental Principles
- •1.1.1.2 Sound Waves
- •1.1.1.3 Generating Ultrasound Waves
- •1.1.1.4.3 Interference
- •1.1.1.5.1 Pulse-Echo Technique
- •1.1.1.5.2 Time Gain Compensation
- •1.1.1.5.3 A-Mode
- •1.1.1.5.4 B-Mode
- •1.1.1.5.5 M-Mode
- •1.1.1.6 Resolution
- •1.1.1.7 Beam Focusing
- •1.1.1.8.2 Linear Arrays
- •1.1.1.8.3 Curved or Convex Arrays
- •1.1.1.8.4 Sector Scanners
- •1.1.1.8.5 Phased Arrays
- •1.1.1.8.6 Mechanical Sector Scanners
- •1.1.1.8.7 Annular Phased Arrays
- •1.1.1.9 Ultrasound Artifacts
- •1.1.1.9.1 Posterior Shadowing
- •1.1.1.9.2 Acoustic Enhancement
- •1.1.1 Gray-Scale Ultrasonography (B-Mode)
- •1.1.1.1 Historical Milestones
- •1.1.1.9.4 Side Lobes
- •1.1.1.9.5 Reverberation Artifact
- •1.1.1.9.6 Geometric Distortion
- •1.1.2.1 Continuous Wave Doppler Ultrasound
- •1.1.2.3 Frequency Processing
- •1.1.2.4 Blood Flow Measurement
- •1.1.3.1 Velocity Mode
- •1.1.3.2 Power Doppler Mode
- •1.1.3.3 B-Flow Mode (Brightness Flow)
- •1.1.3.4 Intravascular Ultrasound
- •1.1.4.2 Mirror Artifact
- •1.1.4.6 Doppler Angle
- •1.1.5 Ultrasound Contrast Agents
- •1.1.5.3.1 Contrast-Enhanced Duplex Ultrasound
- •1.1.5.3.2 Contrast Harmonic Imaging
- •1.1.5.3.3 Stimulated Acoustic Emission Imaging
- •1.1.6.3.1 B-Mode
- •1.1.6.3.2 M-Mode
- •1.1.6.3.3 CW Doppler
- •1.1.6.3.4 PW Doppler
- •1.1.6.3.5 Color Doppler
- •1.1.6.4 Conclusion
- •1.2 Hemodynamic Principles
- •1.2.1 Laminar Flow
- •1.2.2.1 Low-Resistance Flow
- •1.2.2.2 High-Resistance Flow
- •1.2.2.3 Perfusion Regulation
- •1.2.3.1 Poststenotic Parameters
- •1.3 Machine Settings
- •2: Extremity Arteries
- •2.1.1 Vascular Anatomy
- •2.1.1.1 Pelvic Arteries
- •2.1.1.2 Leg Arteries
- •2.1.2.1 Pelvic Arteries
- •2.1.2.2 Leg Arteries
- •2.1.6 Abnormal Findings
- •2.1.6.1 Atherosclerotic Occlusive Disease
- •2.1.6.1.1 Pelvic Arteries
- •2.1.6.1.3 Stenosis Grading
- •2.1.6.1.4 Leg Arteries
- •2.1.6.1.9 Profunda Femoris Artery
- •2.1.6.1.13 Multilevel Obstruction
- •2.1.6.1.14 Arterial Occlusion
- •2.1.6.2 Arterial Embolism
- •2.1.6.3 Aneurysm
- •2.1.6.3.1 True Aneurysm
- •2.1.6.3.2 Pseudoaneurysm
- •2.1.6.4.1 Adventitial Cystic Disease
- •2.1.6.4.2 Popliteal Artery Entrapment Syndrome
- •2.1.6.4.3 Raynaud’s Disease
- •2.1.6.4.5 Buerger’s Disease
- •2.1.6.4.7 Dissection
- •2.1.6.4.8 Arteriovenous Fistulas
- •2.1.7.1 Thromboendarterectomy
- •2.1.7.3 Bypass Graft Surveillance
- •2.2 Arm Arteries
- •2.2.1 Vascular Anatomy
- •2.2.3.1 Atherosclerosis
- •2.2.3.2 Vascular Compression Syndromes
- •2.2.4 Documentation
- •2.2.5 Normal Findings
- •2.2.6.1 Atherosclerosis
- •2.2.6.2 Vascular Compression Syndromes
- •2.2.6.4 Buerger’s Disease
- •2.2.6.5 Raynaud’s Disease
- •2.3 Atlas: Extremity Arteries
- •3.1.2.1.2 Patient Positioning
- •3.1.2.1.3 Examination Technique
- •3: Extremity Veins
- •3.1.1 Vascular Anatomy
- •3.1.2 Examination Protocol
- •3.1.2.1 Thrombosis
- •3.1.2.1.1 Equipment
- •3.1.3 Normal Findings
- •3.1.4 Documentation
- •3.1.5.1.1 Leg Vein Thrombosis
- •3.1.5.2 Varicosis
- •3.1.6.1 Thrombosis
- •3.1.6.1.3 Pulmonary Embolism
- •3.1.6.1.5 Thrombus Age
- •3.1.6.1.6 Recurrent Thrombosis
- •3.1.6.3 Varicosis
- •3.1.6.3.1 Treatment Options
- •3.1.6.4 Varicophlebitis
- •3.1.7 Rare Venous Disorders
- •3.1.7.1 Venous Aneurysm
- •3.1.7.1.1 Sonographic Workup
- •3.1.7.3 Venous Compression
- •3.1.7.4 Venous Adventitial Cystic Disease
- •3.1.8 Vein Mapping
- •3.1.9.1 Deep Vein Thrombosis
- •3.1.9.1.1 Ultrasound Versus Venography
- •3.1.9.3 Varicosis
- •3.2.1 Vascular Anatomy
- •3.2.3 Normal Findings
- •3.2.4 Documentation
- •3.2.5 Clinical Role
- •3.3 Atlas: Extremity Veins
- •4: Arteriovenous Fistulas
- •4.1.1 Background
- •4.2.2 Hemodialysis AV Fistula
- •4.5 Documentation
- •4.7 Hemodialysis Access Complications
- •4.7.1 Hemodialysis Access Stenosis
- •4.7.1.3 Proximal Feeding Artery Stenosis
- •4.7.2.1 Peripheral Ischemia
- •4.7.2.2 Hemodialysis Access Aneurysm
- •4.7.2.3 Inadequate or Excessive Fistula Flow
- •4.7.2.4 Arm Swelling
- •4.8.1 Therapeutic Decision-Making
- •4.8.2 Surveillance Programs?
