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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5191_Библиотеки_им_академика_М_И_Перельмана.pdf
Skin Necrosis andtheNeed
forVascular Assessments
SaritphatOrrapin , KittipanRerkasem ,
andRajgopalMani
6
6.1 Introduction
The vascular assessment in peripheral arterial disease (PAD), which is a condition of atherosclerotic stenosis or occlusion of the peripheral
arteries, plays a vital role in the diagnosis and
treatment of disease. The anatomic location of the
PAD involves carotid artery, vertebral artery, mesenteric artery, renal artery, upper extremity, and
lower extremity artery [1, 2]. The most common
location of symptomatic PAD is lower extremity.
When the perfusion to the lower extremity is
lower than a threshold value of resting metabolic
requirement, the legs and feet turn to skin necrosis
including gangrene and ischemic ulcer. The death
S. Orrapin
Vascular Surgery Division, Department of Surgery,
Faculty of Medicine, Thammasat University,
Pathum Thani, Thailand
Thammasat University– Center of Excellence for
Diabetic foot care (TU-CDC), Thammasat University
Hospital, Thammasat University, Pathum Thani,
Thailand
e-mail: orrapins@tu.ac.th
K. Rerkasem
Research Institute for Health Sciences,
Chiang Mai University, Chiang Mai, Thailand
Department of Surgery, Faculty of Medicine,
Chiang Mai University, Chiang Mai, Thailand
e-mail: kittipan.r@cmu.ac.th
R. Mani (*)
Research Institute for Health Sciences,
Chiang Mai University, Chiang Mai, Thailand
of the cell due to ischemia is the continuing process which is associated with morbidity, amputation, and impaired quality of life. Critical limb
ischemia (CLI) or chronic limb- threatening
ischemia (CLTI) is the advanced stage of atherosclerotic disease due to severe impaired perfusion,
which is a clinical syndrome of PAD in combination with rest pain, gangrene, or ischemic ulcer
more than 2weeks’ duration [1]. There are other
causes of chronic lower extremity ischemia, such
as smoking arterial inammation (thromboangiitis obliterans or Buerger’s disease (TAO)),
chronic arterial embolism, arterial entrapment,
fungal arterial infection, Takayasu’s disease, and
other uncommon arteriopathies such as druginduced arteriopathy [3–7]. The vascular assessment, which ranges from noninvasive methods
such as ankle-brachial index and tissue oxygen
measurement to invasive methods such as angiography, is important to differentiate the cause of
disease, determine the severity of ischemia, surveil the progression of disease and prognosis,
select the medication and modalities of treatment,
and determine the requirement of revascularization procedure [1, 8–10].
6.2 Epidemiology ofPeripheral
Arterial Disease
PAD results from atherosclerotic occlusion of the
blood vessels in the lower and upper limbs symptomatically expressed as pain on exercise that is
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_6
41
42
S. Orrapin et al.
relieved by transient rest: this condition is known
as intermittent claudication (IC). IC worsens with
reduction in blood ow and perfusion leading to
CLTI. This in turn leads to cell death, ulceration,
and necrosis; the pathophysiology of this condition is described in a separate section in this
chapter. PAD presents a signicant clinical burden. Fowkes reported that 202 million people
were living with PAD worldwide: 69.7% of this
population lived in low- to middle-income countries (LMICs) with a breakup of 54.8 million in
Southeast Asia and 45.9 million in the Western
Pacic countries [11]. Fowkes used anklebrachial pressure index (ABI) threshold of ≤0.9
to dene the presence of PAD in 34 studies from
22 high-income countries (HICs) and 12 from
LMICs. Song and Fowkes [11, 12] conducted a
systematic review and meta-analysis on 118 studies and, based on their modeling, estimated the
global population of PAD to be 236.92 million
people in 2015. Both reports found that PAD
increased with age and sex: prevalence of 5.28%
(95% CI 3.38–8.17%) in HIC in 45–49-year-old
women and 5.41% (3.41–8.49%) in men. In the
85–89-year group, prevalence found was 18.38%
(11.16–28.76%) in women and 18.83%
(12.03–25%) in men. In LMIC group countries,
prevalence rates were higher in women than men,
especially in the younger age group, with 6.31%
(4.86–8.15%) in 45–49-year group, which has
implications for planning health care [11].
