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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3722_Библиотеки_им_академика_М_И_Перельмана
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6 Arterial Revascularization
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Fig. 6.60 Mini-crush technique
Crushed side
branch stent
Double barrel•
Neocarina•
157
deployed simultaneously from proximal main
vessel into each respective bifurcating vessel
(side branch, main branch).
• Similar to technique used for aorto-iliac bifurcating lesions with kissing technique used
there.
• Best for shallow angles (60° to 90°).
• Less time-consuming as no need to re-cross
for KBI.
• The downside is that it is theoretically creating a smaller lumen in the proximal main vessel with neocarina.
• Steps: Wire both side branch and main branch
and place appropriately sized stents in each
vessel with proximal ends of both stents protruding in the proximal main vessel.
Simultaneously inate both stents.
6.12 Distal Emboli Management
S.JayMathews
Fig. 6.61 Kissing stent technique
gle layer of stent is left behind in the main vessel proximal to the bifurcation.
• Steps: Side branch is wired, and stent is placed
in the side branch with small portion of proximal portion of stent protruding into main
vessel. Next, the main branch is wired, and
stent is placed in the main branch of bifurcation protruding out into main vessel and
deployed such that it “crushes” the proximal
portion of the side branch stent against the
vessel wall. Finally, the side branch is rewired
and KBI is performed.
6.11.5 Kissing Stent Technique
(Fig.6.61)
• New metallic neocarina created in proximal
main vessel (i.e., TP trunk) as two stents
6.12.1 Introduction
Any peripheral intervention carries the inherent
risk of distal embolization (DE). Mitigation of
this risk involves identifying patients at highest
risk, those who will be most impacted adversely
by embolization, and intraprocedural prevention
strategies.
Embolic debris is seen in most peripheral
arterial interventions, occurring in 70–100% of
cases as seen by examination of embolic protection or by Doppler studies [153]. However, clinically signicant embolic lesions requiring
mechanical or pharmacomechanical treatments
remain low (<3%) [153, 154]. TASC
(Transatlantic Inter- Society Consensus) II D
lesions, angiographic thrombus, and prior history of amputations are independent predictors
of DE [154]. In addition, patients with critical
limb ischemia, greater number of treatment vessels, and emergent cases seem to have higher
DE [153]. The use of atherectomy devices can
also lead to DE [155].
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I. Ali et al.
6.12.2 Prevention
In appropriate patients, distal embolic protection
devices (EPD) may mitigate macroembolic
debris.
• Most embolic protection lter devices feature
a pore-size between 100 to 150 micrometers,
potentially allowing microembolic material
below that size.
• While typically not clinically signicant, this
material can lead to no-reow in various vascular beds. An alternative to traditional EPD
devices is use of external compression.
• The “HIRANODOME” (Interim hemostatic
technique with HIgh pressure for Regional
blood ow in the supercial femoral Artery,
NOninvasive Distal protection Occlusion
MEthod) technique utilizes an external band
to compress the popliteal artery [156].
• Alternatively, the use of pneumatic compression with a blood pressure cuff inated over
the calf may also be effective [157]. With distal
compression during proximal intervention, a
column of static blood is created which can be
removed with manual or mechanical aspiration
thrombectomy. In this fashion, DE can be
reduced. Distal compression carries the advantage of not requiring specialized EPD, trauma
to the intima with inadvertent EPD migration,
or distal “spillover” from a full EPD.
In patients at high risk for DE, prophylactic
EPD may be advised. Some have proposed use of
lters in patients with chronic total occlusion, instent restenosis, thrombotic lesions, calcic
lesions >40 mm, and long-length lesions
(>140mm) [158]. Complex patients with single-
vessel runoff or use of atherectomy devices may
warrant EPD placement.
• While EPD does offer some protection, it is
not without some risk as DE can still occur
despite use (>4% in one series) [159].
• In general, in the presence of acute or subacute
thrombus, thrombectomy should be performed
to reduce the risk of distal embolization and
avoid overwhelming the capabilities of an EPD.
6.12.3 Treatment
Treatment strategies for distal embolization
depend on pathology.
• Macrovascular arterial thrombotic embolization may respond to simple aspiration (manual
or powered).
• Microvascular embolization (<1 mm) may
respond to infusion of thrombolytics for 6 to
24h post-procedure.
• In the setting of extensive thrombosis, it may
be necessary to perform lytic (TPA) infusion
in order to separate out discrete atherosclerotic disease from thrombotic material.
