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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3591_Библиотеки_им_академика_М_И_Перельмана.pdf
348
J. Valakkada et al.
a
d
Fig. 28.1 Diagrammatic representation of common arteriovenous stula congurations (a–d) and ultrasound imaging of a mature AVF (e
and f). Radiocephalic stula at the wrist (a) showing ligated cephalic
vein (arrowhead) with end-to-side anastomosis (arrow) of the cephalic
vein to the radial artery. Brachiocephalic stula (b) shows ligated
cephalic vein (arrowhead) with end-to-side anastomosis (arrow) to the
brachial artery, brachio-basilic stula (c) showing ligated basilic vein
b
e
c
f
(arrowhead) and end-to-side anastomosis (arrow) to the brachial artery.
AV graft (d) with PTFE arteriovenous loop graft (arrow) between the
cephalic vein and brachial artery. Axial grayscale ultrasound image (e)
and long axis color Doppler image with spectral tracing (f) of the draining cephalic vein of a mature brachiocephalic stula showing diameter
of 6.6mm (>6mm) with ow of 830ml/min (>600ml/min)
steal syndrome and ischemic monomeric neuropathy [7].
However, it has the disadvantage of a low rate of maturation
and low ow rates [8, 9]. Brachiocephalic stula (BCF) is
the next choice. However, it can be created upfront in
patients with multiple comorbidities as it has better maturity
and patency rates [10]. Though BCF has the advantage of
the ease of creation, high maturation rate, and good ow
rate, it has a high incidence of arterial steal and symptomatic central venous stenosis due to high ow [11, 12].
Brachial transposed basilic vein stula (BTB) is considered
when both of the above options are not feasible. It can be
done in a single stage or in two stages wherein the basilic
vein is transposed later on to the subcutaneous plane. Both
types of procedures have similar patency and failure rates
[13–15]. A two-stage procedure is usually used in small
basilic veins but has the disadvantage of a delay of 4–8weeks
for stula maturation [15]. The native stula usually matures
in around 4–6 weeks. The anatomical sites of AV stula
with the advantages and disadvantages of each are summarized in Table28.1.
28 Endovascular Interventions inHemodialysis Access Fistulas
Table 28.1 Anatomical sites of AV stula with advantages and disadvantages of each
Access type Common sites of stenosis Advantages Disadvantages
Radiocephalic stula
(RCF)
Brachiocephalic stula
(BCF)
Brachial to transposed
basilic vein stula (BTB)
Juxta- anastomotic site Easy to create
Juxta- anastomotic
Cephalic arch
Proximal swing segment High rates of maturation
Low rate of steal syndrome
Rare ischemic monomelic
neuropathy
Upstream vein will be saved to
create future new access
High rates of maturation
High ow rates
Easy to create
High ow rates
Low rate of maturation
Low ow rate
High chances of steal syndrome
High chances of central venous stenosis
Increased ischemic monomelic neuropathy
Difcult to create
High chances of steal syndrome
High chances of central venous stenosis
Increased ischemic monomelic neuropathy
349
28.3 Clinical Presentation ofDysfunctional
Fistula
28.3.1 Stages oftheFistula
The clinical presentation depends on the stage of the stula
(Table28.2).
Nonmaturation of Fistula It occurs if the arterial and
venous diameters are inadequate or there are early surgical
complications like infection or anastomotic site stenosis.
Maturation time may get prolonged if the veins are small in
caliber and if there is an early draining vein preventing adequate arterialization. They are also seen in diabetics and
patients with severe atherosclerotic narrowing of the arteries.
Early Failure of Matured AVF A matured stula can show
signs of failure such as increased time of dialysis (>4h), prolonged bleeding during dialysis, and reduced thrill. The etiology includes stenosis at the venous side (most common),
anastomotic site, or rarely in the artery proximal to the stula. Stenosis in the venous segment is the most common
cause of a failing stula. Usually, hemodynamically signicant stenosis is dened as 50% luminal narrowing or a
75–80% decrease in the cross-sectional area. Venous stenosis
is mainly due to intimal hyperplasia as a result of endothelial
injury produced by surgical trauma at the time of access creation, inammation, uremia, hypoxia, hemodynamic shear
stress, or vessel wall injury from needle punctures.
Endothelial injury leads to increased leukocyte proliferation
and smooth muscle cell migration from the media to the intimal layer [16].