However, the true prevalence and incidence
rate of PAD may be underestimated due to the
lack of a good screening system, which makes it
impossible to report the exact number of PAD
patients in the group who has no symptoms or
has minor symptoms [13]. According to the data
registry of the Society for Vascular Surgery
(SVS) and the European Society for Vascular
Surgery (ESVS), 80% of PAD patients are
asymptomatic, of which half of them are associated with DM and 10–30% and 20–40% are present with intermittent claudication and atypical
leg pain, respectively [1, 8–10, 14–16].
The associated risk factors for PAD are the
following:
• Smoking 2.72% (95 CI 2.39–3.09%) in HIC,
1.42% (1.25–1.62%) in LMIC
• Diabetes mellitus (DM) 1.86% (1.66–2.14%)
in HIC, 1.47% (1.29–1.68%) in LMIC
• Hypertension 1.55% (1.42–1.71%) in HIC,
1.36% (1.24–1.50%) in LMIC
• Hypercholesterolemia 1.19% (1.07–1.33%) in
HIC, 1.14% (1.03–1.25%) in LMIC
Of these risk factors, the association between
DM and PAD is especially signicant to this
chapter. DM affects platelet aggregation and
increases inammation with raised AGE and reactive oxygen species, endothelial dysfunction, and
vascular smooth muscle cell dysfunction, all of
which are implicated in PAD.Pain is attenuated in
people with diabetes and neuropathy. ABI could
be falsely high (>1.30) owing to the presence of
medial calcinosis. Estimated prevalence could be
inaccurate since ABI relies on detecting two of the
three vessels around the ankle, and the variation
of ABI with vessel narrowing is unknown in some
ethnic minorities. The narrative from these data is
that the PAD is signicant and an increasing burden affecting both genders: it is worse in women
in the younger age range in LMIC and could be
expected to affect daily life considerably: walking
to work, shopping, and life in general would be
affected and likely to get worse [17].
PAD is associated with morbidity and mortality
due to amputation and major adverse cardiovascular
events (MACEs), especially in CLTI. The major
cause of death is acute coronary syndrome (ACS).
Because of atherosclerotic involvement of multiple
vascular beds, 50% of patients with CLTI are coronary artery disease (CAD) and cerebrovascular disease (CVD) [14, 18]. The 5-year mortality rate in
patients with PAD is 10–15%. When diagnosed
with CLTI, the 1-year mortality rate increases to
25%. 6.5% and 4.5% of CLTIs are fatal myocardial
infarction (MI) and fatal stroke, respectively. 25%
of CLTI patients undergo major amputation due to
ischemic limb process or infection [19]. MACE
rapidly increases during the perioperative period
due to the stress from the foot infection or active
comorbid disease and risk of the operation including revascularization, debridement, and amputation.
Poor performance status occurs in patients with loss
of ambulatory state due to amputation, limb ulceration, gangrene, rest pain, or disabling claudication,
all of which are increased risk for MACE.The SVS
6 Skin Necrosis andtheNeed forVascular Assessments
43
Objective Performance Goals (OPGs) established
standardized tools to report benchmark of perioperative outcome including MACE and major
adverse limb events (MALEs) after revascularization procedures in patients with CLTI [20, 21].
6.3 Pathophysiology
ofPeripheral Arterial
Disease
Arterial obstruction can lead to skin necrosis.
Atherosclerosis is the most common cause of
arterial occlusion. Dyslipidemia, obesity, hypertension, DM, and smoking are the risk factors for
the development of atherosclerotic lesions [22].
However, the distribution is different between the
risk factors. For example, in a diabetes patient,
the obstructive lesion is mainly in tibial vessel
occlusion, whereas with smoking, it is in the aortoiliac segment.