• Cholesterol, atheromatous debris, and calcium fragments will not respond to lysis
[160]. A combination of aspiration and
thrombolysis may be effective [161]. In this
situation, direct-powered aspiration devices
like Indigo Lightning 7 or CAT Rx for tibial–
pedal vessels (Penumbra, Inc.) may be effective [162].
• Thrombectomy devices like the Wolf (Boston
Scientic, Inc.) may have greater extraction
force than powered aspiration devices as it uti-
6 Arterial Revascularization
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159
lizes a nitinol weave to ingest mixed morphology material in antegrade fashion.
• Basket embolectomy devices (e.g., Pounce
[Surmodics, Inc.], Excipio SV [Contego,
Inc.], etc.) may also have a role with removal
of calcic debris, but risk further distal
embolization as the device needs to be
Fig. 6.62 Occlusion of the distal popliteal, tibioperoneal
trunk, and proximal anterior tibial arteries due to distal
embolization
advanced beyond the occlusion before
removal.
• Combination aspiration and extraction techniques may be effective. Atherectomy and/or
PTA may restore ow with discrete lesions,
but also carries the risk of further distal embolization. Some operators have proposed using
small underinated balloons (2–3mm in size)
and performing Fogarty embolectomy into an
aspiration catheter.
6.12.4 Case Example
A 75-year-old woman with diabetes, chronic kidney disease, dyslipidemia, and former tobacco
abuse presented with Rutherford 4 symptoms.
During inow intervention of the SFA, she developed DE with occlusion of both the anterior tibial
and tibioperoneal trunk (Fig.6.62). Mechanical
powered aspiration thrombectomy utilizing the
Indigo Lightning 7 catheter (Penumbra, Inc.) was
rst performed into the tibioperoneal trunk. Due
to difculty in crossing due to the presence of tibioperoneal disease, a balloon-assisted tracking
technique was used with an underinated 3mm
balloon (Fig.6.63a). The catheter was advanced
during balloon deation with simultaneous aspiration. Then aspiration was performed into the
anterior tibial artery (Fig.6.63b). There was dissection seen in the tibioperoneal trunk
(Fig.6.64a). Flow restoration was demonstrated
with intact three-vessel runoff after drug-eluting
stent placement into the tibioperoneal trunk
(Fig.6.64b).
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I. Ali et al.
Fig. 6.63 Advancement of the Indigo Lightning 7 catheter (A– tibioperoneal trunk; B– anterior tibial artery)
Fig. 6.64 Final angiography (a– post-thrombectomy; b– post-stenting of the tibioperoneal trunk)
6 Arterial Revascularization
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161
6.13 Blue Toe Syndrome
Management
Sabeen Dhand, MD
Blue toe syndrome is manifested by a cyanotic
toe caused by ischemia from small end artery
occlusion, most commonly due to atheroembolic
disease. Several other conditions may also present with blue discoloration of toes and a careful
history, physical exam, and noninvasive workup
can aid in the diagnosis and management of this
condition. Here, we will discuss the condition as
well as the appropriate workup and management
of syndrome.
Presentation: Sudden onset of a unilateral,
painful blue toe (Fig.6.65). Can also present with
multiple toes and/or involve both feet depending
on the etiology.
Causes: Several causes of blue toe syndrome
exist, which all relate to a common mechanism:
Obstruction of the small digital arteries supplying the toe leading to ischemia [163, 164]. A
careful history from the patient can help determine the etiology of the syndrome.
1. Embolic Disease (most common):
Most embolic causes are related to atherosclerotic and aneurysmal sources. Unstable,
friable plaques can result in fragmentation
and emboli of cholesterol debris and/or brinoplatelet aggregates into the tiny arteries of
the digits. This results in mechanical occlu-
Fig. 6.65 Bluish, purplish discoloration of the rst digit on the left foot
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I. Ali et al.
sion of the digital artery, with development of
ischemia that characteristically presents with
cyanosis and pain [163–166].
Most lesions are from the infrarenal
abdominal aorta to the distal popliteal artery.
Suprarenal lesions usually present with visceral organ ischemia (i.e., splenic or renal
infarct) rather than lower extremity digital
ischemia, although these may still occur [163,
164]. Similarly, intracardiac thrombus and or
valvular vegetative disease can also serve as a
source for emboli [163, 164, 167].