Early draining veins cause shunting of blood reducing the
effectiveness of dialysis. Partial thrombus can also lead to
reduced ow in a matured stula. These patients need to be
picked up early by USG surveillance and treated as they are
prone to acute thrombosis of stula. Patients can present
with acute thrombosis of the stula due to acute hypotension, venous stenosis, venous aneurysm, or infection.
Venous Hypertension
The prevalence of central vein ste-
nosis is about 10% in patients on dialysis AVF access and
13% among patients with tunneled central venous dialysis
catheters [17]. These patients present with limb edema, facial
edema, and dilated veins. They occur commonly due to
venous hypertension resulting from a central vein or proximal cephalic vein stenosis. The prior use of central line catheters in these patients predisposes them to thrombosis or
narrowing of central veins. High-output cardiac failure that
presents similarly albeit with involvement of the contralateral limb and legs needs to be differentiated from venous
hypertension.
Limb Claudication and Ulcer Some patients present with
arterial steal phenomenon manifesting as ischemic pain, gangrenous changes, or altered sensations in the distal limb.
Arterial steal is more common with BCF compared to RCF
owing to the larger diameters of former vessels. It is important to differentiate true steal syndrome from distal atherosclerotic disease presenting as ischemia as there is a limited
role for endovascular intervention in the former. Restoration
of ow or improvement in ischemic symptoms occurs after
compression of the stula points out to an arterial steal.
Other Presentation Uremic mononeuritis can masquerade
the digital ischemic symptoms. Other presentations include
seroma, abscess, hematoma, or pseudoaneurysm at the
venous access site or the anastomotic region.
350
Table 28.2 Clinical presentation with causes of dysfunctional stulas
Clinical presentations Causes USG ndings
Nonmaturing stulas Vascular stenosis (in the outow vein or at
Reduced ow
Reduced thrill
Increased time for hemodialysis
No ow
No thrill
Failure to cannulate
Acute thrombus during hypotensive
phase of dialysis
Limb edema with dilated veins
Increased/prolonged bleeding during
dialysis
Ischemic pain in limb Arterial steal phenomenon True steal: No ow distal to AVF site, but ow
Tingling or mononeuropathy Uremic mononeuritis
the anastomotic site)
Competitive outow veins
Deep outow vein that is nonpalpable
Stenosis at venous site, anastomotic site, or
artery site
Early draining veins
Aneurysmal dilation with partial thrombus
Acute thrombosis
Stenosis
Hypotension phase during dialysis
Infection
Aneurysmal dilatation
Central vein stenosis
High ow stula (may cause high- output
cardiac failure)
Polyneuritis
Periodic limb restlessness
Small vein diameter<6mm
Low ow rate<600ml/min
Distance from skin >6mm
Flow <500ml/min
Any evidence of stenosis in the entire circuit or any
early draining veins present has to be examined
Echogenic thrombus
Extent of occlusion
Dilatation and tortuosity of the outow vein
Central vein stenosis: Flow rate within normal range
or slightly reduced, indirect evidence—Loss of phasic
variation in jugular veins
High ow stula: Flow rate>1.5L/min
reappears after compression of the AVF, ow reversal
in the distal radial artery (from the ulnar artery) may
be seen
Pitfall: Flow reversal seen only in diastolic phase is
usually asymptomatic
Normal Doppler ndings
Nerve conduction studies
J. Valakkada et al.
28.3.2 Imaging Evaluation
Ultrasound Doppler is the preferred imaging modality before
the creation of AVF.Artery diameter >2mm, vein diameter
>2.5mm, depth from the skin less than 5 mm, absence of
early draining vein, and absence of central vein obstruction
need to be conrmed on Doppler prior to the stula creation.
Though the maturity of the stula is assessed based on the
thrill and adequate ow rate during dialysis, ultrasound surveillance is gaining importance in detecting early stula malfunction. Ultrasound criteria for an adequate stula
(Fig.28.1) include access vein diameter >6 mm, ow rate
>600ml/min, and distance from skin ≤6mm (Rule of 6).
Ultrasound is also the initial imaging modality in failing
stulas. A ow rate <300–500ml/min, narrowing in the stula circuit, elevated peak systolic velocity (PSV) at the stenotic site (≥375cm/s), PSV ratio (>2:1) between the stenotic
segment and vein 2cm caudal are signs of signicant venous
stenosis [18]. USG can also reveal acute thrombus forming
secondary due to venous stenosis, acute hypotension, venous
aneurysm, or infection. USG can show indirect evidence of
central vein stenosis by loss of phasic variation in jugular
veins. This phasic variation may be appreciable if compression at AVF site is done. In high ow stula causing highoutput cardiac failure, the ow rate will be in the range of
1500–2000ml/min. It is important to differentiate the etiology in such patients since central vein stenosis requires
angioplasty or stenting of the vessel while high-output stula
requires closure of the stula.