The metabolic abnormality in patients with DM
leads to hyperglycemia, insulin resistance, and
increasing of free fatty acid [23]. Hyperglycemia
increases the oxidative stress by increasing reactive oxygen species (ROS). In addition, the cellular mitogenic pathway activation through the
mitochondrial generation of the superoxide
anion including advanced glycation end products
(AGEs), protein kinase C (PKC) activation, and
nuclear factor kappa B (NF-κB) is induced by
high blood glucose level. In patients with longduration DM, insulin resistance causes endothelial dysfunction, decreasing of nitric oxide (NO)
synthase, expression of adhesion molecules, and
atherosclerotic lesions [23]. In addition, a thrombosis risk in DM increases through the hypercoagulation and platelet aggregation. Insulin
resistance is also promoted in the atherosclerotic
process due to lipid metabolism disturbance such
as high triglycerides (TGs), high apolipoprotein B
(ApoB), small and dense low-density lipoprotein
(LDL), and low high- density lipoprotein (HDL)
cholesterol [1, 16, 24]. In early atherosclerotic
process, the endothelial dysfunction is associated with hypertensive patients. A reduction in
NO results in a reduced vasodilatory response and
thereby inammation, thrombosis, and activate
coagulation cascade [1, 16, 23–26]. The repetitive
blood pressure alterations in hypertensive condition cause ongoing renin-angiotensin system activation, which impacts the atherosclerotic lesions
[1, 16, 24]. Smoking causes an inammation of
vessel wall, which is related to atherosclerotic
plaque formation through interleukin-6, tissue
necrosis factor-α, interleukin-1-β, leukocyte,
C-reactive protein (CRP), and other inammatory markers [1, 16, 24]. The prothrombotic state
of platelet activation and aggregation is created
by increasing of thromboxane A2 (TXA2), von
Willebrand factor (vWF), thrombin, and brin
and decreasing of prostacyclin, antithrombotic,
and brinolytic substances [1, 16, 24].
Detailed postmortem studies of patients of different ages show that atherosclerosis progresses
from small and inconsequential fatty streaks
to brolipid plaque and complicated lesions,
which are the cause of many different clinical disorders such as skin necrosis (gangrene),
myocardial infarction, or stroke. Atherosclerotic
plaques begin with the subendothelial accumulation of lipid-laden foamy macrophages and
T-lymphocytes (T-cells), which form non- stenotic
fatty streaks. This progresses to the formation of
acellular core of lipid cholesterol, bound by a
brous cap that contains vascular smooth muscle
cells (VSMCs) and inammatory cells, especially macrophages, mast cells, and T-cells. In an
advanced lesion, new blood vessels and calcium
hydroxyapatite are present [1, 16, 24].
Although atherosclerosis is a systemic disease involving especially large- and medium-size
arteries, atherosclerotic plaque tends to develop in
certain places such as the carotid artery, the infrarenal aorta, and the arteries of the lower extremities, in particular at the sites of bifurcation, the
ostia, the branchings, and the bends. This suggests
that hemodynamic forces play a role in atherogenesis; many hypotheses have been proposed to
explain this unique focal pattern.
6.4 Atherosclerosis
andSymptomatology
There are two mechanisms by which symptoms
of atherosclerotic lesions can develop. Firstly, by
the time that atherosclerotic lesion has increased
44
in size with the deposition of a necrotic core,
inammatory cells, and a brous cap, the lesion
is so large that the downstream blood supply is
not sufcient. Initially, this usually occurs
because of exertion associated with increased
blood ow demand such as intermittent claudication of the calf. Patients have calf pain when
walking, but the symptom relieves when patients
rest their leg. The muscle contraction during
exercise needs much more energy (blood supply)
than those with resting stage. Then in case the
atherosclerotic lesion causes further obstruction,
this can progress to rest pain and dry gangrene
(skin necrosis). In case this dry gangrene becomes
infected, this leads to wet gangrene, in which
massive and rapid skin necrosis can occur
(Fig. 6.1). The second mechanism begins with
erosion or rupture plaque, resulting in exposure
of the blood to thrombogenic lipid cores.
Consequently, a rapid accumulation of platelets,
deposition of brin, and occlusion of the vessel
by thrombus or distal embolization of thrombotic
material occur, which may lead to very severe
problems suddenly such as acute arterial occlusion (thrombosis). This can cause massive skin
necrosis in the leg (Fig. 6.2). Since these two
S. Orrapin et al.
Fig. 6.1 The foot of a diabetic patient who started with
gangrene in the fth toe; then the infection resulted in
massive skin necrosis of his foot in 5days’ time. This picture shows the foot after the rst debridement due to wet
gangrene and necrotizing fasciitis
ab
Fig. 6.2 Acute thrombosis of the aortoiliac artery shows
xed mottling skin of the foot following acute thrombosis
of the aortoiliac artery (a), and computed tomographic
arteriography demonstrated occlusion of distal aorta and
bilateral common iliac artery with arterial wall calcication (b)
6 Skin Necrosis andtheNeed forVascular Assessments
45
mechanisms can cause massive skin necrosis,
consequently these lead to major amputation of
the leg.