2. Vasculitis:
Inammation of blood vessels results in
vasospasm and/or immune complex deposition, resulting in endothelial proliferation,
eventually narrowing or obstructing digital
arteries. Since vasculitides are systemic,
involvement is usually bilateral and
symmetric. A commonly referred to disorder
includes Raynaud’s disease, although other
examples include microscopic polyarteritis,
polyarteritis nodosa, and system lupus erythematosus [163, 164].
3. Hyperviscosity:
Blood viscosity increases when there is
increased cellularity (red blood cells, platelets, proteins, etc.). This increased thickness
slows down blood ow leading to stasis and
promoting thrombosis of digital arteries.
Conditions include polycythemia, leukemia,
cryoglobulinemia, and macroglobulinemia.
Findings can often involve multiple toes, can
be bilateral, or also involve larger arteries and
organs [163, 164].
4. Hypercoagulability:
Numerous conditions are associated with a
tendency to thrombosis due to abnormal blood
vessels, platelets, or coagulation factors.
Again, thrombosis leads to focal digital ischemia, frequently involving multiple digits or
other vascular territories. Examples include
malignancy, antiphospholipid syndrome,
essential thrombocytopenia, and disseminated
intravascular coagulation [163, 164].
5. Calciphylaxis:
Calcium deposits and accumulates in blood
vessels and the skin, resulting in obstruction
of arteries, as well as skin lesions, including
ulcerations and even gangrene. This condition
is rare and serious, carrying a very high mortality rate [164, 168].
6. Medications:
Anticoagulation and thrombolytics can
destabilize friable plaques and promote fragmentation of cholesterol or brinoplatelet
emboli into distal vascular beds [164, 169,
170]. Corticosteroids have also been shown to
cause blue toes due to inhibited platelet activation in the setting of endothelial damage,
thus exacerbating a hypercoagulable or hyperviscous state [171].
Illicit drug use is also associated with blue
toes, including cocaine and amphetamines, as
result of vasoocclusive disease [172].
7. Iatrogenesis:
A recent angiogram can disrupt atheroscle-
rotic lesions, promoting fragmentation and
embolization. This can be related to the wire
or from intervention, such as angioplasty
[163, 164].
Any podiatric surgery that manipulates the
foot or toes can also damage the vascular bed
within the forefoot, leading to temporary or
permanent digital ischemia [164, 173].
8. Nonocclusive mimickers of blue toe syn-
drome: trauma (ecchymosis, venous hemorrhage), reex sympathetic dystrophy, and
acrocyanosis [164].
6.13.1 Physical Examination
• Initially petechia, then bluish or purplish dis-
coloration, or mottling of the toes.
• Partial or entire involvement of the toe– usu-
ally well demarcated.
• Distribution: single toe, multiple toes, or
bilateral.
• Ulceration or gangrene may be present.
• Sluggish capillary rell.
• Cool to touch.
• Tender to palpation or manipulation.
• Palpable pedal pulses often present.
• Proximal livedo reticularis: blue-red mottling
of the foot or calf (Fig.6.66).
6 Arterial Revascularization
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(Fig. 6.67). Even if a femoropopliteal lesion is
identied on duplex ultrasound, CTA, or MRA is
still recommended, since these modalities better
characterize the morphology and location of the
lesions, which signicantly aids in treatment
planning and device selection (Fig.6.68).
Therefore, when atherosclerotic disease is
suspected as a cause for blue toes, workup should
begin with duplex sonography of the lower
extremities followed by CTA or MRA covering
the entire length of the aorta and the bilateral
lower extremities. Morphology characteristics
that are seen on these studies include severe focal
stenoses/occlusion, noncalcied ulcerated
plaques, and penetrating ulcers [174, 175].
Aneurysms at any location with irregular mural
thrombus are also at risk for peripheral
embolization.
If a cardiac source is suspected, echocardiography (transthoracic or transesophageal) is recommended [163]. In addition, intravascular
ultrasound (IVUS) during endovascular therapy
can also further delineate and characterize vulnerable plaques [176].
In cases where no obvious embolic source is
identied, then other systemic causes of blue toe
syndrome should be investigated, if the history
alone did not easily identify the cause [164].
Fig. 6.66 Livedo reticularis affecting the right foot. This
condition is represented as blue-red mottling of the skin in
a net-like, or reticular, pattern
6.13.1.2 Treatment
The goal of treatment is to control the underlying
source and prevent further embolization, occlusion, and eventual tissue (digit/limb) loss. This
requires medical therapy in combination with
6.13.1.1 Evaluation
A sudden, unilateral blue painful toe should raise
high suspicion for an embolic source [164]. In
these cases, the identication of the offending
endovascular or surgical approaches (for atheroembolic causes).
