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TASC A lesions:
both common iliac arteries (CIA) or short segment stenosis (<3 cm) that involve one or both external iliac arteries (CIA).
TASC B lesions:
the infrarenal aorta, unilateral CIA occlusion, single or multiple stenosis totaling 3-10 cm involving the EIA but not extending into the CFA, unilateral EIA occlusion not involving the origin of the internal iliac or CFA.
TASC C lesions:
bilateral EIA stenosis 3-10 cm long not extending into the CFA, unilateral EIA stenosis extending into the CFA, unilateral EIA occlusion that involves the origins of the hypogastric artery and/or CFA, heavily calcified unilateral EIA occlusion with or without involvement of origins of the internal iliac and/or CFA.
TASC D lesion:
diffuse disease involving the aorta and both iliac arteries requiring treatment, diffuse multiple stenosis involving the unilateral CIA, EIA, CFA; unilateral occlusions of both CIA and EIA; bilateral occlusions of EIA, iliac stenosis in patients with abdominal aortic aneurysm (AAA) requiring treatment and not amenable to endograft placement or other lesions requiring open aortic or iliac surgery.
30 Aortoiliac Disease
335
bypass range from aorta to femoral, aorta to bifemoral, aorta to iliac, femoral to femoral, and axillary to femoral artery bypasses. An aortic bifurcation bypass has a good 5-year patency rate of 90%. Extra-anatomic bypass grafts have poorer outcomes with 5-year patency of 51% and 75% for axillary-unifemoral and axillary-bifemoral bypass grafts, respectively [9].
In 2000, the TransAtlantic Inter-Society Consensus (TASC) guidelines were published in a document that orga­nized aortic and iliac lesions based on anatomic distribution
stenosis involving one or
short (<3 cm) stenosis of
and morphology. They were initially published to denote which lesions were more suitable for endovascular therapy and which ones were better suited to surgical repair. In 2007, the guidelines were revised to expand the role of endovascu­lar therapy (Fig.30.2) [10].
Although the TASC guidelines were developed to help guide endovascular versus surgical therapy, they are seldom used for clinical decision-making. As technology improves and better devices facilitate percutaneous revascularization, most practitioners espouse an endovascular-rst approach.
Fig. 30.2 The 2007 TransAtlantic Inter-Society Consensus (TASC) guidelines
bilateral CIA occlusions,
infra-renal aortoiliac occlusion,
336
A. B. Bhatt and J. F. Benenati
Today, the TASC guidelines are typically used for research purposes and serve as a useful anatomic descriptor of disease distribution.

Interventional Therapy

The approach to aortic and iliac lesions depends largely on the distribution of disease. For example, a patient who has an ostial common iliac artery stenosis will have a different treatment strategy than a patient who has a mid common iliac artery stenosis. It is helpful to group lesions according to their anatomic location as follows: isolated abdominal aorta stenosis, aortic bifurcation, common iliac artery, and external iliac artery.
Abdominal Aorta
Aortic occlusive disease typically involves the infrarenal
Key Point
balloon-expandable stents are commonly used to prevent ow abnormalities at the aortic bifurcation. In patients that have an associated abdominal aortic aneurysm, care should be taken to not place the iliac stents too proximally within the abdominal aorta because this may preclude future endo­vascular repair of the abdominal aortic aneurysm.
Common Iliac Artery
Lesions in the non-ostial segments of the common iliac artery are typically treated with primary stenting. Stent types include balloon-expandable, self-expanding, bare metal, and covered stents. Within the common iliac artery, balloon- expandable stents are usually preferred because they have higher hoop strength than self-expanding stents. The large- scale, multi­center, multinational prospective BRAVISSIMO trial demon­strated a 12-month primary patency rate of 93% in patients with iliac lesions that underwent primary stenting, noting that this was comparable to open surgical bypass [11].
External Iliac Artery
• Endovascular treatment is based on anatomic location:
• Abdominal aorta=angioplasty + uncovered stent
• Aortic bifurcation=kissing iliac stents
• Common iliac artery=balloon-expandable stent
• External iliac artery=self-expandable stents
abdominal aorta, much like aneurysmal disease. It usually occurs below the origin of the inferior mesenteric artery. Unlike aneurysmal disease, percutaneous therapy involves angioplasty with placement of uncovered stents. Typically, balloon-expandable stents are chosen because they provide greater radial force. They can also be overdilated to achieve a larger diameter (Fig.30.3).