6.5 The Eects ofDiabetes
onPAD
andtheDiabeticFoot
DM is the major atherosclerotic risk factor that
increases the risk of PAD.Chronically high blood
glucose levels, increases in free fatty acids, and
insulin resistance can be seen in diabetes patients.
In addition, the increasing of blood glucose level
activates the inammatory response of blood vessels, leading to vasoconstriction and decreasing
of thrombosis threshold [1, 16]. The diabetes
patients are at risk of lower limb amputation
more than normal people about 20 times.
Complications from diabetes are caused by multiple factors such as hypoglycemia and high
blood HbA1c level, as well as lack of knowledge
of improper foot care and socioeconomic conditions of the family [1, 16, 24]. The complications
of DM involve the peripheral artery that feeds the
legs. Both macroangiopathy and microangiopathy cause limited blood supply to the tissue of the
foot. The PAD is the part of macroangiopathy
under atherosclerotic process of medium and
large vessel. The incidence of PAD in patients
with DM is 10–30% [9]. Most common anatomic
distribution of macrovascular involvement by
atherosclerosis in patients with DM is crural
arteries, including tibial and peroneal arteries
leading to diabetic foot ulcer (DFU) and chronic
limb-threatening ischemia (CLTI) [1, 16]. In
addition, the gangrene and skin necrosis can
originate from microvascular involvement, which
causes the capillary basement membrane thickening and decreasing of capillary blood ow and
microcirculation. Another process of diabetic
foot (DF) and DFU is peripheral neuropathy,
which is found in 60% of DM patients and 80%
of patients with DFU.Peripheral motor neuropathy causes foot deformity due to loss of muscle
imbalance, causing bone and joint damage, called
neuro-osteoarthropathy or Charcot foot, found in
2% of all diabetics, or causes deformed feet in
other ways, such as pes cavus, claw toes, at feet,
and hallux valgus [16]. The limited ankle and feet
joint mobility and their deformities cause the
abnormal distribution of foot weight and repeated
minor foot trauma injuries and callous formation
[11, 14, 15]. A disorder of the peripheral sensory
nervous system causes a decrease in the sensation
of the feet [14]. The autonomic nerve involvement causes dry, cracked, and ulcerative skin to
easily become ulcerative or infected in the skin
layer [27]. Both vascular and neurologic involvement of DF causes chronic recurrent and high
risk of infected ulcer in diabetes patients. Chronic
hyperglycemias activate the inammatory process and ongoing cell death processes (apoptosis)
by oxidative stress. The neutrophil dysfunction
associated with hyperglycemia causes the impairment of the immune system, which causes the
infection-prone DFU or diabetic foot infection
(DFI) [28, 29]. Diabetic foot infection (DFI) is
caused by the invasion of microorganisms into
the ulcer or tissues of the feet through the ssures
of the skin in patients with diabetes. The DFI
aggravates the inammatory processes of surrounding tissue, which leads to the tissue loss and
skin necrosis [29–31] (Fig.6.3).
46
Fig. 6.3 The association between atherosclerosis, peripheral arterial disease, and diabetic foot ulcer
S. Orrapin et al.
6.6 Macrovascular
andMicrovascular
Assessment Tools
Vascular assessment techniques of PAD, particularly in gangrene and ischemic ulcer, are based
on the severity and prognosis of disease, risk and
level of amputation limit, prediction of the wound
healing rate, and requirement of revascularization. Both macrovascular assessment technique
such as ABI and computed tomographic
angiography (CTA) and microvascular assessment technique such as skin perfusion pressure
(SPP), transcutaneous oxygen tension (TcPO2),
or transcutaneous oxygen measurement (TCOM)
and other skin perfusion imaging are the modalities to obtain the diagnosis and anatomic distribution of PAD.When the patients indicate to lower
extremity revascularization, urgently assess and
treat patients, which can decrease the risk for
major limb amputation [1, 16, 32, 33]. To prevent
the amputation of lower extremity due to PAD,
do not assume that microangiopathy, when present, is the cause of poor healing in patients with a
chronic recalcitrant ulcer [34]. Although some
techniques are not widely used to evaluate the
perfusion of skin necrosis of the lower extremity,
the appropriate use of any of the following vascular assessment modalities is useful to guide the
physician to appropriate treatment modalities.