- •4.9 Atlas: Arteriovenous Fistulas
- •5: Extracranial Cerebral Arteries
- •5.1.1 Carotid Arteries
- •5.1.2 Vertebral Arteries
- •5.2.1 Carotid Arteries
- •5.2.2 Vertebral Arteries
- •5.3 Documentation
- •5.4 Normal Findings
- •5.4.1 Carotid Arteries
- •5.4.2 Vertebral Arteries
- •5.5.1 Carotid Arteries
- •5.5.1.1 Stenosis Grading
- •5.5.1.2 Plaque Morphology
- •5.5.2 Vertebral Arteries
- •5.6.1 Carotid Arteries
- •5.6.1.1.1 Intima-Media Thickness
- •5.6.1.1.2 Plaque Features
- •5.6.1.1.4 Plaque Thickness
- •5.6.1.1.5 Plaque Morphology: Plaque Surface
- •5.6.1.3 Occlusion
- •5.6.1.3.1 Persistent Primitive Hypoglossal Artery
- •5.6.1.4 Postoperative Follow-Up
- •5.6.1.4.1 Carotid Endarterectomy (CEA)
- •5.6.1.4.2 Carotid Artery Stenting (CAS)
- •5.6.1.4.5 Stent Dislocation
- •5.6.2 Vertebral Arteries
- •5.6.2.1 Stenosis
- •5.6.2.2 Occlusion
- •5.6.2.3 Dissection
- •5.6.2.4 Subclavian Steal Syndrome
- •5.8.1 Dissection
- •5.8.2 Vasculitis
- •5.8.3 Fibromuscular Dysplasia
- •5.8.4 Aneurysm
- •5.8.5 Arteriovenous Fistula
- •5.8.6 Idiopathic Carotidynia
- •5.8.7 Vasospasm
- •5.10 Atlas: Extracranial Cerebral Arteries
- •6.1.1 Vascular Anatomy
- •6.1.1.1 Aorta
- •6.1.1.2 Visceral Arteries
- •6.1.1.3 Renal Arteries
- •6.1.2.1 Aorta
- •6.1.2.2 Visceral Arteries
- •6.1.2.3 Renal Arteries
- •6.1.2.3.1 Ultrasound Technique
- •6.1.3 Normal Findings
- •6.1.3.1 Aorta
- •6.1.3.2 Visceral Arteries
- •6.1.3.3 Renal Arteries
- •6.1.5.1 Aorta
- •6.1.5.1.1 Abdominal Aortic Aneurysm
- •6.1.5.2 Visceral Arteries
- •6.1.5.3 Renal Arteries
- •6.1.6.1 Renal Arteries
- •6.1.6.1.2 Therapy-Oriented Stenosis Grading
- •6.1.6.1.3 Contrast-Enhanced Ultrasound (CEUS)
- •6.1.6.1.5 Diagnostic Algorithm
- •6.1.6.1.6 Renal Artery Occlusion
- •6.1.6.1.7 Transplant Kidney
- •6.1.6.2 Visceral Arteries
- •6.1.6.2.1 Celiac Trunk
- •6.1.6.2.2 Visceral Artery Aneurysm
- •6.1.6.2.3 Dissection
- •6.1.6.2.4 Superior Mesenteric Artery
- •6.1.6.2.5 Acute Mesenteric Artery Occlusion
- •6.1.6.3 Aorta
- •6.1.6.3.2 Abdominal Aortic Aneurysm
- •6.1.6.3.6 Aortic Dissection
- •6.2.1 Vascular Anatomy
- •6.2.1.1 Vena Cava
- •6.2.1.2 Renal Veins
- •6.2.2 Examination Technique
- •6.2.2.1 Vena Cava
- •6.2.2.2 Renal Veins
- •6.2.3.1 Renal Veins
- •6.2.3.2 Portal Venous System
- •6.2.4 Normal Findings
- •6.2.4.2 Portal Venous System
- •6.2.5 Documentation
- •6.2.6.1 Vena Cava
- •6.2.6.1.1 Membranous Vena Cava Obstruction
- •6.2.6.2 Renal Veins
- •6.2.6.3.1 Splenic Vein Thrombosis
- •6.2.6.4.1 Portal Vein Thrombosis
- •6.2.6.4.2 Portal Hypertension
- •6.2.6.4.3 Hepatic Veins

274
aV
Chapter 4 · Arteriovenous Fistulas
PSV 3.7m/s and 0.9m/s
R3
Pp
fA
R1
Pc
A
C
dA
R2
pA
4
a b c
. Fig.4.5 a Diagram of factors aecting peripheral perfusion after creation of an AV stula (for details see text) (fA feeding artery, Pc central
arterial pressure, dA draining artery, Pp peripheral arterial perfusion pressure, pA peripheral arteries, R1 resistance of feeding artery, R2 resistance
of peripheral vessels, R3 total resistance of anastomosed vessel, A anastomosis, aV anastomosed vessel, C collateral) (From Scholz 1998).
b, c High-ow AV stula with a markedly increased peak systolic velocity (PSV) of >350cm/s in a long segment of the brachial artery feeding the
stula. The increase is nonfocal, making stenosis unlikely. The Doppler waveform from the brachial artery (c) shows ow without manual
compression of the AV stula (left) and with compression (right). During compression, ow in the brachial artery becomes more pulsatile, and a
normal PSV of 100cm/s is measured
forearm and hand. Severe dialysis access steal syndrome
(DASS) can cause retrograde ow from the arteries supplying
the hand or an increased ow in the ulnar artery if the stula
is supplied by the arteries of the palmar arch. Hypoperfusion
of the ngers or even of the whole hand may ensue. e risk of
ischemia in the ngers or the hand increases with the severity
of PAOD and the magnitude of stula ow.