Aortic Bifurcation
Atherosclerotic lesions that involve the aortic bifurcation warrant special consideration. When a stenotic lesion involves the origin of the common iliac artery and distal abdominal aorta, kissing iliac stents are typically required (Fig.30.4). Angioplasty and stenting of a lesion in this loca­tion in isolation without treating the contralateral side may cause plaque shifting/embolization and luminal stenosis of the untreated contralateral common iliac artery. Covered
Lesions within the external iliac artery are also typically treated with primary stenting. Unlike the common iliac artery, the external iliac arteries are more tortuous and are subject to more external forces. As a result, self-expanding stents are preferred in this location.
Internal Iliac Artery
The internal iliac arteries are infrequently treated in isolation. They are, however, an important consideration when treating common and extra iliac lesions. One retrospective evaluation found that even when bare metal stents are placed across the origin of the hypogastric arteries, although immediate occlu­sion is rare, their long-term patency is reduced [12]. Typically, as long as one hypogastric artery remains patent, there is enough cross lling within the pelvis to prevent signicant symptomology. If both are occluded, especially acutely, the patient may experience buttock claudication, impotence, and, rarely, pelvic visceral ischemia.
Pre-procedurally, the patient should be medically opti­mized for revascularization. All patients that can tolerate aspirin therapy should be started on a daily baby aspirin. Based on the HOPE and EUROPA trials, all patients with PAD should be started on an ACE inhibitor, irrespective of their blood pressure because ACE inhibitors have been shown to decrease the incidence of stroke and MI, even in PAD patients that are otherwise normotensive. Statin therapy
30 Aortoiliac Disease
337
Fig. 30.3 (a) Patient with Rutherford 3 claudication found to have aor-
tic stenosis. This is a normal segment of the patient’s aorta distal to the renal arteries and the inferior mesenteric artery which is key to safely treating this patient with angioplasty and stent placement. (b) Slightly inferiorly, there is a segment of stenotic infrarenal abdominal aorta (arrow), across which there was a 70mmHg gradient at rest. (c) During treatment, bilateral common femoral arterial accesses are obtained. Through the left groin, a multi-sidehole catheter (arrow) was advanced to facilitate imaging. Through the right groin, a sheath is advanced across the lesion (arrowhead). This sheath will facilitate safe and pre­cise positioning of a balloon-expandable stent. (d) The sheath is
should also be started on all patients with PAD. Routine labs should be checked including a CBC and BMP. In patients with chronic kidney disease, IV hydration can help reduce the risk of contrast-induced nephropathy.
Before the procedure, it is also critical to review the patient’s noninvasive evaluation including available cross­sectional imaging and correlate the ndings with the patient’s
retracted (arrowhead) allowing the balloon-expandable stent to be deployed. As the balloon is inated to deploy the stent (dashed arrow), the multi-sidehole catheter (solid arrow) can be intermittently used for imaging to ensure appropriate deployment of the stent. As the stent is deployed, the catheter is retracted prior to full expansion of the stent. (e) Post-stenting angiogram shows appropriate positioning of the stent below the origin of the inferior mesenteric artery (solid arrow) and above the origin of an inferior accessory right renal artery (dashed arrow). Post-procedure pressure measurements revealed no signicant gradient, with resolution of the pre-procedure 70mmHg gradient across the stenotic segment of the aorta
symptomatology. Pre-procedure CTA is very helpful for planning the treatment approach in aortoiliac disease. Not all stenoses warrant treatment, and oftentimes, intra-procedural digital subtraction angiography, intravascular ultrasound, and pressure measurements will reveal lesions that may not be clinically signicant. Depending on the location of the lesion, the steps of the procedure and devices used will vary.