6.7 Macrovascular Assessments
ofTissue Viability
The ankle-brachial index (ABI), which is the
noninvasive test of chronic arterial occlusion, has
been widely used for diagnosing the PAD [1, 16,
35–37]. Because of the simplicity of the mea-
surement technique, high availability, and less
expensive instrument, the ABI is recommended
as the rst-line screening test in patients who
have high risk or are suspected of PAD [15, 36,
38]. The normal range of ABI is 1–1.3. Diagnosis
of PAD is established by (1) the value of ABI less
than 0.9 or (2) the value of ABI less than 0.9 after
exercise or (3) the decreasing of postexercise ABI
more than 20% by walking on a 3.2km/h speed
treadmill test for 5min with the incline slope of
12° [5, 14, 35, 36, 39]. The sensitivity and specicity of ABI to diagnose PAD are 79% and 96%,
respectively [40].
6 Skin Necrosis andtheNeed forVascular Assessments
47
The ABI measurements are performed using
a handheld sphygmomanometer cuff at the
ankles. Doppler ultrasounds detect the signals
and measure ankle systolic blood pressure at
the position of the posterior tibial artery or dorsalis pedis artery and also the systolic blood
pressure of the brachial artery under supine
position; the ABI calculation is done using the
ipsilateral highest ankle systolic blood pressure
(ankle pressure) divided by the highest brachial
systolic blood pressure [5, 40–42]. Lower ABI
values indicate greater severity of PAD in the
same patient (Table6.1), while patients with an
ABI value greater than 1.3 represent a stiffness
of the arterial wall. The ABI can also determine
the severity of atherosclerosis in other vascular
beds and predict the risk of MACE including
stroke, MI, and cardiovascular death [43]. The
ankle pressure alone is less reliable due to
changes in systemic blood pressure conditions
such as hypertension, hypotension, shock, or
heart failure that affect the ankle pressure. ABI
has often been unreliable, with high false-negative rate of the test particularly for diabetes,
old age, and end-stage renal disease (ESRD)
patients. The false elevation of ankle pressure
due to medial calcinosis causes the overestimation of ABI value and underestimation of severity of PAD (Fig. 6.4). The false elevation of
ankle pressure and ABI value may present
either noncompressible vessel value (ABI
>1.30) or normal range of ABI (ABI 1.00–1.29)
(Fig. 6.4) [1, 16, 34]. Arain’s study included
17,485 consecutive patients who underwent
Table 6.1 The severity of peripheral arterial disease
related with resting and postexercise ankle-brachial index
[5, 36, 39]
Resting
Disease severity
Noncompressible
arteries
Normal 1.00–1.29
Borderline 0.91–0.99
Mild PAD 0.71–0.90 0.51–0.90
Moderate PAD 0.41–0.70 0.16–0.50
Severe PAD
ABI ankle-brachial index; PAD peripheral arterial disease
ABI
≥1.30
≤0.40 ≤0.15
Postexercise
ABI
ABI measurement to identify the incidence of
noncompressible vessel. The result showed that
2781 (16%) had noncompressible vessels [44].