A drop in peripheral perfusion pressure below the critical
threshold with pain and vital risks to nger areas is dependent on several factors (. Fig.4.5):
5 Systemic blood pressure
5 Atherosclerosis of peripheral arteries (micro- and
macroangiopathy) with increased resistance distal to the
venous anastomosis
5 Peripheral resistance distal to the venous anastomosis
5 Collateralization around the stula
5 Width of anastomosis
5 Steal phenomena (DASS)
5 Venous outow resistance
5 Proximal stenosis of feeding artery
Macroangiopathic causes of ischemia of the stula-bearing
arm and excessive blood ow through the stula can be diagnosed by duplex ultrasound. e color duplex examination
for peripheral ischemia focuses on identifying sclerotic stenotic lesions of the arm arteries proximal and distal to the
arteriovenous anastomosis (with a view to performing PTA
or placing a synthetic gra) or on conrming a high-ow stula with arterial steal (DASS). Once excessive stula ow has
been established as the cause of ischemia, real-time measurement of peripheral ow velocity in response to increasing
manual compression of the stula is performed to estimate
the expected eects of dierent surgical revision techniques
(tailoring, banding, or distal revascularization and interval
ligation (DRIL)). Duplex ultrasound can also be used for
intraoperative monitoring of the eects of ow reduction by
cu placement or plication (Aschwanden etal. 2003; Zanow
etal. 2006). Arterial steal results if venous outow is greater
than the capacity of the feeding artery (e.g., due to dilatation). Such a stula draws blood from areas peripheral to the
anastomosis and is characterized by reversed ow in the
feeding artery distal to the venous anastomosis.
Peripheral ischemia occurs in 2–8% of all patients with a
hemodialysis access.
Identifying the underlying cause can
be complex. Underlying causes include DASS due to excessive stula ow and a relevant proximal stenosis of the feeding artery presenting with poor hemodialysis ow. Proximal
stenosis of the feeding artery can be identied by spectral
Doppler interrogation upstream of the venous anastomosis
while the stula is being compressed. During compression of
the stula, the waveform should become triphasic, while a
monophasic ow prole and delayed upstroke suggest stenosis of the feeding artery (. Fig.4.12b, c (Atlas)). e stenosis
is then localized by mapping the feeding artery upstream of
the spectral Doppler sampling site.
e next step is spectral Doppler imaging of the feeding
artery just distal to the venous anastomosis, comparing ow
in this segment without and with compression of the stula
(. Figs.4.17 and 4.19 (Atlas)). Comprehensive assessment of
the hemodynamic situation is crucial for deciding about the
best therapeutic management (DRIL, banding). If the waveform obtained without compression shows two-and-fro ow
(systolic forward ow and diastolic backward ow) or even
persistent ow reversal, then this is diagnostic of arterial steal.
In a patient with peripheral ischemia, this ultrasound nding
is an indication for restricting ow through the vascular
access (e.g., banding) or a DRIL procedure (Anaya- Ayala
etal. 2012; Scali etal. 2013), and no additional diagnostic tests
are necessary. Flow reversal in the distal feeding artery without symptoms of ischemia is observed when there is retrograde lling with backward ow in the brachial artery via the
palmar arch, and these patients do not require treatment.

4.7 · Hemodialysis Access Complications
275
4
In the absence of steal-related ow changes in the artery
distal to the venous anastomosis, manual compression of the
stula will nearly always elicit faster ow (PSV) in this segment and can thus help in estimating a potential benecial
eect of access ow restriction on peripheral perfusion and
in deciding which treatment option will restore adequate
perfusion of the hand (banding or gra interposition to
reduce the lumen; the latter is typically only necessary when
a high PSV of >2m/s is measured in the stula). e eect of
ow-restricting measures can be estimated by pre- and intraoperative determination of ow in the distal feeding artery
and the stula while applying graded compression. Patients
in whom high stula ow has been ruled out as the cause of
ischemia are candidates for a DRIL procedure. Before DRIL
is performed, it is important, especially in diabetics, to evaluate the distal feeding artery down to the nger arteries for
any additional stenotic lesions amenable to treatment (PTA).
e search is best performed by levelwise spectral Doppler
interrogation of the distal radial artery and the nger arteries
with intermittent mapping. e sonographic search for stenosis in this territory is time-consuming and may be limited
in diabetics with severe medial calcication. A supplementary angiogram is helpful for detecting stenotic lesions in this
territory.
is is the only situation that may require an angiographic
examination. Otherwise, the unique hemodynamic information obtained with color duplex imaging is oen superior in
elucidating underlying vascular access problems in patients
with symptoms of ischemia.
When DASS due to excessive stula ow is suspected,
duplex ultrasound can be used to quantify the stula ow
volume (see
increases the risk of peripheral ischemia and high-output
cardiac failure (Bay etal. 1998). In most cases, however, ow
quantication is not necessary, and a treatment decision can
be made based on the spectral Doppler ndings obtained in
the feeding artery distal to the venous anastomosis (including the nger arteries) with and without manual compression of the stula (. Fig.4.17 (Atlas)).