338
A. B. Bhatt and J. F. Benenati
Fig. 30.4 (a) Patient was a Rutherford 3 claudicant with evidence of
inow disease on her noninvasive testing. Her initial angiogram revealed bilateral ostial common iliac artery stenoses (arrows) which had a 40mmHg gradient across them following the administration of intra-arterial nitroglycerine. (b) Access is gained through both common femoral arteries. Because of their location, balloon-expanding stents were used for treatment. Sheaths were advanced centrally across both
stenoses. Image shows left common femoral artery sheath is across the stenosis (arrow). Access was then obtained in the right CFA through which a sheath was placed (dashed arrow). Following access, it was subsequently advanced centrally like the left CFA sheath. (c) Both stents were simultaneously deployed in a kissing fashion. (d) Post­procedure angiogram demonstrates successful treatment of both lesions with no pressure gradient across the stented segments
30 Aortoiliac Disease
339
The How To
1. Most aortoiliac interventions will require a single common femoral artery access, but many will require bilateral groin access and perhaps even radial or brachial artery access. Treating lesions isolated to the abdominal aorta typically requires two accesses, one to place a catheter for angiogra­phy and the other through which to deploy the stent. Having an imaging catheter facilitates pre­cise stent deployment because it allows for real­time imaging as the stent is being deployed. Lesions of the aortic bifurcation require bilateral groin access for kissing stent placement. Lesions of the mid and distal common iliac artery are best treated with ipsilateral access, whereas lesions in the external iliac artery are best treated by access­ing the contralateral groin. Access is obtained using the typical Seldinger technique, and a short sidearm sheath is placed (refer to Chap. 8 for more information).
2. Once access is obtained, a pigtail or other multi­sidehole catheter will be advanced into the abdom­inal aorta, and a pelvic angiogram will be performed in the anteroposterior as well as bilat­eral oblique projections. Imaging in these three projections allows accurate delineation of anatomy
by isolating each segment of the abdominal aorta and iliac vessels. The lesions of interest should be evaluated for severity, length of stenosis or occlu­sion, and the size of the adjacent normal vessel. This allows for accurate sizing of the angioplasty balloons and stents. The oblique views also allow the operator to evaluate the patency of both inter­nal iliac arteries in case one needs to be covered by a stent.
3. Wire access is then obtained across the lesion of interest. A common method by which to do this is
catheter. If an acute occlusion is present and the limb is viable, the occlusion will typically be treated by placing a thrombolysis catheter and administer-
acute thrombus and can unmask any culprit lesions responsible for the acute occlusion.
4. question, trans-stenotic pressure measurements are obtained. A pressure gradient of greater than
rial nitroglycerine can be administered to mimic exercise. In this setting, a gradient of greater than
9].
5. If a severe stenosis is present, balloon angioplasty may be required to facilitate passage of catheters and sheaths. Angiography should be performed after each angioplasty to monitor for complica­tions including rupture. If a rupture is suspected,
tamponade the rupture, and a covered stent should be deployed.
6. If a balloon-expandable stent is to be used, an appropriately sized sheath must be advanced past the lesion through which an undeployed stent can safely be advanced. Once the stent is in position, it is unsheathed (the sheath is retracted proximal
to deploy the stent. If a balloon-expandable stent is advanced through a stenosis without the use of a sheath, the stent can catch on plaque and become dislodged from the balloon. Using a
the stent once it is in position help prevent this complication.
7. If a self-expanding stent is to be used, it can be advanced over the wire without the use of a long delivery sheath. When they are deployed, the leading end of the stent should always be deployed slightly distal to the intended landing zone. As the distal end of the stent is being deployed, the entire stent can be slightly retracted but never advanced [13].
8. When kissing stents are deployed at the aortic bifurcation, sheaths are advanced into the abdomi­nal aorta from each common femoral artery access to facilitate delivery of balloon-expandable stents. Once the sheaths are retracted, the balloon­expandable stents are deployed simultaneously so that each stent ultimately has the same diameter.
9. Once the stent is deployed, a post-deployment angiogram is performed. If needed, balloon­expandable stents can be further dilated using a bigger balloon, but this luminal gain comes at the expense of foreshortening the stent. Self­expanding stents on the other hand cannot be overdilated, so appropriate sizing is critical. Post-dilatation with a non-compliant balloon may allow for more uniform expansion of the stent.
10. should be performed to ensure that the target lesion was adequately treated. The angiogram
-
will also evaluate for iatrogenic complications including dissection or rupture. Post-procedure trans-stenotic pressure measurements can also
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A. B. Bhatt and J. F. Benenati
Following each intervention, patients should again be counseled on managing modiable risk factors. Following stenting, many providers will start patients on a daily baby aspirin if the patient is not already on one. Plavix is typically not used when the aorta or relatively large iliac arteries are stented. If a drugeluting stent is used however, dual anti­platelet therapy should be administered for at least 3 months. Patients with CKD should again receive intravenous hydra­tion following contrast administration. A postprocedure duplex and pulse volume recordings can be ordered to deter­mine efcacy of the procedure and establish a new baseline.