Randhawa’s study, which is a retrospective
observational study, showed that 70% of the
tibial vessels that were considered to be noncompressible are actually occluded or severely
stenotic by angiography [45]. So, patients who
have clinical characteristics that indicate symptomatic PAD with discordant ABI result will
suffer from (1) fainting, or absent pedal pulse,
brittle nail, calf muscle hypotrophy, hairless
leg, IC, and rest pain but will have ABI value
higher than 0.90 [36], (2) ABI values greater
than 1.3, (3) decreasing of the pedal pulse’s
intensity or systolic ankle pressure during leg
lifting, and (4) monophasic or damping of
Doppler waveform with a normal ABI value
should evaluate the additional measurement
such as toe pressure, toe-brachial index (TBI),
pulse volume recorder (PVR), and Doppler
waveform analysis (Fig.6.4) [5, 38]. If TBI is
less than 0.70 or toe pressure is less than 0.4,
the diagnosis of PAD is established [36, 39–41,
46]. Currently, toe pressure and TBI, which are
simplied, quick, and inexpensive tools for
perfusion assessment, are the recommended
tests of forefoot perfusion appropriately to
diagnose and manage CLTI. Comparing with
ABI, toe pressure assessment offers more accuracy in detecting limb ischemia in the presence
of noncompressible or false elevation of ankle
pressure in heavily calcied vessels. However,
toe gangrene, previous toe amputation and
extensive ulcer, and concomitant infection in
the forefoot and toe area are limitations of toe
pressure measurement [1, 47]. The vascular
assessment, which included clinical history
taking, physical examination and perfusion
measurement of the ischemic limb, revealed
that CLTI is a chronic form of limb-threatening
ischemia that can result in severe limb loss due
to inadequate perfusion to gangrene or ischemic ulcers. The SVS Wound, Ischemia, and
foot Infection (WIfI) classication should be
staging to predict a risk of amputation,
likelihood of wound healing, and benet for
48
S. Orrapin et al.
CLTI with Gangrene or
Ischemic ulcer
Normal ABI 0.9–1.29
Ischemic ulcer or
Gangrene on
examination
No
Wound care and
Control infection
Ye s
Vascular assessment
Absent/Faint pulse on
examination
Ye s
AP and ABI
measurement
Abnormal ABI ≤ 0.9
TP and/or TCOM
measurement
WIfI Staging
Obtain Vascular imaging
(CTA/MRA/DSA
of lower extremity)
No
Wound care and
Control infection
ABI ≤ 1.30 or
discordant AP, ABI
and/or Doppler
waveforms
Revascularization
Fig. 6.4 The algorithm of decision-making for revascularization based on vascular assessment and clinical presentation of gangrene and ischemic ulcer in patients with
chronic limb-threatening ischemia. CLTI chronic limbthreatening ischemia; AP ankle pressure; ABI ankle-
revascularization. The aim of revascularization
procedure is to prevent limb amputation
(Fig.6.4) [48–50].
Catheter arteriography by performing plain
radiography or uoroscopy in conjunction with
the administration of contrast media intraarterially can evaluate anatomical characteristics and dynamic blood ow of lower
extremities. Because arteriography can provide
a complete map of the lower limb arteries and
selective catheter placement during lower
extremity arteriography enhances imaging,
reduces contrast material dose, and enhances
sensitivity in patients with CLTI, arteriography
is a gold standard diagnostic tool for PAD
brachial index; TP toe pressure; TCOM transcutaneous
oxygen measurement; CTA computed tomographic arteriography; MRA magnetic resonance arteriography; WIfI
Wound Ischemia foot Infection; DSA digital subtraction
arteriography
patients who have indicated revascularization
including disabling IC and CLTI, particularly
when below-the-knee to pedal artery disease is
suspected (Fig.6.5).
The arteriography shows the intraluminal
anatomical characteristics of the arteries,
including stenosis, occlusion, dissection, and
intimal calcication. Arteriography allows
intervention at the same setting such as balloon
angioplasty with stenting and coil embolization (Fig.6.5). For open vascular bypass procedure, completion arteriography immediately
after an operation is recommended to identify
the occult lesion to prevent restenosis of vascular bypass. Digital subtraction angiography
cd
6 Skin Necrosis andtheNeed forVascular Assessments
ab
49
Fig. 6.5 Digital subtraction arteriography (DSA) demonstrated supercial femoral artery occlusion in chronic
limb-threatening ischemia patient. (a) Arteriography to
evaluate below-the-knee artery; (b) arteriography to eval-
(DSA) is currently developed to remove the
bones and opaque matter, which provides the
intraluminal imaging clearly from an inow
suprainguinal aortoiliac segment to crural and
foot arteries [1, 16, 47]. However, intra- arterial
contrast media injection poses a higher risk of
contrast-induced nephropathy (CIN) than
peripheral vein injections, especially in
patients who have estimated glomerular ltration rate (eGFR) less than 30mL/min/1.73m2.
Because of the high exposure to ionizing radiation and contrast media, the catheter angiography should be preserved in patients who are
candidates for revascularization. In addition,
the risk factors of catheter and wire- associated
complications during arteriography include
arterial dissection, thrombosis, distal embolization, and extravasation and increased risk of
limb loss during the diagnostic procedure [1].