Another cause of peripheral ischemia is ow diversion
through competing veins arising from the access vein.
erefore, the access vein should be examined once excessive
stula ow and arterial inow obstruction have been ruled
out as underlying causes of symptomatic ischemia. Accessory
veins are marked for subsequent surgical ligation to restore
adequate peripheral perfusion.
4.7.2.2 Hemodialysis Access Aneurysm
Because of the supercial location of the hemodialysis access,
occlusion or aneurysm can be diagnosed clinically. Duplex
ultrasonography may be performed to conrm the clinical
diagnosis and to identify the origin and extent of an aneurysm (suture aneurysm, puncture aneurysm) for planning
the therapeutic procedure.
Pseudoaneurysm (or false aneurysm) is a typical punc-
ture complication developing when blood escapes through a
defect in the arterial wall. e resulting subcutaneous blood
7 Sect. 4.4). A volume ow rate>1200mL/min
collection has a persisting communication with the artery.
Color duplex ultrasound identies a pseudoaneurysm as a
perivascular space with pulsatile ow. A pseudoaneurysm of
the arterialized access vein is typically associated with
obstructed venous drainage (stenosis or partial thrombosis
of the access vein or axillary vein). Sonographic demonstration of to-and-fro ow identies the neck of the pseudoaneurysm. Occasionally, thrombin injection is a treatment option
but requires even greater care than in native arteries to avoid
thrombin escape into the blood bloodstream and drainage
toward the heart. Precautions include complete manual compression of the stula during thrombin instillation and
restriction of arterial inow by placement of a tourniquet.
Aer these precautions, ultrasound-guided thrombin instillation should begin in the periphery (5000IU in 5mL 0.9%
NaCl) monitoring clot formation by color duplex ultrasound
. Fig.4.11a, b (Atlas)). A suture aneurysm is a pseudoaneu-
(
rysm due to suture failure and is commonly associated with
infection (
pouchings that develop on the basis of degeneration of the
wall of the arterialized vein. ey are dened as circumscribed increases in diameter to over 15mm or to twice the
diameter of the proximal segment. Fistula dilatation is common due to turbulent ow (especially distal to a narrowed
segment) and an increased wall pressure resulting from arterialization of the access vein. Such dilatations may extend
over a considerable length of the draining vein when a hemodialysis access has been used for many years (. Fig.4.3).
4.7.2.3 Inadequate or Excessive Fistula Flow
A wide range of stula ow rates, from 500 to 1200mL/min,
is deemed acceptable for hemodialysis. Rates exceeding
1600mL/min (Grosser etal. 1991) or 20% of the cardiac output can cause complications such as cardiac insuciency or
ischemia distal to the vascular access. Estimation of the volume ow rate through the stula may be helpful in various
situations such as assessment of the outcome of stula banding or other ow-restricting measures. As discussed above,
various methods exist to quantify stula ow volume (see
7 Sect. 4.4). eoretically, the most accurate method is to
calculate the dierence between ow volumes in the feeding
artery proximal and distal to the arteriovenous anastomosis.
Practically and technically, it is easier and more accurate to
calculate stula ow volume from measurements in the ipsilateral and contralateral brachial artery or from measurements taken without and with compression of the stula
(. Fig.4.10e–g). e latter is the most accurate method. A
volume ow rate of less than 300mL/min is widely assumed
to be inadequate for eective hemodialysis, and low ow or a
decrease in stula ow volume over time is regarded as a predictor of hemodialysis access failure.
beginning in the feeding artery (for details see 7 Sect. 4.7.1).
Increased pulsatility in the brachial artery suggests obstruction of the stula or venous outow, and the next step is to
examine the venous anastomosis (especially in patients with
. Fig.4.11d (Atlas)).
True vascular access-related aneurysms are focal out-
Poor stula ow should prompt a search for stenosis,

276
Chapter 4 · Arteriovenous Fistulas
4
a b
. Fig.4.6 a Retrograde arterialization via backward supply to an accessory branch with reduction of stula ow: such accessory branches can
be identied sonographically and marked for ligation (According to Scholz 1998). b Brescia-Cimino stula at the wrist with inadequate ow for
hemodialysis. Once stenosis has been ruled out, the examiner must search for accessory branches that divert blood away from the main vein.
Such branches need to be ligated to ensure adequate blood ow through the access vein. In the case shown, ultrasound identied an accessory
vein with relevant ow. The spectral display shows an increase in PSV within the access vein from 50cm/s (due to ow diversion) to 75cm/s (with
manual compression of the accessory vein)
a Brescia-Cimino stula). If there is no ow obstruction at
this site, the length of the access segment is scanned, with a
focus on stenosis or partial thrombosis. If ow in the stula
is more pulsatile than expected, the examiner should proceed
to search for a ow obstruction of the draining veins, especially the axillary and subclavian veins.
Central venous obstruction with impaired venous
drainage can lead to congestion and edema. Aected patients
may present with arm swelling, especially when there is poor
collateralization and stula ow is high. In these patients, a
careful evaluation of the axillary and subclavian veins is warranted to search for venous narrowing. is is accomplished
by spectral Doppler evaluation of the axillary vein in the
infraclavicular fossa. Normal venous ow in this region
should show both respiratory phasicity and atrial pulsatility
(W-shaped waveform). Obstructed central venous drainage
is suggested when, compared with the contralateral arm, this
ow modulation is lost or markedly damped during manual
compression of the stula. Compression is necessary to
avoid misinterpretation because phasicity and pulsatility of
venous ow may also be modulated by high stula ow. Also
in the infraclavicular fossa, the cephalic vein termination is
evaluated for stenosis and the axillary vein for thrombotic
deposits.
Luminal narrowing of the draining vein is seen in up to
40% of hemodialysis patients but may be asymptomatic if
collaterals are present (Hecking etal. 2006; Neville et al.