Key Point
The best DSA projection for imaging each vessel:
• Abdominal aorta=AP
• Internal iliac artery=contralateral oblique
• Femoral bifurcation=ipsilateral oblique
Key Point
A pressure gradient of >10 mmHg at rest or >10– 15 mmHg after nitroglycerine administration is con­sidered a signicant stenosis and warrants treatment.
Blue Toe Syndrome
Treating patients with blue toe syndrome requires pre- procedure imaging to identify lesions responsible for producing athero­sclerotic emboli. Historically, these lesions were treated with surgical exclusion and bypass or endarterectomy. Today, these lesions can be successfully treated with angioplasty and stenting much like any other vascular lesion [14, 15].

References

1. Fowkes FG, Rudan D, Rudan I, Aboyans V, Denenberg JO, etal.
Comparison of global estimates of prevalence and risk factors for peripheral artery disease in 2000 and 2010: a systematic review and analysis. Lancet. 2013;382(9901):1329–40. https://doi.
org/10.1016/S0140-6736(13)61249-0.
2. Olin JW, White CJ, Armstrong EJ, Kadian-Dodov D, Hiatt WR. Peripheral artery disease. J Am Coll Cardiol. 2016;67(11):1338–57. https://doi.org/10.1016/j.jacc.2015.12.049.
3. Aboyans V, Desormais I, Lacroix P. The general prognosis of patients with peripheral arterial disease differs according to the disease localization. J Vasc Surg. 2010;51(6):1585–6. https://doi.
org/10.1016/j.jvs.2010.04.008.
4. McDermott MM, Greenland P, Liu K, Guralnik JM, Criqui MH, Dolan NC, et al. Leg symptoms in peripheral arterial dis­ease: associated clinical characteristics and functional impair­ment. JAMA. 2001;286(13):1599–606. https://doi.org/10.1001/
jama.286.13.1599.
5. Abu Dabrh AM, Steffen MW, Undavalli C, Asi N, Wang Z, Elamin MB, etal. The natural history of untreated severe or criti­cal limb ischemia. J Vasc Surg. 2015;62(6):1642–51. https://doi.
org/10.1016/j.jvs.2015.07.065.
6. Crawford JD, Perrone KH, Wong VW, Mitchell EL, Azarbal AF, Liem TK, Moneta GLA. Modern series of acute aortic occlu­sion. J Vasc Surg. 2014;59(4):1044–50. https://doi.org/10.1016/j.
jvs.2013.10.080.
7. Okazaki J, Guntani A, Homma K, Kyuragi R, Kawakubo E, Maehara Y. Fibromuscular dysplasia of the lower extremities. Ann Vasc Dis. 2011;4(2):143–9. https://doi.org/10.3400/avd.
cr.10.01027.
8. Chi Y.Safety and efcacy of cilostazol in the management of inter­mittent claudication. Vasc Health Risk Manag. 2008;4:1197–203.
https://doi.org/10.2147/vhrm.s3160.
9. Neisen M. Endovascular management of aortoiliac occlusive dis­ease. Semin Interv Radiol. 2009;26(04):296–302. https://doi.org/1
0.1055/s-0029-1242199.
10. Jaff MR, White CJ, Hiatt WR, Fowkes GR, Dormandy J, et al. An update on methods for revascularization and expansion of the TASC lesion classication to include below-the-knee arteries: a supple­ment to the inter-society consensus for the management of peripheral arterial disease (TASC II): the TASC Steering Committee. Catheter Cardiovasc Interv. 2015;86(4):611–25. https://doi.org/10.1002/
ccd.26122.
11. Bosiers M, Deloose K, Callaert J, Maene L, Beelen R, Keirse K, etal. BRAVISSIMO: 12-month results from a large scale prospec­tive trial. JCardiovasc Surg. 2013;54(2):235–53.
12. Lee HJ, Armstrong E, Salhan N, Realyvasquez AJ, Laird JR, Humphries M.Patency of the internal iliac artery after placement of common and external iliac artery stents. JVasc Surg. 2015;61(6).
https://doi.org/10.1016/j.jvs.2015.04.131.
13. Aggarwal V, Waldo S, Armstrong E. Endovascular revascu­larization for aortoiliac atherosclerotic disease. Vasc Health Risk Manag. 2016;12:117–27. https://doi.org/10.2147/vhrm.
s98721.