Carbon dioxide arteriography (CO2 arteriography) by using carbon dioxide directly into the
arteries can be used in patients with a chronic
kidney disease to prevent CIN and allergy to contrast media. The carbon dioxide replaces the
blood in artery temporarily. However, the use of
CO2 arteriography has certain limitations, including low quality of the artery image that is less
uate below-the-knee and foot arteries; (c) balloon angioplasty of proximal supercial femoral artery; (d) after
supercial femoral artery stenting
clear than contrast media intra-arterially. So, CO2
arteriography is usually used as an additional
agent in conjunction with regular contrast media.
CO2 angiography is generally considered inferior
to iodinated angiography but can still provide
useful diagnostic images by using power injection and adjust the 30° Trendelenburg patient’s
position during intervention to increase carbon
dioxide concentration and reduce the velocity of
blood ow, respectively [51, 52].
Computed tomographic arteriography (CTA)
can provide a more detailed overview of the
lower limb vascular and conrm an uncertain
PAD diagnosis or verify the severity and an anatomic distribution of the arterial occlusive lesion
before revascularization (Fig. 6.6). In addition,
the CTA composite is used for the extraluminal
and intraluminal study. For extraluminal study,
CTA can evaluate the source of external compression, associated organ or structural abnormalities, inammation of the vessel wall, and
surrounding structure. CTA has advanced in
terms of high accuracy and acquisition times. The
development of the CTA in modern era creates a
multiple-plane view with high-resolution image
and three-dimensional (3D) reconstructions. The
sensitivity and specicity of the arterial occlusive
50
S. Orrapin et al.
Fig. 6.6 Computed tomographic arteriography (CTA) of
aortoiliac occlusive disease (AIOD) in chronic limbthreatening ischemia patient with bilateral groin calcica-
disease of CTA in the aortoiliac segment are 95%
and 96%, respectively, and those of the femoropopliteal segment are 97% and 94%, respectively,
and below-the-knee arteries are 95% and 91%,
respectively [53, 54]. However, the limitations of
the study on the CTA include the image interference on artifact, calcied artery, and limited evaluation or overestimation of below-the-knee artery
lesion, especially in concomitant proximal artery
occlusive disease. Because of the potentially
nephrotoxic contrast agents and radiation exposure of CTA, the CTA should be performed in
patients who are candidates for revascularization
or who had uncertain PAD diagnosis by other
modalities of investigation. Thus, the clinical
value of CTA in the CLTI target population
remains uncertain. Below-the-knee and belowthe- ankle artery runoff vessel usually gets a complete evaluation on catheter angiography or DSA
or foot magnetic resonance arteriography (MRA)
due to less reliability for CTA imaging of belowthe- knee artery [1].
Magnetic resonance arteriography (MRA) is a
noninvasive imaging method with non-exposure
to ionizing radiation, which can create the 3D
images of the entire arterial map. So, the MRA is
tion (right and left, Fig. 6.5, of axial view CTA) and
occlusion of aortoiliac segment with heavy calcication
(central, Fig.6.5, of CTA reconstruction)
suitable for patients with CLTI who have plans
for revascularization, unaffected by arterial calcication. Both sensitivity and specicity of MRA
are 93–100% [40]. However, MRA interpretation
depends on the availability of subspecialist vascular radiologist or expert interventionist. The
overestimation with the false-positive result of
the stenotic lesion is higher in MRA imaging
when compared with CTA and DSA.In addition,
venous contamination can obscure arteries below
the knee. CLTI patients with pacemakers, debrillators, and other metallic implantation such as
cerebral clips are contraindicated to perform
MRA. In addition, the metallic material can
cause artifacts that mimic vessel occlusions. If
MRA cannot provide the adequate below-theknee and below-the-ankle imaging, the foot
MRA or catheter arteriography is the choice of
further investigation to identify the occult lesion
[1, 16]. Contrast-enhanced MRA (CE-MRA)
using gadolinium-based contrast agents is generally preferred because of the high contrast-tonoise ratio, better spatial resolution, more rapid
acquisition, and less artifact. In addition, timeresolved techniques can improve image ow patterns and increase the accuracy to identify