Treatment starts with antiplatelet therapy and
anticoagulation.
lesion with noninvasive imaging is vital to determine management and prevent further embolization and ischemia.
Duplex ultrasonography is widely available
and good at identifying disease in the femoropopliteal segment. However, since up to 40% of
the offending lesions may originate in the aorta
• Primary choices usually include aspirin and
heparin, which can be used as a bridge to oral
anticoagulation of choice.
• Other antiplatelet agents, such as clopidogrel
or dipyridamole, have also been used [164,
167, 177].
or iliac arteries, additional evaluation with computed tomography angiogram (CTA) or magnetic
resonance angiogram (MRA) is necessary [164]
Following the identication and characteriza-
tion of the offending lesion, denitive treatment
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I. Ali et al.
Fig. 6.67 (a) Axial and (b) sagittal views of a computed
tomography angiogram of the thoracic aorta demonstrating an irregular adherent plaque in a patient presenting
with renal infarcts and tissue loss involving the bilateral
can be performed via an endovascular or surgical
approach.
feet. The remainder to the patient’s aorta and lower
extremity arteries did not demonstrate suspicious lesions
to account for the emboli
or stent graft is utilized to stabilize and exclude
the lesion [178]. Adjunctive therapies such as
atherectomy and thrombectomy can also be uti-
• Thoracic and abdominal aortic syndromes are
typically treated via an endovascular approach,
if possible. A stent graft is utilized, excluding
the offending lesion, whether it be eccentric
mural thrombus in an aneurysm, adherent aortic thrombus, or a penetrating ulcer (Fig.6.69).
• Femoropopliteal aneurysms, however, are
usually treated surgically with ligation and
bypass, although endovascular options with
stent grafting are also possible in appropriate
candidates.
lized with caution [167, 177, 179–181]. Embolic
protection devices can be used to prevent further
embolization during various endovascular therapies (Fig. 6.70). Surgical options still include
endarterectomy or bypass to isolate and exclude
the source of emboli.
If severe tissue loss and gangrene are present,
amputation is often necessary to prevent further
complications. Healing of the surgical wound in
these limb salvage cases is particularly likely in
patients who have undergone treatment of the
underlying disease. Following surgical treatment,
Atherosclerotic lesions with friable plaques
are now most exclusively treated via an endovascular approach. In most cases, a bare metal stent
medical treatment with anticoagulation and antiplatelets is continued throughout the patient’s
lifetime.
ab
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Fig. 6.68 (a) Coronal reformatted images from a com-
puted tomography angiogram (CTA) and (b)
3- dimensional (3D) reconstruction of the same segment
demonstrating a focal occlusion of the distal supercial
femoral artery, in a patient presenting with blue toe syndrome. Case courtesy by Dr. Alok Bhatt and Dr. Gregg
Khodorov
166
Fig. 6.69 Thoracic aortic endograft placement for treatment of an irregular aortic plaque resulting in peripheral
embolization
I. Ali et al.
6.14 Drug-Eluting Technology
AishwaryaRaja and EricSecemsky
6.14.1 Paclitaxel: Where Are
WeNow?
6.14.1.1 Introduction toPaclitaxel
Endovascular therapy utilizing traditional
uncoated percutaneous transluminal angioplasty
(PTA) and bare metal stents (BMS) has been
shown to have a restenosis rate as high as 40–60%
by 1year [182]. Inspired by the success of drugcoated devices in percutaneous coronary intervention, researchers have used paclitaxel, a
highly lipophilic compound with rapid uptake
into tissues and long-term anti-proliferative
effects on vascular smooth muscle cells and
broblasts, to coat peripheral balloons and stents
and halt the restenotic process [183].
abc
Fig. 6.70 (a) Preintervention angiogram of a focal occlu-
sion in a patient with ipsilateral blue toe syndrome (CTA
shown in Fig.6.4); (b) endovascular recanalization of the
occlusion with angioplasty followed by bare metal stent
placement, utilizing a distal embolization protection
device (EPD,*) during treatment; (c) physical examination of the EPD demonstrates a tiny embolus which is an
example of the friability of the offending lesions seen this
syndrome. Case courtesy of Dr. Alok Bhatt and Dr. Gregg
Khodorov
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