CT venography is recommended only in the evaluation of
the central veins wherein the ultrasound ndings are inconclusive. CT can identify the site and extent of occlusion, the
presence of any distal stump, and the status of the contralateral brachiocephalic and subclavian veins. The patient can
undergo dialysis after CT scan to reduce the risk of contrastinduced osmotic uid overload. The use of contrast MRI is
not recommended due to the risk of nephrogenic systemic
brosis. Invasive angiogram is done if therapeutic procedure
is planned. It can also demonstrate the steal syndrome or distal arterial disease and delineate distal vasculature anatomy
for surgical reconstruction.
28.3.3 Pre-procedure
andIntraproceduralCare
There are some hemodynamic and physiological changes in
ESRD patients that need to be kept in mind during endovascular interventions (Table28.3). These patients have altered
hemodynamics with mild uid volume overload. So cautious
28 Endovascular Interventions inHemodialysis Access Fistulas
Table 28.3 Hemodynamic issues in patients on hemodialysis
Parameters Signicance
Fluid overload Patient is already in uid overload status
Serum potassium (K
Pulmonary edema Presents with dyspnea, may develop due to excess uid administration
Acidosis Metabolic acidosis with compensatory respiratory alkalosis
Contrast No risk of contrast-induced nephropathy as the kidneys are already nonfunctioning
Coagulation Functional thrombocytopenia: Aspirin is not required to prevent restenosis after angioplasty or stenting
Fluid restriction should be done before, during, and after the procedure
Usual volume of uids for 24hours: Urine output +500ml
+
) Thrombolysis and any declotting procedures may aggravate hyperkalemia
Pre-procedure dialysis has to be done to maintain K
ECG monitoring to detect tall T waves indicating hyperkalemia
High ceiling loop diuretics (e.g., furosemide) decreases the preload by shifting uid to the peripheral venous
compartment in the setting of pulmonary edema
May present with breathing difculty which has to be differentiated from dyspnea due to pulmonary edema
Risk of uid overload present: Iso-osmolar contrast agents preferred
Vicarious excretion of contrast through the bowel or liver can occur in ESRD patients
Prolonged heparin T
: Judicious use of heparin, avoid newer anticoagulants
1/2
+
levels within normal range
351
use of intravenous uids is necessary to prevent volume
overload and pulmonary edema. The daily uid requirement
is calculated by adding 500ml (which is required for basic
metabolism/sweating) to the 24-h urine output volume. In
addition, the dyspnea of pulmonary edema needs to be differentiated from compensatory nonlabored hyperventilation
in metabolic acidosis. As the kidney has no diuretic function,
only high ceiling loop diuretics (like furosemide) can be
given to decrease pulmonary edema which decreases preload
by shifting the uid to the peripheral venous compartment.
Fluid overload can be caused by using hyperosmolar contrast
agents. Hence iso-osmolar contrast agents (iodixanol) are
preferred which will reduce the volume overload to some
extent. These patients have platelet dysfunction [19] and
aspirin or other antiplatelet agents may increase the risk of
bleeding. Judicious usage of heparin is needed as its half-life
is prolonged in CKD patients. It is wise to avoid newer oral
anticoagulants that have renal excretion.
28.4 Endovascular Management
28.4.1 Nonmature Fistulas
The treatment is directed to the cause of nonmaturation. Any
early draining vein can be ligated surgically or coiled
(Fig. 28.2) via the endovascular route [20]. Poor arterial
inow can be corrected by balloon angioplasty of the feeding
artery. Balloon-assisted maturation of the stula can be done
if the parent vein is small caliber (<2 mm) (Fig. 28.2).
However, any nonmature stula requiring ≥2 interventions is
a poor prognostic indicator for maturation. In case of deep
nonpalpable vein, surgical transposition of the vein to a
supercial location should be done.
28.4.2 Anastomotic andJuxta-Anastomotic
Venous Stenosis
Management includes venoplasty (Fig.28.3) or stenting for
the stenosis. The access can be preferable venous access.
Depending on the site of stenosis, retrograde or antegrade
venous access can be created. Arterial access is used only if
it is difcult to cross the anastomotic site from the venous
end (Fig.28.4). It is preferable to use a micropuncture set
needle (21G) under USG guidance for access. It is better not
to have access above the elbow in radio cephalic stula, as it
may prevent the future creation of BCF.