14. Renshaw A, Mccowen T, Waltke EA, Wattenhofer SP, Tahara RW, Baxter BT.Angioplasty with stenting is effective in treating blue toe syndrome. Vasc Endovasc Surg. 2002;36(2):155–9. https://doi.
org/10.1177/153857440203600210.
15. Matchett WJ, Mcfarland DR, Eidt JF, Moursi MM.Blue toe syn­drome: treatment with intra-arterial stents and review of therapies. JVasc Interv Radiol. 2000;11(5):585–92. https://doi.org/10.1016/
s1051-0443(07)61610-8.

Infrainguinal Disease

DylanSuttle andLukeR.Wilkins

Pathophysiology

Peripheral artery disease (PAD) describes the presence of atherosclerotic lesions involving arteries of the upper or lower extremities. PAD more frequently involves the lower extremities and has a spectrum of disease patterns ranging from asymptomatic, mild stenosis to extremely painful total vessel occlusion, potentially resulting in limb loss. The pres­ence of PAD dramatically increases mortality risk by related diseases such as coronary artery disease, cerebrovascular disease, and other major arterial diseases such as abdominal aortic aneurysm [1]. The prevalence of PAD increases with age after the fourth decade; 10–15% of the population in the fth decade is affected. PAD has a slight predilection for men over women and nonwhite ethnicity over white.
Risk factors for PAD are no different than those for ath­erosclerosis in general as discussed in the chapter on aor­toiliac disease. Risk factors include cigarette smoking, age, hypertension, renal insufciency, hyperlipidemia, male gen­der, diabetes mellitus, obesity, family history, physical inac­tivity, and hyperhomocysteinemia [26]. Smokers have four times increased risk for developing PAD; the risk of develop­ing PAD is proportional to the number of cigarettes smoked [1]. Patients with diabetes mellitus are twice as likely to have PAD; every 1% increase in hemoglobin A1c increases the risk for PAD by 26% [7].
In order to grasp IR techniques employed in treatment of PAD, it is important to understand the anatomic and physio­logic aspects of arteries as well as the pathogenesis of athero-
D. Suttle University of Virginia Health System, Department of Radiology and Medical Imaging, Interventional Radiology, Charlottesville, VA, USA e-mail: ds8de@virginia.edu
L. R. Wilkins ( Department of Radiology and Medical Imaging, University of Virginia Health System, Charlottesville, VA, USA e-mail: lrw6n@virginia.edu
*)
31
sclerotic lesions. The artery wall consists of intima, media, and adventitia [8]. The intima contains endothelial cells, smooth muscle cells, and macrophages. The macrophages and other immune cells play a key role in consuming circulat­ing oxidized lipoproteins, thereby creating foam cells and building the foundation for an atheroma, which ultimately leads to arteriosclerosis [9]. The American Heart Association has dened six types of atherosclerosis (Table 31.1). Only types V and VI are detectable on angiography [6]. While almost all PAD is caused by atherosclerosis, it is important to be aware of other disease processes that can cause peripheral artery narrowing or occlusion (Table31.2) [1].
As previously mentioned, PAD exists along a spectrum from asymptomatic to life-threatening manifestations. Symptoms typically begin with claudication and progress to rest pain and ischemic skin lesions. The Rutherford criteria (see Table 30.1, Chap. 30 on aortoiliac disease) delineate the severity of lower extremity ischemia based on symptoms and objective criteria [10].
Asymptomatic Disease (Rutherford Category0)
The incidence of PAD is believed by some to be grossly underestimated due to the initial asymptomatic presentation of the disease, and the vast majority of patients with PAD are asymptomatic. The body’s ability to grow new, collateral ves­sels portends an indolent, asymptomatic presentation despite signicant arteriosclerosis. Many patients who present with severe, acute ischemia requiring below-the-knee amputation were asymptomatic 6months prior to presentation [11].