2004). Venous obstruction oen occurs secondary to a central venous intervention or placement of a central venous
catheter. With 93% sensitivity and 94% specicity, color
duplex ultrasonograpy has replaced venography in diagnosing obstructed venous drainage (Grogan etal. 2005). Color
duplex imaging is also the method of choice for postinterventional evaluation of the access vein and central
venous outow. e primary patency rate aer PTA alone is
only 7–43% versus 11–70% for PTA with stenting (Mickley
2006). In patients with a synthetic dialysis access, narrowing
primarily occurs at the site of the venous (distal) anastomosis and is due to intimal hyperplasia (Gaanterman et al.
1995; Roy-Chaudhury etal. 2001). In a study of 38 patients
with clinically suspected hemodialysis access gra stenosis
examined by Doppler ultrasound and angiography, Robbin
etal. (1998) found ultrasound to reliably depict stenoses of
access gras and draining veins using PSV criteria. A focal
two- to three-fold PSV increase was associated with 75% or
greater stenosis.
Vascular access thrombosis can progress to partial or
even complete occlusion. It has many causes including preexisting stenosis, puncture complications (dissection, wall
hematoma), stula infection, and local compression, and the
risk is higher in patients with episodes of hypovolemia or
hypotension.
Another cause of
low stula ow (once stenosis has been
ruled out) is diversion of blood through collateral veins
coursing parallel to the access vein. Dilated accessory veins
with large ow volumes can cause arm swelling. If the
branches arise close to the venous anastomosis, patients may
develop symptomatic arterial steal. Inadequate dialysis ow,
new-onset steal-related symptoms (especially if they develop
some time aer creation of the dialysis stula) (. Fig.4.19a-d
(Atlas)), and arm swelling should prompt a color duplex
examination to search for branching veins along the length of
the access vein (in transverse orientation). Flow velocity and
diameter of the branch vein are measured to determine the
amount of blood diverted from the hemodialysis access vein.
In addition, a branch vein can be compressed to estimate the
ow increase likely to occur in the access segment aer ligation. A relevant branch vein identied sonographically can
then be marked for ligation (
. Fig. 4.6). e presence of
branch veins may also be the reason that an AV stula fails to
mature. In this case, ligation will lead to maturation within a
short time.

4.8 · Diagnostic Role ofDuplex Ultrasound Compared withOther Modalities
277
4
Flow volumes of over 1500–2000mL/min may occur in
patients with a more proximal hemodialysis access (bend of
the elbow) if the cephalic vein is dilated and the anastomosis
is too wide. Such high ow rates can lead to high-output cardiac insuciency, especially in patients with compensated
cardiac insuciency or pre-existing cardiac damage.
Quantication of the stula ow volume by duplex ultrasound (the most reliable method for this purpose) can help
avoid this complication, allowing identication of candidates
for banding and assessment of the adequacy of ow reduction aer treatment.
4.7.2.4 Arm Swelling
Venous outow obstruction in patients with a hemodialysis
access may be due to (partial) central vein thrombosis or
terminal stenosis of the cephalic vein (. Figs.4.15 and 4.18
(both Atlas)) and can present with arm swelling. Obstructed
central venous drainage is suggested when there is increased
pulsatility of ow in the access near the anastomosis and is
conrmed by compression ultrasound or duplex ultrasound with the transducer in the infraclavicular fossa
(incomplete compressibility of the vein with marginal ow
around the clot). In patients with a loop gra, venous outow obstruction may also be due to a stenosis upstream of
the venous anastomosis. If no outow obstruction is identied, the examiner proceeds to scan the length of the stula
in the transverse plane beginning at the venous anastomasosis to look for large-caliber accessory veins arising
from the access vein. (
When pressure in an accessory vein is high, it not only
drains blood to the heart but also diverts blood to the forearm and hand. Venous ow reversal is identied sonographically, and these veins are then marked for surgical
ligation.
Other complications cause circumscribed swelling. An
example is pseudoaneurysm at puncture sites, which is identied on color ow images by the characteristic to-and-fro
ow through a persisting communication with the parent
vessel. Like a pseudoaneurysm developing as a complication
of femoral artery puncture, a hemodialysis-access-related
pseudoaneurysm can be treated by ultrasound-guided
thrombin instillation. However, to prevent drainage of
thrombin toward the center, even greater precautions should
be taken including short manual compression of the access
segment downstream of the aneurysm during instillation
. Fig.4.11a, b (Atlas)).
(
4.8 Diagnostic Role ofDuplex Ultrasound
. Figs.4.16 and 4.19 (both Atlas)).
Compared withOther Modalities
Gray-scale ultrasound identies both morphologic vascular
changes of a hemodialysis access (dilatation, aneurysm, narrowing, thrombosis) and perivascular lesions (hematoma,
abscess). (Color) duplex imaging provides quantitative information on stula ow and identies stenoses of the access
vein and inow artery. Ultrasonography thus enables more
comprehensive evaluation of suspected hemodialysis access
complications and their dierential diagnosis than the mere
visualization of vascular morphology by angiography.
Angiography has the advantage of providing a better overview of the vascular anatomy around an AV stula, but evaluation of complex vascular patterns may be impaired by
overlying vessels. Sonographically detected pathology such
as stenosis, length of dilated segment, or venous short circuits can be directly marked on the skin for surgical management. Ultrasound has 91–98% sensitivity and specicity in
identifying arterial and venous stenosis, and provides unique
information on the complex hemodynamic situation around
an AV hemodialysis access and its pathology. is information is more relevant for deciding about the best treatment
strategy in patients with hemodialysis access problems or
complications (e.g., low ow, peripheral ischemia, arm
swelling) than the morphologic information provided by
angiography.