The choice of the balloon is based on the adjacent normal
vein and the length of the stenosis. It should be 20–30%
larger than the diameter of the normal vein adjacent to the
stenosis. Balloon length should match the length of the stenosis. It minimizes barotrauma to the adjacent normal vein
thereby reducing the risk of restenosis. As these stenoses are
rm due to neointimal hyperplasia, often high/ultrahigh
pressure balloons were needed (rated burst pressure of
≥20atm, ultrahigh pressure balloons of >30atm). In recalcitrant lesions, cutting balloon angioplasty can be done, and it
has shown signicantly higher patency rates than conventional balloon angioplasty in a few studies [21]. There are
multiple diverse results of long-term patency of drug-coated
balloons in such stenosis [22–24]. In case of immediate
recoil of the vein or multiple episodes of restenosis, stenting
can be performed using self-expanding stents and interwoven stents with good midterm patency. Chan et al. [25]
showed an increase in access ow and primary patency in AV
grafts, but no differences in primary patency of AV stulae
after stent placement. A covered stent can be placed for longer patency, and in cases of venous rupture not respond to
prolonged balloon ination. The cephalic vein entry to the
352
bc
J. Valakkada et al.
a
def
Fig. 28.2 Nonmaturing stula. Digital subtraction angiogram images
(a–c) of a patient who presented with a nonmaturing right brachiocephalic stula due to small caliber cephalic vein (arrows in a). Balloonassisted maturation of the stula (arrow in b) was done via the radial
artery access with opening (arrow in c) of the stula. DSA images (d–f)
of a patient who presented with difculty in vascular access of his left
subclavian vein is also prone to stenosis and kinking.
Venoplasty at this segment is more prone to rupture and
recoil (Fig.28.5).
Technique-related complications include vein rupture
[26, 27] during balloon ination and can be treated with
manual compression, balloon tamponade, or graft placement. Venous thrombosis caudal to the sheath can be treated
with mechanical aspiration or heparin injection. Distal arterial emboli if symptomatic should be removed by using different techniques including aspiration or mechanical
thrombectomy.
brachiocephalic stula showing stenosis at the anastomotic site (arrowhead in d) and an early draining vein (arrow in d). Balloon angioplasty
of the stenotic segment (arrowhead in e) with coiling of the early draining vein (arrow in f) was done after which there was a reappearance of
thrill with increased ow through the stula
28.4.3 Acute Thrombosis
Acute thrombosis is associated with underlying venous
stenosis in about 85–90% of cases [28]. Apart from endothelial injury, other mechanisms like elevated anti-protein
C and anti-protein S antibodies contribute to thrombosis
[29]. Treatment involves thrombectomy or thrombolysis
(Fig.28.6). If the thrombus is acute (<2weeks old), most
of the thrombus can be removed by thrombolysis.
However, as the age of the thrombus increases, the addition of a mechanical device may be needed in addition to
28 Endovascular Interventions inHemodialysis Access Fistulas
353
a
d
Fig. 28.3 Venous stenosis. Digital subtraction angiogram images (a
and b) of a patient who presented with a failing brachiocephalic stula
showing multifocal stenosis at the anastomotic site and in the draining
cephalic vein (arrows in a and b) with good opening of the stenotic segments after balloon angioplasty (arrow in b). DSA images (c–f) of a
patient with a failing left radiocephalic stula due to short-segment
b
e
c
f
cephalic vein stenosis (arrow in c). The chronic stricture did not yield
with balloon venoplasty (arrow in d) after which a cutting balloon
(arrow in e) was used. Post-venoplasty angiogram showed complete
opening of the stenotic segment (arrow in f) with good ow across the
cephalic vein
the pharmacotherapy. Pharmaco-mechanical thrombectomy (PMT) involves the injection of a lytic agent with
suction of the thrombus. Underlying stenotic lesions that
are unmasked after de- clotting should be treated using
angioplasty. Failure of thrombolysis occurs in long seg-
ment thrombus, large thrombus load, chronic thrombus,
venous pouches with thrombus, and pseudoaneurysm with
thrombus. Coagulopathy, stula site infection, and intracardiac right to left shunt are absolute contraindications
for thrombolysis.