Claudication (Rutherford Categories 1–3)
Claudication is muscular pain in one or both legs during exer­cise which is relieved by rest [2, 12]. Like other manifestations of ischemia, it results from decreased blood ow and inability
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_31
341
342
D. Suttle and L. R. Wilkins
Table 31.1 American Heart Association types of atherosclerotic
lesions [8]
Lesion type Main histology I Isolated macrophage foam cells II Fatty streak, mainly intracellular lipid accumulation III Type II with small extracellular lipid pools IV Atheroma, type II with core of extracellular lipid V Fibroatheroma, lipid core, and brotic layer can be
VI Complicated, surface defect, thrombus
Table 31.2 Causes of peripheral artery narrowing and occlusion
Causes of peripheral artery narrowing and occlusion Arteritis Atherosclerosis Coarctation of the aorta Cystic adventitial disease of the popliteal Embolic disease Fibromuscular dysplasia Iliac artery syndrome
(cyclists) Popliteal entrapment Primary vascular tumors Remote arterial trauma Thrombosed popliteal artery aneurysm
calcic
Irradiation injury (usually iliac artery)
to meet the oxygen demands of the large, lower extremity muscle groups. While claudication is the classic symptom of lower extremity PAD, it is variable and may be present during certain episodes of exercise and absent in others. Claudication typically has a detrimental effect on lifestyle due to hindering mobility. Individuals with lower extremity PAD are more likely to have non-claudication- related, symptomatic issues, such as arthritis, and overall increased functional disability [13, 14].
Key Point
Claudication is dened as muscular pain in the leg dur­ing exercise that is relieved by rest. Critical limb isch­emia is more severe and includes rest pain, ischemia skin changes and acute limb ischemia.
Critical Limb Ischemia: Skin Lesions (Rutherford Categories 5–6)
Ischemic skin lesions are further on the continuum of CLI.These typically occur on the feet and can be initiated by a slight insult to skin integrity. Poor perfusion results in poor healing and subsequent development of ulceration. Ischemic ulcers may progress to frank gangrene. Beware of other lower extremity skin lesions such as diabetic ulcers and venous stasis ulcers in the evaluation of CLI.Diabetic ulcers are due to neuropathy and often result from a pivotal event such as wearing shoes that are too tight or stepping on a sharp object. Venous stasis ulcers classically occur on the lower leg above the medial malleolus.
Acute Limb Ischemia
Acute limb ischemia (ALI) results from sudden obstruction of vascular ow. This can occur in a variety of settings including atherosclerotic plaque rupture with acute throm­botic event, embolic event from a site proximal to the affected vessel, severe vasospasm, arterial dissection, acute arterial compression, or secondary to aneurysm thrombosis [14]. Acute embolic events are often much more profound due to the lack of matured collateralization that typically occurs in chronic disease associated with local thrombosis [13]. The “six Ps” are helpful to remember the presentation of ALI: pain, pallor, paresthesias, poikilothermia, pulselessness, and paralysis. The latter two symptoms are late ndings indica­tive of severe and potentially irreversible ischemia [10]. When evaluating a patient with acute embolic ischemia, it is prudent to consider the source of the embolus (e.g., left atrium) to prevent further showering of emboli.
Key Point
The six Ps of acute limb ischemia:
Critical Limb Ischemia: Rest Pain (Rutherford Category 4)
Critical limb ischemia (CLI) is dened by symptoms beyond claudication (e.g., rest pain, ischemic skin lesions, and acute limb ischemia). Rest pain is a similar sensation as claudica­tion but occurs in the absence of exercise. This pain often occurs at night when the feet are in a nondependent position with relief upon lowering the limb below the level of the heart. Rest pain may also be described by patients as a con­stant, diffuse pain throughout the day with waxing and wan­ing severity. If a patient’s initial presentation for the diagnosis of CLI is rest pain, they have a grim prognosis of a 20% mortality rate in 1year [1].
• Pain
• Pallor
• Paresthesias
• Poikilothermia
• Pulselessness
• Paralysis

Clinical Indication

History and physical exam are invaluable in the work-up of lower extremity PAD. Evaluation for the risk factors described above should certainly be obtained, as well as a
31 Infrainguinal Disease
343
detailed description of symptoms and any past surgical his­tory should intervention be warranted. Inspection of the patient’s skin should be focused on integrity of the skin and presence or absence of lower extremity hair. Examining the feet allows assessment of capillary rell time, temperature, and pulses. The femoral, popliteal, dorsalis pedis (DP), and posterior tibial (PT) pulses should be obtained bilaterally, regardless of the patient’s presentation. Diagnosis by pulse examination alone, due to inherent limitations, tends to over­diagnose PAD; therefore, more objective measurements such as Doppler are more sensitive and can assist in stratifying location and degree of stenosis [15].