4.8.1 Therapeutic Decision-Making
Color duplex ultrasound is an excellent tool for the pretherapeutic evaluation of patients with an occluded BresciaCimino stula, providing valuable information for deciding
between surgical and interventional management. Over
time, a hemodialysis access may degenerate with alternating
widening and constriction. ese changes are detectable by
ultrasound, also in patients with large arms. Luminal narrowing due to scar formation at puncture sites is sonographically characterized by a thin lumen and thickened
walls, which may additionally appear more echogenic. e
ultrasound ndings thus guide the treatment decision,
allowing identication of patients whose vascular access
problems can be managed by an endovascular procedure
with thrombectomy and those requiring surgical revision
with placement of a synthetic gra (narrowing due to scar
formation). Surgical revision is also necessary in patients
with ectatic/aneurysmal dilatation and thrombotic deposits
on the walls in conjunction with thromboembolic occlusion. Hemodynamic assessment with dierentiation of
excessive versus normal stula ow is the basis for selecting
the best therapeutic strategy when patients present with
peripheral ischemia (
e decision as to when a stenosis should be treated may
be dicult, especially in patients with a Brescia-Cimino stula that has been used for many years. Because of the degenerative changes of such stulas, characterized by the
alternation of narrowed and widened segments, higher cutos (absolute PSV or PSV ratio) than in native arteries are
required to identify therapeutically relevant stenosis. Blood
ow velocity alone is no reliable measure in a natural stula
and should always be interpreted in conjunction with stula
adequacy. Conversely, in a synthetic gra with its invariable
diameter, the PSV ratio allows reliable stenosis grading.
At the anastomosis of both native stulas and synthetic
gras, the PSV ratio is an unreliable parameter. Here, an
7 Sect. 4.7.2.1).

278
Chapter 4 · Arteriovenous Fistulas
absolute PSV of 2.5m/s suggests stenosis with beginning
hemodynamic relevance. Again, this says nothing about the
therapeutic relevance of the stenosis. On the contrary, as
long as there is adequate ow for hemodialysis, a relative
stenosis may even be desirable to prevent dialysis access
steal syndrome (DASS) with symptomatic peripheral ischemia. In these patients, elimination of the stenosis may even
be contraindicated and can inadvertently induce ischemia,
4
especially if preinterventional spectral Doppler interrogation already shows to-and-fro-ow in the feeding artery
distal to the arteriovenous anastomosis. erefore, to make
the right therapeutic decision, it is crucial to always interpret the hemodynamic sonographic ndings in conjunction
with the patient’s clinical presentation or hemodialysis
access problems.
e results of a recent study (Schäberle and Leyerer 2014)
in 51 patients with common hemodialysis access problems
(37% peripheral ischemia, 53% poor stula ow, 10% arm
swelling) conrm that the three-point ultrasound protocol
presented above (
7 Sect. 4.2.2.1) allows reliable pretherapeu-
tic identication of underlying causes and initiation of
appropriate treatment. In 47 of the 51 patients (92%), this
protocol resulted in adequate management of the underlying
problems without a need for revision of the therapeutic
approach. is study also showed the structured protocol to
be time-ecient, requiring on average 8minutes for diagnostic workup of hemodialysis access problems.
studies but on experience and data obtained in the follow-up
of synthetic bypass gras for steno-occlusive disease in
peripheral arteries of the leg.
Another issue is whether the more or less aggressive reintervention policy is justied in all patients in whom routine
surveillance reveals relevant hemodialysis-access-related stenosis. As discussed above, it is not always necessary or even
desirable to treat a stenosis as long as there is adequate stula
ow for hemodialysis. In certain scenarios, the elimination of
a stenosis might even cause a steal eect with symptomic
peripheral ischemia. While the controversy about routine
surveillance remains to be solved, it is undisputed, though,
that signs of hemodialysis access problems such as reduced
blood ow should prompt timely sonographic evaluation tailored to the clinical situation.
Timely workup is the basis for adequate and individualized management. e following listing summarizes the
hemodialysis access problems and underlying causes that are
amenable to sonographic workup and dierentiation (with
gure references in brackets):
Inadequate or low stula ow
5
5 Decreased inow due to stenosis of the feeding artery
(. Fig.4.12 (Atlas))
5 Stenosis of the anastomosis or access vein
(. Figs.4.13 and 4.15 (Atlas), . Fig.4.4)
5 Decreased drainage due to proximal venous outow
obstruction (stenosis or (partial) thrombosis)
(. Figs.4.15 and 4.18 (Atlas))
5 Partial thrombosis of access vein with reduction of
4.8.2 Surveillance Programs?
patent lumen
5 Has stula maturation occurred? (. Fig.4.21 (Atlas))
ere is an ongoing controversy about the benet of routine
duplex ultrasound surveillance in preventing thrombosis
and prolonging vascular access survival in hemodialysis
patients (Vachharajani 2012). It is undisputed, though, that
duplex ultrasound is highly accurate in detecting vascular
access stenosis (Finlay etal. 1993; Older etal. 1998; Doelman
et al. 2005), and there is published evidence showing the
benet of early revision for imminent access failure diagnosed on the basis of sonographic ow measurement (Bay
etal. 1998) or stenosis detection and grading (Older etal.
1998). is position is conrmed by a recent study showing
that, while surveillance programs result in a 2.6% higher rate
of stula interventions, they also reduce the stula thrombosis rate by 8.4% (Jiang etal. 2013). Despite the high diagnostic accuracy of ultrasound in identifying the etiologies of
vascular access problems (aneurysm, stenosis, partial thrombosis) (Pietura etal. 2005; Doelman etal. 2005), the authors
5 Inadequate stula ow due to diversion of blood ow
into (parallel) accessory veins (. Figs.4.6 and4.16
(Atlas))
5 Peripheral ischemia
5 Hyperfunctioning stula (DASS) (. Fig.4.5;
. Figs.4.10, 4.14, 4.17, and 4.20 (Atlas))
5 Arterial stenosis (. Fig.4.12 (Atlas))
5 (Prominent accessory vein (. Figs.4.6,4.16
4.20 (Atlas)))
and
5 Arm swelling
5 Stenosis/rombus of draining vein (. Figs.4.15,
4.18, 4.19, and 4.20 (Atlas))
5 Prominent accessory vein with blood ow (retro-
grade) parallel to stula ow (. Figs.4.16, 4.19, and
4.20 (Atlas))
5 Degenerative dilatation (. Fig.4.11 (Atlas)), pseudo-
aneurysm
(. Fig.4.11 (Atlas)), infection
of a large meta- analysis (Tonelli et al. 2008) and a recent
review (Paulson etal. 2013) conclude that surveillance programs are not justied because they do not lower the risk of
access loss.