354
J. Valakkada et al.
a
bc
def
Fig. 28.4 Access routes. Digital subtraction angiogram showing various access routes for performing endovascular interventions in a failing
hemodialysis stula: Radial artery access (arrow in a) for a failing radiocephalic stula due to stenosis in the juxta anastomotic cephalic vein
(arrowhead in b). Balloon angioplasty of the stenotic segment (arrowhead in b) was done with a satisfactory opening (arrowhead in c) and
good ow through the stula. Combined femoral vein (arrow in d) and
radial artery access (arrow in e) for a failing radiocephalic stula due to
stenosis in the cephalic vein. Brachial artery access (arrow in f) for
venoplasty of a stenotic cephalic vein in a failing brachiocephalic
stula
bc
ef
28 Endovascular Interventions inHemodialysis Access Fistulas
a
355
d
Fig. 28.5 DSA and venogram images (a to d) of a patient with right
brachiocephalic stula who presented with right upper limb edema and
decreased ow rate through the stula on ultrasound showing short segment tight stenosis (arrow in a) of the cephalic vein at the cephalic arch,
proximal to where it drains into the subclavian vein (arrowhead in a)
which did not yield to balloon venoplasty (arrow in b), following which
a cutting balloon (arrow in c) was used. Post-procedure angiogram
showed good opening of stenotic segment (arrow in d). DSA image
showing extravasation of contrast (arrow in e) after attempting to cross
a stenotic segment in the cephalic vein at the cephalic arch. A balloon
was inated at the site of contrast extravasation for 5min, after which
venograms revealed cessation of the extravasation (arrow in f)
356
bc
J. Valakkada et al.
a
d
Fig. 28.6 Acute thrombosis. DSA images (a to c) show acute throm-
bosis of the cephalic vein in left radiocephalic stula (arrow in a).
Suction thrombectomy was done with post-procedure angiograms
showing signicant reduction in the thrombus load (arrow in b) and
aspirated thrombi (c). Axial ultrasound image (d) and DSA image
e
28.5 Central Venous Stenosis
These patients require opening of the stenotic or occluded
segment (Fig.28.7). A short segment stenosis or occlusion
can be effectively managed by angioplasty alone with large
f
(arrow in e) showing thrombosis of the juxta anastomotic cephalic vein
of a brachiocephalic stula. 5 mg Alteplase was instilled along the
length of the thrombus. Post-thrombolysis venogram showed near total
lysis of the thrombus with good opacication of the distal cephalic vein
(arrow in f)
diameter balloons (12–20mm) if recoil is not present post
angioplasty. The access can be from the venous end of stula
or common femoral vein or both depending on the site of the
occlusion and the presence of a favorable stump for parking
the catheter and negotiating the guidewire. Multiple tech-
28 Endovascular Interventions inHemodialysis Access Fistulas
357
ab
d
Fig. 28.7 Central vein stenosis. An ESRD patient on maintenance
hemodialysis presented with left upper limb edema and pulsatile thrill
felt over his left brachiocephalic stula indicating patency. DSA images
showing stenosis of the left brachiocephalic vein (arrow in a), and stent
was placed. Moderate residual stenosis (arrow in b) persisted after
stenting for which balloon angioplasty was performed with satisfactory
niques like sharp recanalization, long Chiba needle, ColaPinto needle, radiofrequency wires, and inside-out access
catheter system have been tried to increase the success rate
of recanalization [30]. Similar to juxta-anastomotic stenosis,
high-pressure balloons and cutting balloons may be
attempted. Various techniques are employed for the long segment stenosis (Fig.28.8). Failed angioplasty or recoil mandates the placement of a stent [5]. A self-expanding stent is
better than balloon mounted stent as it prevents elastic recoil,
and its lumen increases over time [31]. Stent graft patency
e
opening of the stenotic segment (arrow in c). The patient presented
3months later with similar symptoms. Venogram revealed in-stent stenosis (arrow in d) for which balloon angioplasty (arrow in e) was performed. Post-procedure venogram showed a signicant reduction of the
stenosis (arrow in f)
rates at 3, 6, 12, and 24months were 97%, 81%, 67%, and
45%, respectively, compared to bare metal stents (40–50%
over 1year) [32]. Acute complications during the procedure
include venous rupture, cardiac tamponade, hemothorax,
stent migration, and post-stent pulmonary edema. Late complications include in-stent restenosis due to intimal hyperplasia. The patients can be placed on active surveillance and
primary-assisted angioplasty to improve the patency rates.
Occluded stents can be treated with balloon angioplasty
(secondary-assisted angioplasty).
c
f