Key Point
When evaluating a patient with PAD, evaluate the fol­lowing pulses bilaterally:
• Femoral
• Popliteal
• Dorsalis pedis (DP)
• Posterior tibial (PT)
Pulses can be absent, monophasic, biphasic, or tri­phasic (normal) based on the waveform. They are graded on intensity from 0 (absent) to 4+ (bounding).
There are two inexpensive non-imaging-based tests which
are used for the initial evaluation of most lower extremity PAD. Ankle-brachial index (ABI) objecties the presence and degree of lower extremity drop in blood pressure (Table31.3, Fig.31.1) [16]. ABI is simply a ratio of the high­est systolic pressure obtained from the ankle (either DP or PT) of the affected leg to the highest systolic pressure of either arm. ABI should be obtained for each lower extremity. ABIs are typically calculated with a sphygmomanometer and Doppler, but if a Doppler is unavailable, a stethoscope over the artery of interest has proven accurate in the initial work-up [17]. The presence of PAD is a marker of diffuse vascular disease: in general, the lower the ABI, the greater the risk of a cardiovascular event [2]. In patients with diabe­tes mellitus or otherwise non-compressible arteries, toe­brachial index may be used and follows the same concept as ABI but is performed with a miniature sphygmomanometer
Table 31.3 Interpreting ankle-brachial index (ABI)
Result Interpretation >1.30 Non-compressible (diabetes mellitus, calcic medial
sclerosis)
0.91–1.30 Normal
0.41–0.90 Mild to moderate PAD, claudication
0.00–0.40 Severe PAD, rest pain
for the big toe. Toe systolic pressure is typically greater than 50 mm Hg. Patients with a toe systolic pressure less than 30mm Hg typically are unable to heal lower extremity ulcers or surgical incisions [13]. Exercise testing is another method of ABI calculation by which the patient exercises for 5min or until the pain is reproduced, at which time the ABI is cal­culated. A decrease in ABI by 15–20% during exercise is diagnostic for PAD [1].
Pulse volume recordings measure the global perfusion of an extremity. Multiple cuffs are applied and inated at low pressure in sequence along an extremity. Subtle changes in pressure in the cuff with each heart beat are graphed. Changes in waveform indicate decreased perfusion and can reveal the general location of an occlusion [13].
Imaging studies provide assessment of the degree of vas­cular calcication, the precise location and size of lesions, targets for revascularization, and localization of collateral vessels. Cross-sectional imaging (e.g., ultrasound, CTA, and MRA) have largely replaced angiography as a primary imag­ing choice for workup and diagnosis.
Duplex ultrasound determines morphology of a lesion and calculates blood ow velocities and turbulence within a vessel (Fig.31.2). Increasing ow velocity indicates a higher degree of stenosis until the narrowing becomes so severe that ow is nearly obstructed. It is particularly useful in monitor­ing patency of bypass grafts. Computed tomography angiog­raphy (CTA) provides a timely assessment and mapping of lower extremity arteries (Fig.31.3). It requires the use of intravenous iodinated contrast, which may be contraindi­cated in patients with renal failure. Additionally, it subjects the patient to ionizing radiation exposure. Magnetic reso­nance angiography (MRA) is highly sensitive for the evalua­tion of luminal stenosis (Fig.31.4). Intravenous gadolinium is typically used. It is possible to obtain MRA without gado­linium, but this requires much longer image acquisition sequences termed time of ight, which some patients may not be able to tolerate. MRA is the most expensive of these imaging studies and may not be as widely available as CTA or ultrasound [13].
Angiography has evolved into a secondary imaging choice for evaluation of lower extremity arterial stenosis. Most patients undergoing angiography have had noninvasive imaging workup prior to arriving in the uoroscopy suite. Typically, the right femoral artery is accessed using the Seldinger technique. An abdominal aortogram is performed rst to evaluate for concomitant visceral and subsequently iliac and pelvic occlusive disease. Attention is then turned to the lower extremities, and time-delayed exposures after bolus contrast injections are performed to evaluate the entire lower extremity. Manipulations of the patient’s leg position and angle of the C-arm are employed to provide optimal visualization of all the extremity arterial branches. The
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Fig. 31.1 Ankle brachial
index. ABIs of a 53-year-old male with left leg claudication. (a) Pre-stent placement ABI.Notice the right leg has biphasic waveforms and an ABI of
0.92, while the left leg has monophasic waveforms and ABI of 0.41, indicating moderate PAD. (b) Status post left SFA stent placement the left ABI returns to normal
D. Suttle and L. R. Wilkins