Nevertheless, there are proponents of surveillance programs for native stulas, while it is undisputed that regular
monitoring of synthetic access gras does not signicantly
improve outcome. is conclusion is not based on scientic
Hemodialysis patients may present with complex clinical
problems as a result of the intricate hemodynamic patterns
that may develop in and around their vascular access over
time. Such cases require an individual sonographic approach
to obtain a comprehensive overview of the vascular situation
including possible dierential diagnoses, which is essential
for identifying the best therapeutic strategy.

4.9 · Atlas: Arteriovenous Fistulas
279
4.9 Atlas: Arteriovenous Fistulas
. Table4.5 lists the gures presented in the Atlas. e gures illustrate normal ndings, methodology, and vascular abnor-
malities in patients with an arteriovenous stula.
. Table4.5 Arteriovenous stulas– gures
Entity/Pathology Figure
4
Spontaneous AV stula
Iatrogenic AV stula
Hemodialysis access– normal ndings and volume ow measurement
Hemodyalisis access complications– high-ow stula, peripheral ischemia; volume ow measurement
Fistula ow volume calculation from measurement in the feeding artery (brachial artery) without and
with stula compression
Aneurysm of hemodialysis access– puncture aneurysm, suture aneurysm, degenerative dilatation
Stenosis of proximal feeding artery
Anastomotic stenosis
Hemodialysis access complication– peripheral ischemia, arterial steal
Hemodialysis access complication– reduced stula ow, terminal cephalic vein stenosis
Hemodialysis access complication– peripheral ischemia
Peripheral ischemia after creation of hemodialysis access– accessory vein ligation
Peripheral ischemia– arterial steal with retrograde ow in palmar arch
Outow obstruction– central vein thrombosis downstream of hemodialysis access
Peripheral ischemia– to-and-fro ow, anastomotic stenosis, accessory vein
Hemodialysis access complication– progressive swelling of forearm and hand
Failure of stula maturation due to stenosis close to anastomosis
. Fig.4.7 (Atlas), page 280
. Fig.4.8 (Atlas), page 280
. Fig.4.9 (Atlas), page 281
. Fig.4.10 (Atlas), page 282
. Fig.4.10 (Atlas), page 283
. Fig.4.11 (Atlas), page 284
. Fig.4.12 (Atlas), page 285
. Fig.4.13 (Atlas), page 285
. Fig.4.14 (Atlas), page 286
. Fig.4.15 (Atlas), page 286
. Fig.4.16 (Atlas), page 287
. Fig.4.16 (Atlas), page 287
. Fig.4.17 (Atlas), page 288
. Fig.4.18 (Atlas), page 288
. Fig.4.19 (Atlas), page 289
. Fig.4.20 (Atlas), page 290
. Fig.4.21 (Atlas), page 290

280
bc
Chapter 4 · Arteriovenous Fistulas
4
a
. Fig.4.7a–c (Atlas) Spontaneous AV stula.
a Ultrasound examination to rule out thrombosis in a patient with leg swelling. The color ow image obtained while scanning the veins at the
pelvic level shows a color bruit in the surrounding tissue, consistent with perivascular tissue vibration caused by an AV stula. There is highly
turbulent ow in the feeding common iliac artery (CIA) and in the internal iliac artery. The Doppler waveform from the internal iliac artery near the
stula shows the high diastolic ow typical of a short circuit between the arterial and venous system. The arched internal iliac artery is depicted
with turbulent ow to the level of the stula (mosaic of colors). Turbulent ow is also depicted in the common iliac vein (CIV) posterior to it. The
elongated external iliac artery (EIA) is seen anteriorly.
b Unlike the internal iliac artery supplying the stula, the external iliac artery (EIA) shows pulsatile, triphasic ow on color duplex and in the
Doppler waveform. Using intermittent spectral Doppler interrogation along the internal iliac artery and vein, the examiner can gradually
approach the site of the stula, which is identied by an abrupt increase in peak systolic and especially diastolic velocities.
c Contrast medium ow in angiography reveals the AV short circuit in the pelvis. Ultrasonography is superior to angiography in precisely localizing
the stula. The arrows indicate the iliac artery and vein
abc
de f
. Fig.4.8a–f (Atlas) Iatrogenic AV stula.
a There is continuous diastolic ow in the common femoral artery on the right compared to the contralateral side. The time-averaged velocity
(TAV) is 47.6cm/s with a peak systolic velocity (PSV) of 117cm/s and an end-diastolic velocity (EDV) of 10cm/s.
b Comparison with the unaected side shows ow in the left common femoral artery to be triphasic with a PSV of 99.8cm/s and a TAV of
22.9cm/s. The common femoral artery diameter is the same on both sides.
c The common femoral vein on the right has a pulsatile ow prole (with ow toward the center displayed in blue) characteristic of an arterialized
vein draining an AV stula (. Fig.4.2d).
d The case presented is a typical example of a iatrogenic AV stula as a complication of cardiac catheterization. This type of iatrogenic stula
nearly always develops between the supercial femoral vein and the profunda femoris artery and typically occurs when the access site in the
groin is chosen too low. The search for the stula reveals the connection between the profunda femoris artery (A.P.F; blue ow away from
transducer) to the supercial femoral vein (V.F.S) with a high-frequency ow signal (aliasing, red) and a ow velocity of over 3.5m/s. Anteriorly, the
supercial femoral artery is depicted (A.F.S; red, toward transducer).
e The Doppler waveform from the profunda femoris artery (A.P.F) proximal to the AV stula shows a large diastolic ow component and the same
ow prole as the common femoral artery.
f Distal to the AV stula (see d), the profunda femoris artery (A.P.F; coded in blue) shows a triphasic prole without end-diastolic ow. This change
in ow pattern proves that the AV stula is located between the two sampling sites (in e and f)

4.9 · Atlas: Arteriovenous Fistulas
. Fig.4.9a–c (Atlas) Hemodialysis access– normal ndings and
volume ow measurement.
a Oblique image of the anastomosis of a Brescia-Cimino stula
(end-of-vein-to-side-of-artery anastomosis) in the bend of the elbow
with marked turbulence at the anastomosis. Stretched brachial artery
coursing posterior to the anastomosis.
b The color ow image (left) shows the proximal brachial artery with
ow coded in red and mild aliasing on the left and the distal brachial
artery on the right (coded blue). The sharp transition from red to blue
appears to indicate ow reversal but is due to a change in ow
direction relative to the transducer. In the color ow image, faster
blood ow in the feeding artery is indicated by brighter colors. The
Doppler waveform from the feeding artery (right) shows a large
diastolic ow component (end-diastolic velocity (EDV) of 95cm/s).
With a calculated average ow velocity of 108cm/s and a brachial
artery diameter of 4.8mm, the ow volume in the feeding artery is
1170mL/min.
c The brachial artery segment distal to the AV stula has the typical
ow prole of arm arteries: triphasic waveform without an enddiastolic component. The ow volume calculated for the brachial artery
segment just distal to the venous anastomosis is 129mL/min
(0.16cm2×60×13cm/s). The stula ow volume, calculated as the
dierence in ow volumes between the brachial artery upstream and
downstream of the venous anastomosis, is 1040mL/min
281
a
4
b
c

282
cd
Chapter 4 · Arteriovenous Fistulas
4
a
. Fig.4.10a–j (Atlas) Hemodyalisis access complications– high- ow stula, peripheral ischemia; volume ow measurement.
Excessive stula ow can lead to dialysis access steal syndrome (DASS) with ischemia of the hand or cardiac insuciency. Since hemodialysis
patients often have considerable comorbidity, the stula must be examined as a possible cause of newly occurring signs of cardiac insuciency.
Duplex ultrasound is the simplest and most reliable method for estimating the ow volume in the AV stula. A more reliable method for determining stula ow volume (compared with the method illustrated in . Fig.4.9b, c) is measurement of the ow volume in the brachial artery in both
arms with calculation of the stula ow volume as the dierence between the stula-bearing arm and the non-stula-bearing arm.
a When this feature is available, the system’s software calculates the mean time-averaged velocity (TAV) from the Doppler waveform recorded
with an angle of less than 60° (144cm/s in this case).
b At the same site, the vessel diameter is measured in the B-mode scan (6.5mm). For accurate calculation of the vascular cross-sectional area, the
systolic and diastolic diameters have to be measured (using the leading-edge method, . Fig. 1.28) and weighted at a ratio of 1:2. This is done in
the time-motion mode with an angle of insonation perpendicular to the vessel (i.e., as close to 90° as possible). In the example, a ow volume of
2778mL/min is calculated from the mean TAV and cross-sectional area.
c The same measurements are performed in the brachial artery of the non-stula-bearing arm, where the ow prole is triphasic with a mean TAV
of 21.9cm/s.
d After calculation of the mean cross-sectional area from the systolic and diastolic diameters, a mean ow volume of 108mL/min is calculated.
The example also illustrates the ow-induced dilatation of the arterial vessels as a cause of increased ow in long-standing AV stulas (the
diameter dierences between the views with spectral Doppler displays (a, c) and those with time-motion displays (b, d) are due to the use of
dierent scales).
e–j Fistula ow volume calculation from measurement in the feeding artery (brachial artery) without and with stula compression.
e Patient presenting with peripheral ischemia and clinical dilation of the access vein 11years after establishment of an AV stula in the bend of
the elbow. Sonographic measurement reveals dilatation of the feeding brachial artery with a systolic diameter of 6.8mm and diastolic diameter of
6.4mm, from which a vascular cross-sectional area of 0.34cm2 is calculated (with 1:2 weighting of systolic and diastolic diameters).
f Without compression of the stula, the brachial artery upstream of the AV anastomosis has a time-averaged velocity (TAV) of 120cm/s with a
ow prole characteristic of an artery feeding an AV stula.
g With manual compression of the stula, TAV determined at the same site in the brachial artery is 10cm/s, and the waveform is triphasic (which is
the pattern characteristic of high-resistance ow in peripheral arteries). The stula ow volume calculated from these measurements is high and is
diagnostic of a hyperfunctioning AV stula: 0.34 × (120–10)=37.4cm3/s or 2.24l/min (cross-sectional area multiplied by (TAV without stula
compression minus TAV with stula compression)).
h Distal to the AV anastomosis, the brachial artery shows retrograde ow with a monophasic waveform, consistent with arterial steal.
i With manual compression of the AV stula, there is normal ow to the periphery with a triphasic waveform in the distal brachial artery.
j Dilated access vein with large caliber variation (in part with oval vessel cross-section) and turbulent ow, which precludes reliable direct ow
volume determination in the access vein
b

4.9 · Atlas: Arteriovenous Fistulas
283
4
diameter
B-mode
e
distal to
AV anastomosis
time-motion display
without fistula
compression
brachial arterybrbbr
f
distal to
AV anastomosis
without
fistula compression
with
fistula compression
hi
. Fig.4.10 (continued)
brachial artery
with fistula
compression
g
access vein
j
Соседние файлы в папке Библиотека им академика М.И. Перельмана
